Curso OBESIDADE

Curso Avançado em
Obesidade Infanto-Juvenil
Prof. Dr. Carlos Alberto Nogueira de Almeida
Associação Brasileira de Nutrologia
Universidade Federal de São Carlos
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ Consequências para a saúde
➡ Diagnóstico da obesidade
➡ definição
➡ classificação
➡ Abordagem clínica
➡ história clínica
➡ exame físico (antropometria e composição corporal)
Roteiro ➡
➡ exames subsidiários
Diagnóstico das principais comorbidades
➡ psicossociais
➡ cardiometabólicas
➡ outras
➡ Tratamento
➡ nutricional
➡ atividade física
➡ farmacoterapia
➡ comorbidades
➡ abordagem familiar
➡ Prognóstico e tracking
Curso Avançado em Obesidade
Infanto-Juvenil ➡ Atualização científica
➡ Avaliação
2
Nogueira-de-Almeida - 7 de novembro de 2018
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
Retra
to da
Saúde
2018
2018
Excesso de peso
1
Excesso de peso (pré-obesidade + obesidade) Obesidade por

nível educacional por região
em Portugal
38,5%
58,6%
NACIONAL 56,3%
57% 13,2%
de excesso de peso
53,6%
nenhum/1.º ciclo ensino secundário
do ensino básico
53,4%
Adultos (M) Adultos (F) Criança Idosos
59% 55% 25% 81%
de excesso de peso de excesso de peso de excesso de peso de excesso de peso 55,5%
Fonte: DGS, 2017

Fig. 10. Prevalência de excesso de peso (pré-obesidade e obesidade), em Portugal.
4
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
6
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
Caso Clínico 1
• Menina
• 6 anos exatos
• Peso: 30 kg
• Estatura: 124 cm
• Diagnóstico da obesidade, etapas:
➡cálculo do IMC
➡Plotagem do IMC na curva de IMC
➡Diagnóstico de acordo com pontos de corte
8
Menina, 6 anos, 30 kg, 124 cm, IMC de 19,5 kg/m2 Caso Clínico 1
Obesidade
Sobrepeso
Sobrepeso vs Obesidade
10
Valores das distribuições das dosagens de laboratoriais dos 84
sujeitos, categorizados segundo o diagnóstico de sobrepeso ou
obesidade. Ribeirão Preto (SP), outubro de 2004 a outubro de 2005
Exames Laboratoriais Sobrepeso versus obesidade

Glicemia de jejum p = 0,858 (bicaudal) n.s.
OGTT p = 0,3917 ( bicaudal) n.s.
Colesterol total p = 0,3387 ( bicaudal), n.s.
LDL-colesterol p = 0,3206 (bicaudal), n.s.
HDL-colesterol
Menores de 10 anos
p = 0,0476 (bicaudal) *
Maiores de 10 anos
p = 0,1890 (bicaudal) n.s.
Triglicérides
Menores de 10 anos p = 0,0672 (bicaudal) n.s.
Maiores de 10 anos p = 0,1891 (bicaudal) n.s.
De Almeida CAN (Rev. Paulista de Pediatria 2010)
11
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
12
Menina, 6 anos, 30 kg, 124 cm, IMC de 19,5 kg/m2 Caso Clínico 1
Estatura Elevada
13
Leptina
Sinaliza para SNS

- Gordura suficiente -
Atingido percentual necessário

Reduz ingesta alimentar
para início da puberdade
Reduz deposição de gordura Início da puberdade
14
IMC é suficiente?
• Individual versus populacional
• Composição Corporal
➡ Exame clínico
➡ Circunferência abdominal
➡ Dobras cutâneas
➡ Bioimpedanciometria
15
Circunferência Abdominal
Local de medida:
Ponto médio entre
a última costela e a
crista ilíaca
16
76
Anexo 9 - Distribuição em percentis da circunferência abdominal segundo gênero e idade
BRANCOS NEGROS
Meninos Meninas Meninos Meninas
Idade Percentil Percentil Percentil Percentil
(anos) N 50 90 n 50 90 N 50 90 N 50 90
5 28 52 59 34 51 57 36 52 56 34 52 56
6 44 54 61 60 53 60 42 54 60 52 53 59
7 54 55 61 55 54 64 53 56 61 52 56 67
8 95 59 75 75 58 73 54 58 67 54 58 65
9 53 62 77 84 60 73 53 60 74 56 61 78
10 72 64 88 67 63 75 53 64 79 49 62 79
11 97 68 90 95 66 83 58 64 79 67 67 87
12 102 70 89 89 67 83 60 68 87 73 67 84
13 82 77 95 78 69 94 49 68 87 64 67 81
14 88 73 99 54 69 96 62 72 85 51 68 92
15 58 73 99 58 69 88 44 72 81 54 72 85
16 41 77 97 58 68 93 41 75 91 34 75 90
17 22 79 90 42 66 86 31 78 101 35 71 105
Fonte: Freedman, 1999.
17
Circunferência
Abdominal
18
Dobras Cutâneas
• 50% do tecido adiposo encontra-se no sub-cutâneo
• Funções
– Estimar o percentual de gordura corporal
– Avaliar a distribuição da gordura corporal
19
Dobras Cutâneas
2 Dobras cutâneas: Tríceps, subescapular
(S= somatória das D.C. Tríceps e Subescapular)
•Rapazes Brancos
•Pré-Púbere=G% = 1,21 (S) - 0,008 (S)² - 1,7
•Púbere = G% =1,21 (S) - 0,008 (S)² - 3,4
•Pós-Púbere = G% =1,21 (S) - 0,008 (S)² - 5,5
•Rapazes Negros
•Pré-Púbere=G% = 1,21 (S) - 0,008 (S)² - 3,5
•Púbere = G% =1,21 (S) - 0,008 (S)² - 5,2
•Pós-Púbere = G% =1,21 (S) - 0,008 (S)² - 6,8
•Moças de qualquer raça e nível de maturidade
•G% = 1,33 (S) - 0,013 (S)² - 6,8
Obs: Quando o (S) for maior que 35 mm, será utilizada uma única equação para cada sexo,
para qualquer raça e nível de maturidade:
•Rapazes
•G% = 0,783 (S) +1,6
•Moças
•G% = 0,546 (S) +9,7
20
Faixas de Percentual de Adiposidade
% GORDURA % GORDURA
CLASSIFICAÇÃO
MENINOS MENINAS
Muito baixo 8-9 7 - 11
Baixo 10 - 12 12 - 17
Ideal 13 - 20 18 - 25
Moderadamente alto 21 - 24 26 - 29
Alto 25 - 30 30 - 38
Muito alto 31 - 42 39 - 43
Meninos e meninas (abaixo de 18 anos, Lohman TG, 1987)
21
Bioimpedanciometria
• Princípio: O fluxo de eletricidade é facilitado através de tecidos
hidratados e livres de gordura e na água extracelular, em
comparação com o tecido gorduroso.
• Resistência: Medida de oposição pura ao fluxo de corrente

elétrica através do corpo
• Reactância: Oposição ao fluxo de corrente causado pela

capacitância* produzida pela membrana celular
• Preparo
22
Resistência & Reactância
• Massa Gorda
– Tecido adiposo
Resistência
• Massa Magra
– Água Reactância
– Tecido muscular
– Tecido ósseo
– Tecido conjuntivo
– Epitélios
– Sangue
23
Preparo para BIA

• Fazer jejum nas 4 horas que antecedem o exame;
• Não realizar qualquer atividade física além daquelas que normalmente executa no dia-
a-dia, nas 24 horas que antecedem o exame;
• Durante as 24 horas que antecedem o exame, paciente deve estar bem hidratado.
Isso pode ser conseguido ingerindo-se, nesse período, pelo menos 2 litros de água.
• Durante as 24 horas que antecedem o exame paciente não deve fazer uso de
produtos que contenham cafeína, como por exemplo, café, alguns refrigerantes,
alguns remédios para dor-de-cabeça, líquidos energéticos, etc;
• No momento do exame, paciente não poderá estar usando qualquer objeto metálico,
como brincos, percings, anéis, etc;
• No momento do exame, paciente não poderá estar usando aparelhos elétricos como
marcapassos;
• Evitar período pré menstrual
24
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
25
Excesso de adiposidade corporal
Obesidade sem Resistência Obesidade Metabólica

Insulínica (Com Resistência Insulínica)
Sindrômica Epigenética Induzida Clássica
Ag. Infecciosos Somática
Neurológica
Endocrinológica Fármacos
Distúrbios do sono
Psicossocial
Nogueira-de-Almeida CA, Rêgo CMBSS, et al 2018, Revista Medicina Ribeirão Preto USP, v51(2):138-152
26
• Menino, 12 anos, busca atendimento encaminhado pelo
pediatra por excesso de peso Caso Clínico 2
• Crescimento e desenvolvimento sem maiores
intercorrências
• tem alergia respiratória diagnosticada há 2 anos em uso
de tratamento tópico e sistêmico
• antropometria, exames e curva de IMC mostrados abaixo.
Peso 72 kg
Estatura 158 cm
Circ. Abdominal 93
% gordura (BIA) 37%
Glicemia 92
Insulina 8
Colesterol total 202
HDL 53
LDL 133
Triglicerídeos 77
27

intercorrências
Peso 72 kg
Estatura 158 cm
Circ. Abdominal 93
% gordura (BIA) 37%
Glicemia 92
Insulina 8
HDL 53
LDL 133
Triglicerídeos 77
28
intercorrências
% GORDURA % GORDURA Peso 72 kg

CLASSIFICAÇÃO
MENINOS MENINAS
Estatura 158 cm
Muito baixo 8-9 7 - 11
Circ. Abdominal 93
Baixo 10 - 12 12 - 17 % gordura (BIA) 37%
Glicemia 92
Ideal 13 - 20 18 - 25
Insulina 8
Moderadamente
21 - 24 26 - 29
alto Colesterol total 202
Alto 25 - 30 30 - 38 HDL 53
LDL 133
Muito alto 31 - 42 39 - 43
Triglicerídeos 77
29

intercorrências
Peso 72 kg
Estatura 158 cm
Circ. Abdominal 93
% gordura (BIA) 37%
Glicemia 92
Insulina 8
HDL 53
LDL 133
Triglicerídeos 77
30
intercorrências
Peso 72 kg
Estatura 158 cm
Circ. Abdominal 93
% gordura (BIA) 37%
Glicemia 92
Insulina 8
HDL 53
LDL 133
Triglicerídeos 77
31
Obesidade sem Resistência Obesidade Metabólica

Insulínica (Com Resistência Insulínica)
Sindrômica Epigenética Induzida Clássica
Ag. Infecciosos Somática
Neurológica
Endocrinológica Fármacos
Distúrbios do sono
Psicossocial
Nogueira-de-Almeida 2016, submmited
32
intercorrências
Peso 72 kg
Estatura 158 cm
Circ. Abdominal 93
% gordura (BIA) 37%
Glicemia 92 •Obesidade induzida por fármaco

Insulina 8 •Dislipidemia (LDL elevado)
HDL 53
LDL 133
Triglicerídeos 77
33
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
34
Dislipidemia
Obesidade na infância e adolescência
Anexo 19 – Valores do perfil lipídico de crianças

(acima de 2 anos) e adolescentes
Lipoproteínas (mg/dL) Desejáveis Limítrofes Aumentados
Colesterol total < 150 150-169 >170
LDL-C < 100 100-129 >130
HDL-C > 45
Triglicerídios < 100 100-129 >130
Fonte: IV Diretriz Brasileira sobre Dislipidemias e P revenção de Aterosclerose, 2007.
35
Hiperglicemia
Prevalence of hyperglicemia: 383 OBESE children, 7-18 years old
100%
Boys Girls
75%
50%
25%
6,4% 4,7%
0%
glicemia > 100
Nogueira-de-Almeida et al, 2016, Rev. Medicina USP, 49:504-510
98 36 Manual de Orientação – Departamento de Nutrologia

Resistência Periférica à Insulina
Prevalence of insulin resistance: 383 children, 7-18 years old, Brazil
100%
Boys Girls Total

75%
50% 44,1% 39,2% 42,7% 40,5%

33,1% 37,8%
25%
0%
Insulinemia > 15 HOMA > 3.16
Nogueira-de-Almeida et al, 2016, Rev. Medicina USP, 49:504-510
37
glicemia
Nogueira-de-Almeida et al,
J Pediatr (Rio J). 2008;84(2):
insulinemia 136-140
HOMA
38
Detection of insulin resistance using fixed or age
related cut off points of fasting insulin
100%
Fixed Age Related
75%
50% 57,6% 57,8%

44,1%
25% 33,1%
0%
Boys Girls
Nogueira-de-Almeida et al, 2018, PGHN, v.21(1):59-67
39

Fasting insulinemia
Cuartero et al; An Pediatr.2007;66:481-90 - Vol. 66 Núm.5
40
Nogueira-de-Almeida et al,
J Pediatr (Rio J). 2008;84(2):136-140
41
80
Anexo 13 – Distribuição em percentis da pressão arterial segundo percentis de estatura e idade (sexo masculino)
PA sistólica (mmHg) PA diastólica (mmHg)
Idade PA Percentil de altura Percentil de altura
(anos) percentil
5 10 25 50 75 90 95 5 10 25 50 75 90 95
1 50 80 81 83 85 87 88 89 34 35 36 37 38 39 39
90 94 95 97 99 100 102 103 49 50 51 52 53 53 54
95 98 99 101 103 104 106 106 54 54 55 56 57 58 58
99 105 106 108 110 112 113 114 61 62 63 64 65 66 66
2 50 84 85 87 88 90 92 92 39 40 41 42 43 44 44
90 97 99 100 102 104 105 106 54 55 56 57 58 58 59
95 101 102 104 106 108 109 110 59 59 60 61 62 63 63
99 109 110 111 113 115 117 117 66 67 68 69 70 71 71
3 50 86 87 89 91 93 94 95 44 44 45 46 47 48 48
90 100 101 103 105 107 108 109 59 59 60 61 62 63 63
95 104 105 107 109 110 112 113 63 63 64 65 66 67 67
99 111 112 114 116 118 119 120 71 71 72 73 74 75 75
4 50 88 89 91 93 95 96 97 47 48 49 50 51 51 52
90 102 103 105 107 109 110 111 62 63 64 65 66 66 67
95 106 107 109 111 112 114 115 66 67 68 69 70 71 71
99 113 114 116 118 120 121 122 74 75 76 77 78 78 79
5 50 90 91 93 95 96 98 98 50 51 52 53 54 55 55
90 104 105 106 108 110 111 112 65 66 67 68 69 69 70
95 108 109 110 112 114 115 116 69 70 71 72 73 74 74
99 115 116 118 120 121 123 123 77 78 79 80 81 81 82
6 50 91 92 94 96 98 99 100 53 53 54 55 56 57 57
90 105 106 108 110 111 113 113 68 68 69 70 71 72 72
95 109 110 112 114 115 117 117 72 72 73 74 75 76 76
99 116 117 119 121 123 124 125 80 80 81 82 83 84 84
7 50 92 94 95 97 99 100 101 55 55 56 57 58 59 59
90 106 107 109 111 113 114 115 70 70 71 72 73 74 74
95 110 111 113 115 117 118 119 74 74 75 76 77 78 78
99 117 118 120 122 124 125 126 82 82 83 84 85 86 86
8 50 94 95 97 99 100 102 102 56 57 58 59 60 60 61
90 107 109 110 112 114 115 116 71 72 72 73 74 75 76
95 111 112 114 116 118 119 120 75 76 77 78 79 79 80
99 119 120 122 123 125 127 127 83 84 85 86 87 87 88
9 50 95 96 98 100 102 103 104 57 58 59 60 61 61 62
90 109 110 112 114 115 117 118 72 73 74 75 76 76 77
95 113 114 116 118 119 121 121 76 77 78 79 80 81 81
99 120 121 123 125 127 128 129 84 85 86 87 88 88 89
10 50 97 98 100 102 103 105 106 58 59 60 61 61 62 63
90 111 112 114 115 117 119 119 73 73 74 75 76 77 78
95 115 116 117 119 121 122 123 77 78 79 80 81 81 82
99 122 123 125 127 128 130 130 85 86 86 88 88 89 90
11 50 99 100 102 104 105 107 107 59 60 61 62 63 63 63
90 113 114 115 117 119 120 121 74 75 75 76 77 78 78
95 117 118 119 121 123 124 125 78 79 80 81 82 82 82
99 124 125 127 129 130 132 132 86 87 88 89 90 90 90
12 50 101 102 104 106 108 109 110 59 60 61 62 63 63 64
90 115 116 118 120 121 123 123 74 75 75 76 77 78 79
95 119 120 122 123 125 127 127 78 79 80 81 82 82 83
99 126 127 129 131 133 134 135 86 87 88 89 90 90 91
13 50 104 105 106 108 110 111 112 60 60 61 62 63 67 67
90 117 118 120 122 124 125 126 75 75 76 77 78 79 79
95 121 122 124 126 128 129 130 79 79 80 81 82 83 83
99 128 130 131 133 135 136 137 87 87 88 89 90 91 91
14 50 106 107 109 111 113 114 115 60 61 62 63 64 65 65
90 120 121 123 125 126 128 128 75 76 77 78 79 79 80
95 124 125 127 128 130 132 132 80 80 81 82 83 84 84
99 131 132 134 136 138 139 140 87 88 89 90 91 92 92
15 50 109 110 112 113 115 117 117 61 62 63 64 65 66 66
90 122 124 125 127 129 130 131 76 77 78 79 80 80 81
95 126 127 129 131 133 134 135 81 81 82 83 84 85 85
99 134 135 136 138 140 142 142 88 89 90 91 92 93 93
16 50 111 112 114 116 118 119 120 63 63 64 65 66 67 67
90 125 126 128 130 131 133 134 78 78 79 80 81 82 82
95 129 130 132 134 135 137 137 82 83 83 84 85 86 87
99 136 137 139 141 143 144 145 90 90 91 92 93 94 94
17 50 114 115 116 118 120 121 122 65 66 66 67 68 69 70
90 127 128 130 132 134 135 136 80 80 81 82 83 84 84
95 131 132 134 136 138 139 140 84 85 86 87 87 88 89
99 139 140 141 143 145 146 147 92 93 93 94 95 96 97
Fonte: National High Blood Pressure, 2004.
42
Hipertensão Arterial
43
Doença Gordurosa Hepática Não Alcoólica

• As lesões hepáticas que acompanham a obesidade são decorrentes de mecanismos combinados, que envolvem
a resistência insulínica e o estresse oxidativo
• Esses mecanismos têm influência de fatores genéticos, que podem predispor ao aparecimento dessa doença,
como o alelo PNPLA3, as variantes da apoproteína C3 e as adipocitocinas (adiponectina e leptina)
• Tais lesões, que se iniciam com a simples infiltração gordurosa no fígado, podem progredir, evoluindo para
esteato-hepatite (20% dos casos) e cirrose hepática (2% dos casos)
• O padrão-ouro de diagnóstico da lesão hepática é a biópsia
• AST e ALT estão elevadas mas nunca mais que 4 vezes os valores normais
• Índice AST/ALT em geral menor que 1 (OBS: valors maiores que 1 são encontrados geralmente na
esteatohepatite alcoólica)
• Como diagnóstico diferencial deve-se considerar: uso de drogas hepatotóxicas, intoxicações, doenças
metabólicas e hepatites virais.
ZAMIN JR., Idilio et al . A importância do índice AST/ALT no diagnóstico da esteatohepatite não-alcoólica. Arq. Gastroenterol., São Paulo , v. 39, n. 1, p. 22-26, Mar. 2002
44
Comorbidades Psicossociais
• Alvos de agressões, mentiras ou rumores
• Vítimas de provocação
• Criticados em atividades esportivas
• Vitimização e agressão
– Física nos meninos
– Verbal nas meninas
• Isolamento e marginalização
• Estresse
• Comportamentos de risco:
– Drogas
– Álcool
– Promiscuidade sexual
• Depressão
TDH-AFH, BSS-R & PHA, 2004, Texas Department of Health
45
Wardle et al (1995)
46
Menina de 9 anos e 11 meses, com Caso Clínico 3
os seguintes dados:
Peso 55,7
Estatura 138,5
P Estatura 53,9
Circ. Abdominal 89,5
Pressão arterial 125 / 84
Glicemia 86 Qual o diagnóstico?

Insulina 36
HDL 42
LDL 87
Triglicerídeos 157
47

os seguintes dados:
Peso 55,7
Estatura 138,5
P Estatura 53,9
Glicemia 86
Insulina 36
HDL 42
LDL 87
Triglicerídeos 157
48
os seguintes dados:
Peso 55,7
Estatura 138,5
P Estatura 53,9

Glicemia 86
Insulina 36

HDL 42
LDL 87
Triglicerídeos 157
Table 2 49
BLOOD PRESSURE LEVELS FOR THE 90TH AND 95TH PERCENTILES OF BLOOD
PRESSURE FOR GIRLS AGE 1 TO 17 YEARS BY PERCENTILES OF HEIGHT
Menina de 9 anos e 11 meses, com Height

Systolic BP (mm Hg)
Caso Clínico 3 Diastolic BP (mm Hg)
Age Percentiles* ➞5% 10% 25% 50% 75% 90% 95% 5% 10% 25% 50% 75% 90% 95%
BP†
os seguintes dados:
➞
1 90th 97 98 99 100 102 103 104 53 53 53 54 55 56 56

95th 101 102 103 104 105 107 107 57 57 57 58 59 60 60
2 90th 99 99 100 102 103 104 105 57 57 58 58 59 60 61
95th 102 103 104 105 107 108 109 61 61 62 62 63 64 65
3 90th 100 100 102 103 104 105 106 61 61 61 62 63 63 64
95th 104 104 105 107 108 109 110 65 65 65 66 67 67 68
4 90th 101 102 103 104 106 107 108 63 63 64 65 65 66 67
95th 105 106 107 108 109 111 111 67 67 68 69 69 70 71
Peso 55,7 Table 2
5 90th 103 103 104 106 107 108 109 65 66 66 67 68 68 69
95th 107 107 108 110 111 112 113 69 70 70 71 72 72 73
Estatura 138,5 BLOOD PRESSURE LEVELS FOR THE 90TH AND 95TH PERCENTILES OF BLOOD
6 90th 104 105 106 107 109 110 111 67 67 68 69 69 70 71
PRESSURE
95th GIRLS
FOR108 109 A GE 1
110 17 Y114
111TO112 114BY PERCENTILES
EARS 71 71 72OF H
73EIGHT
73 74 75
P Estatura 53,9 7 90th 106 107 108 109 110 112 112 69 69 69 70 71 72 72
95th 110 110 Systolic
112 BP 113 (mm
114Hg)115 116 73 73 Diastolic
73 74 BP (mm
75 Hg)76 76
Height
Circ. Abdominal 89,5 Age
8 Percentiles*
90th ➞5%
108 10%
109 25%
110 50%
111 75%
112 90%
113 95%
114 5%
70 10%
70 25%
71 50%
71 75%
72 90%
73 95%
74
BP†
95th 112 112 113 115 116 117 118 74 74 75 75 76 77 78
➞
Pressão arterial 125 / 84 91 90th

90th 97 110
110 98 112
99 113
100 114
102 115
103 116
104 53
71 53
72 53
72 54
73 55
74 56
74 56
75
95th
95th 101 114
114 102 115
103 117
104 118
105 119
107 120
107 57
75 57
76 57
76 58
77 59
78 60
78 60
79
Glicemia 86 102 90th
90th 99 112
112 99 114
100 115
102 116
103 117
104 118
105 57
73 57
73 58
73 58
74 59
75 60
76 61
76
95th
95th 102 116
116 103 117
104 119
105 120
107 121
108 122
109 61
77 61
77 62
77 62
78 63
79 64
80 65
80
Insulina 36 113 90th
90th 100 114
114 100 116
102 117
103 118
104 119
105 120
106 61
74 61
74 61
75 62
75 63
76 63
77 64
77
95th
95th 104 118
118 104 119
105 121
107 122
108 123
109 124
110 65
78 65
78 65
79 66
79 67
80 67
81 68
81
124 90th
90th 101 116
116 102 118
103 119
104 120
106 121
107 122
108 63
75 63
75 64
76 65
76 65
77 66
78 67
78
95th
95th 105 120
120 106 121
107 123
108 124
109 125
111 126
111 67
79 67
79 68
80 69
80 69
81 70
82 71
82
HDL 42
135 90th
90th 103 118
118 103 119
104 121
106 122
107 123
108 124
109 65
76 66
76 66
77 67
78 68
78 68
79 69
80
LDL 87
95th
95th P90
121 PAs
107 122
107 108 =
123 125113
110 111
126 112 128
127 113 69
80 70
80 70
81 71
82 72
82 72
83 73
84
146 90th
90th 104 120
119 105 121
106 122
107 124
109 125
110 126
111 67
77 67
77 68
78 69
79 69
79 70
80 71
81
95th
95th 108 124
123 109 125
110 126
111 128
112 129
114 130
114 71
81 71
81 72
82 73
83 73
83 74
84 75
85
Triglicerídeos 157
157 90th
90th P90
121 PAd
106 121
107 108 =
122 12473125
109 110 112 127
126 112 69
78 69
78 69
79 70
79 71
80 72
81 72
82
95th
95th 110 125
124 110 126
112 128
113 129
114 130
115 131
116 73
82 73
82 73
83 74
83 75
84 76
85 76
86
168 90th
90th 108 122
122 109 123
110 125
111 126
112 127
113 128
114 70
79 70
79 71
79 71
80 72
81 73
82 74
82
95th
95th 112 126
125 112 127
113 128
115 130
116 131
117 132
118 74
83 74
83 75
83 75
84 76
85 77
86 78
86
179 90th
90th 110 123
122 110 124
112 125
113 126
114 128
115 128
116 71
79 72
79 72
79 73
80 74
81 74
82 75
82
95th
95th 114 126
126 114 127
115 129
117 130
118 131
119 132
120 75
83 76
83 76
83 77
84 78
85 78
86 79
86
10 percentile
*Height 90th 50
112 112
determined
95th percentile
114 115
by standard
116 determined
116 117 by119
116curves.
growth 117 118
120measurement.
121 122
73
77
73
77
73
77
74
78
75
79
76
80
76
80
†Blood pressure a single
11 90th 114 114 Nogueira-de-Almeida
116 117 118 119 120 74 74 75 - 775de76novembro
77 77 de 2018
95th 118 118 119 121 122 123 124 78 78 79 79 80 81 81
os seguintes dados:
Peso 55,7
Estatura 138,5
P Estatura 53,9

Glicemia 86
Insulina 36

HDL 42
LDL 87
Triglicerídeos 157
51

os seguintes dados:
Peso 55,7
Estatura 138,5
P Estatura 53,9 •Obesidade

Pressão arterial 125 / 84 •Hipertensão arterial

Glicemia 86
Insulina 36 •Resistência insulínica

HDL 42 •Dislipidemia
LDL 87
Triglicerídeos 157
52
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
53
Conceito de dietorerapia
A dietoterapia é uma ferramenta que usa alimentos e
nutrientes para tratamento e prevenção de
enfermidades, levando o organismo a adquirir os
nutrientes necessários para boa perfomance e saúde.
54
Dietoterapia para obesidade
• Ajustes na dieta já existente
• Orientações qualitativas
• Orientações quantitativas
• Inclusão de alimentos funcionais
• Orientações psicológicas de comportamento

alimentar
• Plano alimentar ("dieta", "cardápio", etc)
55
Etapas para montagem do

plano alimentar
• Quantas calorias serão prescritas ?
• Quais os hábitos alimentares da criança ?
• Que comorbidades estão presentes ?
• O plano será do tipo fechado ou por grupos ?
56
Calorias do plano
Nível de Atividade Fìsica
Moderadamento
Grupo Idade (anos) Sedentário Ativo
ativo
Crianças 2-3 1.000 1.000-1.400 1.000-1.400
4-8 1.200 1.400-1.600 1.400-1.800

Meninas 9-13 1.600 1.600-2.000 1.800-2.200
14-18 1.800 2.000 2.400
4-8 1.400 1.400-1.600 1.600-2.000

Meninos 9-13 1.800 1.800-2.200 2.000-2.600
14-18 2.200 2.400-2.800 2.800-3.200
•O objetivo final pode ser reduzir em 20% o gasto energético estimado;
•Para as crianças muito obesas, por estarem habituadas a ingerir quantidades

elevadas de alimentos, pode-se começar sem redução do gasto energético
estimado e, aos poucos, retirar de 5 em 5% até chegar aos 20%.
57
Exemplo
• Menino, 14 anos, sedentário, peso de 72 kg e estatura de 160 cm
• Gasto energético estimado: 2.200 calorias
• Prescrição: 2.200 – 20% (440) = 1760 cal
Nível de Atividade Fìsica

Moderadamento
Grupo Idade (anos) Sedentário Ativo
ativo
Crianças 2-3 1.000 1.000-1.400 1.000-1.400
4-8 1.200 1.400-1.600 1.400-1.800

Meninas 9-13 1.600 1.600-2.000 1.800-2.200
14-18 1.800 2.000 2.400
4-8 1.400 1.400-1.600 1.600-2.000

Meninos 9-13 1.800 1.800-2.200 2.000-2.600
14-18 2.200 2.400-2.800 2.800-3.200
58
Equações especí-icas para obesos
PARA MENINOS COM SOBREPESO E OBESOS DE 3 A 18 ANOS:
PARA MANUTENÇÃO DO PESO EM MENINOS COM SOBREPESO E OBESOS DE 3-18 ANOS:
= 114 – 50,9 x idade (anos) + AUvidade Física x (19,5 x peso [kg] + 1161,4 x altura [m])
Coeficiente de aUvidade `sica (AF):
AF = 1,00 (sedentário) 114 - (50,9 x 14) + 1 x 19,5 x 72 + 1.161,4 x 1,6
AF = 1,12 (aUvidade leve)
= 2.664 calorias
AF = 1,24 (aUvidade moderada)
= - 20% = 2.131 calorias
AF = 1,45 (aUvidade intensa)
PARA MENINAS COM SOBREPESO E OBESAS DE 3 A 18 ANOS:

PARA MANUTENÇÃO DO PESO EM MENINAS COM SOBREPESO E OBESAS DE 3-18 ANOS:
= 389 – 41,2 x idade (a) + AUvidade Física x (15,0 x peso [kg] + 701,6 x altura [m])
Coeficiente de aUvidade `sica (AF):
AF = 1,00 (sedentário)
AF = 1,18 (aUvidade leve)
AF = 1,35 (aUvidade moderada)
AF = 1,60 (aUvidade intensa)
59
Plano fechado
versus
Plano por grupos
60
Plano por grupos
REFEIÇÃO GRUPO No. DE PORÇÕES
Cereais, tubérculos 1
Gorduras e óleos 2
Café da manhã
Laticínios 1
Lanche da manhã Frutas 2
SBP, 2011 Leguminosas 1

Almoço
Carnes e ovos 1
Folhas e legumes 6
Gorduras e óleos 2
Lanche da tarde
Frutas 2
Leguminosas 1
Jantar
Carnes e ovos 1
Folhas e legumes 6
Ceia Laticínios 1
61
Plano por grupos

REFEIÇÃO GRUPO No. DE PORÇÕES
Café da manhã
Gorduras e óleos 2 Plano Padrão:
Laticínios 1
Lanche da manhã Frutas 2

• 1.100 calorias
Cereais, tubérculos 1 • Macronutrientes equilibrados:

Leguminosas 1
Almoço ‣ 55 a 65 % de CH
Carnes e ovos 1
Folhas e legumes 6 ‣ 20 a 30% de LP

‣ 10 a 20% de PT
Lanche da tarde Gorduras e óleos 2
Frutas 2
• Oferta adequada de micronutrientes
Cereais, tubérculos 1 • Necessário:

Leguminosas 1
Jantar ‣ ajuste calórico
Carnes e ovos 1
Folhas e legumes 6 ‣ ajuste para comorbidades

Ceia Laticínios 1 Tucunduva et al.
Rev. Nutr., Campinas, 16(1):5-19, 2003
62
Check-list
1 a 18 anos Check-list
Cereais, pães, tubérculos e raízes
4 (1) (2) (3) (4)
Verduras e legumes
3 (1) (2) (3)
Frutas
4 (1) (2) (3) (4)
Leites, queijos e iogurtes

2 (1) (2)
Carnes e ovos
2 (1) (2)
Leguminosas
2 (1) (2)
Óleos e gorduras
4 (1) (2) (3) (4)
Alimentos de consumo ocasional

1 (1)
Prof. Dr. Carlos Alberto Nogueira-de-Almeida – www.clinicanutre.com

63
Menino de 12 anos e 6 meses trazido pela mãe porque estava

sofrendo na escola com apelidos. É moderadamente ativo e no
Caso Clínico 4
caso novo obtiveram-se os seguintes dados:
• Obesidade de acordo com IMC

• Circunferência abdominal elevada O emagrecimento
• Comorbidades:
melhora todos os
‣bullying na escola
aspectos encontrados no
‣hipertensão arterial
diagnóstico.
‣Resistência insulínica
‣Dislipidemia com Mas… o que mais pode
✓ CT elevado ser feito dentro do
✓LDL elevado planejamento alimentar ?
✓TG elevado
64
Condutas genéricas para dislipidemia
• Restrição calórica
• Redução do percentual de lipídeos da dieta de 30 para 25%, sendo:
‣ 10 % polinsaturados
‣ 10% monoinsaturados
‣ 5% saturados
‣ 0 % trans
‣ Rodízio de carnes/ovos (gado, porco, aves, peixes e ovos)
‣ 50% dos cereais na forma integral
‣ Carboidratos de menor índice glicêmico, reduzindo acentuadamente CH simples
‣ Laticínios semi-desnatados
‣ Peixes ricos em ômega 3
‣ Frutas, verduras e legumes em abundância
‣ Fibras (idade + 5 até o limite de 25 gramas)
‣ Fitosterois: 2 gramas por dia (em alimentos fortificados)
‣ Atividade física
65
Condutas nutrológicas para Resistência Insulínica
• Restrição calórica
• Fracionamento da dieta
‣ 50% dos cereais na forma integral
• Carboidratos de menor índice glicêmico
• Redução acentuada de CH simples
• Peixes ricos em ômega 3
• Frutas, verduras e legumes em abundância
• Fibras (idade + 5 até o limite de 25 gramas)
• Atividade física com bastante componente muscular
66
1ª consulta 2ª consulta 3ª consulta 4ª consulta
Idade 12 A + 6 M 13 A + 7 M 14 A + 7M 15 A + 4 M
Peso 66,7 67,5 68,2 67,3
Estatura 147,5 155,1 158 160,1
P Estatura 24,2 24,4 11,8 8,7
IMC 30,7 28,1 27,3 26,3
P IMC 99,9 99,3 98,3 96,3
Z IMC 2,98 2,44 2,13 1,79
Circ. Abdominal 101 86 88,1 84,5
Pressão arterial 160/80 106/75 106/60 106/57
Glicemia 90 90 -- --
Insulina 30,9 12 -- --
Colesterol total 192 145 -- --
HDL 53 43 -- --
LDL 117 86 -- --
Triglicerídeos 110 79 -- --
67
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
68
Retra
to da
Saúd
e 20
18
2018
7
5 1
21
EU28 PT
46 33 2017 Variação 2017 Variação
2017-2013 2017-2013
68 6 7 -1 5 -3
33 = 21 +1
14 -3 6 -2
46 +4 68 +4
0 = 0 =
14
EU28 Anel Exterior pt Anel interior Evolução 12/2017 (EB88.4) - 11-12/2013 (EB80.2)
Fonte: Eurobarómetro sobre desporto e atividade física (Special Eurobarometer 472), 2017
Fig. 12. Frequência de prática desporto ou exercício físico, em Portugal e na Europa
69
Criança de 10 anos de idade, sexo

Caso Clínico 5
feminino, escore z de IMC + 2,5, com
Curso de Capacitação em
Obesidade Infanto Juvenil da Abran
dislipidemia e resistência insulínica,
sedentária.
Como você fará a prescrição de
atividade física para tratar
essa criança?
70
Lancet, maio de 2010
71
72
Etapas a serem gradualmente alcançadas
1. Restringir tempo em atividades sedentárias: máximo 2 horas por dia de tela
2. Tirar do sedentarismo: oportunidade para lazer, mudanças de hábitos, estímulo a

brincadeiras ativas, games com movimento.
3. Atividade física visando prevenção de doenças crônicas: 30 minutos por dia consecutivos
ou não
4. Atividade física visando prevenção de DCV e de ganho de excessivo de peso: 60 minutos

por dia de atividade moderada a intensa, com atividades de resistência óssea e muscular
pelo menos 3 vezes por semana
5. Atividade física visando redução da gordura corporal: 60 a 90 minutos de atividade

moderada a intensa todos os dias, com atividades de resistência óssea e muscular pelo
menos 3 vezes por semana
73
Programa para emagrecimento

• Periodicidade
– 5 a 7 dias por semana
• Todos os dias
– atividade aeróbica moderada a vigorosa
• 3 vezes por semana

– exercícios de resistência óssea e muscular
74
Atividade Aeróbica
MODERADA VIGOROSA
Skate (recreativo) Jogos ativos de correr e perseguir
Caminhada (recreativo) Futebol
Bicicleta (recreativo) Passeio de bicicleta
Patins (recreativo) Pular corda
Artes marciais
Corrida
Basquete
Natação
Tênis
75
MITOS SOBRE ATIVIDADES ENVOLVENDO FORÇA

MUSCULAR
• Atrapalha crescimento
– Nenhuma comprovação quando feito corretamente
• Haverá lesão da cartilagem de crescimento

– Nunca foi cientificamente demonstrado
• A quantidade de testosterona é insuficiente para permitir

exercícios de força
– Testosterona não é necessária para isso
• É insegura
– Nenhuma comprovação quando feito corretamente.
• É indicada somente para atletas

– Os benefícios à saúde são para todos
76
Como fazer... Na prática
üProporcione instrução qualificada e supervisão;
üGaranta ambiente seguro e livre de riscos;
üEnsine as crianças os benefícios e as preocupações associadas ao treinamento de força;
üComece cada sessão com 5 a 10 minutos de aquecimento;
üComece com carga leve e 10 a 15 repetições em uma variedade de exercícios;
üProgrida para 2 ou 3 séries de 6 a 15 repetições, dependendo das necessidades e objetivos;
üRealizar 8-12 exercícios para cada segmento corporal: superior, inferior e médio;
üAumentar o peso gradualmente à medida que melhora a capacidade;
üFoco na técnica correta e não na quantidade de peso levantada;
üPeriodicidade: duas a três vezes por semana em dias não consecutivos;
üTreino individualizado para monitorar o progresso;
üManter atividade sempre nova e desafiadora, variando o programa de treinamento.
77
Atividade de Atividade de
Resistência Óssea Resistência Muscular
Jogos como “amarelinha” Jogos de força, como “cabo-de-guerra”

Saltitar ou saltar Flexões
Pular corda Exercícios com peso
Corrida
Arvorismo
Tênis
Escalada em parece
Basquete
Balanço em playgrounds ou barras
Futebol
Abdominais
Voleibol
Condicionamento (ginástica) Exercícios usando o peso do corpo
78
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
79
Menina de 9 anos e 11 meses, encaminhada por colega pediatra Voltando ao

para emagrecimento. Saudável, sedentária e no caso novo
obtiveram-se os seguintes dados:
Caso Clínico 3
Peso 55,7 Obesidade

Estatura 138,5
Percentil da Estatura 53,9

Hipertensão arterial

Resistência insulínica
Glicemia 86 Dislipidemia
Insulina 36
HDL 42
LDL 87
Triglicerídeos 157
80
Evolução do caso
visita 1 visita 4 visita 5
Idade 9A + 10M 10 A + 5M 10 A + 11M
Peso 55,7 51,3 53,6
Estatura 138,5 141,5 145,1
P Estatura 53,9 49,7
IMC 29 25,6 25,4
P IMC > 97 99,4
Z IMC 3,15 2,49
Circ. 89,5 79,3 83

Abdominal
Pressão 125 / 84 100/75 100/75
arterial
Glicemia 86 78 82 Foi associada metformina,
Insulina 36 18 15
Colesterol 161 157 500 mg na versão XR junto ao

total
HDL 42 53
jantar e mantido por 6 meses
LDL 87 87
Triglicerídeo 157 82
s
81
Evolução do caso
visita 1 visita 4 visita 5 visita 12
Idade 9A + 10M 10 A + 5M 10 A + 11M 15A + 2M
Peso 55,7 51,3 53,6 60,6
Estatura 138,5 141,5 145,1 160,5
P Estatura 53,9 49,7
IMC 29 25,6 25,4 23,7
P IMC > 97 99,4 83,3
Z IMC 3,15 2,49 0,96
Circ. 89,5 79,3 83 78

Abdominal
Pressão 125 / 84 100/75 100/75 100/68
arterial Família reorientada e mantida
Glicemia 86 78 82 80
Insulina 36 18 15 11 metformina, 500 mg na versão XR

Colesterol 161 157 158
total junto ao jantar e mantido por mais
HDL 42 53 55
LDL 87 87 88 6 meses
Trigliceríde 157 82 75
os
82
Opções Farmacológicas
• 8 estudos bem conduzidos:
– 1 com orlistate
– 4 com sibutramina
– 3 com metformina
Michael Freemark
Pharmacotherapy of childhood
obesity
Diabetes Care, 2007
83
• 64 estudos (5.230 participantes)

• Em 10 estudos sobre farmacoterapia:
– Referências a sibutramina, orlistate e
metformina Luttikhuis et al
Interventions for treating
– Conclusão dos autores: para os obesity in children
Cochrane Database Syst Rev
adolescentes, é possível o uso de 2010 (edited)(1)
farmacoterapia como coadjuvante,
pesando-se riscos e benefícios
84
Pharmacological treatment of obesity in children and adolescents: current status and
perspectives.
Expert Opinion on Pharmacotherapy, december, 2010
Natalia Catoira, Mara Nagel, Guillermo Di Girolamo, Claudio D Gonzalez
REFERÊNCIAS A SIBUTRAMINA, ORLISTATE E METFORMINA
ü The efficacy of these drugs is modest;
ü Our knowledge of their efficacy and safety comes from clinical trials affected by
insufficient follow-up (1 year or less);
ü very often, these trials are of limited power;
ü Further data from larger and longer well-designed clinical trials would be
advisable.
85
Managing childhood obesity: when lifestyle change is not enough.

Hearnshaw C, Matyka K.
Diabetes Obes Metab, 2010 Nov;12(11):947-57
• 76 artigos avaliados:
– Farmacoterapia
– Cirurgia
• “The study design of many was inadequate and the role of
pharmacotherapy or surgery in childhood obesity remains
unclear”
86
Journal of Obesity
Volume 2011, Article ID 928165, 13 pages doi:10.1155/2011/928165
• Basicamente fala de metformina, sibutramina e
orlistate como opções possíveis
• Sugere-se leitura por descrever várias outras
possibilidades presentes e futuras.
87
557859
research-article2014
AOPXXX10.1177/1060028014557859Annals of PharmacotherapyBoland et al
Review Article
Annals of Pharmacotherapy
Pharmacological Management of Obesity in

1–13
© The Author(s) 2014
Reprints and permissions:
Pediatric Patients sagepub.com/journalsPermissions.nav
DOI: 10.1177/1060028014557859
aop.sagepub.com
Cassie L. Boland, PharmD1, John Brock Harris, PharmD1,

and Kira B. Harris, PharmD1
Abstract
Objective:To review current evidence of pharmacological options for managing pediatric obesity and provide potential
areasConclusions:
for future research.Lifestyle
Data Sources: interventions
A MEDLINE searchremain (1966the treatment
to October 2014)ofwaschoice
conducted inusing
pediatric
the following
keywords: exenatide, liraglutide, lorcaserin, metformin, obesity, orlistat, pediatric, phentermine, pramlintide, topiramate, weight loss,
obesity,
and butStudy
zonisamide. concomitant
Selection pharmacotherapy
and Data Extraction:may Identifiedbe articles
beneficial in some
were evaluated forpatients. Orlistat
inclusion, with priority
given to randomized controlled trials with orlistat, metformin, glucagon-like peptide-1 agonists, topiramate, and zonisamide
inshould be considered
human subjects as second-line
and articles written therapywere
in English. References for also
pediatric
reviewedobesity. Evidence
for additional suggests
trials. Data Synthesis:
Whereas lifestyle modification is considered first-line therapy for obese pediatric patients, severe obesity may benefit from
pharmacotherapy.
that other diabetesOrlistatand
is the only Food and Drug
antiepileptic Administration
medications may (FDA)-approved
also provide medication for pediatric
weight-loss obesity
benefits,
and reduced body mass index (BMI) by 0.5 to 4 kg/m2, but gastrointestinal (GI) adverse effects may limit use. Metformin
has demonstrated BMI reductionsbut of 0.17
safety kg/m2, with
to 1.8should bemild GI adverse
further effects usually managed with dose titration.
evaluated.
2
Exenatide reduced BMI by 1.1 to 1.7 kg/m and was well-tolerated with mostly transient or mild GI adverse effects.
Topiramate and zonisamide reduced weight when used in the treatment of epilepsy. Future studies should examine efficacy
and safety of pharmacological agents in addition to lifestyle modifications for pediatric obesity. Conclusions: Lifestyle
interventions remain the treatment of choice in pediatric obesity, but concomitant pharmacotherapy may be beneficial in
some patients. Orlistat should be considered as second-line therapy for pediatric obesity. Evidence suggests that other
diabetes and antiepileptic medications may also provide weight-loss benefits, but safety should be further evaluated.
Keywords 88
exenatide, liraglutide, lorcaserin, metformin, obesity, orlistat, pediatric, phentermine, pramlintide, topiramate,
Nogueira-de-Almeida weight
- 7 de loss,
novembro de 2018
zonisamide
Mead E, Atkinson G, et al. Drug interventions for the
treatment of obesity in children and adolescents.
Cochrane Database Syst Rev. 2016 Nov
• pharmacological interventions: metformin, sibutramine, orlistat and

fluoxetine
• pharmacological interventions may have small effects in reduction in BMI

and bodyweight in obese children and adolescents
• Trials were generally of low quality with many having a short or no post-
intervention follow-up period and high dropout rates
• many of these drugs are not licensed for the treatment of obesity in
children and adolescents
89
• Metformina
• Sibutramina
• Orlistate
• Fluoxetina
• Sertralina
• Topiramato
• Exenatide
• Fitoterápicos
90
Metformina
Obesity Insulin
resitance
Insulin Resistance: A Vicious Circle Of Excess Fat; Wood P, Diabetes in control 2007, issue 351
91
92
Size of treatment P
effect value
Weight (kg) –4.35 0.02
Weight z-score –0.09 0.009
BMI (kg/m2) –1.26 0.002
BMI z-score –0.12 0.005
Waist circumference (cm) –2.8 0.003
Waist circumference z-score –0.05 0.005
Fasting insulin (mU/liter) –2.2 0.011
Fasting glucose (mmol/liter) –0.2 0.048
Insulin sensitivity [(mU/ +0.17 0.506

liter)–1·min–1]
Sg (min–1) +0.0004 0.853
AIR (mU/liter–1·min) –121.4 0.189
DI –93.9 0.451
Kg –0.03 0.550
93
Use of metformin in obese adolescents with hyperinsulinemia: a 6-month,

randomized, double-blind, placebo-controlled clinical trial.
Atabek et al, J Pediatr Endocrinol Metab, 2008
• 120 adolescentes de 9 a 17 anos, PIMC>95

• Todos com dieta, exercício e terapia comportamental
• 90 tratados com 500 mg de metformina, 30 com placebo
• 6 meses de estudo
• Grupo tratado com metformina teve melhora:
– Maior queda no IMC
– Redução da insulinemia
94
Metformin XR Treatment of Adolescent
Obesity
95
Metformin XR Treatment of Adolescent Obesity
Possível crítica ao estudo:

foi dada metformina para todos os participantes e não somente
para aqueles portadores de resistência insulínica
96
Metformin in Obese Children and Adolescents: The MOCA Trial
(J Clin Endocrinol Metab 98: 322–329, 2013)
Design:
Prospective, randomized, double-blind, placebo-controlled trial.
The study was conducted at six pediatric endocrine centers in the United Kingdom
Single Intervention: metformin
151 obese hyperinsulinemic children (8-18 years)
– 74 metformin
– 77 placebo
Results:
Metformin was associated with a significant reduction in BMI-SDS compared with
placebo at 6 months.
Conclusions:
Metformin therapy has a beneficial treatment effect over placebo for BMI-SDS 3
months, with changes in BMI-SDS sustained at 6 months.
97
Metformina
• Não é “remédio para emagrecer”
• Só é indicada em casos específicos
• Pode levar à Acidose Lática
• Dose: 500 a 1700 mg/dia
98
Sibutramina
99
Sibutramina
100
Sibutramina
Table I
Included studies
1st or 2nd efficiency

Trial Interventions n Months measures about the
reduction of obesity
1 Diet + Sibutramine. 10-15 mg/d 43 12 %* initial BMI (p)
Berkowitz et al. (April 2003) Diet + Placebo 1-6 A † initial weight (p)
2 39
Diet + Sibutramine 6-12 A waist circumf ‡ (p)
A initial BMI (p)
1 Diet + Sibutramine. 10 mg/d 368
% initial BMI (s)
Berkowitz et al. (July 2006) 12 A initial weight (s)
2 Diet + Placebo 130 % initial weight (s)
A waist circumf (s)
Daniels et al. (June 2007) 12 A initial BMI (p)
2 Diet + Placebo 130
A initial BMI (p)
1 Sibutramine 10 mg/d 23
% initial BMI (p)
García Morales et al. (July 2006) 6 A initial weight (p)
A waist circumf (s)
2 Placebo 23
% waist circumf (s)
A initial BMI (p)
1 Sibutramine 10 mg/d 30 % initial BMI (s)
A initial weight (p)
Godoy-Matos et al. (March 2005) 6 % initial weight (s)
A waist circumf (s)
2 Placebo 30 A hip circumf (s)
A waist/hip (s)
Diet + Sibutramine . 10 mg/d 1-3
1 12 A initial BMI (p)
Only diet 3-6
Van Mil et al. (April 2007)
Diet + Placebo 1-3
2 12 A initial weight (s)
Only diet 3-6
Orlistat 120 mg A initial BMI (p)
1 357
3 times daily A initial weight (s)
Chanoine et al. (June 2005) 12
(Nutr Hosp. 2011;26:451-457)
2
; DOI:10.3305/nh.2011.26.3.5123
Placebo 182
A waist circumf (s)
A hip circumf (s)
1 Orlistat
101 120 mg 20
Maahs et al. (January 2006) 3 times daily 6 A initial BMI (p)
2 Placebo 20
Sibutramina
1 Diet + Orlistat 22 A initial BMI (p)
Ozkan et al. (December 2004) 120 mg 3 times daily 12 A initial weight (p)
2 Diet 20 % initial weight (p)
*% = Porcentaje change in …, †A = Absolute change in…, ‡ Circumf = Circumference
month. Regarding the duration of the trials with sibu- most baseline characteristics of the groups were tabu-
tramine, some lasted 6 months and others 12 months. In lated and homogeneous. Also multicenter studies of
connection with orlistat, sample sizes ranged from 539 Berkowitz 2006, Daniels 2007 and Chanoine 2005
patients of multicenter study of Chanoine 2005,13 to 40 stratified randomization, to minimize any selection
and 42 teenagers in the other two publications Table III bias . These three, like the work of Berkowitz in 2003,
included. In the 3 cases the doseAbsolute
14-15
was 120 mg change in initial detailed
3 times BMI (kg/m 2
)
correctly the mechanisms of blinding, which
daily and ranged between 6 and 12 months. limits detection bias and gives them a bonus point in
Trial The trials were funded Treatment group
by pharmaceutical compa- the chosen Comparator
rating scale. All trials described p-valor vs placebo
the loss of
nies manufacturing theSibutramine
Berkowitz et al.* drugs under (n =investigation.
368) - 3.1 The follow Placebo
up; the (n
above,
= 130)as well as Garcia-Morales
- 0.3 p <2006
0.001
16
majority reached a moderate to high methodological and Godoy-Matos 2005, 17

analyzed by intention to
Daniels et al.†quality according toSibutramine (n = 368)as
Jadad endpoints, - 2.9
can± 0.15
be seen in treat,Placebo (n = 130) - 0.3
thus sheltering from± 0.24 p < 0.001
attrition bias. In general, the
Godoy-Matostableet al. II. All studies Sibutramine
mentioned(nrandomization,
= 30) - 3.6 ± 2.5 and in resultsPlacebo
were (n = 30) - 0.9properly.
expressed ± 0.9 p < 0.001
Van Mil et al. Sibutramine 3 months (n = 11) - 1.5 ± 1.1 Placebo 3 months (n = 12) - 1.1 ± 1.6 p > 0.05
Chanoine et al.‡ Orlistat (n = 352) - 0.55 Placebo (n = 181) + 0.31 p = 0.001
Maahs et al. Review sibutramine and Orlistat
orlistat (n = 20) - 1.3 ± 1.6 Nutr Hosp. 2011;26(3):451-457
Placebo (n = 20) - 0.8 ± 3 453
p = 0.39
in obese adolescents
Oskan et al. Orlistat (n = 22) - 4.09 ± 2.9 Diet (n = 20) + 0.11 ± 2.49 p < 0.001
The results are expressed as mean change ± SD, except in those cases:
*Mean change.
†
Conclusions:
Mean change ± SE. Sibutramine in combination with a hypocaloric diet and changes in
‡
Change least squares mean.
lifestyle in obese adolescents achieve a short-term loss of weight greater than that
Table IV
Absolute change in initial weight (kg)
achieved through the dietary-behavioral therapy alone.
Trial Treatment group Comparator p-valor vs placebo
Berkowitz et al. Sibutramine (n = 43) - 7.8 ± 6.3 Placebo (n = 39) - 3.2 ± 6.1 p = 0.001
Berkowitz et al.* Sibutramine (n = 281) - 6.5 ± 0.31 Placebo (n = 79) + 1.9 ± 0.56 p < 0.001
García Morales et al.† Sibutramine (n = 23) - 7.3 (4.6, 9.9) Placebo (n = 23) - 4.3 (1.7, 6.9) p > 0.05
Godoy-Matos et al. Sibutramine (n = 30) - 10.3 ± 6.6 Placebo (n = 30) - 2.4 ± 2.5 p < 0.001
Van Mil et al. (Nutr Hosp.
Sibutramine2011;26:451-457)
3 months (n = 11) - 2.81 ± 3.37 ; DOI:10.3305/nh.2011.26.3.5123
Placebo 3 months (n = 12) - 2.05 ± 3.54 p > 0.05
Chanoine et al. ‡ Orlistat (n = 352) + 0.53 Placebo (n = 181) + 3.14 p < 0.001
Oskan et al. Orlistat (n = 22) - 6.27 ± 5.4 102 Diet (n = 20) + 4.16 ± 6.45 p < 0.001
Sibutramina
• Somente acima de 18 anos
• Ações esperadas:
– Indução da saciedade
– Redução da fome
– Aumento do gasto energético
• Dose inicial de 10 mg
• Dose máxima de 15 mg
103
Orlistate
• Única medicação anti-obesidade aprovada pelo FDA
(EUA) para adolescentes (acima de 12 anos)
• Ação: inibição da lipase pancreática
• Dose 120 mg três vezes ao dia (café, almoço e

jantar)
• As seguintes drogas podem ter sua absorção

alterada pelo uso do orlistat:
• Ciclosporina – é preciso um intervalo de pelo

menos 3 horas entre a administração do orlistat e da
ciclosporina.
• Levotiroxina – é preciso um intervalo de pelo
menos 4 horas entre a administração do orlistat e
da levotiroxina.
• Multivitamínicos – é preciso um intervalo de pelo
menos 2 horas entre a administração do orlistat e de
multivitamínicos.
• Análogos da vitamina D – é preciso um intervalo
de pelo menos 2 horas entre a administração do
orlistat e dos análogos da vitamina D.
104
Orlistate
Jama 2005; 293: 2873-2883

105
Orlistate
Randomized, double-blind, placebo-controlled trial of orlistat for weight loss in adolescents.
Maahs D et al - 2006
METHODS:
6-month randomized, double-blind, placebo-controlled trial to compare the effects of orlistat (120 mg orally
3 times a day) and placebo on reduction of body mass index (BMI). Forty adolescents between 14 and 18
years of age with a mean BMI of 40 kg/m2.
RESULTS:
1) No statistically significant difference was noted between the 2 study groups for decrease in BMI from
baseline to 6 months (P = 0.39).
2) Laboratory measurements did not differ between the 2 groups. In comparison with the placebo group,
the orlistat group had increased adverse events, primarily gastrointestinal symptoms and findings.
CONCLUSION:
In this study of obese adolescents, orlistat did not significantly reduce BMI in comparison with placebo at 6
months.
106
2 Diet + Placebo 130 % initial weight (s)
A waist circumf (s)
Daniels et al. (June 2007) 12 A initial BMI (p)
2 Diet + Placebo 130
A initial BMI (p)
1 Sibutramine 10 mg/d 23
% initial BMI (p)
A waist circumf (s)
2 Placebo 23
Orlistate
% waist circumf (s)
A initial BMI (p)
1 Sibutramine 10 mg/d 30 % initial BMI (s)
A initial weight (p)
Godoy-Matos et al. (March 2005) 6 % initial weight (s)
A waist circumf (s)
Table I
2 Placebo 30 A hip circumf (s)
Included studies A waist/hip (s)
Diet + Sibutramine . 10 mg/d 1-3 1st or 2nd efficiency
Trial 1 Interventions n12 Months A initial
measures BMI
about the(p)
Only diet 3-6
Van Mil et al. (April 2007) reduction of obesity
Diet + Placebo 1-3
2 12 A initial weight (s)
1
Only diet
Diet + Sibutramine. 10-15 mg/d 43
3-6
12 %* initial BMI (p)
Berkowitz et al. (April 2003) Orlistat
Diet 120 mg
+ Placebo 1-6 A initial
A † initial BMI(p)
weight (p)
21 357
39
Chanoine et al. (June 2005) Diet3+times daily
Sibutramine 6-12
12
A initial
A waist weight
circumf ‡ (s)
(p)
A waist circumf (s)
2 Placebo 182
AA initial BMI (p)(s)
hip circumf
% initial BMI (s)
Berkowitz et al. (July 2006) 1 Orlistat 120 mg 20 12 A initial weight (s)
Maahs et al. (January 2006) 2 3 times
Diet daily
+ Placebo 130 6 A initial
% initial BMI(s)
weight (p)
2 Placebo 20 A waist circumf (s)
Table III
11 Diet + Orlistat
Diet + Sibutramine. 10 mg/d 22
368 A initial BMI (p)
Daniels
Ozkan etetal.
al.(December
(June 2007)2004)
2 Absolute 120 changetimesindaily
mg+3Placebo
Diet initial BMI 130
(kg/m2 )
AAinitial1212
initialBMI (p) (p)
weight
2 Diet 20 % initial weight (p)
Trial Treatment
*% = Porcentaje change in …, †A = Absolute group
1 change Sibutramine
in…, ‡ 10 mg/d
Circumf = Circumference Comparator % initial BMI (p)
23
A initial BMI (p)
p-valor vs placebo
Berkowitz et al.* Sibutramine (n = 368) - 3.1 Table III Placebo (n = 130) - A
0.3waist circumf (s) p < 0.001
duration of2(n
Daniels et al.†month. Regarding theSibutramine = Absolute
the trials-with
368)
Placebo
2.9 ±change
0.15 in most
sibu- initial
baseline 23 2
BMIPlacebo
(kg/m ) = 130)of
characteristics
(n the%
- 0.3 ±groups were tabu-
0.24 circumf
waist (s) p < 0.001
tramine, some lasted 6 months and others 12 months. In lated and homogeneous. Also multicenter studies of
Godoy-Matosconnection
et al. with orlistat,Sibutramine
sample sizes (n =ranged
30) - 3.6from± 2.5
539 Berkowitz 2006, Placebo (n = 30)
Daniels 2007- 0.9and
±A0.9
initial BMI (p)
Chanoine 2005 p < 0.001
Trial Treatment
1 group Sibutramine 10 mg/d 30 Comparator % initial BMI (s) p-valor vs placebo
Van Mil et al.patients of multicenter study of3Chanoine
months (n2005, to 40± 1.1 stratifiedPlacebo
randomization, to =minimize ±any selection
13
Sibutramine = 11) - 1.5 3 months (n 12) A- 1.1
initial1.6
weight (p) p > 0.05
Berkowitz and 42 teenagers in 2005)
the other two publications bias . These three, like the(n6==work
130) of Berkowitz in 2003,
Chanoine etetal.al.*
Godoy-Matos
‡ et al. (March Sibutramine
included.14-15 In the 3 cases theOrlistat
dose(n was
(n = 368)
= 352)
120 mg
- 3.1
- 0.55
3 times detailed correctly
Placebo
Placebo (n
the mechanisms181) +- 0.3
%
0.31
of
initial weight
blinding,
A waist circumf (s)
(s)
which
pp<=0.001
0.001
Daniels
Maahs etetal.
al.† daily and ranged between Sibutramine 2(nmonths.
6 and 12(n
Orlistat ==20)
368)- 1.3
- 2.9± ±1.60.15
Placebo limits detection Placebo
30bias(nand
Placebo =(n130) 20)- 0.3
=gives 0.8±A±0.24
-them a3 bonus
hip point
circumf (s) in p p< =0.001
0.39
Godoy-Matos
Oskan et al. nies etThe
al. trials were funded by pharmaceutical
Sibutramine
Orlistat (n (n = 30) - 3.6±compa-
= investigation.
22) - 4.09 ±2.9
2.5 the chosen rating scale.
Placebo
Diet (n =(n =All
20) 30)trials
- 0.9±described
+ 0.11
A waist/hip
±2.49
0.9 the (s)
loss of pp<<0.001
0.001
manufacturing the drugs under The follow up; the above, as well as Garcia-Morales 2006 16
Van Mil et al. majority reachedSibutramine

a moderate 3tomonths (nDiet
= 11)+ Sibutramine
1high methodological - 1.5 ± 1.1 . 10and
mg/d Placebo 3 months
Godoy-Matos 12 2005,17
1-3(n = 12) - 1.1 ± 1.6
A initial BMI (p) p > 0.05
The results are Van
expressed as Only diet 3-6 analyzed by intention to
‡ Mil et
quality al.mean
(Aprilchange
according 2007) ± SD,endpoints,
to Jadad except in those
as cases:
can be seen
Chanoine et al. Orlistat (n = 352) - 0.55Diet +inPlacebo treat, thus sheltering
Placebo from
(n =
1-3attrition
181) + bias. In general, the
0.31 p = 0.001
*Mean change.table II. All studies mentioned randomization,
2 and 12
in diet results were expressed
Only properly.
3-6
A initial weight (s)
Maahs
†
Mean et al. ± SE. Orlistat in combination
change
Conclusions: Orlistat (n = 20)with- 1.3 ±a1.6hypocaloric diet andPlacebo changes (n = 20) in -lifestyle
0.8 ± 3 in obese adolescents p = 0.39
Changeetleast Orlistat 120 mg A initial BMI (p)
al. squares mean.
‡
Oskan Orlistat (n1 = 22) - 4.09 ± 2.9 3 times daily Diet
357 (n = 20) + 0.11 ± 2.49
A initial weight (s) p < 0.001
Chanoine et al. (June 2005) 12
achieve A waist circumf (s)
The results areaexpressed
short-term
Review as mean loss
sibutramine andof
change weight
except2 ingreater
orlistat
± SD, than
those cases: Nutrthat
Hosp.achieved
Placebo through
2011;26(3):451-457
182 the dietary-behavioral
A hip circumf (s)
therapy
453 alone.
*Mean change. in obese adolescents
†
Mean change ± SE. 1 Table
Orlistat 120 mg IV 20
‡
Maahs et al. (January 2006)
Change least squares mean. Absolute3 times
change dailyin initial weight (kg) 6 A initial BMI (p)
(Nutr Hosp. 2011;26:451-457) ; DOI:10.3305/nh.2011.26.3.5123
2 Placebo 20
Trial Treatment
1 group Diet + Orlistat 22 Comparator A initial BMI (p) p-valor vs placebo
Ozkan et al. (December 2004) 120 mg 3 times daily 12 A initial weight (p)
Berkowitz et al. Sibutramine2 (n = 43) - 7.8 ± 6.3 107IV
DietTable Placebo
20 (n = 39) - 3.2%± initial
6.1 weight (p) p = 0.001
Berkowitz et *% al.*= Porcentaje change in …,
Sibutramine
A = Absolute(n
†
= Absolute
281)
change in…, - 6.5
‡
±change
Circumf 0.31 in initial weight
= Circumference (kg)(n = 79) + 1.9 ± 0.56
Placebo p < 0.001
García Morales et al.† Sibutramine (n = 23) - 7.3 (4.6, 9.9) Placebo (n = 23) - 4.3 (1.7, 6.9) p > 0.05
Trial Treatment group Comparatorof the groups were tabu- p-valor vs placebo
Godoy-Matosmonth. et al. Regarding the duration
tramine, some lasted 6 months
of the trials
Sibutramine (n
and others
= 30) -with sibu-
10.3
12 months.
± 6.6
In
most baseline characteristics
Placebo
lated and homogeneous.
(n = 30) - 2.4 ± 2.5 p < 0.001
Berkowitz et al. Sibutramine (n = 43) - 7.8 ± 6.3 Placebo (n =Also 39) -multicenter
3.2 ± 6.1 studies of p = 0.001
Fluoxetina
Van Mil et al.connection with orlistat,
Sibutramine
sample3 months (n = 11)
sizes ranged from- 2.81
539± 3.37 Berkowitz Placebo
2006, 3Daniels
months (n = 12)
2007 and- 2.05 ± 3.54 2005
Chanoine p > 0.05
Berkowitz et al.*
patients of multicenterSibutramine (n = 281)
study of Chanoine - 6.513 ±to0.31
2005, Placebo (n = 79) + 1.9 ± 0.56 p < 0.001
Chanoine et al. and
‡
42† teenagers Sibutramine
Orlistat (n = 352)
in the other(n two
+ 0.53 40
publications
stratified randomization,
bias . These three,
Placebo
like the
to minimize
(nwork
= 181) 3.14any selection
+Berkowitz
of(1.7, in 2003,
p < 0.001
García Morales et al. = 23) - 7.3 (4.6, 9.9) Placebo (n = 23) - 4.3 6.9) p > 0.05
Oskan et al. included.14-15 In the 3 casesOrlistat
the dose(nwas
= 22)
120 - 6.27
mg 3±times5.4 detailed correctlyDiet
the(nmechanisms
= 20) + 4.16 ±of6.45 blinding, which p < 0.001
Godoy-Matosdaily et al.and ranged between Sibutramine (n = 30) - 10.3 ± 6.6
6 and 12 months. limits detection Placebo
bias and(n =gives
30) -them
2.4 ± a2.5
bonus point in p < 0.001
The results
Van Mil etare
al. expressed as mean
The trials werechange
funded± SD,
Sibutramine byexcept
monthsin those
(n =cases:
3pharmaceutical 11)compa-
- 2.81 ± 3.37 the chosen rating3scale.
Placebo monthsAll(ntrials
= 12)described the loss of
- 2.05 ± 3.54 p > 0.05
*Mean change nies± SE.manufacturing the drugs under investigation. The follow up; the above, as well as Garcia-Morales 2006 16
Chanoine
†
Mean changeet al. ‡
majority
(95% CI) reached a moderate Orlistat (n =methodological
to high 352) + 0.53 and Godoy-Matos Placebo
2005,(n17=analyzed
181) + 3.14 by intention to p < 0.001
‡
Changeetleast
Oskan qualitymean.
al. squares according to Jadad endpoints,
Orlistat as can
(n = 22) be ±seen
- 6.27 5.4 in treat, thus sheltering
Diet (nfrom
= 20)attrition
+ 4.16 ±bias.
6.45In general, the p < 0.001
table II. All studies mentioned randomization, and in results were expressed properly.
*Mean change ± SE.
†2006, the p-value was > 0’05 between groups (sibu-
Mean change (95% CI)sibutramine and orlistat
Review
Adverse effects
Nutr Hosp. 2011;26(3):451-457 453
• ISRS
‡
tramine,
Change leastplacebo),
squares mean.
in obese but < 0’05 in the intra-group (initial
adolescents
weight, final weight) of sibutramine. Concerns about the increase in blood pressure and
2 orlistat studies found a significantly better weight heart rate observed in some adults after treatment with
variation
2006, after 12was
the p-value months
> 0’05with the drug
between than(sibu-
groups with Adverse effectsled to the multicenter study of Daniels
sibutramine
• Aprovado pelo FDA a partir de 7 anos de idade para
placebo. placebo), but < 0’05 in the intra-group (initial
tramine, 2007, which evaluated carefully the cardiovascular
weight, final weight) of sibutramine. safety of thisabout
Concerns product
theinincrease
obese adolescents.
in blood pressureTrial ended
and
tratamento de depressão e TOC
2 orlistat studies found a significantly better weight
Quality of after
variation life 12 months with the drug than with
after rate
heart 12 months,
observedand smalladults
in some averages
afterdecreases were
treatment with
objectified for
sibutramine ledeach variable
to the in the sibutramine
multicenter study of Danielsgroup
placebo. and inwhich
2007, the placebo group,
evaluated with nothe
carefully significant differ-
cardiovascular
Only one clinical trial, published by García Morales ences of
safety between groupsin(systolic
this product blood pressure:
obese adolescents. -2.1 vs
Trial ended
• Existe na versão gotas
in July 2006, assessed the changes in the quality of life -2.1 12
after mmHg;months, diastolic blood
and small pressure:
averages -0.1 vswere
decreases -1.1
Quality of life that treat their obesity with a drug such
of adolescents mmHg; heart
objectified for rate
each-0.2 vs -1.8
variable in bpm). Furthermore,
the sibutramine groupin
as sibutramine. This study used SF-36, which is aimed bothingroups,
and these reductions
the placebo group, with in no
vitalsignificant
signs werediffer-
higher
at Only
people 14 years
one! clinical andpublished
trial, has a route from 0Morales
by García (worst among
ences those who
between managed
groups (systolic a decrease in BMI
blood pressure: ! 5%
-2.1 vs
• Doses inicias de 5 a 10 mg chegando na dose terapêutica
health)
in to 100assessed
July 2006, (best health status). in
the changes It showed improve-
the quality of life compared
-2.1 mmHg; with patientsblood
diastolic that managed
pressure:a-0.1 vs -1.1in
reduction
ment
of in the quality
adolescents of life,
that treat theirwith no significant
obesity with a drugdiffer-
such their BMI
mmHg; " 5%.
heart -0.2 2vsmulticenter
rate The trials with sibu-
-1.8 bpm). Furthermore, in
que não deve ultrapassar 20 mg
as
at
sibutramine.
ence between the
people
group: mean
This
! 14scores
study used group
sibutramine
yearson andthehas
SF-36,and
a route
SF-36
which
from
in the
theisplacebo
aimed
0 (worst
sibutramine
both groups,
tramine these reductions
(Berkowitz in vital2007,
2006, Daniels signs were higher
996 patients
among
between those
the whotwo)managed
reporteda adecrease
similar inincidence
BMI ! 5% of
health) to 100 (best
group increased fromhealth
78 status). It showed
(SD = 13’3) improve-
at baseline to compared with patients
adverse effects that managed
for sibutramine and aplacebo,
reductiononlyin
ment in the= quality
84’8 (SD 7’4) at of
thelife,
endwith nostudy,
of the significant differ-
whereas the their BMI " 5%.
tachycardia The 2statistically
differed multicenterbetween
trials with thesibu-
two
ence between
respective theinsibutramine
values the placebogroup
group and
werethe
82’8placebo
(SD = tramine (Berkowitz
groups (the 2 papers 2006, Daniels
published 13%2007,for996 patients
sibutramine
group:
10’3) andmean87’3scores
(SD =on the SF-36 in the sibutramine
7 ‘6). between
comparedthe withtwo)
6%reported a similar
for placebo). Otherincidence of
side effects
group increased from 78 (SD = 13’3) at baseline to adverse effects for sibutramine and placebo, only
84’8 (SD = 7’4) at the end of the study, whereas the tachycardia differed statistically between the two
respective values in the placebo group were 82’8 (SD = 108 groups (the 2 papers published 13% for sibutramine
Review
10’3) andsibutramine
87’3 (SDand = 7 orlistat
‘6). Nutr Hosp. 2011;26(3):451-457
compared with 6% for placebo). Other side effects 455
in obese adolescents Nogueira-de-Almeida - 7 de novembro de 2018
Sertralina
• ISRS
• Aprovado pelo FDA a partir de 6 anos de idade para

tratamento de TOC
• Doses inicias de 25 chegando na dose terapêutica que

não deve ultrapassar 50 mg
109
Topiramato
• O topiramato é uma droga uUlizada principalmente no tratamento de epilepsia
• Contudo, foi observado que os pacientes que o uUlizavam apresentavam, como

efeito colateral, perda de peso (devido à perda de apeUte ou mesmo à fissura
por carboidratos)
• Em virtude disso, começou-se a estudar esta droga como adjuvante no

tratamento da obesidade grave, especialmente nos casos de compulsão. No
entanto, em pediatria, ao prescrever para obesidade, deve-se sempre
considerar o outro efeito adverso, que é possibilidade de lenUdão ao
aprendizado
• Dose: 3 a 7 mg/kg/dia
Fox CK et al. Topiramate for weight reducUon in adolescents with severe obesity. Clinical Pediatrics,1-6,2014
110
Exenatide
6
• Agonista GLP-1
Table 2. (continued)
• Mecanismo de ação: aumento da secreção de lepUna Number
a parUr de sinalização do trato Change
of Baseline Obesity
digestório,
in Change in
Study Design Duration Study Population Patients (n) Therapy Treatment Groups BMI (kg/m2) Weight (kg)
levando a redução do apeUte, diminuição da ingesta energéUca e retardo no esvaziamento gástrico.
Yanovski et al, 201143 R, DB, PC 6 Months, then 6-12 Years old (mean = 100 Lifestyle MET 1000 mg bid −0.78a 1.47a
6
OL MET for 6 approximately 10 years modifications PBO 0.32 4.85

• Dose: 10 μg duas vezes ao dia months old) insulin resistant, and
Downloaded from aop.sagepub.com at GEORGIAN COURTDownloaded
mean BMI = 34.6 kg/m2, multivitamin

predominantly non-
Hispanic
44
Kendall et al, 2013 R, DB, PC 6 Months 8-18 Years old (mean 151 Lifestyle MET 1500 mg/d Mean Mean
= 13.7 years old), modifications and PBO difference: difference:
Table 2. (continued)
BMI >98th percentile −1.07a −2.6a
(mean BMI = 36.5 kg/
2
m ), F > M, impaired Number of Baseline Obesity Change in Change in
Study Design Duration Studytolerance
glucose Population or Patients (n) Therapy Treatment Groups BMI (kg/m2) Weight (kg)
Yanovski et al, 201143 R, DB, PC 6 Months, then 6-12hyperinsulinemia
Years old (mean = 100 Lifestyle MET 1000 mg bid −0.78aa 1.47aa
Kelly et al, 201247 R, OL, 6 OL
Months
MET for 6 9-16 Years old, extreme
approximately 10 years2 12 Lifestyle
modifications PBO Exenatide 10 µg bid −1.7
0.32 −3.9
4.85
controlled, months obesity (BMI ≥35
old) insulin resistant,kg/m ; modifications
and and PBO
2
UNIV on November
crossover, mean = 36.7 kg/m

mean BMI = 34.6 kg/m , ), F 2
multivitamin
pilot >M
predominantly non-
Kelly et al, 201348 R, DB, PC, MC 3 Months, then 12-19 Years old, severe
Hispanic 26 Lifestyle Exenatide 10 µg bid −1.13a −3.26a
from aop.sagepub.com
Kendall et al, 201344 R, DB, PC 6 3Months

months OL 8-18obesity old ≥35
Years(BMI (mean kg/m2; 151 modifications MET
Lifestyle and1500
PBOmg/d Mean Mean
exenatide =mean
13.7=years kg/m2)
42.5 old),
19, 2014
modifications and PBO difference: difference:

extension BMI >98th percentile −1.07a −2.6a
(mean BMI = 36.5 kg/
Abbreviations: BMI, body mass index; R, randomized; DB, double blind; PC, placebo controlled; F, female; M, male; MET, metformin; PBO, placebo; NR, not reported; MC, multicenter; FL, fluoxetine;
m2), F > M, impaired
at GEORGIAN COURT UNIV on November 19, 2014
OL, open-label.
a
p<0.05
glucose tolerance or
hyperinsulinemia
Kelly et al, 201247 R, OL, 6 Months 9-16 Years old, extreme 12 Lifestyle Exenatide 10 µg bid −1.7a −3.9a
controlled, obesity (BMI ≥35 kg/m2; modifications and PBO
crossover, mean = 36.7 kg/m2), F
48
Poland et al. Annals of Pharmacotherapy 2014; 1-13
pilot >M
Kelly et al, 2013 R, DB, PC, MC 3 Months, then 12-19 Years old, severe 26 Lifestyle Exenatide 10 µg bid −1.13a −3.26a
3 months OL obesity (BMI ≥35 kg/m2; modifications and PBO
exenatide mean = 42.5 kg/m2)
extension
111
Abbreviations: BMI, body mass index; R, randomized; DB, double blind; PC, placebo controlled; F, female; M, male; MET, metformin; PBO, placebo; NR, not reported; MC, multicenter; FL, fluoxetine;
OL, open-label.
a
p<0.05
Fitoterápicos
• Sem evidências cienuficas na faixa etária pediátrica
Greydanus et al. Pediatr Clin N Am 58 (2011) 139–153

doi:10.1016/j.pcl.2010.10.007
112
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
113
Menina, 11 anos, escore z de IMC +2,4 trazida à Caso Clínico 6

consulta para seguimento de obesidade. Já em
tratamento tradicional há 1 ano de obesidade com
dislipidemia e hipertensão.
Ao exame apresentou PA de 162/96
Na reavaliação laboratorial, observou-se
• LDL de 192 mg/dL
• TGP (ALT) de 49 U/L e TGO (AST) de 43 (índice
AST/ALT = 0,88)
• Insulinemia de 19
Quais suas condutas?
114
RELATO DE CASO
Consenso da Associação Brasileira de

Nutrologia sobre manejo da dislipidemia
secundária à obesidade infanto-juvenil
1
Carlos Alberto Nogueira-de-Almeida
2
Elza Daniel de Mello
3
Patrícia Piccoli de Mello
4
Paula Daniel de Mello
5
Renato Augusto Zorzo
6
Durval Ribas Filho
1
MD, MSc, PhD, Universidade de Ribeirão Preto, ABRAN
2
MD, MSc, PhD, Universidade Federal do Rio Grande do Sul, ABRAN
3
MD, MSc, Universidade Federal do Rio Grande do Sul
4
AC, University of Cologne
5
MD, MSC, Universidade Federal de São Carlos
6
MD, MSC, PhD, Faculdade de Medicina da Fundação Padre Albino, ABRAN
CARLOS ALBERTO NOGUEIRA-DE-ALMEIDA
RESUMO
Objetivo
Figura 1 - Etapas
Estabelecer da opção
consenso terapêutica
sobre o manejodedaacordo com valores
dislipidemia de LDL-colesterol
secundária e presença de fatores de risco
à obesidade infanto-juvenil.
Métodos 115
(valores de LDL expressos em mg/dL).
Foi realizada pesquisa bibliográfica nas bases de dados Medline, Scielo e LILACS. Com base nas
evidências científicas, o grupo de trabalho estabeleceu as condutas recomendadas pelo Departamento
de Nutrologia Pediátrica da ABRAN.
Resultados
Os autores redigiram o consenso que foi aprovado pela Diretoria da Associação Brasileira de Nutrologia
- ABRAN.
Conclusões
São apresentadas, com base nas evidências científicas, as recomendações para a condução dos casos
de dislipidemia associados à obesidade na infância e adolescência.
Palavras-Chave: Dislipidemia, lipídeos, aterosclerose, crianças e adolescentes.
INTRODUÇÃO ção infanto-juvenil, que apresenta prevalência de

sobrepeso de 31,6% nos Estados Unidos1. No
A obesidade é um fenômeno global, cuja pre- Brasil, segundo os últimos dados do IBGE, 51,4%
valência vem aumentando nas últimas décadas, dos meninos e 43,8% das meninas entre 5 e 9 anos
chegando a assumir caráter de epidemia. Dados de idade apresentam excesso de peso, números que
recentes confirmam o crescimento acelerado de indi- mostram a importância desta entidade mórbida na
víduos com excesso de peso também na popula- esfera da saúde pública1, 2. O acúmulo de gordura
International Journal of Nutrology, v.10, n.4, p. 161-178, Set / Dez 2017 161
116
risco cardiovascular. do VET
O presente consenso propõe o tratamento da 12%) e
dislipidemia associada à obesidade em duas etapas: indicam
gordura
Etapa 1 a popul
Terapia não farmacológica, que envolve tratamento alteraçõ
nutrológico e estímulo à prática de atividade física. puberal5
166 International
es Etapa 2
m Tratamento medicamentoso.
ão
os A figura 1 apresenta esquematica
es etapas se deve adotar de acordo co
117
Os LDL-colesterol e presença
Dislipidemia – Tratamento de fatores d
Nutrológico
es
• Conduta inicial:
de Etapa 1 – Terapia
– Ingestão calórica suficiente para não farmacológica
crescimento
DA A– Ingestão
terapêutica
diária e variada de:não farmacológica é
se duas
• Frutas, verduras e legumes: 5 ou mais porções diárias
partes
• Substituição que
de carboidratos devem
simples por complexos ser impleme
7
. taneamente: nutroterapia e orientaçõe
• Preferência de carnes magras, de aves ou de peixes
– Reavaliar em 3 meses
ia de atividade física (AF).
to
o, 1) Nutroterapia 1
os 118
Dislipidemia – Tratamento Nutrológico
• Em caso de insucesso:
– Calorias derivadas de lipídeos
• Inferior a 30% (sugere-se 25%)
• 5% de saturada
• 10% poli-insaturada (peixes, frutos do mar, soja, grãos)
• 10% monoinsaturada (abacate, canola, oliva, girassol, etc)
• < 200 mg/dia de colesterol
• Nada de trans
119
2
Dislipidemia – Tratamento Nutrológico
• Em caso de insucesso (continuação):

– Aumentar o consumo de fibras solúveis
• Idade + 5 anos, máximo 25 gramas/dia
– Reduzir carboidratos simples
– Limitar consumo de bebidas adoçadas
– Álcool com moderação (adolescentes)
– Elevar consumo de ômega 3
• Peixes 2 vezes por semana
– Reavaliar em 3 meses
120
2
Dislipidemia - Terapia farmacológica
Classe Mecanismo de ação Dose
↓ síntese endógena de colesterol por inibição SinvastaUna: 10-40mg /dia

HGM-CoA redutase; LovastaUna: 10-40mg /dia
Esta?nas AtorvastaUna: 10-20mg /dia
↑ aUvidade receptores de LDL-colesterol no PravastaUna: 20-40mg/dia
`gado
Inibidores Inibidor específico da absorção do colesterol, EzeUmiba: 10mg/dia

absorção do agindo sobre a borda estriada do enterócito
colesterol
Agem no intesUno se ligando aos ácidos biliares e ColesUramina: 4-16g/dia
Sequestradores evitando sua reabsorção, promovendo excreção
ColesUpol: 5-20g/dia
de ácidos biliares e remoção do ciclo do colesterol
(resinas) Não há absorção sistêmica
↓ síntese de VLDL-colesterol 10-20mg/dia

Fibratos
Melhoram função endotelial Ácidos graxos ômega-3:
Nutracêu?cos 2-4g/dia
121
Tratamento não farmacológico
• Para todas as crianças com pressão arterial acima do
percentil 90
• Emagrecimento
• Redução na ingestão de sal
• Atividade física
– Evitar esportes competitivos
122
Tratamento farmacológico
• Indicações
– Hipertensão sintomática
– Hipertensão secundária
– Evidência de lesão em órgão alvo
– Diabetes tipo 1 ou 2
– Hipertensão persistente, não responsiva às condutas não-
farmacológicas
– Iniciar sempre com um agente e combinar depois, se necessário
123
Tratamento farmacológico
Aspectos Atuais da Hipertensão Arterial Pediátrica
90
Tabela 4. Medicamentos orais mais utilizados para o tratamento da hipertensão arterial crônica pediátrica8.
Medicamento Dose Inicial (mg/kg/dose) Dose máxima (mg/kg/dia) Intervalo
Amlodipina
(6-17 anos) 2,5 mg/dia 5 mg/dia 24h
Nifedipina XL 0,25 – 0,5 3 (máx: 120mg/dia) 12 – 24h
Captopril
Criança 0,3 – 0,5 6 8h
Neonato 0,03 – 0,15 2 8 – 24h
Enalapril 0,08 0,6 12 – 24h
Losartan 0,7 (máx: 50mg/dia) 1,4 (máx: 100mg/dia) 24h
Propranolol 1–2 4(máx: 640mg/dia) 8 – 12h
Atenolol 0,5 – 1 2 (máx: 100mg/dia) 12 – 24h
Furosemide 0,5 – 2 6 4 – 12h
Hidroclorotiazida 1 3 (máx: 50mg/dia) 12h
Triamterene 1–2 3 – 4 (máx: 300mg/dia) 12h
Espironolactona 1 3,3 (máx: 100mg/dia) 6 – 12h
Clonidina
(≥ 12 anos) 0,2mg/dia 2,4mg/dia 12h
Prazosin 0,05 – 0,1 0,5 8h
Hidralazina 0,75 7,5 (máx: 200mg/dia) 6h
Minoxidil
< 12 anos 0,2 50mg/dia 6-8h
≥ 12 anos 5mg/dia 100mg/dia
máx: máximo; h: horas
A tabela 4 demonstra as doses pediátricas atua- 124 hipertensiva se caracteriza por elevação também impor-
lizadas para os hipotensores mais prescritos para o Nogueira-de-Almeida
tante de pressão arterial em paciente sob- risco
7 dedenovembro
evolução de 2018
tratamento da hipertensão crônica. Crianças com hiper- para lesão progressiva de órgãos-alvo, mas sem evidência
Doença Hepática Gordurosa Não Alcoólica
• low energy-dense diet
• diet low in sugar (particularly fructose)
• Diet low in fat
• Diet high in fibre
• Low glycaemic index diet
• Significant quantity of fruit and vegetables
• Addition of ω-3 polyunsaturated fatty acids (found in ‘oily’ fish)
• Simply eating breakfast is known to help achieve a healthy metabolic state
Mann JP, Goonetilleke R,

McKiernan P. Arch Dis Child 2015 doi:10.1136/ archdischild-2014-307985
125
Menina, 11 anos, escore z de IMC +2,4 trazida à consulta para seguimento

de obesidade. Já em tratamento tradicional há 1 ano de obesidade com
Caso Clínico 6
dislipidemia e hipertensão.
Ao exame apresentou PA de 162/96
Na reavaliação laboratorial, observou-se
• LDL de 192 mg/dL
• TGP (ALT) de 49 U/L e TGO (AST) de 43 (índice AST/ALT = 0,88)
• Insulinemia de 19
• Manter programa de emagrecimento (dieta + atividade física)
• Iniciar medicação anti-hipertensiva ou referir ao cardiologista
• Iniciar sinvastativa 10 mg/dia por 3 meses
• Iniciar metformina 500 mg por dia
• Enriquecer dieta com fibras, frutas, verduras, legumes, fibras e ômega 3
• Reavaliação laboratorial em 3 meses
126
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
127
Menina de 9 anos, escore z de IMC elevado (+2,1), obesidade

Caso Clínico 7
predominantemente abdominal, acantose nigicans em pescoço e axilas.
Segundo a mãe, veio por insistência do pediatra, já que não concorda que
a criança precise de um nutrólogo. Refere já ter feito exame de sangue

apenas uma vez, um “hemograma completo”, que estava normal. Sobre a
alimentação, diz que a família tem uma rotina alimentar muito saudável. A
criança sempre comeu uma dieta bem equilibrada, pelo menos em casa,
Que aspectos
mas não garante o mesmo na casa dos coleguinhas, junto aos avós e na
escola. A criança não faz esporte mas “não para um minuto, correndo o dia psicossociais
todo”. Os pais são saudáveis e magros, assim como o irmão mais velho
(que é atleta), por isso na família não há a preocupação com restrição relevantes você
quanto à aquisição de qualquer alimento, sendo a dispensa cheia sempre.
vê nesse caso e
Como trabalham muito, os pais dedicam pouco tempo para levar a criança
para atividades físicas programadas e, nos raros momentos de folga, como conduziria
costumam sair para jantar. A família tem um orçamento folgado, sem
o tratamento ?
restrições financeiras. Os pais acreditam que, com essa idade, a filha já
tem condições de se responsabilizar pela alimentação, de modo que evitam
colocar regras e limites para não serem opressores.
128
Aspectos psicossociais relevantes para o
tratamento da obesidade e papel da família
• Ajudar a família a reconhecer a obesidade (gráficos, tabelas, etc)
• Obesidade como doença
• Comorbidades
• Leitura realista da situação
• Preparação do núcleo familiar para o tratamento
• Divisão de responsabilidades
• Orçamento
• Responsabilidade da criança
• Limite
• Hábito alimentar dos coabitantes
• Atividade física
• Gerenciamento das atividades fora de casa
• Tolerância
De Almeida CCJN & Nogueira-de-Almeida CA.
• Dias de exceção Acompanhamento psicológico da criança obesa.
In: Nutrição em Pediatria, 2a. ed, Manole: 2017
129
Situações de risco
• Mãe ansiosa e bebê voraz
• Pais negligentes
• Competição
• Simbiose
• Culpa por ausência
• Sistemas familiares obesogênicos
De Almeida CCJN - Aspectos psicossociais da obesidade.

E-book Obesidade SBP 2019 - in press
130
Journal of Tropical Pediatrics, 2017, 0, 1–4
doi: 10.1093/tropej/fmx027
Case report
CASE REPORT
Obesity as a Presentation of Munchausen

Syndrome by Proxy
by Carlos Alberto Nogueira-de-Almeida,
Carla Cristina J. N. de Almeida, Nat!alia Inocêncio Pereira,
Nilton Antonio de Souza Filho, and Valmir Aparecido de Oliveira
University of Ribeir~ao Preto, S~ao Paulo 14027-150, Brazil
Correspondence: Carlos Alberto Nogueira-de-Almeida, University of Ribeir~ao Preto, Rua Eugênio Ferrante, 170, Jd. Nova Aliança Sul, Ribeir~ao
Preto, S~ao Paulo 14027-150, Brazil. Tel: þ55 16 992217498; E-mail <dr.nogueira@me.com>
ABSTRACT
Objective: To describe a case of an obese child whose weight gain was related to the Munchausen
Syndrome by proxy (MSP).
Methods: This is a case report including information regarding the child’s clinical history and the
Carlos Alberto Nogueira-de-Almeida – www.clincanutre.com
mother’s behavior. The common features of the syndrome are confronted with the description of
the case, seeking to demonstrate the similarities. 131
Results: The description ratifies the diagnosis based on the signs and symptoms presented by the
child (<5 years old, frequent contacts with health system, symptoms witnessed only by the mother,
➡ Introdução
confusing findings, not helped by treatments, emotionally distant father) and the attitude of the
mother (concerned, interested in procedures, comfortable in the medical setting, higher medical
➡ epidemiologia
knowledge, hostile when thwarted). ➡ etiopatogenia
Conclusion: The case presented points to a new etiology, the MSP, to be considered within the set
➡ Consequências
of factors currently known to cause and maintain obesity in childhood.para a saúde
K E Y W O R D S : obesity, Munchausen syndrome by proxy, child, victimization, child abuse
➡ definição
➡ classificação
INTRODUCTION and this leads professionals to seek unusual explana-
Obesity is a great challenge for pediatricians owing tions. The treatment usually depends on a good
to its high prevalence and difficulties in the definition diagnosis, which
➡ história may be challenging, as new etiologi-
clínica
of causal factors. It is a disease that originates from a cal possibilities
➡ exame físico arise every day e[5].
(antropometria composição corporal)
Roteiro
combination of genetic and environmental factors
[1] and metabolic programming may influence the
phenotypic expression [2]. Although the increase in
fat storage is owing to positive energy balance [3],
First described in
1977, Munchausen Syndrome
by proxy (MSP) is a psychiatric disorder listed in the
➡ Diagnóstico das principais comorbidades
DSM V as Factious Disorder Imposed on Another
[6].➡ Itpsicossociais
appears when someone intentionally causes
sometimes the clinical history does not show an symptoms on another person, who will then be con-
excess of food intake or a sedentary behavior [4], sidered sick [7]. A lot of specific clinical findings
➡ outras
➡ Tratamento
V ➡ nutricional
C The Author [2017]. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com " 1
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
132
133
134
135
136
137
138
Tracking
• Seguir pela curva

– Objetivo: atingir o escore z alvo ou a composição
corporal adequada
• Readequar o plano a cada 4-6 meses
• Atenção ao crescimento físico
• Atenção às deficiências
• Re-avaliação de parâmetros laboratoriais
• Fase de manutenção
139
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
140
Classificação
Controvérsias Aleitamento
materno
Farmaco-
terapia Prevenção
Obesidade
Microbiota Infantil causas
Atividade física Consequências
Tratamento Cognição e SNC
141
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
142
Nogueira-de-Almeida et al, 2018, Medicina (Ribeirão Preto, Online) 2018; 51(2)
143
144
Wiklund P, Törmäkangas T, Shi Y, Wu N, Vainionpää A, Alen M, Cheng S. Normal-weight obesity
and cardiometabolic risk: A 7-year longitudinal study in girls from prepuberty to early
adulthood. Obesity (Silver Spring). 2017 Jun;25(6):1077-1082
Excesso de adiposidade
corporal – e não de peso –
leva a maiores riscos
cardiometabólicos.
145
146
Yoon DY, Lee YA, Lee J, Kim JH, Shin CH, Yang SW. Prevalence and Clinical Characteristics of Metabolically Healthy
Obesity in Korean Children and Adolescents: Data from the Korea National Health and Nutrition Examination
Survey. J Korean Med Sci. 2017 Nov;32(11):1840-1847
Estudo coreano mostrando que 68,8% dos adolescentes

obesos, com idades entre 10 e 19 anos, apresentam resistência
insulínica (HOMA-IR > percentil 95).
147
Scinta W, Bayes H, Smith N. Insulin Resistance and Hunger in Childhood Obesity: A

Patient and Physician's Perspective. Adv Ther. 2017 Oct;34(10):2386-2391
Resistência insulínica provoca fome e o uso

de metformina reduz a fome
148
Ubiña-Aznar E, Tapia-Ceballos L, Rosales-Zabal JM, Porcel-Chacón R, Poveda-Gómez F, Lozano-Calero C, Ortiz-
Cuevas C, Rivas-Ruiz F, Sánchez Cantos A, Navarro Jarabo JM. Insulin resistance and the metabolic syndrome are
related to the severity of steatosis in the pediatric population with obesity. Rev Esp Enferm Dig. 2017 Nov;109(11):
772-777
A presença de resistência insulínica é fator de risco para DHGNA

e o valor de corte de HOMA > 4,9 pode ser usado como
indicador da presença desse quadro.
149
Thota P, Perez-Lopez FR, Benites-Zapata VA, Pasupuleti V, Hernandez AV. Obesity-related

insulin resistance in adolescents: a systematic review and meta-analysis of observational
studies. Gynecol Endocrinol. 2017 Mar;33(3):179-184
Hiperinsulinismo é extremamente frequente

entre crianças obesas
150
Dalla Valle M, Laatikainen T, Lehikoinen M, Nykänen P, Jääskeläinen J. Paediatric obesity
treatment had better outcomes when children were younger, well motivated and did not have
acanthosis nigricans. Acta Paediatr. 2017 Nov;106(11):1842-1850
Crianças obesas com acantose nigricans

respondem pior ao tratamento de
obesidade
151
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
152
Total (%) 22.4 22.5 16.9 0.039
Girls (%) 24.4 24.6 11.5 0.122
Boys (%) 20.1 20.1 21.2 0.862
Obesity (IMC ≥ p95)
Total (%) 15.9 15.9 18.6 0.039
Girls (%) 13.1 13.0 0.724 15.4
Oyarzún MF, Barja S, Domínguez MA, Villarroel L, Arnaiz P, Mardones F.
[Breastfeeding, obesity and metabolic syndrome at school age]. Rev Chil Pediatr. 0.751
Boys (%) 19.1 19.0 21.2
2018
*p < 0.05 (Pearson Chi-squared test). Apr;89(2):173-181
Differences between children that were breastfed (BF) and non-breastfed (non-BF).
Prevalência de obesidade maior entre crianças

não amamentadas e a duração do aleitamento
correlacionou-se a menor risco de obesidade e
complicações metabólicas.
Figure 1. Prevalences of cardio-
vascular risk factors and Metabolic
Syndrome, according to the breast-
feeding (BF) antecedent. GLI: Glyce-
mia ≥ 100 mg/dL; TG: Triglycerides
≥ 110 mg/dL; HDL: Cholesterol HDL
≤ 40 (mg/dL); WC: Waist circumfe-
rence ≥ percentile 90; BP: Blood
pressure (systolic or diastolic) ≥ 90th
percentile; CT: Total cholesterol
≥ 200 mg/dL; LDL-C: LDL choleste-
rol > 130 mg/dL; IR: insulin resistan-
ce ≥ 90th percentile; MS: Metabolic
Syndrome. Sin differences significa-
tive entre ambos groups. Pearson
Chi squared test (P > 0.05).
176 Prof. Dr. Carlos Alberto Nogueira de Almeida
153
Badillo-Suárez PA, Rodríguez-Cruz M, Nieves-Morales X. Impact of Metabolic Hormones

Secreted in Human Breast Milk on Nutritional Programming in Childhood Obesity. J
Mammary Gland BiolJ Mammary
Neoplasia. 2017 Sep;22(3):171-191
Gland Biol Neoplasia
Hormônios como leptina, insulina,

grelina, adiponectina, resistina,
obestatina, IGF1, apelina, nefastina,
entre outros, tem sido detectados no
leite humano e podem ajudar a explicar
o efeito protetor contra a obesidade na
medida em que participam do controle
de fome, saciedade e homeostase
energética.
Fig. 1 Hypothesis explaining how the maternal metabolic status may decrease during pregnancy of mothers with different nutritional
alter infant metabolism, leading to weight gain and increasing the risk conditions are shown in red, whereas events that are favored or

of obesity in childhood and adulthood. These alterations may be related increased are shown in blue. Finally, parameters that are maintained as
with appetite deregulation. Hormones and physiological parameters that normal are shown in green
154
TGF-β2-RIII in milk samples from a Sumatran orangutan may override hormonal signals in milk. Infants and toddlers
(Pongo abelii) and from a gorilla (Gorilla gorilla) are modi- living in Nubri (high pressure) likely have less energy avail-
fied during lactation, for instance; adiponectin, EGF, and able for growth given high infectious disease burdens and
TGF-β2 concentration in the milk sample declined with infant thermal stress, and consequently, these factors hide associa-
Wang L, Collins C, Ratliff M, Xie B, Wang Y. Breastfeeding Reduces
Childhood Obesity Risks. Child Obes. 2017 Jun;13(3):197-204
Aleitamento materno no primeiro mês e aleitamento por

mais de 6 meses protegem contra obesidade em estudo
longitudinal de seguimento até os 12 anos de idade
155
Uwaezuoke et al. Relationship Between Exclusive Breastfeeding and Lower Risk of

Childhood Obesity: A Narrative Review of Published Evidence.
Clin Med Insights Pediatr. 2017
et al Uwaezuoke et al 5
Redução de risco de obesidade em diversos estudos

Tablebreastfeeding
s reporting causality between exclusive 1. Studies reporting
and lower risk of childhood
causality obesity. breastfeeding and lower risk of childhood obesity.
between exclusive
AR), COUNTRY OF AUTHORS (YEAR),

STUDY DESIGN OBESITYCOUNTRY OF
RISK REDUCTIONSTUDY DESIGN OBESITY
ODDS RISK
RATIO REDUCTION
(95% CONFIDENCE OD
ORIGIN INTERVAL [CI]) INT
014),29 China Zheng et al13%

Longitudinal (2014), 29 China
(breastfeeding Longitudinal
duration: 3–5 months) 13%(0.77–0.99)
0.87 (breastfeeding duration: 3–5 months) 0.8
27% (breastfeeding duration: ⩾6 months) (breastfeeding duration: ⩾6 months)
27%(0.56–0.95)
0.73 0.7
l (2013),19 USA Anderson et

Cross-sectional al (2013),
Not 19 USA
provided Cross-sectional Not(CI:
0.79 provided
0.69–0.91)a 0.7
(breastfeeding duration: ⩾6 months) (breastfeeding duration: ⩾6 months)
d Reilly (2002),20 UK Armstrong Not

Cross-sectional and provided
Reilly (2002),20 UK Cross-sectional Not(0.61–0.80)
0.70 provided b 0.7
07),73 Brazil and SystematicHorta et al (2007),

review/ 73 Brazil and
Not provided Systematic review/ 0.78
Not(0.72–0.84)
provided 0.7
Switzerland
meta-analysis meta-analysis
4),75 China Yan et al (2014),

Meta-analysis 75 China
Not provided Meta-analysis Not(0.74–0.81)
0.78 provided 0.7
005),76 UK SystematicOwen
reviewet al Not
(2005),76 UK
provided Systematic review Not(0.33–0.55)
0.43 provided c 0.4
0.88 (0.85–0.90)d 0.8
2005),74 Germany Harder et al4%

Meta-analysis (2005),74 Germany
(breastfeeding duration:Meta-analysis
1–3 months) 4% (0.74–0.88)
0.81 (breastfeeding duration: 1–3 months) 0.8
aAdjusted for child’s race/ethnicity, maternal age, maternal smoking, and child’s birth weight.
d’s race/ethnicity, maternal age, maternal smoking, and child’s birth weight.
Prof. Dr.status,
bAdjusted for socioeconomic Carlosbirth
Alberto Nogueira
weight, de Almeida
and sex.
oeconomic status, birth weight, and sex.
cSmall sample size (n < 500).
ze (n < 500).
dLarge sample size (n ⩾ 500). 156
ze (n ⩾ 500).
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
157
Pietrobelli A, Agosti M; MeNu Group. Nutrition in the First 1000 Days: Ten Practices to Minimize
Obesity Emerging from Published Science. Int J Environ Res Public Health. 2017 Dec 1;14(12)
1. Envolvimento do pai e da mãe

2. Monitorização da gestação
3. Aleitamento materno
4. Alimentação complementar entre 4 e 6 meses e não uso de leite de vaca
antes do primeiro ano
5. Exposição precoce a frutas e vegetais e não uso de sal, açúcar e sucos
6. Respeito ao apetite da criança evitando alimentação coercitiva
7. Cuidado com excesso de proteína animal
8. Oferta adequada de ácidos graxos essenciais
9. Pais como modelo
10. Atividade física e sono adequados
158
Pacheco LS, Blanco E, Burrows R, Reyes M, Lozoff B, Gahagan S. Early Onset Obesity
and Risk of Metabolic Syndrome Among Chilean Adolescents. Prev Chronic Dis. 2017
Oct 12;14:E93
Coorte chilena:
Início precoce de obesidade (5 anos de idade) eleva muito o
risco de obesidade e síndrome metabólica aos 17 anos de
idade
159
Chen G, Chiang WL, Shu BC, Guo YL, Chiou ST, Chiang TL. Associations of caesarean delivery and
the occurrence of neurodevelopmental disorders, asthma or obesity in childhood based on
Taiwan birth cohort study. BMJ Open. 2017 Sep 27;7(9):e017086
Coorte chinesa envolvendo 24.200 nascimentos:

Associação robusta entre nascimento por cesariana e
obesidade aos 5 anos de idade
160
Genoni G, Menegon V, Secco GG, Sonzini M, Martelli M, Castagno M, Ricotti R, Monzani A, Aronici M, Grossini E, Di
Mario C, Bona G, Bellone S, Prodam F. Insulin resistance, serum uric acid and metabolic syndrome are linked to
cardiovascular dysfunction in pediatric obesity. Int J Cardiol. 2017 Dec 15;249:366-371
Ácido úrico como marcador de disfunção

cardiovascular (espessamento de VE e de íntima
da carótida) entre crianças obesas
161
Leonard SA, Rasmussen KM, King JC, Abrams B. Trajectories of maternal weight from
before pregnancy through postpartum and associations with childhood obesity. Am J
Clin Nutr. 2017 Nov;106(5):1295-1301
Obesidade no período fértil da mulher leva a maior

risco de obesidade dos futuros filhos, incluindo
períodos:
➢ pré-concepcional
➢ Gestacional
➢ manutenção pós gravídica de excesso de peso
162
Oostvogels AJJM, Hof MHP, Gademan MGJ, Roseboom TJ, Stronks K, Vrijkotte TGM. Does
maternal pre-pregnancy overweight or obesity influence offspring's growth patterns from birth
up to 7years? The ABCD-study. Early Hum Dev. 2017 Oct;113:62-70
Obesidade da mãe antes de engravidar

eleva a velocidade de ganho de peso e
o IMC da criança em estudo de 7 anos
de seguimento
t and obese mothers. Prof. Dr. Carlos Alberto Nogueira de Almeida

ng, hypertension and diabetes during pregnancy and gestational age at birth. Growth
ns and their 95% confidence intervals can be found online Supplementary163Table 3.
d not study growth patterns per parental BMI group [6–8,28]. Al-
Paz Levy D, Sheiner E, Wainstock T, Sergienko R, Landau D, Walfisch A. Evidence that children
ough these studies found
born atan effect
early of(37-38
term maternal BMI onare
6/7 weeks) weight and/orrisk for diabetes and obesity-related
at increased
MI of the child, no effect on height was shown [6,7], or studied [8,28].
disorders. Am J Obstet Gynecol. 2017 Nov;217(5):588.e1-588.e11
Growth is an interplay of genetic and environmental factors [29]. In
search OBSTETRICS
in studies, variability in weight and height at birth up to age 12 years ajog.org
Coorte israelense envolvendo 225.260
s the and
Weibull
offspringpara-
weight
FIGURE partos:
of mothers with overweight and obesity. Scores were adjusted for
model of gestational
g pregnancy, long-termage at birth. Bold values are significant different (p < 0.05)
Survival curves of hospitalization incidence according to gestational age
tabolic morbidity in Parto que ocorre no limite inferior do
age of 18 years) ac-
nal age at birth. Thetermo (< 39 semanas) eleva risco de
Girls
or maternal clusters Weight

Height obesidade aos 18 BMI anos.
, hypertensive disor-
Maternal
, maternal Maternal
diabetes, Maternal Maternal Maternal Maternal
verweight obesity overweight obesity overweight obesity
ncy obesity, −0.03
− 0.01
smoking, 0.06 0.15 0.14 0.25
tion
.01 of labor,0.13
mode of 0.14 0.35 0.16 0.29
cesarean),
.03 SGA,
0.23 and a 0.17 0.42 0.18 0.33
0.24 term 0.19
.06 score. Early
ar 0.39 0.23 0.42
.09 0.34 0.26 0.57 0.29 0.52
a significant and in-
.11 0.39 0.31 0.69 0.33 0.6
tion
.13
with long-term
0.43 0.36 0.71 0.38 0.69
etabolic
.14 morbidities,
0.53 0.39 0.91 0.44 0.78
azard
.15 ratio 0.66
(aHR) of 0.39 1.21 0.48 0.87
e1.34), and more so A, Total endocrine and metabolic
Prof. Dr. hospitalizations in children
Carlos Alberto Nogueira deaccording
Almeida to gestational age at birth (for
HR, 1.30; 95% CI, early term group: mean survival, 17.93 years; 95% confidence interval [CI], 17.92e17.94; for full-
term group: mean survival, 17.956 years;164 95% CI, 17.95e17.96; log rank P < .001). B, Over-
remained unchanged
weight- and obesity-related hospitalizations in children according to gestational age at- birth
Nogueira-de-Almeida 7 de(for early de 2018
novembro
icity as a potential
Kim J, Lee I, Lim S. Overweight or obesity in children aged 0 to 6 and the risk of adult
metabolic syndrome: A systematic review and meta-analysis. J Clin Nurs. 2017 Dec;
26(23-24):3869-3880
Revisão sistemática com metanálise

demonstrando que o início da obesidade nos
primeiros 2 anos de vida está correlacionado com
obesidade e síndrome metabólica na adultícia
165
Oelsner KT, Guo Y, To SB, Non AL, Barkin SL. Maternal BMI as a predictor of methylation
of obesity-related genes in saliva samples from preschool-age Hispanic children at-risk
for obesity. BMC Genomics. 2017 Jan 9;18(1):57
IMC materno elevado leva a metilação de genes

ligados à obesidade na criança.
166
Singer K, Lumeng CN. The initiation of metabolic inflammation in
childhood obesity. J Clin Invest. 2017 Jan 3;127(1):65-73
Processo inflamatório ligado à obesidade inicia-se na infância
The Journal of Clinical Investigation R E V I E W S E R I E S : M E TA B O L I S M A N D I N F L A M M AT
increase in ATM infiltration and ampl

tion of immune responses associated
hypomethylation in innate pattern rec
tion genes such as Tlr1 and Tlr2 (36).
The clinical evidence that ob
during pregnancy can lead to proin
matory activation in the fetus is some
sparse (37). In obese mothers, plac
inflammatory macrophages are incre
and produce proinflammatory cytok
although fetal blood leukocytes do
appear to be altered (38, 39). Mat
obesity and overweight status are
Figure 2. A developmental framework for theDr.
Prof. initiation
CarlosofAlberto
metainflammation.
Nogueira deThroughout
Almeida the life- risk factors for increased serum in
course there are multiple initiating events that can lead to the expansion of adipose tissue and sys- matory markers in preterm infants
temic chronic inflammation. These include programmed inheritance 167 (orange), environmental factors not in term newborns (40). After ad
(green), intrinsic growth rates of the child (red), and adipose tissue metabolic impairments (purple).
ing for childhood BMI, C-reactive pr
(CRP) levels were increased in 12-
Lind MV, Larnkjær A, Mølgaard C, Michaelsen KF. Dietary protein intake old andchildren
qualityborn in to mothers with h
earlyand
In mice life: impact
humans, on growth
qualitative and obesity.
and quantitative changes Curr Opin Clin
in ATMs Nutr Metab
pre-pregnancy BMIs,Care. 2017 that
suggesting Jan;maternal obesity may
occur in obesity that are mediated by proliferation 20(1):71-76
and leukocyte the immune system in the long term (41).
trafficking from the circulation (20, 21). Events that precede and In terms of inflammation and disease risk, low birth w
may amplify ATM recruitment include the activation of convention- (LBW) is a well-documented and strong risk factor for meta
al CD4+ T cells and the accumulation of adipose tissue neutrophils disease — a concept encompassed in the Barker hypothesis
Excesso de consumo de proteína nos
(22–24). Recruited ATMs prominently express the marker CD11c in ing poor in utero growth to CVD and diabetes (42–44). In rod
mice and
dois home to crown-like
primeiros anosstructures
de vida (CLSs), whichde
é fator form around intrauterine growth
Dietary restriction
protein intake in (IUGR) is associated
early life and obesitywith
risk incre
Lind
dead or dying adipocytes and are a recognized sign of adipose tissue inflammatory markers in the circulation of the offspring (45
dysfunction in many contexts (25,
risco para obesidade futura26). ATMs assume phenotypic Proposed mechanisms for this effect include alterations in th
High protein intake
changes characterized by lysosomal activation and the formation of cadian clock and downregulation of Pparg and Ppara with I
a metabolically activated phenotype distinct from classical (M1) or (48). Longitudinal studies such as the Bogalusa Heart Study
alternative (M2) activation (13, 27). Adaptive immunity is Highalso trig-
intake of show that LBW induces chronic elevations in wbc counts
High intake of
gered by chronic inflammation via the function of ATMs BCAA and adi- inflammatory biomarkers methionine
such as CRP in childhood (49, 50).
pose tissue dendritic cells as antigen-presenting cells (28, 29). This ilar to LBW, high birth weight is associated with increased
promotes Th1 immunity in adipose tissue by stimulating conven- visceral adiposity and insulin resistance; however, the evid
tional T cell activation at the expense of Tregs (24,and 30).
Increased IGF-1
insulin that this
andoccurs
increase in association
Satiety of BCAA
degradation with elevated levels of inflamm
Alterations of methyl donor
metabolism and epigenetic
secretion
biomarkers such as CRP isprocesses
in acylcarnitines
not strongly supported (51, 52). T
When does metainflammation begin? findings suggest that for some children the initiating even
The increase in obesity prevalence at all ages suggests Growth metainflammation
that the Excessive may occur in the postnatal setting and less
Lower b-oxidation
stimulation
initiating events for metainflammation may occur in the earliest
through mammalian the prenatal environment.
adipogenesis
target of rapamycin
developmental stages. This concept is emphasized in the devel- Perinatal/infancy period. The transition from the intra
opmental origins of health and disease paradigm, which postu- ine to the extrauterine environment during the perinatal p
Increased risk of obesity development
lates that prenatal and perinatal factors influence adult diseas- is characterized by intense remodeling of both metabolic p
es such as diabetes and obesity via epigenetic and physiologic ology and the immune system. These two processes interse
FIGURE 1. Current hypotheses on how high-protein intake in childhood might increase obesity risk. The figure
programming (31). There is evidence
constructed based ontocurrent
Prof. support
Dr. Carlos the induction
Alberto
hypothesis of de
Nogueira
[1,19 &
,20,25 places
Almeida
,26,27].
& like the gut where the establishment of the intestinal m
metainflammation in all developmental stages, with the poten- biome after birth is coupled to the development of the imm
tial for life-long consequences
protein contenton metabolic
of the diet regulation
with. as wellit besystem
168Should pre- that is permissivea towards
Furthermore, colonization in of
better understanding early
thelifem
as immune responses to non-metabolic
ferred to include more stimulifat,(Figure 2). These
especially The
long chain immune
Nogueira-de-Almeida
anismssystem in infants
involved - 7anddeisnovembro
immature
which and over time
de 2018
population group tr
unsaturated fat or should the focus be on providing especially vulnerable to high-protein intak
Rayfield S, Plugge E. Systematic review and meta-analysis of the association between
maternal smoking in pregnancy and childhood overweight and obesity. J Epidemiol
Community Health. 2017 Feb;71(2):162-173
Revisão sistemática com

Figure 2 Pooled unadjusted OR for maternal prenatal smoking and childhood overweight.
metanálise:
Mães que fumam antes de
engravidarem elevam risco de
obesidade nos futuros filhos
Figure 3 Pooled adjusted OR for maternal prenatal smoking and childhood overweight.
This systematic review highlights maternal smoking in and a smoke-free environment for all will be an important part
pregnancy as an important factor contributing toward the of this. 169
childhood obesity pandemic. This reinforces the need for In conclusion, this systematic review has confirmed evidence for
ongoing public health interventions regarding smoking an association between maternal smoking in pregnancy
cessation in all countries, particularly focusing on women of and childhood overweight and obesity. This knowledge is relevant
child bearing age. The pathway to childhood overweight is to all from policymakers to those healthcare professionals in
multifactorial, but also largely preventable. Estimates show that regular contact with women of child bearing age. Smoking cessa-
40% of childhood obesity could be prevented through a com-
Classificação
tion is of benefit to the long-term health of the mother, it benefits
bination of healthy eating promotion, active living and the ces- the growing fetus during pregnancy and now this study confirms
sation of smoking during pregnancy.23 Prevention of childhood evidence of benefit to her offspring’s future health and well-being
through removing this increased risk of overweight.Aleitamento
Controvérsias
obesity should start at the earliest possible stage of development
Rayfield S, Plugge E. J Epidemiol Community Health 2017;71:162–173. doi:10.1136/jech-2016-207376

materno
171
Farmaco-
terapia Prevenção
Obesidade
170
Forejt M, Brázdová ZD, Novák J, Zlámal F, Forbelská M, Bienert P, Mořkovská P, Zavřelová M, Pohořalá A, Jurášková
M, Salah N, Bienertová-Vašků J. Higher Energy Intake Variability as Predisposition to Obesity: Novel Approach Using
Interquartile Range. Cent Eur J Public Health. 2017 Dec;25(4):321-325
Variabilidade elevada no
consumo calórico das
refeições principais eleva
risco de obesidade
171
Foucan L, Larifla L, Durand E, Rambhojan C, Armand C, Michel CT, Billy R, Dhennin V, De Graeve F, Rabearivelo I,
Sand O, Lacorte JM, Froguel P, Bonnefond A. High Prevalence of Rare Monogenic Forms of Obesity in Obese
Guadeloupean Afro-Caribbean Children. J Clin Endocrinol Metab. 2018 Feb 1;103(2):539-545
15% de prevalência de
obesidade monogênica em
população específica
(descendentes afro-
caribenhos) de Gaudalupe
172
Kowal M, Matusik S, Pilecki MW, Kryst Ł, Sobiecki J, Woronkowicz A. Overweight and
obesity risk factors in children aged 3-7 years: a prospective study in the city of Kraków.
Ann Hum Biol. 2017 Dec;44(8):693-703
Fatores causais identificados em estudo

prospectivo de Krakov:
✓ Peso ao nascer elevado
✓ Aleitamento materno muito prolongado
✓ Consumo de álcool pela mãe
✓ Baixa escolaridade materna
✓ Baixa idade materna
✓ IMC paterno elevado
173
Bharati S, Pal M, Shome S, Roy P, Dhara P, Bharati P. Influence of socio-economic

status and television watching on childhood obesity in Kolkata. Homo. 2017 Dec;
68(6):487-494
Amostra de 5.216 crianças de Calcutá.

Associação positiva entre obesidade e:
✓ tempo de TV
✓ consumo de fast-food
174
Li M, Xue H, Wang W, Wen M, Wang Y. Increased obesity risks for being an only child
in China: findings from a nationally representative study of 19,487 children. Public
Health. 2017 Dec;153:44-51
Filho único com 36% mais

chance de apresentar
sobrepeso e 43% mais chance
de ser obeso
175
Felső R, Lohner S, Hollódy K, Erhardt É, Molnár D. Relationship between sleep duration

and childhood obesity: Systematic review including the potential underlying
mechanisms. Nutr Metab Cardiovasc Dis. 2017 Sep;27(9):751-761
Revisão sistemática com metanálise.

Sono de curta duração eleva risco de obesidade através de aumento do sedentarismo, do
desenvolvimento de resistência insulínica e da piora da qualidade da dieta.
176
Ács O, Péterfia B, Hollósi P, Luczay A, Török D, Szabó A. Methylation Status of
CYP27B1 and IGF2 Correlate to BMI SDS in Children with Obesity. Obes Facts.
2017;10(4):353-362
Taxa de obesidade mostra correlação

com metilação do DNA:
Hipometilação dos genes do IGF2 e
hipermetilação do CYP27B1 podem influenciar
positivamente a taxa de IMC observada em
crianças obesas
177
Ouyang S, Tang R, Liu Z, Ma F, Li Y, Wu J. Characterization and predicted role of

microRNA expression profiles associated with early childhood obesity. Mol Med Rep.
2017 Oct;16(4):3799-3806
Metilação dos miRNA levando a desregulação

da atividade e obesidade de surgimento
precoce em crianças
178
Zhang MX, Cheng H, Zhao XY, Wu LJ, Yan YK, Mi J. [Effect of genetic polymorphisms
on change in body mass index and obesity status during childhood]. Zhonghua Yu
Fang Yi Xue Za Zhi. 2017 Jul 6;51(7):635-641
Polimorfismos em genes ligados à

obesidade são capazes de prever o maior
risco de a criança se tornar obesa. Quanto
mais alelos de risco, maior a
susceptibilidade.
179
Peacock-Chambers E, Radesky JS, Parker SE, Zuckerman B, Lumeng JC, Silverstein M.

Infant Regulatory Problems and Obesity in Early Childhood. Acad Pediatr. 2017 Jul;
17(5):523-528
Dados relativos a 5.750 crianças estudadas.

Dificuldades nas capacidades regulatórias aos 9
meses de idade associam-se a elevado risco de
obesidade na idade pré-escolar.
180
Song QY, Song JY, Wang Y, Wang S, Yang YD, Meng XR, Ma J, Wang HJ, Wang Y. Association Study of Three Gene
Polymorphisms Recently Identified by a Genome-Wide Association Study with Obesity-Related Phenotypes in
Chinese Children. Obes Facts. 2017;10(3):179-190
Primeira demonstração de novo

polimorfismo (SNP) ligado ao fenótipo de
obesidade: rs564343
181
Sakamoto N, Gozal D, Smith DL, Yang L, Morimoto N, Wada H, Maruyama K, Ikeda A, Suzuki Y, Nakayama M,
Horiguchi I, Tanigawa T. Sleep Duration, Snoring Prevalence, Obesity, and Behavioral Problems in a Large Cohort of
Primary School Students in Japan. Sleep. 2017 Mar 1;40(3)
✓ Pouco sono leva a obesidade

✓ Obesidade eleva risco de distúrbios do
sono
✓ Ambos estão relacionados a problemas
comportamentais na escola
182
Turel O, Romashkin A, Morrison KM. A model linking video gaming, sleep quality,
sweet drinks consumption and obesity among children and youth. Clin Obes. 2017
Aug;7(4):191-198
Uso de videogame por 4 horas antes de ir para cama,

associado a uso de bebidas adoçadas durante o jogo e
posterior má qualidade de sono:
Associação com adiposidade abdominal
183
Petrov ME, Vander Wyst KB, Whisner CM, Jeong M, Denniston M, Moramarco MW, Gallagher MR, Reifsnider E.
Relationship of Sleep Duration and Regularity with Dietary Intake Among Preschool-Aged Children with Obesity
from Low-Income Families. J Dev Behav Pediatr. 2017 Feb/Mar;38(2):120-128
Entre famílias de baixa renda americanas

(Texas):
Menos horas de sono associadas a aumento
da gordura corporal.
Consumo reduzido de carboidratos e
aumentados de gorduras e proteínas.
184
Li L, Zhang S, Huang Y, Chen K. Sleep duration and obesity in children: A systematic
review and meta-analysis of prospective cohort studies. J Paediatr Child Health. 2017
Apr;53(4):378-385
Sleep duration and obesity

metanálise:
Pouca duração do sono
relacionada a obesidade.
Fig. 2 Forest plot of the associa

sleep duration and risk of obesi
The pooled relative risk (RR) based
was (RR: 1.45; 95% confidence
P = 0.003), and the heterogeneit
cant (I2 = 94.6%, P < 0.001). †Sho
of age-specific sleep recommenda
after screening the titles and abstracts. Then, we assessed them in 44 200 children (15 cohorts from 12 studies) w
more detail and obtained 34 relevant studies that met our inclu- the final analysis.19,20,22–31 Among the studies,
sion criteria. However, two reports were excluded because of ducted in the USA, and the other studies we
duplicate publication using the same study population. Therefore, Australia, Canada and the UK. The follow-up
Prof. Dr. Carlos Alberto Nogueira deincluded
32 studies were Almeidain our analysis (12 studies with 15 cohorts from 2 years to 15 years; most studies used q
related to risk of obesity and 24 studies related to BMI). assess sleep duration, three studies used sleep d
185 one cohort used polysomnograms.27 Height a
Meta-analysis results of the association between
measured using standard methods in most stu
sleep duration and obesity
studies that used self-reporting.25,26 Different stan
Table 1 summarises the characteristics of included studies regard- to define short or long sleep duration due to
Kenney EL, Gortmaker SL. United States Adolescents' Television, Computer, Videogame,
ing the association between sleep duration and obesity. A total of changes in sleep needs. The definition of obes
Smartphone, and Tablet Use: Associations with Sugary Drinks, Sleep, Physical Activity,
and Obesity. J Pediatr. 2017 Mar;182:144-149
Table 2 Meta-analysis of the association between sleep curtailment and obesity among children by subgroups
Subgroup No. of studies RR (95% CI) Pz I2 (%)

Amostra nacional representativa americana, envolvendo 24.800
Age
adolescentes. Pre-schoolers
Primary-schoolers
8
3
1.30 (1.17–1.44)
1.40 (1.09–1.81)
<0.001
0.009
22.7
35.0
Adolescents 2 1.27 (1.07–1.50) 0.006 0.0
Associação forte entre uso de smartfones, tablets, computadores e
Region
USA 9 1.27 (1.16–1.40) <0.001 13.5
videogames com obesidade. Others
Sample size
4 1.44 (1.19–1.74) <0.001 0.0
<5000 10 1.30 (1.17–1.44) <0.001 24.0

Dados explicativos: aumento no consumo de bebidas adoçadas,
3 curta
1.31 (1.14–1.52)
≥5000 <0.001 0.0
Sleep period
duração de sono e sedentarismo. 24 h 2 1.43 (1.01–2.02) 0.05 39.7
Per night 11 1.30 (1.19–1.41) <0.001 7.6
Years of follow-up
<5 5 1.53 (1.26–1.84) <0.001 0.0
≥5 8 1.25 (1.14–1.38) <0.001 0.0
Quality†
<6 2 1.14 (0.91–1.43) 0.25 0.0
≥6 11 1.33 (1.22–1.46) <0.001 3.8
†Scores of Newcastle-Ottawa Scale13 to evaluate the quality of each study; CI, confidence interval; RR, relative risk.
4 Journal of Paediatrics a
© 2017 Paediatrics and Child Health Division (The Royal Australasian
186
Wu Y, Gong Q, Zou Z, Li H, Zhang X. Short sleep duration and obesity among children:
A systematic review and meta-analysis of prospective studies. Obes Res Clin Pract.
2017 Mar - Apr;11(2):140-150
Revisão sistemática
com metanálise:
Curta duração do sono
associada a aumento
do risco de obesidade.
187
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
188
Wójtowicz J, Łempicka A, Łuczyński W, Szczepański W, Zomerfeld A, Semeran K, Bossowski A. Central aortic
pressure, arterial stiffness and echocardiographic parameters of children with overweight/obesity and arterial
hypertension. Adv Clin Exp Med. 2017 Dec;26(9):1399-1404
Crianças obesas apresentam aumentam da pressão aórtica (sistólica e
diastólica) e aumento da espessura do ventrículo esquerdo.
189
Zulkipli MS, Dahlui M, Jamil N, Peramalah D, Wai HVC, Bulgiba A, Rampal S. The association
between obesity and dengue severity among pediatric patients: A systematic review and meta-
analysis. PLoS Negl Trop Dis. 2018 Feb 7;12(2):e0006263

metanálise:
Obesidade aumenta a
gravidade da dengue em
crianças
190
Lechuga-Sancho AM, Gallego-Andujar D, Ruiz-Ocaña P, Visiedo FM, Saez-Benito A, Schwarz M, Segundo C, Mateos
RM. Obesity induced alterations in redox homeostasis and oxidative stress are present from an early age. PLoS One.
2018 Jan 25;13(1):e0191547
Crianças obesas com resistência periférica à insulina

apresentam mais estresse oxidativo
191
Zabarsky G, Beek C, Hagman E, Pierpont B, Caprio S, Weiss R. Impact of Severe

Obesity on Cardiovascular Risk Factors in Youth. J Pediatr. 2018 Jan;192:105-114
108
Os riscos metabólicos
associados à obesidade
aparecem antes de se
chegar aos graus mais
severos.
192
Green WD, Beck MA. Obesity Impairs the Adaptive Immune Response to Influenza
Virus. Ann Am Thorac Soc. 2017 Nov;14(Supplement_5):S406-S409
Obesidade prejudica a reposta imune ao vírus influenza por alteração da

resposta imune celular.
Obesos vacinados tem o dobro de chance de desenvolver gripe comparados
aos magros vacinados, mesmo apresentando a mesma resposta sorológica.
193
Pont SJ, Puhl R, Cook SR, Slusser W; SECTION ON OBESITY; OBESITY SOCIETY. Stigma
Experienced by Children and Adolescents With Obesity. Pediatrics. 2017 Dec;140(6).
pii: e20173034
A estigmatização das pessoas com obesidade é generalizada e causa danos. O estigma do

peso é muitas vezes propagado e tolerado na sociedade por causa das crenças de que o
estigma e a vergonha motivam as pessoas a perder peso. No entanto, em vez de motivar
mudanças positivas, esse estigma contribui para comportamentos como compulsão
alimentar, isolamento social, evitação de serviços de saúde, diminuição da atividade física
e aumento do ganho de peso, que pioram a obesidade.
194
Jing L, Nevius CD, Friday CM, Suever JD, Pulenthiran A, Mejia-Spiegeler A, Kirchner HL, Cochran WJ, Wehner GJ,
Chishti AS, Haggerty CM, Fornwalt BK. Ambulatory systolic blood pressure and obesity are independently associated
with left ventricular hypertrophic remodeling in children. J Cardiovasc Magn Reson. 2017 Nov 9;19(1):86
Crianças obesas apresentam hipertrofia do ventrículo

esquerdo relacionados ao grau de obesidade e à pressão
arterial
195
An R, Yan H, Shi X, Yang Y. Childhood obesity and school absenteeism: a systematic

review and meta-analysis. Obes Rev. 2017 Dec;18(12):1412-1424

metanálise:
Risco de faltas à escola de 27%
entre crianças com sobrepeso e
de 54% entre as obesas
196
Durbin C, Egan R, Gervasi K, Nadeau N, Neal E, Reich S, Gregory T. The effects of
obesity on pulmonary function in children. JAAPA. 2017 Sep;30(9):30-33
Obesidade prejudica o sistema respiratório:

✓ Função pulmonar
✓ Tolerância a exercício
✓ Trocas gasosas
✓ Musculatura respiratória
197
Umer A, Kelley GA, Cottrell LE, Giacobbi P Jr, Innes KE, Lilly CL. Childhood obesity and
adult cardiovascular disease risk factors: a systematic review with meta-analysis.
BMC Public Health. 2017 Aug 29;17(1):683
Revisão sistemática com metanálise:

Obesidade na infância leva a maiores
riscos cardiovasculares no adulto:
✓ Maior pressão arterial
✓ Hipertrigliceridemia
✓ Menor HDL
198
Pan L, Li X, Feng Y, Hong L. Psychological assessment of children and
adolescents with obesity. J Int Med Res. 2018 Jan;46(1):89-97
Crianças obesas quando em tratamento, estão mais propensas

a instabilidade emocional, impulsividade e problemas
emocionais e psicológicos extremos.
199
Pogodina A, Rychkova L, Kravtzova O, Klimkina J, Kosovtzeva A. Cardiometabolic Risk

Factors and Health-Related Quality of Life in Adolescents with Obesity. Child Obes.
2017 Dec;13(6):499-506
Adolescentes
CHILDHOOD OBESITY obesos apresentam
Month 2017 pior qualidade de vida
Discussion
We demonstrated that 70.6% of all
least one CRF in addition to being ob
mon CRF was hypertension. Lipid an
tabolism disorders were diagnosed les
The prevalence of CRFs among ob
been shown in other research studies
et al. found similar results as our sample
at 07/20/17. For personal use only.
were diagnosed at a higher frequency w

is worth noting that wherein other su
diagnosis of dyslipidemia more often i
the frequency of hypertension diagnosis
Figure 1. HRQL scores in adolescents with obesity compared to in
population. *Common population mean values (adapted from pub-
that of our survey.24,25 The higher freque
lished data33). AMean values for the group of adolescents with obesity, diagnosis as observed in the aforementio
with 95% confidence intervals. HRQL, health-related quality of life. may possibly be connected to the inclu
with severe obesity, whereas our sam
Our logistic regression Prof.analysis demonstrated that re-
Dr. Carlos Alberto Nogueira de Almeida adolescents diagnosed with a moderate
gardless of the presence of any CRF, female sex was asso- is also worth noting that the percentage
ciated with lower HRQL scores in the physical 200 functioning among our study population that also h
domain [odds ratio (OR) 3.1; 95% CI 1.03–9.5, p = 0.04]. Nogueira-de-Almeida
(in addition- to
7 de novembro
obesity) wasde comparabl
2018
Brener A, Bello R, Lebenthal Y, Yackobovitch-Gavan M, Phillip M, Shalitin S. The
Impact of Adolescent Obesity on Adult Height. Horm Res Paediatr. 2017;88(3-4):
237-243
Adolescentes obesos apresentam maior

riso de redução de estatura final
201
Al-Shorman A, Al-Domi H, Faqih A. Markers of subclinical atherosclerosis in

schoolchildren with obesity and metabolic syndrome. Swiss Med Wkly. 2017 Jun
21;147:w14446
Escolares obesos apresentam marcadores de inflamação e

disfunção endotelial, sem relação com grau da obesidade ou
marcadores de síndrome metabólica
202
Kelishadi R, Roufarshbaf M, Soheili S, Payghambarzadeh F, Masjedi M. Association of
Childhood Obesity and the Immune System: A Systematic Review of Reviews. Child
Obes. 2017 Aug;13(4):332-346
Revisão de revisões:
• Obesidade altera sistema imune como um todo:
✓ Níveis de citocinas e proteínas
✓ Número de células imunológicas
✓ Comportamento das células imunológicas
✓ Pode causar ou exacerbar: asma, alergia, dermatite atópica e apneia do
sono
✓ Pode prejudicar a reação imunológica desejável nas vacinas
✓ Pode reduzir a reação a antígenos bacterianos
203
Jimenez-Rivera C, Hadjiyannakis S, Davila J, Hurteau J, Aglipay M, Barrowman N, Adamo

KB. Prevalence and risk factors for non-alcoholic fatty liver in children and youth with
obesity. BMC Pediatr. 2017 Apr 26;17(1):113
Estudo prospectivo envolvendo 97 crianças e adolescentes (8-17 anos):

DHGNA é altamente prevalente em crianças obesas e sua presença está
associada especialmente ao aumento dos triglicerídeos
204
Quek YH, Tam WWS, Zhang MWB, Ho RCM. Exploring the association between
childhood and adolescent obesity and depression: a meta-analysis. Obes Rev. 2017
Jul;18(7):742-754
Estudo de metanálise:
Crianças e adolescentes obesos são mais sujeitos a desenvolverem sintomas
depressivos e depressão
205
de Groot CJ, van den Berg A, Ballieux BEPB, Kroon HM, Rings EHHM, Wit JM, van den
Akker ELT. Determinants of Advanced Bone Age in Childhood Obesity
. Horm Res Paediatr. 2017;87(4):254-263
Crianças obesas apresentam avanço na idade óssea e esse efeito é mediado

pelo aumento do sulfato de dehidroepiandrosterona (DHEA)
*DHEA: precursor da androstenediona - este, por sua vez precursor

da testosterona e dos estrógenos estrona e estradiol
206
Dibeklioglu SE, Çevik BŞ, Acar B, Özçakar ZB, Uncu N, Kara N, Çaycı Ş, Çakar N. The
association between obesity, hypertension and left ventricular mass in adolescents. J
Pediatr Endocrinol Metab. 2017 Feb 1;30(2):167-174
Obesidade em adolescentes é fator de risco para hipertrofia do

ventrículo esquerdo, independentemente da presença de hipertensão
arterial.
Sugere-se avaliação cardiológica de rotina em adolescentes obesos.
207
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
208
Tee JYH, Gan WY, Tan KA, Chin YS. Obesity and unhealthy lifestyle associated with
poor executive function among Malaysian adolescents. PLoS One. 2018 Apr
17;13(4):e0195934
Entre adolescentes obesos apresentam prejuízo das funções cerebrais

executivas.
Quadro pode ser atenuado por: melhora da qualidade do sono, regularidade
no jantar e nível elevado de atividade física.
209
Santana CCA, Hill JO, Azevedo LB, Gunnarsdottir T, Prado WL. The association
between obesity and academic performance in youth: a systematic review. Obes Rev.
2017 Oct;18(10):1191-1199
Revisão sistemática:
No presente, as evidências são insuficientes para estabelecer
um link direto entre obesidade e queda na performance
acadêmica entre crianças em idade escolar.
210
Martin A, Booth JN, McGeown S, Niven A, Sproule J, Saunders DH, Reilly JJ. Longitudinal
Associations Between Childhood Obesity and Academic Achievement: Systematic Review with
Focus Group Data. Curr Obes Rep. 2017 Sep;6(3):297-313
31 estudos, sendo 17 coortes revistos não conseguiram
demosntra relação entre obesidade infantil e queda no
desempenho escolar.
211
Cheke LG, Bonnici HM, Clayton NS, Simons JS. Obesity and insulin resistance are
associated with reduced activity in core memory regions of the brain.
Neuropsychologia. 2017 Feb;96:137-149
Obesidade está associada a queda na atividade funcional do

SNC em áreas ligadas a memória episódica.
A resistência insulínica parece ser a chave explicativa desse
prejuízo.
212
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
213
Nielsen TRH, Fonvig CE, Dahl M, Mollerup PM, Lausten-Thomsen U, Pedersen O, Hansen T, Holm
JC. Childhood obesity treatment; Effects on BMI SDS, body composition, and fasting plasma lipid
concentrations. PLoS One. 2018 Feb 14;13(2):e0190576
Mesmo em crianças obesas que, durante um adequado tratamento

multiprofissional, apresentam aumento do escore z de IMC, as estratégias
usadas garantem melhora da composição corporal e do perfil lipídico.
214
Qi L, Guo Y, Liu CQ, Huang ZP, Sheng Y, Zou DJ. Effects of bariatric surgery on glycemic and lipid
metabolism, surgical complication and quality of life in adolescents with obesity: a systematic
review and meta-analysis. Surg Obes Relat Dis. 2017 Dec;13(12):2037-2055

✓ 49 estudos envolvidos, com 3.007 pacientes incluídos com idades entre 14
e 20 anos;
✓ 3 cirurgias mais comuns: Y de Roux, banda ajustável, sleeve gastrectomia;
✓ Redução média de 31% do IMC e melhora dos perfis glicêmico e lipídico;
✓ Melhores resultados com Y de Roux
215
Coutant R, Bouhours-Nouet N, Donzeau A, Fauchard M, Decrequy A, Malka J, Riquin E, Beaumesnil M, Sallé A, Briet
C, Topart P, Schmitt F. Bariatric surgery in adolescents with severe obesity: Review and state of the art in France.
Ann Endocrinol (Paris). 2017 Oct;78(5):462-468
Na França: cirurgia bariátrica efetiva com efeitos adversos mínimos no curto

prazo.
Perda média com Y de Roux: 16,6 kg/m2
Perda média com Sleeve: 14,1 kg/m2
Perda média com banda: 11,6 kg/m2
216
Wong MS, Jones-Smith JC, Colantuoni E, Thorpe RJ Jr, Bleich SN, Chan KS. The Longitudinal
Association Between Early Childhood Obesity and Fathers' Involvement in Caregiving and
Decision-Making. Obesity (Silver Spring). 2017 Oct;25(10):1754-1761
Estudo de seguimento longitudinal:

Aumento do envolvimento do pai (cuidado em geral e ajuda na
tomada de decisões) reduz risco de obesidade entre crianças de
2 a 4 anos.
217
Morgan PJ, Young MD, Lloyd AB, Wang ML, Eather N, Miller A, Murtagh EM, Barnes AT, Pagoto
SL. Involvement of Fathers in Pediatric Obesity Treatment and Prevention Trials: A Systematic
Review. Pediatrics. 2017 Feb;139(2). pii: e20162635
As estratégias atuais de tratamento da obesidade não tem
envolvido o pai.
São necessárias abordagens inovadoras que permitam maior
participação e engajamento do pai.
218
O'Connor EA, Evans CV, Burda BU, Walsh ES, Eder M, Lozano P. Screening for Obesity and Intervention for Weight
Management in Children and Adolescents: Evidence Report and Systematic Review for the US Preventive Services
Task Force. JAMA. 2017 Jun 20;317(23):2427-2444
Tempo total de interveção que leva a sucesso no tratamento da
obesidade é de no mínimo 26 horas.
219
Della Corte C, Mosca A, Vania A, Alterio A, Iasevoli S, Nobili V. Good adherence to the
Mediterranean diet reduces the risk for NASH and diabetes in pediatric patients with obesity:
The results of an Italian Study. Nutrition. 2017 Jul - Aug;39-40:8-14
Estudo italiano:
Dieta Mediterrânea é segura, barata e eficaz para
tratamento da obesidade e da DHGNA
220
f IGB [18, 19] and bariatric surgery [22, 23].
e present study, no serious complications during IGB to be infrequent [20]. A recent review of the literature [24],
nt or retrieval were reported, and there were no mor- including 26 studies (n = 6101), found serious complications
The IGB treatment can therefore be considered safe. associated with IGB to be rare: mortality (0.05%), gastric
sible explanation for the absence of complications in ulcers (0.3%), gastric perforation (0.1%), and balloon migra-
sent study was the small number of participants. tion (0.09%).
Fittipaldi-Fernandez RJ, Guedes MR, Galvao Neto MP, Klein MRST, Diestel CF. Efficacy
r, severe complicationsof are reported inBalloon
Intragastric the literature Weight
Treatment for loss hasObesity.
Adolescent traditionally
ObesbeenSurg.the main
2017 outcome
Oct;
measure of
27(10):2546-2551efficacy in IGB treatment and is frequently
evaluated as weight loss (kg), change in BMI (kg/m2),
Success rates of %TWL, and %EWL. The %EWL during the 6 months
Patients
of IGB use observed Estudo in brasileiro:
our study was 56.94%. This
(n = 27)
percentage is similar
Tratamento to that found
de adolescentes cominbalão
the intra-
group of ad-
%TWL olescents included in the study conducted by Sallet
gástrico colocado por via endoscópica
et al. (2014) [13] (57.4%, n = 21), but was higheré seguro e than
<10% 7 (25.92%)
≥10% 20 (74.08%)
that obtained eficaz
in theapósstudies conducted
6 meses de uso. by Reece et al.
%EWL (n; %)
(2016) [18] (9.55%, n = 12) and Karagiozolou-
OBS: estudo não mostra resultados
Lampoudi et al. (2009) [17] (14.29%, após an retirada
= 14). The
<20% 4 (14.81%)
great divergence in thedoresultsbalão. of these studies conduct-
20–50% 10 (37.04%)
ed with teenagers may be attributed to the small number
>50% 13 (48.15%)
of participants in each study. In studies conducted with
BMI/age index (n; %)
adults, the %EWL also varies but is lower than 50%:
>p97 16 (59.26%)
33.9% [25], 32.1% [26], 41.6% [27], 39.7% [28], 36.2%
>p85–p97 7 (25.93%)
[24], and 36.5% [29].
>p50–p85 3 (11.11%)
In the studies conducted with adolescents, we were not able
<p50 1 (3.70%)
to find information about %TWL. The %TWL achieved by
TBWL total weight loss, EWL excess our adolescent patients (16.35%) was higher than that ob-
weight loss, BMI body mass index served in the meta-analysis conducted with adult patients
221
Rajjo T, Mohammed K, Alsawas M, Ahmed AT, Farah W, Asi N, Almasri J, Prokop LJ,
Murad MH. Treatment of Pediatric Obesity: An Umbrella Systematic Review. J Clin
Endocrinol Metab. 2017 Mar 1;102(3):763-775
Várias estratégias de tratamento se mostram isoladamente
eficazes, entretanto as abordagens com vários componentes
parecem levar aos melhores resultados.
222
Browne AF. Therapeutic Options to Treat Pediatric Obesity.
Gastrointest Endosc Clin N Am. 2017 Apr;27(2):313-326
O melhor tratamento da obesidade infantil é aquele que a

considera como doença crônica e, portanto, o cuidado deve ser
contínuo e envolver aspecto multidisciplinar.
223
He B, Long W, Li X, Yang W, Chen Y, Zhu Y. Sugar-Sweetened Beverages Consumption Positively

Associated with the Risks of Obesity and Hypertriglyceridemia Among Children Aged 7-18 Years
in South China. J Atheroscler Thromb. 2018 Jan 1;25(1):81-89
Estudo transversal envolvendo 2.032 crianças:

Consumo de bebidas adoçadas eleva risco de obesidade (OR
2,08) e hipertrigliceridemia (OR 1,70).
224
Greenhill C. Obesity: Assessing the long-term outcomes of bariatric
surgery in adolescents. Nat Rev Endocrinol. 2017 Mar;13(3):125
Benefícios da cirurgia bariátrica na adolescência superam os

efeitos adversos (deficiências nutricionais e perda excessiva de
peso), mas faltam estudos de seguimento de longo prazo.
225
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
226
tes nos jovens com sobrepeso e obesidade com- estudo corrobora os resultados prévios33, haja
parados aos eutróficos (17,1 e 18,2 vs 15,5%). vista que indivíduos com sobrepeso e obesida-
Na análise ajustada, jovens com sobrepeso e obe- de reduziram a prevalência de PAE de 50% para
sidade da amostra total e os não praticantes de 37% em três meses, e para 29%, em seis meses de
esportes apresentaram razão de prevalência de intervenção por meio da atividade física. Dessa
possuir PAE, que variou de 1,60 a 2,15 superior, forma, a prática esportiva regular torna possível
comparados
Coledamaos seus Ferraiol
DHC, pares eutróficos, resultados
PF, Pires aosGreca
R Júnior, jovens expostos à um dos
JPA, Oliveira AR.principais determi-and obesity
Overweight
que corroboram com os descritos previamen- nantes da PAE, que é o sobrepeso
are not associated to high blood pressure in young people sport practitioners. Cien e a obesidade,
te9-11,18,22,26. Para os jovens praticantes
Saude de esportes apresentarem
Colet. 2017 prevalência semelhante aos seus
Dec;22(12):4051-4060
não foram encontradas associações significativas. pares eutróficos.
Esses resultados demonstram epidemiologica- Apesar de o delineamento do presente estudo
mente a proteção cardiovascular que os indiví- ser transversal, os resultados corroboram parcial-
duos com sobrepeso e obesidade praticantes de mente os estudos experimentais e ensaios clíni-
esportes estudados apresentaram comparados a cos aleatórios realizados Estudo brasileiro:
previamente. Já foram
seus pares não praticantes. descritas reduções significativas na pressão arte-
Sobrepeso e obesidade não se associam a
Os resultados apresentados, quando analisa- rial em programas de treinamento com duração
da a amostra total, corroboram com os estudos de três33 a seis hipertensão arterial
meses34. Ainda, quando
programas o adolescente
de exer-
prévios que demonstraram não haver associação cícios eficazes em reduzir a pressão arterial de jo-
entre atividade física com a PAE em jovens9,11,21-23. vens apresentam,simultaneamente
no mínimo, trêspratica
sessões atividade
sema- física
No presente estudo foi utilizada a prática espor- nais e com duração superior a 60 min35. Provavel-
esportiva.
Tabela 4 . Análise multivariada entre a associação do sobrepeso e da obesidade com a pressão arterial elevada.
Todos * Não Praticantes ** Praticantes ***
Variáveis % % %
RP (IC95%) RP (IC95%) RP (IC95%)
Eutrófico 15,2 1,00 15,1 1,00 15,5 1,00
Sobrepeso 25,7 1,60 (1,02-2,52)a 29,7 1,80 (1,05-3,14)c 17,1 1,01 (0,36-2,82)e
Obesidade 29,5 1,93 (1,15-3,25)b 33,3 2,15 (1,10-4,16)d 18,2 1,09 (0,48-2,48)f
RP: Razão de prevalência; IC95% - Intervalo de confiança de 95%; * - Ajustado para sexo e idade; ** - Ajustado para sexo, idade
e escolaridade paterna; *** - Ajustado para sexo e comportamento sedentário. DEFF: a = 1,07; b = 0,83; c = 1,23; d = 1,16; e = 1,20;
f
= 0,36.
227
Foster C, Moore JB, Singletary CR, Skelton JA. Physical activity and family-based
obesity treatment: a review of expert recommendations on physical activity in youth.
Clin Obes. 2018 Feb;8(1):68-79
Apenas 33% dos adolescentes americanos conseguem

atender à recomendação de pelo menos 60 minutos de
atividade física diária.
228
Oliveira LC, Ferrari GLM, Araújo TL, Matsudo V. Overweight, obesity, steps, and
moderate to vigorous physical activity in children. Rev Saude Publica. 2017 Apr
27;51(0):38
Estudo brasileiro:
Para prevenir sobrepeso e obesidade em crianças:
✓ Meninos: 10.500 passos por dia
✓ Meninas: 8.500 passos por dia
✓ Meninos: 66 minutos por dia de atividade física moderada/vigorosa
✓ Meninas: 46 minutos por dia de atividade moderada/vigorosa
229
González-Ruiz K, Ramírez-Vélez R, Correa-Bautista JE, Peterson MD, García-Hermoso A. The

Effects of Exercise on Abdominal Fat and Liver Enzymes in Pediatric Obesity: A Systematic
Review and Meta-Analysis. Child Obes. 2017 Aug;13(4):272-282
8 GONZÁLEZ-RUIZ ET AL.
Figure 4. Changes in intrahepatic fat in individual studies of exercise group vs. control group.

Discussion Atividade física, especialmente fat, including VAT. The authors concluded that these ef-
aeróbica, efetiva para
fects reduce VAT with >30 cm2tratar
in women and >40 cm2 in
Within the last decade, an increasing number of studies men, after a mean of 12 weeks.
have demonstrated that exercise training programs DHGNA. are In adults, another meta-analysis37 reported significant
beneficial for pediatric obesity. This systematic review and differences in the VAT levels after combined aerobic and
meta-analysis generated novel evidence that exercise strength training in overweight compared with nonexercise
training can help reduce the risk for NAFLD progression controls. These discrepancies can likely be explained by
by targeting hepatic lipid composition; this effect appears the wide range of characteristics of the participants (>35
to be mediated by changes on VAT, SAT, or GGT in years old), study duration, intervention program (i.e.,
overweight/obese pediatric subjects. Similar conclusions treadmill and/or elliptical, weight machines), and extent of
have been suggested in previous narrative reviews36 and change in VAT across these studies. This is consistent
systematic review and meta-analysis in the Prof.adult
Dr. Carlos Alberto with
popula- Nogueira
thedesignificant
Almeida effects of physical activity interven-
12
tion. tions on body fat levels among children and adolescents
Our pooled analysis demonstrated that general exercise230 with obesity.38
reduced VAT and SAT. Similar conclusions were reported Nogueira-de-Almeida
In this context, - 7 de novembro
practice guidelines de 2018
from the American
Nemet D. Childhood Obesity, Physical Activity, and Exercise.
Pediatr Exerc Sci. 2017 Feb;29(1):60-62
Pokemón Go é um jogo de smartphone que usa realidade aumentada, onde

os jogadores são incentivados a sair e caminhar distâncias significativas para
pegar o Pokemon. Os relatórios iniciais sugeriam aumentos no número de
passos por dia, mas esse efeito do jogo não foi sustentado.
231
Goldfield GS, Kenny GP, Alberga AS, Tulloch HE, Doucette S, Cameron JD, Sigal RJ. Effects of
aerobic or resistance training or both on health-related quality of life in youth with obesity: the
HEARTY Trial. Appl Physiol Nutr Metab. 2017 Apr;42(4):361-370
Em adolescentes obesos é fundamental incluir exercícios

de resistência junto aos aeróbicos.
232
García-Hermoso A, Ramírez-Vélez R, Ramírez-Campillo R, Peterson MD, Martínez-Vizcaíno V. Concurrent aerobic
plus resistance exercise versus aerobic exercise alone to improve health outcomes in paediatric obesity: a
systematic review and meta-analysis. Br J Sports Med. 2018 Feb;52(3):161-166

Atividade física aeróbica associada a exercícios de resistência
melhoram a composição corporal, o perfil metabólico e o
estado inflamatório em população obesa pediátrica.
233
Mitchell JA, Dowda M, Pate RR, Kordas K, Froberg K, Sardinha LB, Kolle E, Page A.
Physical Activity and Pediatric Obesity: A Quantile Regression Analysis. Med Sci
Sports Exerc. 2017 Mar;49(3):466-473
Associação extremamente forte entre aumento de atividade

física moderada a vigorosa e redução do tempo de TV no
sucesso do tratamento da obesidade.
234
. The
reported method to assess energy consumption that
study is highly subjective (especially among children and
maso adolescents with obesity) (38,39), and its use in all
(23).
the selected studies facilitates comparisons.
se in As Schwartz
suggested byPerreira
C, King NA, Mayer in theJE, mid-1950s,
B, Blundell it isreview and meta-analysis of
Thivel D. A systematic
n un- energy and macronutrient intake responses to physical activity interventions in children and
commonly believed thatwithindividuals
adolescents obesity. Pediatrincrease their
Obes. 2017 Jun;12(3):179-194
19).

metanálise:
Ativiade física estruturada
0.207
reduz a ingestão energética
s re-
entre adolescentes obesos
tions
1.261
roge-
.903;
uded
e re-
s the
with
ke of Prof. Dr. Carlos Alberto Nogueira de Almeida
2.5 g, Figure 2 Effect size forest plot for absolute energy intake
235
(mean ± 95% confidence intervals).
Classificação
l Association for the Study of Obesity ••, ••–•• Aleitamento

Controvérsias
materno
Farmaco-
terapia Prevenção
Obesidade
236
237
Hou YP, He QQ, Ouyang HM, Peng HS, Wang Q, Li J, Lv XF, Zheng YN, Li SC, Liu HL, Yin
AH. Human Gut Microbiota Associated with Obesity in Chinese Children and
Adolescents. Biomed Res Int. 2017;2017:7585989
Microbiota é diferente entre adolescentes obesos e não obesos.

Bifidobactérias e lactobacilos aumentaram nos adolescentes
obesos à medida que emagreceram e podem ser usasdos como
marcadores de melhor saúde entre adolescentes obesos.
238
Murugesan S, Nirmalkar K, Hoyo-Vadillo C, García-Espitia M, Ramírez-Sánchez D, García-
Mena J. Gut microbiome production of short-chain fatty acids and obesity in children.
Eur J Clin Microbiol Infect Dis. 2018 Apr;37(4):621-625
Ácidos graxos de cadeia curta produzidos pela microbiota podem atuar como
reguladores de processos fisiológicos e patológicos ralcioandos à obesidade
em crianças.
Adicionalmente, a produção excessiva de ácidos graxos de cadeia curta por
determinada microbiota representa fonte de calorias adicionais, podendo
contribuir para o balanço energético positivo.
239
Nagata S, Chiba Y, Wang C, Yamashiro Y. The effects of the Lactobacillus casei strain
on obesity in children: a pilot study. Benef Microbes. 2017 Aug 24;8(4):535-543
Estudo piloto:
Lactobacilo casei strain contribuiu para
a perda de peso e melhorou o perfil
lipídico em crianças obesas.
240
Nicolucci AC, Hume MP, Martínez I, Mayengbam S, Walter J, Reimer RA. Prebiotics
Reduce Body Fat and Alter Intestinal Microbiota in Children Who Are Overweight or With
Obesity. Gastroenterology. 2017 Sep;153(3):711-722
Estudo randomizado controlado com placebo:

Prebiótico (inulina) reduziu peso corporal, percentual de gordura e níveis
séricos de interleucina 6 em criaças obesas
241
Hume MP, Nicolucci AC, Reimer RA. Prebiotic supplementation improves appetite
control in children with overweight and obesity: a randomized controlled trial. Am J
Clin Nutr. 2017 Apr;105(4):790-799
Suplementação com
prebiótico (inulina) melhora
o controle do apetite em
crianças obesas
242
Ville AP, Heyman MB, Medrano R, Wojcicki JM. Early Antibiotic Exposure and Risk
of Childhood Obesity in Latinos. Child Obes. 2017 Jun;13(3):231-235
Uso de antibióticos antes dos

seis meses de idade associou-
se com aumentos do risco de
rápido ganho de peso (OR:
6,42) e obesidade aos 2 anos
(OR: 6,15).
243
Riva A, Borgo F, Lassandro C, Verduci E, Morace G, Borghi E, Berry D. Pediatric obesity is

associated with an altered gut microbiota and discordant shifts in Firmicutes
populations. Environ Microbiol. 2017 Jan;19(1):95-105
Disbiose (aumento de firmicutes e redução de bacterioidetes) e elevada

atividade fermentativa (aumento da produção de ácidos graxos de cadeia
curto com aproveitamento energético) podem estar envolvidos na etiologia
da obesidade.
244
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
245
O'Connor EA, Evans CV, Burda BU, Walsh ES, Eder M, Lozano P. Screening for Obesity and Intervention for Weight
Management in Children and Adolescents: Evidence Report and Systematic Review for the US Preventive Services
Task Force. JAMA. 2017 Jun 20;317(23):2427-2444
Metformina eficaz no tratamento
246
Chao AM, Wadden TA, Berkowitz RI. The safety of pharmacologic treatment for
pediatric obesity. Expert Opin Drug Saf. 2018 Apr;17(4):379-385
Recentes estudos farmacocinéticos em populações pediátricas

com liraglitude têm demonstrado segurança e tolerabilidade
similares ao perfil demonstrado para adultos.
247
Pastor-Villaescusa B, Cañete MD, Caballero-Villarraso J, Hoyos R, Latorre M, Vázquez-Cobela R, Plaza-Díaz J,

Maldonado J, Bueno G, Leis R, Gil Á, Cañete R, Aguilera CM. Metformin for Obesity in Prepubertal and Pubertal
Children: A Randomized Controlled Trial. Pediatrics. 2017 Jul;140(1). pii: e20164285
Metformina apresentou bom resultado para o tratamento da obesidade em crianças pré-

puberes, mas não em púberes.
OBS: critério de inclusão não exigia a presença de RPI
248
Danne T, Biester T, Kapitzke K, Jacobsen SH, Jacobsen LV, Petri KCC, Hale PM, Kordonouri O. Liraglutide in an
Adolescent Population with Obesity: A Randomized, Double-Blind, Placebo-Controlled 5-Week Trial to Assess Safety,
Tolerability, and Pharmacokinetics of Liraglutide in Adolescents Aged 12-17 Years. J Pediatr. 2017 Feb;
181:146-153.e3
Liraglutide com mesma eficácia,

segurança e telerabilidade que em
adultos.
Autores sugerem mesmas
dosagens para adolescentes.
249
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
250
Dembélé B, Sossa Jérôme C, Saizonou J, Makoutodé PC, Mongbo Adé V, Guedègbé Capo-Chichi J, Dona Ouendo ME.
[Coexistence of maternal overweight or obesity and stunted children in south-western Benin households]. Sante
Publique. 2018 Jan Feb;30(1):115-124
Coexistência da mesma casa de mães

DOUBLE FARDEAU NUTRITIONNEL DANS LES MÉNAGES AU BÉNIN
obesas e crianças desnutridas.
I : Prévalence de DFN/SORCE selon l’environnement

à Comè, l’alimentation dans les ménages
actéristiques sanitaires de Comè, Bénin 2015
DFN/SORCE
es Effectif %
n % p
’hygiène du ménage 0,000

ne élevée 97 27,3 97 15,3
ne moyenne 127 35,5 127 11,5
ne basse 133 37,2 133 8,9
e déplacement 0,000
93 26,0 93 12,2
Figure 1 : Statuts nutritionnels de la mère et du dernier enfant
53 14,9 53 7,5 de moins de cinq ans dans les ménages de Comè, Bénin 2015
197 55,1 197 11,8 251
e 14 4,0 14 19,8
rgé depuis www.cairn.info - University of Virginia - - 128.143.7.175 - 03/08/2018 11h20. © S.F.S.P.

e résidence 0,000 (35-49 ans) présentaient trois fois plus de risqueand
quethe
celles
Archibald AJ, Dolinsky VW, Azad MB. Early-Life Exposure to Non-Nutritive Sweeteners
129 36,1 129 13,7 de la première
Developmental Origins of Childhood Obesity: tranche from
Global Evidence (< 25Human
ans) (ORand=Rodent
3,014 ;Studies.
IC95 % =
228 63,9 228 10,3 Nutrients.[2,395-3,794]).
2018 Feb 10;10(2). pii: E194
Celles dont le ménage disposait d’une
déquate 0,544 voiture avaient un risque significativement plus élevé
de surpoids ou d’obésité que celles qui avaient un vélo
39 22,5 39 8,6
(OR = 1,750 ; IC95 % = [1,209-2,534]). Pour l’instruction,
134 77,5 134 9,3
par rapport à celles de niveau secondaire, les femmes de
184 – 184 –
niveau primaire avaient un risque supérieur (OR = 1,389 ;
’insécurité alimentaire Sem evidências entre 0,000 o consumo de edulcorantes
IC95 % = [1,043-1,850]), de même que nocelles
início
sansda
instruc-
rité modérée 65 18,3 65 7,7 tion (OR = 1,209 ; p = 0,163). Les femmes d’ethnie Fon se
rité légère 158 44,1 vida158 e10,7
programação metabólica
distinguaient para
des autres parobesidade.
un risque élevé (OR = 1,417 ;
IC95 % = [1,203-1,668]). La taille de la mère était corrélée
é alimentaire 134 37,6 134 14,4
au risque de surpoids ou d’obésité. Les femmes de petite
ds de naissance 0,078 taille (≤ 155 cm) avaient le risque le plus élevé par rapport
41 17,7 41 12,6 à celles qui se situaient dans la normale ou celles qui avaient
191 82,3 191 10,2 une grande taille (OR = 0,803, OR = 0,896). Les femmes de
statut social élevé avaient un risque plus important que
é 0,710
celles avec un statut social faible (OR = 1,208 ; IC95 % =
48 13,8 301 11,5
[1,012-1,442]). Le risque était de 2,523 (IC95 % = [2,045-
301 86,2 48 11,0 3,113]) pour les femmes en sécurité alimentaire par rapport
8 – 8 – à celles en insécurité alimentaire modérée.
ion 0,695
274 78,7 74 11,8
Facteurs
Prof. Dr. Carlos associés
Alberto au retard
Nogueira de croissance
de Almeida des enfants
74 21,3 274 11,5
9 – 9 – 252 III montre un effet cumulatif de l’âge sur le
Le tableau
Nogueira-de-Almeida
retard de croissance chez - 7 de
les enfants de moins de cinq
novembro
ans. de 2018
de CPN adéquat 0,007
Gui ZH, Zhu YN, Cai L, Sun FH, Ma YH, Jing J, Chen YJ. Sugar-Sweetened Beverage Consumption and Risks of Obesity
and Hypertension in Chinese Children and Adolescents: A National Cross-Sectional Analysis. Nutrients. 2017 Nov
30;9(12). pii: E1302
Estudo chinês de abrangência nacional:

Consumo de bebidas adoçadas não apresentou relação com obesidade e
hipertensão.
Observou-se associação com adiposidade abdominal.
OBS: mais da metade das crianças chinesas consomem regularmente bebidas
adoçadas.
253
Zhao Y, Wang L, Xue H, Wang H, Wang Y. Fast food consumption and its associations with obesity
and hypertension among children: results from the baseline data of the Childhood Obesity
Study in China Mega-cities. BMC Public Health. 2017 Dec 6;17(1):933
Dados de 1.626 pares criança/pais na China:

Nenhuma correlação entre uso de fast-food e desfechos desfavoráveis à
saúde (peso, IMC, circunferência abdominal e pressão arterial)
254
Prevalence Ratios (95%CI) level
Crude 0.79 (0.66–0.95) 0.72 (0.60–0.86) norm
Model 1 0.80 (0.65–0.97) 0.76 (0.63–0.91) lowe
Model 2 0.79 (0.65–0.97) 0.73 (0.60–0.88) no co
Fernández MR, GoettemsModel 3
ML, Demarco 0.79 (0.65–0.97)
FF, Corrêa MB. Is obesity0.73 (0.60–0.88)
associated to Brazi
dental caries in Brazilian schoolchildren? Braz Oral Res. 2017 Nov 6;31:e83
Model 1: Adjusted for socioeconomic variables (type of school, appr
family income and mother’s education); Model 2: Adjusted for revie
Model 1 + demographic variable (sex and age); Model 3: Adjusted
Estudo brasileiro:
for Model 2 + oral health variable [(Gingival inflammation signi
(Bleeding sites)] + diet. by B
Crianças que praticavam menos de 300 minutos por semana de
howe
atividade e crianças com sobrepeso ou obesidade apresentaram betw
Table 3. Crude (c) and adjusted (a) rate ratios (RR) for dental
menos
caries cáries
severity dentárias.
(mean DMFT) and interest variables in Brazilian and
schoolchildren. Poisson regression analysis. (n = 1,210). child
Body mass index (obese/ Physical activity norm
Variable overweight vs eutrophic) (inactive vs active)
revie
Rate ratios (95%CI)
and d
Crude 0.72 (0.57–0.90) 0.78 (0.62–0.98) the u
Model 1 0.74 (0.58–0.94) 0.86(0.68–1.09) Confl
Model 2 0.73 (0.57–0.94) 0.83(0.65–1.06) denti
Model 3 0.73 (0.57–0.94) 0.83(0.65–1.06) child
Model 1: Adjusted for socioeconomic variables (family income signi
Prof. mother’s
and Dr. Carlos Alberto Nogueira
education); Modelde Almeida
2: Adjusted for Model 1 +
demographic variable (sex and age); Model 3: Adjusted for Model
for th
255
2 + oral health variable [(Gingival inflammation (Bleeding sites)]. linea
howe
Poti JM, Braga B, Qin B. Ultra-processed Food Intake and Obesity: What Really weig
Matters for Health-Processing or Nutrient Content? Curr Obes Rep. 2017 Dec;6(4):
Discussion 420-431 It
mech
Dental
Em relação à obesidade cariesnão
infantil, andhá
childhood obesity
evidências are complex
suficientes not a
conditions influenced by multiple factors. Since consu
comprovando quecaries
o grauisdeassociated
processamento with poor do alimento possaand
dietary habits both
ser consideradoinappropriate
fator causal; diets promote obesity,
provavelmente, this study
os efeitos One
aimed to investigate the association between dental over
deletérios se caries
referem, andna verdade,
obesity. à sua composição
Nevertheless, the results of this betw
cross-sectional
nutricional. study provide no evidence that Usua
overweight children are at increased risk for dental carbo
caries. Indeed, while not entirely consistent, the data can l
from this survey suggest that overweight status meal
may be associated with a somewhat decreased risk in su
for caries. Overweight/obese children had a lower line
experience of dental caries than children who had cons
normal weight after adjusting for well-known risk
or fre
factors for caries. These findings confirm the data denta
256
Melis Yavuz H, Selcuk B. Predictors of obesity and overweight in preschoolers: The
role of parenting styles and feeding practices. Appetite. 2018 Jan 1;120:491-499
O risco de obesidade em pré-escolares foi 4,71 vezes maior nas

crianças em que as mães usavam estilo parental autoritário
(a mãe define o que, quando e quanto).
257
Kim HY, Jung HW, Hong H, Kim JH, Shin CH, Yang SW, Lee YA. The Role of Overweight and
Obesity on Bone Health in Korean Adolescents with a Focus on Lean and Fat Mass. J
Korean Med Sci. 2017 Oct;32(10):1633-1641
A obesidade na adolescência leva a melhor saúde

óssea.
258
Hazzard VM, Hahn SL, Sonneville KR. Weight misperception and disordered weight
control behaviors among U.S. high school students with overweight and obesity:
Associations and trends, 1999-2013. Eat Behav. 2017 Aug;26:189-195
Não perceber a própria obesidade, protege crianças em idade

de escolar contra a adoção de comportamentos não saudáveis
visando emagrecimento.
259
Lundbäck V, Ekbom K, Hagman E, Dahlman I, Marcus C. Thyroid-Stimulating Hormone,

Degree of Obesity, and Metabolic Risk Markers in a Cohort of Swedish Children with
Obesity. Horm Res Paediatr. 2017;88(2):140-146
Estudo envolvendo 3.459 crianças suecas:

Observada associação positiva forte entre TSH e:
✓ IMC
✓ Insulinemia
✓ HOMA
✓ colesterol total
✓ triglicerídeos
260
Bobowski N, Mennella JA. Personal Variation in Preference for Sweetness: Effects
of Age and Obesity. Child Obes. 2017 Oct;13(5):369-376
Independente da idade, a preferência por doces não se mostrou

CHILDHOOD OBESITY October 2017
diferente entre crianças obesas e não obesas
Figure 3. Most preferred levels of sucrose and sucralose among all and among o
Prof.6
means Dr. Carlos Alberto
standard Nogueira de Almeida
error.
261
there was no difference in most preferred level of sucrose or which unl
sucralose between obese and nonobese children (Fig. 3a, point scal
Mack I, Bayer C, Schäffelersucrose:
N, Reiband N, Brölz E, 800
obese, Zurstiege
mM;G, Fernandez-Aranda
nonobese, 747F, mM;GawrilowF(1,
C, degrees of
Zipfel S. Chances and Limitations of Video Games in the Fight against Childhood Obesity-A
Systematic36df) = 0.29,
Review. = 0.59;
Eur Eat pDisord Rev. sucralose: obese, 1.05 mM; non-
2017 Jul;25(4):237-267 When te
obese, 1.09 mM; F(1, 32df) = 0.06, p = 0.81) or adults controls to
(Fig. 3b, sucrose: obese, 533 mM; nonobese, 662 mM; F(1, we validat
25df) = 0.98, p = 0.33; sucralose: obese, 0.79 mM; non- pared resp
obese, 0.99 mM; F(1, 24df) = 1.3, p = 0.27). vergence.
PEMS/KPEMS
Extensa revisãoscores were not associated with most
sistemática: responses
preferred levels of sucrose (all p’s > 0.38) or sucralose (all lose on th
Uso de videogames p’s > 0.35). However,
ativos não funciona para=controle
social (r(33df) 0.34, p = 0.05)
da and forced-cho
conformity (r(33df) = 0.48, p = 0.04) subscale scores, both shown to b
of which
obesidade represent
entre externally
crianças de 7 driven motives for palatable
a 15 anos. a taste sti
food intake, were positively associated with BMI z-scores that childr
in children only. for KCl, s
scale to in
responses.
Discussion developme
The liking that children have for higher concentrations to measure
of sucrose than do adults generalized to the sweet taste with few m
of the NNSs sucralose and aspartame. However, not method us
all psychophysical methods were sensitive enough to evidenced
reveal such age-related differences in taste hedonics. methods v
Regardless of age, there was no association between related dif
obesity and the level of sweetness most preferred. Rather, The pre
among children,262BMI was positively associated with dren most
externally driven motives forNogueira-de-Almeida
eating palatable- 7foods, in- desucrose
de novembro 2018 tha
Amer A, Abusamaan M, Li X, Fischer H. Does Pacifier Use in Infancy Decrease the
Risk of Obesity? Clin Pediatr (Phila). 2017 Oct;56(11):1018-1022
Uso de chupeta, independente do tipo de alimentação,
associou-se a menor incidência de obesidade aos 9 e 15
meses de idade.
263
Alberga AS, Prud'homme D, Sigal RJ, Goldfield GS, Hadjiyannakis S, Gougeon R, Phillips P, Malcolm J, Wells GA,
Doucette S, Ma J, Kenny GP. Does exercise training affect resting metabolic rate in adolescents with obesity? Appl
Physiol Nutr Metab. 2017 Jan;42(1):15-22
Apesar de levar a aumento da massa magra, 6 meses de

atividade física aeróbica e/ou de resistência, com modesta
restrição calórica, não levou a aumento da TMB em
adolescentes obesos, quando comparada com apenas dieta.
264
Classificação
materno
Farmaco-
terapia Prevenção
Obesidade
265
➡ Introdução
➡ epidemiologia
➡ etiopatogenia
➡ definição
➡ classificação
Roteiro ➡
➡ psicossociais
➡ outras
➡ Tratamento
➡ nutricional
➡ farmacoterapia
➡ comorbidades
➡ Avaliação
266
Obrigado!
dr.nogueira@me.com
www.clinicanutre.com
P r o f . D r. C a r l o s A l b e r t o N o g u e i r a d e A l m e i d a
Universidade Federal de São Carlos – UFSCAR
Associação Brasileira de Nutrologia - ABRAN
267

Revisão
Classificação da obesidade infantil

Classification of childhood obesity
Carlos Alberto Nogueira-de-Almeida1, Elza Daniel de Mello2, Graziela Aparecida N. de Almeida Ribeiro3,
Carla Cristina João N. de Almeida4, Mário Cícero Falcão5, Carla Maria Barreto da Silva de Souza Rêgo6
RESUMO
Importância do Problema: A obesidade na infância e na adolescência é considerada, atual-
mente, grave problema de saúde pública com prevalência crescente em todo o mundo.
Objetivo: atualizar a classificação da obesidade infantojuvenil publicada originalmente em 2004,
incorporando as novas evidências científicas. Métodos: revisão da Literatura Científica que abor-
dou os fatores etiopatogênicos da obesidade, buscando-se aprimorar a classificação anteriormen-
te publicada incluindo os novos conhecimentos científicos. Resultados: apresentação de uma
classificação que sugere como primeira estratégia a definição da presença de resistência periféri-
ca à insulina e, a seguir, sugere a divisão em quatro subgrupos de obesidade: sindrômica, epige-
nética, induzida (endocrinológica, neurológica, distúrbios do sono, fármacos e agentes infeccio-
sos) e clássica (somática e psicossocial). Conclusão: a classificação permite auxiliar o clínico na
tomada de decisões e na individualização do tratamento.
Palavras Chave: Obesidade. Classificação. Criança. Adolescente. Resistência à Insulina.

Obesidade Pediátrica.
ABSTRACT
Importance of the Problem: obesity in childhood and adolescence is currently considered a
serious public health problem with a growing prevalence worldwide. Objective: to update the
classification of child and adolescent obesity originally published in 2004, incorporating the new
scientific evidence. Methods: a review of the Scientific Literature that addressing etiopathogenic
factors of obesity, in order to improve the previously published classification including the new
scientific knowledge. Results: a classification that suggests as the first strategy the definition of
the presence of peripheral resistance to insulin and then suggests the division into four subgroups
of obesity: syndromic, epigenetic, induced (endocrinological, neurological, sleep disorders, drugs
and infectious agents) and classical (somatic and psychosocial). Conclusion: this classification
could help the clinicians to make decisions and to personalize the treatment.
Keywords: Obesity. Classification. Child. Adolescent. Insulin Resistance. Pediatric Obesity.
1. Doutor, Docente, Departamento de Medicina da Uni- CORRESPONDÊNCIA:

versidade Federal de São Carlos (UFSCAR), Brasil Carlos Alberto Nogueira-de-Almeida
2. Doutora, Docente, Curso de Medicina da Universida- Rua Eugênio Ferrante, 170
de Federal do Rio Grande do Sul, Brasil CEP 14027-150 - Ribeirão Preto, SP, Brasil
3. Doutora, Docente, Centro Universitário Barão de Mauá dr.nogueira@me.com
4. Especialista em Psicologia, Centro de Investigação
em Nutrologia e Saúde, Brasil Recebido em 13/11/2017
5. Doutor, Docente, Faculdade de Medicina da USP, Brasil Aprovado em 30/05/2018
6. Doutora, Docente, Faculdade de Medicina da Univer-
sidade do Porto, Portugal.
Local onde o trabalho foi desenvolvido: Departamento de Medicina da UFSCAR.
Medicina (Ribeirão Preto, Online.) 2018;51(2):138-52 http://dx.doi.org/10.11606/issn.2176-7262.v51i2p138-152

Classificação da obesidade infantil.
INTRODUÇÃO países desenvolvidos como naqueles em desen-

volvimento.4 Estima-se que no mundo 41 milhões
No ano de 2004, momento em que a epide- de crianças menores de cinco anos estejam obe-
mia de obesidade começa a ficar evidente em todo sas.5 O Brasil enfrenta de forma evidente um pro-
o mundo e, paralelamente, cresce o número de cesso de transição nutricional. Ao mesmo tempo
publicações científicas sobre o tema, o Centro de em que a desnutrição energético-proteica tem
Estudos em Saúde e Nutrição Infanto-juvenil da apresentado queda em sua prevalência, o sobre-
Universidade de Ribeirão Preto (CESNI) publicou peso e a obesidade rapidamente se candidatam
uma proposta de classificação clínica,1 que foi tema ao posto de maior problema nutricional do país.
de editorial no mesmo número do periódico.2 Pos- Apesar de não existirem dados atualizados,
teriormente, ela foi adotada em alguns serviços a última Pesquisa de Orçamentos Familiares6 mos-
e incluída em livros de texto.3 Àquela época, cer- trou que, para as crianças com idades entre cin-
tos aspectos da classificação, como a importân- co e nove anos, a prevalência de sobrepeso/obe-
cia dada à resistência insulínica, eram bastante sidade saltou, entre 1989 e 2009, de 13,8% (me-
inovadores e, até mesmo, polêmicos, conforme ninos) e 10,4% (meninas) para 51,4% e 43,8%,
se pode verificar à leitura do editorial escrito por respectivamente e, entre os adolescentes, de
Damiani.2 Basicamente, o que se propôs naquele 20,8% (meninos) e 18,1% (meninas) para 27,6%
momento foi que o profissional que atende a cri- e 23,4%, respectivamente.
ança obesa busque levantar todos os possíveis Para a criança, a obesidade representa,
quadros que pudessem atuar como disparadores muitas vezes, o fator desencadeante para uma
ou mantenedores da adiposidade excessiva. De série de comorbidades que interferem na saúde
acordo com os conhecimentos disponíveis à épo- atual e podem persistir até a vida adulta. Essas
ca, propôs-se que classificação em dois grandes comorbidades, que antes se acreditavam presen-
grupos: com e sem resistência periférica à insuli- tes apenas nos adultos, já são demonstradas em
na. O primeiro foi chamado de Obesidade Meta- crianças e adolescentes, aparecendo já na fase
bólica. O outro grupo foi subdividido em Obesida- de sobrepeso,7 em todas as classes sociais.8 Den-
de Sindrômica, Obesidade Induzida Endocrinoló- tre elas, destacam-se4,8-11: dislipidemias, resistên-
gica, Obesidade Induzida Neurológica, Obesida- cia insulínica, problemas ortopédicos, hipertensão
de Induzida por Fármacos, Obesidade Alimentar arterial, esteatose hepática, modificações da ge-
Somática e Obesidade Alimentar Psicossomática ometria cardiovascular, alterações hepáticas, au-
Por outro lado, fatores hoje bem estuda- mento da espessura carotídea, entre outras.
dos, como a programação metabólica, a microbio- A abordagem terapêutica da obesidade é
ta, as infecções virais e a importância do sono, bastante desafiadora, especialmente para o pro-
eram bem menos conhecidos. Em 2010, Han e co- fissional que atua em ambulatório. Uma das for-
laboradores4 publicaram no periódico Lancet uma mas de otimizar o tratamento é classificar ade-
proposta de classificação bastante semelhante à quadamente cada caso. Pacientes obesos tem em
anteriormente sugerida em 2004 por nosso gru- comum o aumento da adiposidade corporal, que
po. Esses autores também se basearam funda- pode ser entendido como um aspecto fenotípico
mentalmente na ideia de que a obesidade é uma de expressão comum a numerosos quadros clíni-
doença de origem variada, podendo estar asso- cos que, de alguma forma, promovem balanço
ciada a: medicações obesogênicas, doenças hor- energético positivo. Mas é certo que, por exem-
monais (hipotireoidismo, deficiência de hormônio plo, uma criança que acumulou gordura excessiva
de crescimento, doença de Cushing e pseudohi- devido ao uso de um fármaco obesogênico será
poparatireoidismo), alterações hipotalâmicas, qua- tratada de forma distinta daquela que apresenta
dros genéticos (Pradder-Willi, Bardet-Biedl, entre uma síndrome genética.
outros) e problemas relacionados ao estilo de vida O presente artigo descreve uma classifica-
(dieta e atividade física). ção etiopatogênica da obesidade e incorpora e
Atualmente, os números da obesidade são atualiza a proposta anteriormente publicada, 1
impactantes e sua prevalência aumentou subs- mantendo o mesmo objetivo de ser uma ferra-
tancialmente nas últimas três décadas, tanto nos menta para a tomada de decisão terapêutica.
Medicina (Ribeirão Preto, Online.) 2018;51(2):138-52 139

Nogueira-de-Almeida CA, Mello ED, Ribeiro GANA, Almeida CCJN, Falcão MC, Rêgo CMBSS.
A figura 1 mostra, de forma esquemática a constantemente atualizada e que, no presente

classificação e, a seguir, serão discutidos cada um artigo, foi obtida nas bases de dados Scielo e
de seus tópicos. Pubmed, nas línguas portuguesa, espanhola e
inglesa, referentes ao período compreendido en-
MATERIAL E MÉTODOS tre 1980 e 2018.
A presente classificação tem sua origem prin- Excesso de adiposidade corporal

cipal na experiência de seus autores nos serviços A primeira etapa de classificação da crian-
em que atuam. O embasamento teórico dessas ça passa pela confirmação de que, efetivamente,
práticas fundamenta-se em bibliografia científica trata-se de obesidade. O passo inicial é a utiliza-
Sobrepeso/obesidade Sobrepeso/obesidade
sem resistência insulínica com resistência insulínica
Sindrômica Epigenética Associada a Psicossocial Somática
Modificações da microbiota Agentes infecciosos
Distúrbios Problemas
Distúrbios do sono Uso de fármacos
Figura 1. Classificação da obesidade.
140 http://www.revistas.usp.br/rmrp / http://revista.fmrp.usp.br

ção de peso e estatura para cálculo do índice de sar de bastante adequado, do ponto de vista téc-
massa corporal (IMC) e plotagem na curva de es- nico, a utilização prática, para estudos popula-
cores z.12 Valores acima do escore z +2 para cri- cionais, esbarra na dificuldade da avaliação dos
anças abaixo de 5 anos ou +1 para aquelas com critérios de Tanner de todos os pacientes envol-
mais de 5 anos devem ser considerados eleva- vidos.
dos, mesmo que configurem apenas sobrepeso, Estudo anterior, 22 conduzido apenas com
uma vez que as comorbidades já aparecem nes- escolares e adolescentes eutróficos, mostrou que
sa fase.7 a insulinemia de jejum varia de maneira significa-
Considerando-se que, nem todo excesso de tiva entre as idades propostas, de forma a pres-
peso significa aumento da adiposidade, é impor- supor a necessidade de uma curva, com valores
tante confirmar o diagnóstico com algum tipo de ascendentes até os 13-15 anos, com posterior
avaliação de composição corporal, podendo-se queda, tanto para meninos como para meninas.
utilizar o exame físico ou medidas específicas, tais Sendo assim, de acordo com recente publicação
como circunferência abdominal, dobras cutâneas, de nosso grupo, 23 sugere-se que a insulinemia
bioimpedanciometria ou outros métodos de ava- de jejum seja o critério utilizado na prática clínica
liação corpórea.12 para definição de resistência insulínica, com os
seguintes pontos de corte:
Sobrepeso/obesidade com
⇒ 7 a 8,9 anos: 7,92 µU/mL (meninos) e
resistência insulínica
6,70 µU/mL (meninas)
O aumento do índice de massa corporal
correlaciona-se fortemente com o agravamento ⇒ 9 a 10,9 anos: 8,69 µU/mL (meninos) e
da resistência insulínica13 e, apesar da dificulda- 11,99 µU/mL (meninas)
de em diagnosticar essa condição na infância,14 ⇒ 11 a 12,9 anos: 12,18 µU/mL (meninos) e
especialmente do ponto de vista clínico, dois 13,26 µU/mL (meninas)
parâmetros podem ser usados15: a determinação
⇒ 13 a 14,9 anos: 13,74 µU/mL (meninos) e
da insulinemia de jejum e o cálculo de homeostasis
14,85 µU/mL (meninas)
model assessment (HOMA-IR). Em ambos os ca-
sos, a informação obtida será semelhante, uma ⇒ 15 a 17,9 anos: 10,27 µU/mL (meninos) e
vez que, na faixa etária pediátrica, a glicemia 13,13 µU/mL (meninas)
apresenta pouca variação e o HOMA-IR leva em
conta, justamente, insulinemia e glicemia.14 Ain- Mais importante que o simples diagnóstico
da não foram definidos valores de corte interna- da resistência periférica à insulina, justifica-se sua
cionais em relação à insulinemia de jejum e HOMA- categorização como primeira etapa, dadas as con-
IR para a faixa etária pediátrica. Desde a publica- sequências para a saúde da criança, que nem
ção de Tem e McLaren,16 o valor de 15 microUI/mL sempre estão correlacionadas à gravidade do
tem sido usado, mas ainda sem validação. Ou- excesso de peso e aparecem, muitas vezes, de
tros pontos de corte, como 12, 27 e 30 também forma precoce, mesmo nos casos mais leves.24
já foram sugeridos.17 O exame físico revela predominância de
Durante a puberdade, ocorrem eventos que adiposidade nas regiões abdominais e cervical
se assemelham a uma “resistência insulínica fisi- posterior, estatura elevada e acantose nigricans4.
ológica”.18,19,20 Sendo assim, seria imperativo que A maior parte das comorbidades se apresenta de
os pontos de corte fossem definidos respeitan- forma mais prevalente ou, pelo menos, mais gra-
do-se a variação biológica desse indicador. Re- ve, na presença de resistência insulínica.25 Podem-
centemente, Cuartero e colaboradores21 propu- se destacar: diabetes, dislipidemia, hipertensão
seram o uso do percentil 90 baseado em levan- arterial, síndrome dos ovários policísticos, doen-
tamento que incluiu 372 indivíduos com idades ça hepática gordurosa, aceleração da puberdade
entre um mês e 18 anos, no qual observaram e estrias.25 Por fim, é importante destacar o efei-
variação importante desses indicadores em rela- to “círculo vicioso”, uma vez que a obesidade pre-
ção ao estadiamento puberal, idade e sexo. Ape- cipita e agrava a resistência periférica à insulina

a qual, por sua vez, devido possivelmente à hi- Por outro lado, a obesidade pode aparecer
perinsulinemia, leva a processo anabólico, com au- também como resultado de diversas doenças
mento do apetite e da adipogênese.26 Esse últi- genéticas mais específicas, em que apenas um
mo aspecto pode ser, inclusive, demonstrado por defeito encontrado é suficiente para predispor à
um ensaio clínico recente que utilizou como inter- adiposidade excessiva.
venção única a prescrição de metformina (que O exemplo mais clássico é a mutação no
atua reduzindo a resistência insulínica) para cri- gene OB que leva à deficiência na produção de
anças obesas, obtendo-se emagrecimento, mes- leptina, principal hormônio responsável pelo con-
mo na ausência de outras medidas, como dieta trole do balanço energético. Trata-se de quadro
ou aumento da atividade física.27 Devido às maio- bastante raro, mas dramático, na medida em que
res complexidade e gravidade dessa forma de a obesidade resultante é extremamente grave31.
apresentação da obesidade, o tratamento é sem- Deve-se citar também o gene FTO, já bastante es-
pre mais difícil e demorado. tudado, onde indivíduos com determinadas vari-
antes apresentam quadro de obesidade clássica.32
Sobrepeso/obesidade sem Outras síndromes genéticas cursam com
resistência insulínica obesidade,33 tais como: síndrome de Prader Wili,
Nesses casos, apesar de quase sempre Bardet-Biedl, Alström, WAGR, Cohen, Alstrom,
presentes, as comorbidades são menos frequen- Borjeson-Forssman-Lehmann, Beckwith-
tes e graves, sendo que crianças com escores z Wiedemann e Down. Observa-se associação com
maiores tendem a apresentar mais problemas malformações congênitas (leves ou graves), dis-
associados. 28 Por outro lado, nesse grupo, en- morfias faciais, distúrbios de crescimento (hiper
contram-se muitas crianças que, excetuando-se ou hipocrescimento), atraso de desenvolvimento
o excesso de peso, parecem absolutamente nor- neuro-psicomotor, deficiência mental, história fa-
mais. Muitos pacientes têm melhor adesão ao tra- miliar sugestiva, lembrando que a ausência de
tamento convencional, respondendo de forma casos familiares não afasta o fator genético e
mais rápida às medidas terapêuticas. consanguinidade. 34
A segunda etapa da classificação, mostra- A história de excesso de peso pode ser
da a seguir, aplica-se aos dois casos descritos neonatal (onde devem ser avaliadas as síndromes
acima, sugerindo-se que, para efeito de denomi- de hipercrescimento) ou aparecer com o avançar
nação, sejam utilizados todos os aspectos, por da idade.34 No exame físico, encontram-se mal-
exemplo, “obesidade com resistência insulínica formações leves e/ou graves, dismorfias faciais,
associada a distúrbio do sono” ou ainda “obesi- baixa ou alta estatura e alterações neurológicas.34
dade psicossocial sem resistência insulínica”. No caso específico da Síndrome de Prader-
Willi, 33,35
encontram-se hipotonia e dificuldades de
Obesidade sindrômica alimentação no primeiro ano de vida e, posterior-
Sabe-se que a obesidade, de uma maneira mente, aparecem hipogonadismo, retardo men-
geral, apresenta forte componente genético, sen- tal, redução na velocidade de crescimento e hi-
do que muitos autores consideram que se trata perfagia intensa35. O controle da obesidade pode
de uma doença de etiologia poligênica clássica, ser difícil, quando a hiperfagia de origem central
em que o fenótipo final será a resultante da com- está presente, como na síndrome de Prader-Willi,
binação entre diversos genes.29,30 ou a hipotonia, no caso da síndrome de Down,
Já foram, por exemplo, identificados genes que reduz o gasto calórico basal36. Além disso, a
envolvidos em baixa taxa de metabolismo basal, deficiência mental pode atuar como um fator que
baixo efeito termogênico dos alimentos, baixo grau interfere no controle da dieta36. Na maioria das
de oxidação das reservas gordurosas, altos níveis vezes, a doença de base não pode ser tratada e
de atividade da lipase lipoproteica, baixos graus a abordagem da obesidade deve ser feita por
de mobilização lipídica, inadequada regulação cen- educação do paciente e da família, restrição die-
tral de fome/saciedade, baixo grau oxidativo da tética, exercícios físicos e, eventualmente, medi-
musculatura esquelética, dentre outros.29,30 camentos que, em geral, tem pouca efetividade.

Obesidade epigenética Observou-se também que não somente a

subnutrição intrauterina poderia reprogramar os
Programação metabólica é definida como o genes, mas vários outros agravos, nutricionais ou
resultado de “modificações não estruturais do não, em períodos críticos, de elevada plasticidade,
material genético, consequentes de insulto ou como os primeiros 1000 dias de vida (período
estímulo aplicado em um período crítico ou sensí- gestacional mais os dois primeiros anos de vida).47
vel, com potencial de efeito duradouro ou persis- Hoje se reconhece que muitos aspectos li-
tente sobre a estrutura ou a função de um orga- gados à saúde da mãe, podem, adicionalmente,
nismo”.37 interferir nessa programação.48 Hofman e colabo-
O mecanismo genético de programação radores49 propõe que o ambiente adverso, que
metabólica é a epigenética, que é definida como leva ao insulto inicial capaz de fazer a programa-
“todas as mudanças reversíveis e herdáveis no ção metabólica, ocorre de forma diferente de acor-
genoma funcional que não alteram a sequência do com o perfil de nascimento. Nas crianças de
de nucleotídeos do DNA”.38 Há três mecanismos termo, mas com restrição de crescimento intrau-
epigenéticos principais: a metilação, as mudan- terino, o agravo ocorreria na fase pré-natal; por
ças químicas nas histonas e a atuação dos RNAs outro lado, no caso dos prematuros, aconteceria
não-codificantes.39 nos primeiros meses de vida. De fato, vários es-
A metilação é um processo onde radicais tudos têm mostrado que o perfil pós-natal de cres-
metil são adicionados a trechos específicos da cimento e ganho de peso acelerados observados
molécula de DNA, alterando a expressão de de- em crianças nascidas prematuramente, mas tam-
terminado gene. As histonas são estruturas em bém em crianças de termo quando alimentados
volta das quais o DNA se organiza e, modificações inadequadamente, leva a diminuição da sensibi-
em sua configuração espacial, são capazes de lidade à insulina, alterações de padrões de cres-
controlar a transcrição. Por fim, os RNAs não- cimento e aumento da adiposidade.39
codificantes são pequenas fitas de nucleotídeos Cabe destacar que um dos fatores mais
capazes de modular a expressão dos genes por relevantes, que leva a crescimento pós-natal ace-
meio do silenciamento transcricional ou pós-trans- lerado e obesidade futura é o excesso de consu-
cricional. mo de proteínas nos primeiros meses de vida,50
A demonstração mais evidente de progra- sendo esse um exemplo clássico de como se pode
mação metabólica ocorre com a obesidade,38 uma atuar na prevenção da obesidade, estimulando o
vez que fetos submetidos à subnutrição intrau- aleitamento materno ou, na impossibilidade des-
terina conseguem se adaptar para sobreviver, te, prescrevendo fórmulas infantis com teor pro-
mas, para isso, são reprogramados para serem teico adequado e evitando-se o uso de leite de
conservadores de energia.40 Após o nascimento, vaca não modificado.
se a restrição alimentar cessa, o novo perfil feno- Muitas vezes, a procura por explicações
típico leva ao acúmulo excessivo de gordura.41 quando a obesidade já se encontra instalada é
Os estudos posteriores às demonstrações difícil e leva a resultados surpreendentes. Noguei-
de Barker40,42,43 mostraram que não se tratava ra-de-Almeida e colaboradores,51 em artigo publi-
apenas de uma simples habilidade para conser- cado em 2015, mostraram que a ingestão calórica
var energia, mas a todo um conjunto de mudan- e o padrão de atividade física eram semelhantes
ças no perfil metabólico, essenciais na fase in- quando crianças obesas eram comparadas a seus
trauterina, mas inadequadas no meio externo.44 pares eutróficos. Sendo assim, parece que a bus-
Várias dessas mudanças acabam repercutindo na ca pelos fatores causais precoces pode ser a cha-
vida adulta, 45 gerando diversos quadros, tais ve para a melhor compreensão da obesidade.
como: maior pressão arterial, risco elevado de Nesse sentido, o reconhecimento da pro-
diabetes, dislipidemias, redução na densidade gramação metabólica, que pode ocorrer no co-
óssea, respostas inadequadas ao estresse, me- meço da vida, é fundamental para que todas as
nor elasticidade arterial, alterações de perfis hor- medidas sejam tomadas, tanto do ponto de vista
monais e, até mesmo, maior propensão a algu- de saúde pública, como no atendimento individu-
mas doenças psíquicas 46. al, para que a criança possa viver em um ambien-

te adequado. Do ponto de vista nutricional, esse o desenvolvimento de gordura marrom63 e já foi

trabalho começa com a atuação do pediatra an- demonstrado que, na dependência do perfil da
tes do nascimento, junto à gestante.52 Depois, microbiota, pode ocorrer recuperação de calorias
dentro da proposta da Puericultura, inclusive nos da fibra dietética através de fermentação em áci-
programas de saúde da família,53 com o estímulo dos graxos de cadeia curta.64
ao aleitamento materno e, enfim, completa-se
com a adequada orientação à família sobre fór-
Obesidade associada a distúrbios
mulas infantis, alimentação complementar, suple-
endocrinológicos
mentação de micronutrientes e importância da Trata-se de quadro de obesidade associa-
atividade física. do a doenças do sistema endócrino como hipoti-
reoidismo, hipercortisolismo, pseudohipoparati-
Obesidade associada a modificações de reoidismo, deficiência de hormônio de crescimen-
microbiota to e síndrome dos ovários policísticos (SOP). Mui-
A microbiota intestinal pode afetar o peso tas vezes não é possível definir relação de causa
corporal. Este aspecto é muito estudado em ani- e os quadros, quando diagnosticados, podem
mais e acredita-se que o mecanismo seja seme- aparecem juntos.65 De qualquer forma, mesmo
lhante nos seres humanos, ou seja, efeitos so- que não possa ser considerado como fator etio-
bre o metabolismo energético, grau de inflama- lógico, o distúrbio endocrinológico deverá ser ade-
ção e alteração da permeabilidade intestinal.54,55 quadamente abordado para que não se configu-
Recentemente vários pesquisadores têm re como elemento perpetuador da obesidade.65
sugerido que existe relação entre as bactérias O quadro clínico depende da doença de
residentes no trato intestinal e o potencial de base e um dos principais achados é a baixa esta-
ganho de peso. Estudos em animais sugerem que tura, comum à maior parte das doenças endocri-
a administração de antibióticos no início da vida nológicas que cursam com obesidade.66 É impor-
predispõe à obesidade mais tarde,56 mas exis- tante lembrar que, muitas vezes, a própria obe-
tem estudos observacionais em humanos que sidade aparece como o primeiro sintoma a levar
também apoiam esta possibilidade.57-60 O estudo a família a procurar ajuda. Nesses casos, é de
de Gerber et al,61 que inclui mais de 142.000 cri- extrema importância que o clínico esteja atento
anças, encontrou associação persistente, pro- à história, levando em conta uma série de sinto-
gressiva e reversível entre o uso de antibióticos mas que podem revelar a doença de base.
e subsequentes alterações do IMC. Portanto, este Nos casos de hipotireoidismo, pode-se en-
é mais um motivo para o uso racional de antibió- contrar mixedema, atraso da idade óssea, letar-
ticos em pediatria: prevenir alteração de flora in- gia, pele seca, bradicardia e bradipnéia.67 O hi-
fantil e o desenvolvimento de obesidade. percortisolismo leva a hirsutismo, fácies cushin-
Também são encontrados estudos em mo- góide, distribuição centrípeta da adiposidade, es-
delos animais que sugerem que modificações in- trias, acne, pletora, osteoporose e exacerbação
duzidas na microbiota intestinal podem ser res- de caracteres masculinos.68 O pseudohipoparati-
ponsáveis por alguma perda de peso e melhorias reoidismo cursa com resistência à ação do para-
na sensibilidade à insulina, especialmente após tormônio, anomalias dentárias, pele seca, unhas
a cirurgia de bypass gástrico.62 Ainda não está quebradiças e tetanias.69 A deficiência de hormô-
claro se esses mecanismos são relevantes para nio de crescimento mostra basicamente baixa
a gênese da obesidade e mesmo sua epidemia estatura evidente e redução na velocidade de
em humanos. Obviamente, não se trata de indi- crescimento.70 A SOP é doença exclusiva de me-
car ou supervalorizar as cirurgias, mas sim de ninas e ocasiona hirsutismo, distúrbios menstru-
chamar atenção para o sucesso de pesquisas com ais, acne e alopecia,71 sendo que a ocorrência de
probióticos e mesmo transplantes de fezes, já hiperinsulinismo e resistência periférica à insuli-
usados para o manejo da obesidade. na é frequente.72
Outros estudos em animais sugerem que A etapa primordial do tratamento é o con-
certas misturas de bactérias residentes induzem trole da doença de base, com reposição hormonal

nos casos de hipotireoidismo e deficiência de hor- Em Pediatria, esta condição pode ser ob-
mônio de crescimento. O controle do hipercorti- servada especialmente em pacientes com cranio-
solismo depende da etilogia, podendo ser cirúr- faringioma, um tumor embrionário localizado na
gico nos casos dos adenomas. A SOP necessita região do hipotálamo/hipófise, que causa danos
de tratamento apropriado que permita a ovula- ao hipotálamo devido ao próprio tumor ou pelo
ção adequada, sendo que, nos casos em que há tratamento (excisão cirúrgica e radioterapia). É
concomitância de resistência periférica à insuli- uma neoplasia de natureza benigna, pouco fre-
na, a metformina tem sido utilizada com resulta- quente, responsável por 1% a 3% de todos os
dos satisfatórios.73 tumores intracranianos.
A relação entre hormônios e obesidade é Outros fatores também podem fazer parte
bastante complexa. Muitas doenças genéticas (tais da etiologia da obesidade hipotalâmica 74 , tais
como a deficiência congênita de leptina) apresen- como: tumores (epitelioma, angiosarcoma, coles-
tam interface hormonal evidente. De igual forma, teatoma, pinealoma, greminoma, endotelioma,
é provável que muitas crianças obesas apresen- ependimoma, glioma, meningioma, macroadeno-
tem defeitos de produção ou de sinalização de ma hipofisário, teratoma, metástases); inflamação
hormônios ainda não completamente estudados, (sarcoidose, tuberculose, aracnoidite, histiocitose
mas sabidamente ligados aos processos de fome, X, encefalites); síndromes genéticas (síndrome de
saciedade e balanço energético, tais como grelina, Prader-Willi, síndrome de Bardet-Biedl); trauma-
peptídeo YY (PYY), pró-ópio-melanocortina (PONC), tismo craniano; neurocirurgia; radioterapia crania-
transcrito regulador de cocaína e anfetamina na; aneurisma cerebral; drogas psicotrópicas.
(CART), neuropeptídio Y (NPY), peptídeo relacio- O mecanismo proposto para a obesidade
nado ao gene agouti (AgRP), hormônio concen- hipotalâmica tem sido descrito como um desequi-
trador de melanina (MCH), orexina, galanina, áci- líbrio da ação de hormônios orexígenos e anore-
do gama-aminobutírico (GABA), entre outros.66 À xígenos decorrentes dos fatores acima mencio-
medida que distúrbios endocrinológicos específi- nados, que levam à sinalização hipotalâmica dis-
cos desses hormônios forem descobertos, é pos- funcional da homeostase energética. Embora al-
sível que, dentro da classificação proposta, pas- guns estudos tenham demonstrado que estraté-
sem a figurar no presente tópico. Entretanto, até gias terapêuticas não farmacológicas, como die-
a presente data, isso ainda não é possível. ta e atividade física, estejam associadas com
melhora na composição corporal e retardo no
Obesidade associada a problemas ganho de peso, ainda são necessários mais es-
neurológicos tudos para estabelecer a terapia mais adequada
A obesidade de origem hipotalâmica é do- para esses indivíduos.75
ença rara em seres humanos. Ocorre quando exis-
te lesão na região ventromedial ou paraventricular Obesidade associada a distúrbios do sono
do hipotálamo ou na amígdala cerebral. Essas Há algum tempo já é reconhecida a impor-
regiões do cérebro são responsáveis pela inte- tante influência do sono na gênese e na manu-
gração de informações metabólicas sobre reser- tenção da obesidade. Revisão sistemática de 25
vas de nutrientes com impulsos sensoriais afe- estudos publicados entre 2006 e 2011 envolven-
rentes sobre a disponibilidade de alimentos. do crianças e adolescentes entre zero e 19 anos
Quando ocorre lesão, podem causar alte- de idade, verificou que 100% dos estudos mos-
rações metabólicas, como hiperfagia, hiperinsuli- travam associação estatisticamente significativa
nemia, prejuízo da termogênese dos alimentos, entre curta duração do sono e obesidade.76
além de desordens funcionais no sistema nervo- Acredita-se que problemas de sono possam
so autônomo; esses aspectos estão associados estar relacionados à obesidade desde o início da
com a gênese de obesidade. Esta condição pode vida.77 Vários fatores são reconhecidos como cau-
ser causada por trauma, tumor, doença inflama- sadores desse efeito, tais como: aumento da
tória, cirurgia de fossa posterior ou aumento da fome; aumento da oportunidade de comer, ter-
pressão intracraniana. 74 morregulação prejudicada, maior fadiga, aumen-

to dos hormônios ligados ao estresse e aumento ciação de outros fármacos que antagonizem o
da produção de grelina.78 efeito obesogênico, como o uso de topiramato ou
É bastante difícil estabelecer a quantidade metformina, em pacientes em tratamento de es-
de sono ideal para uma criança, sendo reconhe- quizofrenia ou outras doenças psiquiátricas.81,83,85
cido o fato de haver grande variação individual.
Por outro lado, sabe-se que o peso abdominal da
Obesidade associada a agentes
criança obesa exerce, na posição horizontal, for-
infecciosos
te pressão sobre o diafragma, que é o principal Alguns agentes infecciosos já foram asso-
músculo respiratório, fazendo com que ele dimi- ciados com a obesidade, especialmente o adeno-
nua sua capacidade de trabalho. Esse fato leva à vírus.86,87 Estudos em humanos, incluindo um pe-
dificuldade respiratória importante, com períodos queno ensaio em gêmeos, mostrou associação
curtos de completa parada na respiração, conhe- entre anticorpos para o adenovírus 36 e estado
cidos como apneia. Esses períodos, apesar de de obesidade em adultos, mas essa associação
sutis, fazem a criança acordar dezenas de vezes não foi confirmada em outros estudos.88,89 Possí-
no decorrer da noite, dificultando o aprofunda- veis explicações para as observações em huma-
mento do sono. Muitas vezes a irritabilidade e a nos incluem uma verdadeira associação causal, a
sonolência diurna observadas em algumas crian- vulnerabilidade à infecção por adenovírus ou a
ças obesas devem-se a esse fato.79 presença de fatores de confusão não medidos.
Sendo assim, fica claro que a relação entre Em estudo transversal de 124 escolares e
sono e obesidade ocorre por um círculo vicioso, adolescentes com idade entre oito e 18 anos,90
em que os dois quadros se retroalimentam, tor- os anticorpos para o subgrupo D do adenovírus
nando o tratamento ainda mais difícil, uma vez tipo 36 foram encontradas em 19 indivíduos. Quin-
que os mecanismos desse processo ainda não ze (78%) dos 19 indivíduos soropositivos eram
são totalmente conhecidos80. obesos (IMC ≥ percentil 95) e a presença destes
anticorpos foi significativamente mais frequente
Obesidade associada ao uso de fármacos entre indivíduos obesos que entre os não obe-
É um quadro desencadeado e/ou mantido sos (22 versus 7%); entre as crianças obesas,
pela utilização de fármacos atuando como orexí- aquelas que eram soropositivas tinham maiores
genos, agravando a resistência insulínica, aumen- peso, IMC, circunferência da cintura e relação cin-
tando a deposição de gordura ou reduzindo o tura-altura quando comparadas com as
metabolismo basal. Em geral, a anamnese revela seronegativas. Embora estes resultados sugiram
a relação entre o uso do fármaco e o surgimento possível ligação entre o adenovirus 36 e a obesi-
ou o agravamento da obesidade. dade, ainda não foi definitivamente estabelecida
Os fármacos habitualmente envolvidos são: uma relação causal, mas apenas associação.
corticoides, antipsicóticos (valproato de sódio, clo-
zapina, olanzapina, risperidona, quetiapina, clor-
Obesidade psicossocial
promazina), antidepressivos (amitripitilina, imipra- A obesidade nestes casos está associada
mina, nortriptilina), antihistamínicos, estabilizado- ao aumento da ingestão de alimentos diante de
res do humor (carbonato de lítio, ácido valpróico e estados emocionais diversos. A fim de tentar ex-
carbamazepina), anticonvulsivantes (gabapentina, plicar este fato, primeiramente é preciso pontuar
carbamazepina), alguns antineoplásicos, insulina, a importância da alimentação durante a infância,
secretagogos de insulina, antihipertensivos (pro- bem como a relação entre mãe/cuidador e a crian-
pranolol, clonidina) e contraceptivos.66,81-84 ça.
No exame físico podem-se observar sinais Ao nascer, mais do que ser alimentado fisi-
relativos à doença que levou à utilização do fár- camente e consequentemente ter suas necessi-
maco ou sinais causados pelo próprio medicamen- dades nutricionais satisfeitas, a criança necessi-
to. A suspensão ou substituição da droga está ta receber afeto, atenção e cuidado, o que favo-
sempre indicada, apesar de não ser sempre pos- recerá o estabelecimento do vínculo entre mãe/
sível. Em alguns casos, têm-se sugerido a asso- cuidador e criança, suprindo assim suas necessi-

dades emocionais. À medida em que esse vínculo Assim, as necessidades de afeto e atenção
vai se construindo de maneira inadequada ou con- vão encontrar respaldo nas mais diversas formas.
flituosa, a criança pode se tornar mais vulnerável A experiência vivenciada na prática clínica, quan-
ao desenvolvimento de doenças, entre elas a do se pensa em obesidade, permite listar uma
obesidade. Neste caso, pode ocorrer, por exem- série de combinações e possibilidades, que se
plo, superalimentação por parte da mãe/cuidador materializam em alguns esteriótipos, amplamen-
em função da sua dificuldade em distinguir a fome te observados, sendo os mais comuns descritos
da criança de outras necessidades. abaixo 95,96,97:
Assim, ao invés de oferecer atenção, afeto, - Cuidador ansioso e criança voraz: trata-se do
carinho, cuidado e acolhimento necessários ao modelo clássico e, talvez, o mais frequente. Aqui,
filho, são oferecidos alimentos como tentativa de a impossibilidade de contenção adequada às
suprimir o desconforto da criança. Esta aprende necessidades reais do filho, leva a mãe ou cui-
assim que, diante de conflitos e dificuldades o dador a responder a qualquer estímulo com ali-
alimento minimiza o sofrimento emocional.91,92 mentação o que acarretará, ainda nos primei-
A Teoria do Apego de Bowlby93 oferece su- ros meses de vida, em ganho excessivo de
porte à hipótese anteriormente destacada na peso. 98 Esse modelo, entretanto, pode ser
medida em que aponta que todo ser humano transposto para qualquer idade. Dessa forma,
busca a proximidade de pessoas significativas são comuns crianças, adolescentes e adultos
diante de situações de ameaça ou de necessida- vorazes e intolerantes à frustração que, ao não
des diversas. Ao se aproximar dessas pessoas e encontrarem contenção adequada para suas
obter o cuidado e o afeto necessários, o indiví- angústias, utilizam-se do alimento como sub-
duo tenderia a se sentir mais seguro. Ao contrá- terfúgio.
rio, quando não há disponibilidade dessas figu- - Pais negligentes: dentro dessa categoria, en-
ras significativas ou quando essas não são capa- contram-se genitores completamente alheios
zes de oferecer o suporte necessário ou adequa- aos cuidados dos filhos. Quase sempre dele-
do, podem ocorrer dificuldades em lidar com tais gam a função a um terceiro, que podem ser
situações de ameaça, insegurança e necessida- avós ou cuidadores, e se esquivam de quais-
de, predispondo o indivíduo ao desenvolvimento quer responsabilidades na criação, educação e
de doenças como a obesidade. Neste caso, o ali- cuidado dos filhos. Os motivos que levam a tal
mento é utilizado como forma de minimizar os conduta podem ser os mais variados, indo de
conflitos emocionais. depressão, que nesse caso falta condição psí-
Com base nesta teoria, destaca-se a im- quica para serem cuidadores, até mesmo medo,
portância de figuras representativas para a cri- narcisismo ou execução de tarefas cotidianas,
ança, podendo ser os pais ou os cuidadores. Nos onde o filho é algo que não pode atrapalhar a
dias de hoje, com as mudanças que estão sendo vida, pois sempre vai existir uma boa razão para
vivenciadas na família, além do tradicional papel que a criança fique em segundo plano.
da mãe, o pai têm surgido como pessoa significa- - Competitividade: a competição entre pai ou
tiva nos cuidados com os filhos, alcançando lugar mãe e filho ou filha é outro estereótipo comum.
de destaque na conformação familiar, colocando- Tornar-se pai e mãe exige, além de disponibili-
se como figura emocionalmente disponível, sen- dade física, condições psíquicas. O crescimento
sível e que promova segurança, favorecendo o dos filhos, ao mesmo tempo em que é deseja-
aprendizado de estratégias de autorregulação do e bem-vindo, aguça nos pais o sentimento
emocional e de respostas adequadas aos pro- de declínio das próprias condições físicas, acar-
blemas psicológicos, contribuindo para minimizar retando em possível boicote dos genitores, por
os riscos da obesidade psicossocial.94 vezes inconsciente, a tudo o que possa permi-
Apesar de ser reconhecida a importância da tir crescer e aflorar dos filhos. Como resultado,
proximidade de pessoas significativas, como an- qualquer tipo de abordagem, médica, nutricio-
teriormente salientado, existem características nal e psicológica visando emagrecimento tor-
psíquicas individuais de cada pessoa. na-se difícil.99

- Culpa pela ausência: considera-se culpa pela Obesidade somática

ausência à situação em que os pais, por razões
diversas, concretas ou abstratas, como por Trata-se de quadro eminentemente ligado
exemplo, trabalho, compensam seus filhos com ao balanço energético, em que o excesso de te-
comida. Nesse cenário, a criança pode até ter cido adiposo deve-se ao consumo inadequado de
tido regras alimentares cumpridas ao longo do calorias frente ao gasto energético105. Na anam-
dia ou da semana, mas a chegada do genitor nese percebe-se história de consumo alimentar
ausente provoca ruptura nas regras e rotinas excessivo e/ou de sedentarismo. Observam-se os
alimentares. Se as ausências forem frequentes, maus hábitos alimentares, como abusos de óleo,
a falta de regra alimentar será constante.100 açúcar e sal no preparo dos alimentos, ausência
- Simbiose: nesse quadro, o que une pai e mãe de horários para as refeições e simultaneidade
ao filho ou filha, é sempre uma característica de alimentação com outras atividades como as-
comum mantida por ambos, como um pacto ve- sistir à televisão, passeios e reuniões sociais.
lado sendo, no presente caso, a semelhança que O inquérito alimentar quase sempre revela
interessa é o comer em si, que acaba originan- consumo calórico excessivo e a avaliação da ati-
do ou mantendo o quadro de obesidade. Assim, vidade física em geral indica sinais de comporta-
a relação se mantém perfeita enquanto o refe- mento eminentemente sedentário.
rido pacto não seja rompido por uma das par- Ocorre, quase sempre, a partir de um mo-
tes. Nesse caso, se quem tentar quebrar o elo mento bem determinado, sendo comum observar-
for a criança, a mesma sentirá dificuldade maior se fator desencadeante a partir do qual o balan-
pois, além de ter que passar por reeducação ço energético passou a ser positivo.
alimentar, ainda terá que estabelecer nova for- Ao exame físico, a criança apresenta aspec-
ma de vínculo com o genitor, suportando os ata- to saudável, não se encontrando outros sinais além
ques e boicotes constantes do mesmo. do panículo adiposo aumentado que, em geral,
- Sistemas familiares obesogênicos: como o pró- está bem distribuído ou mais concentrado no ab-
prio nome indica não se trata de característica dome. Raramente estão presentes estrias. A pres-
ligada a apenas um dos genitores, mas de toda são arterial tende a ser normal ou pouco elevada.
família. Nesse caso, o sistema familiar, como um A estatura é pouco elevada ou segue o canal fa-
todo, é comprometido, quando o assunto é ali- miliar. O perfil lipídico encontra-se quase sempre
mentação. Todos os membros possuem sobre- dentro da normalidade, podendo-se observar, nos
peso ou obesidade e a alimentação é sempre casos mais graves, pequenos aumentos nos va-
desregrada e hipercalórica, ao mesmo tempo lores de colesterol ou triglicerídeos, que rapida-
em que a prática de atividade física costuma mente respondem à dietoterapia. A resistência
ser desvalorizada. 95,101,102 insulínica é frequente apenas nos casos mais gra-
- Depressão: ao lado de sintomas mais comuns à ves, com boa resposta ao emagrecimento.
depressão, como tristeza, apatia, irritabilidade, O tratamento é clássico, com associação de
isolamento, pode existir, concomitantemente, a dieta hipocalórica, reeducação alimentar e aumen-
perda ou ganho de peso.103 Assim, frente a uma to da atividade física, uma vez que na faixa etária
criança ou adolescente com sobrepeso/obesi- pediátrica, as opções farmacológicas para a obe-
dade ou com dificuldades alimentares, a depres- sidade somática são praticamente inexistentes.106
são tem que ser investigada e, eventualmente,
tratada. CONSIDERAÇÕES FINAIS
Apesar da complexidade das relações en-
tre obesidade e saúde mental,104 aprender a iden- Existem várias classificações de obesidade,
tificar essas combinações ou situações psicosso- tais como primária ou secundária (a primária im-
ciais permite ao profissional atuar, muitas vezes, plica em ingestão alimentar excessiva pura, e a
diretamente no fator desencadeante ou mante- secundária na pré-existência de alguma doença
nedor da obesidade, o que resulta em maior pro- que leve ao excesso de peso); exógena, por au-
babilidade de êxito no tratamento. mento da ingestão ou endógena, quando estão

presentes anomalias endócrinas, genéticas, etc. 5. Nishtar S, Gluckman P, Armstrong T. Ending child-
hood obesity: a time for action. Lancet.
O Código Internacional de Doenças limita-se a di- 2016;387:825-7.
vidir obesidade devida a excesso de calorias e 6. IBGE. Pesquisa de orçamentos familiares 2008-2009
- Análise do consumo alimentar pessoal no Brasil.
obesidade induzida por drogas. Estas classifica-
In: rendimento Cdte, editor. Rio de Janeiro: IBGE;
ções têm como base a fisiopatogenia, em última 2011. p. 150.
análise, pois discriminam se o aumento de tecido 7. Ricco RC, Ricco RG, Nogueira-de-Almeida CA, Ramos
APP. Comparative study of risk factors among chil-
adiposo deve-se ao excesso do alimento ou a dren and adolescents with an anthropometric diag-
outros fatores que levam ao acúmulo de gordura. nosis of overweight or obesity. Rev Paul Pediatr.
2010;28:320-5.
Há dificuldades de se classificar a obesidade atra-
8. Nogueira-de-Almeida CA, Pires LA, Santos RG. Com-
vés da etiopatogenia, pois essa escolha torna o paração de indicadores de perfis glicêmico e lipídico
atendimento dispendioso, com inúmeras aborda- entre crianças e adolescentes obesos egressos de
serviço público ou privado da cidade de Ribeirão
gens laboratoriais, as quais nem sempre estão dis- Preto (SP). Medicina (Ribeirão Preto. Online). 2016;
poníveis na saúde publica ou mesmo privada. Não 49:504-10.
há dúvida de que a abordagem terapêutica de 9. Nogueira-de-Almeida CA, Garcia J, Caixe SH,

Benedeti AC. Ultrasonographic assessment of the
preferência deverá ser multiprofissional, common carotid intima-media complex in normal
enfatizando aspectos nutricionais, psicológicos, weight children and in overweight/obese children.
The FASEB Journal. 2016;30:1165.3-.3.
socioculturais, integrando família e cuidador, uma 10. Nogueira-de-Almeida CA, Caixe SH, Benedeti ACGS,
vez que os tratamentos medicamento e cirúrgico Garcia J. Echocardiography evaluation as a marker
of cardiovascular risk on obese children and ado-
nem sempre serão a primeira escolha. lescents. The FASEB Journal 2016 30: (Suppl. 1)
Sabe-se que, especialmente na área cientí- 126.1.
fica, toda classificação sempre será sujeita a críti- 11. Nogueira-de-Almeida CA, Benedeti AC, Garcia J,
Caixe SH. Correlation between ultrasonographic
cas. Nesse caso, uma restrição possível à propos- measures of the abdominal adiposity and indica-
ta relatada neste artigo é a dificuldade em se ca- tors of obesity in normal and overweight/obesity
children. The FASEB Journal. 2016;30:1165.4-.4.
racterizar a resistência periférica à insulina, além
12. Nogueira-de-Almeida CA, Mello E. Avalliação do es-
de ainda persistirem dúvidas na literatura científi- tado nutrológico. In: Nogueira-de-Almeida CA, Mello
ca sobre seu papel, havendo tanto relatos de que E, editors. Nutrologia Pediátrica: Prática Baseada em
Evidências. 1 ed. São Paulo: Manole; 2016. p. 12-
ela antecede a obesidade como de que ela é ape- 38.
nas mais uma consequência dessa condição. 13. Nogueira-de-Almeida CA, Mello ED. Correlation of
body mass index Z-scores with glucose and lipid
A classificação apresentada não pretende
profiles among overweight and obese children and
acrescentar fatos novos ao já extenso, apesar adolescents. J Pediatr (Rio J). 2018; 94:308-12.
de incompleto, conhecimento sobre a obesidade 14. Romualdo MC, Nobrega FJ, Escrivao MA. Insulin re-
sistance in obese children and adolescents. J Pediatr
na infância. Objetiva apenas organizar os conhe- (Rio J). 2014;90:600-7.
cimentos existentes, com a finalidade principal de 15. Nogueira-de-Almeida CA, Pinho AP, Ricco RG, Pepato
facilitar a tomada de conduta, reforçando a regra MT, Brunetti IL. Determination of glycemia and
insulinemia and the homeostasis model assessment
cada vez mais aceita de que o tratamento das (HOMA) in schoolchildren and adolescents with nor-
doenças em geral, e da obesidade em especial, mal body mass index. J Pediatr (Rio J). 2008;
84:136-40.
deve ser individualizado.
16. Ten S, Maclaren N. Insulin resistance syndrome in
children. J Clin Endocrinol Metab. 2004;89:2526-39.
17. Brasil AR. Crianças e adolescentes com sobrepeso
REFERÊNCIAS BIBLIOGRÁFICAS ou obesidade: avaliação da reação infalmatória atra-
vés da dosagem de proteína C reativa ultra sensí-
1. Nogueira-de-Almeida CA, Baptista MEC, de Almeida vel e prevalência de síndrome metabólica. Belo
GAN, de Faria Ferraz VE. Obesidade infanto-juvenil: Horizonte, 2006; Dissertação (mestrado) – UFMG,
uma proposta de classificação clínica. Pediatr. (São Faculdade de Medicina.
Paulo). 2004;26:257-67.
18. Cook S, Weitzman M, Auinger P, Nguyen M, Dietz
2. Damiani D. Editorial: Obesidade infanto-juvenil: uma WH. Prevalence of a metabolic syndrome pheno-
proposta de classificação clínica. Pediatr. (São Pau- type in adolescents: findings from the third National
lo). 2004;26:1. Health and Nutrition Examination Survey, 1988-
3. Nogueira-de-Almeida CA, Mello ED. Nutrologia 1994. Arch Pediatr Adolesc Med. 2003;157:821-7.
Pediátrica - Prática Baseada em Evidências: Manole; 19. Moran A, Jacobs DR, Jr., Steinberger J, Hong CP,
2016. Prineas R, Luepker R, et al. Insulin resistance dur-
4. Han JC, Lawlor DA, Kimm SY. Childhood obesity. Lan- ing puberty: results from clamp studies in 357 chil-
cet. 2010;375:1737-48. dren. Diabetes. 1999;48:2039-44.

20. Sinaiko AR, Steinberger J, Moran A, Prineas RJ, 36. Foerste T, Sabin M, Reid S, Reddihough D. Under-
Vessby B, Basu S, et al. Relation of body mass in- standing the causes of obesity in children with tri-
dex and insulin resistance to cardiovascular risk fac- somy 21: hyperphagia vs physical inactivity. J Intel-
tors, inflammatory factors, and oxidative stress lect Disabil Res. 2016;60:856-64.
during adolescence. Circulation. 2005;111:1985-91. 37. Lucas A, Gore SM, Cole TJ, Bamford MF, Dossetor
21. Cuartero BG, Lacalle CG, Lobo CJ, Vergaz AG, Rey JF, Barr I, et al. Multicentre trial on feeding low
CC, Villar MJA, et al. Índice HOMA y QUICKI, insuli- birthweight infants: effects of diet on early growth.
na y peptido C en ninos sanos. Puntos de corte de Arch Dis Child. 1984;59:722-30.
riesgo cardiovascular. An Pediatr (Barc). 2007; 66: 38. Desai M, Jellyman JK, Ross MG. Epigenomics, ges-
481-90. tational programming and risk of metabolic syn-
22. Nogueira-de-Almeida CA, Pinho AP, Ricco RG, Pepato drome. Int J Obes. (Lond). 2015;39:633-41.
MT, Brunetti IL. Determination of glycemia and 39. Williams TC, Drake AJ. What a general paediatri-
insulinemia and the homeostasis model assessment cian needs to know about early life programming.
(HOMA) in schoolchildren and adolescents with nor- Arch Dis Child. 2015;100:1058-63.
mal body mass index. J Pediatr (Rio J). 2008; 84:
136-40. 40. Barker DJ, Eriksson JG, Forsen T, Osmond C. Fetal
origins of adult disease: strength of effects and bio-
23. Nogueira-de-Almeida CA, de Mello ED. Different Cri- logical basis. Int J Epidemiol. 2002;31:1235-9.
teria for the Definition of Insulin Resistance and Its
Relation with Dyslipidemia in Overweight and Obese 41. Merkestein M, Cagampang FR, Sellayah D. Fetal
Children and Adolescents. Pediatr Gastroenterol programming of adipose tissue function: an evolu-
Hepatol Nutr. 2018;21:59-67. tionary perspective. Mamm Genome. 2014;25:413-
23.
24. Pinho AP, Brunetti IL, Pepato MT, Nogueira-de-
Almeida CA. Síndrome metabólica em adolescen- 42. Barker DJ, Winter PD, Osmond C, Margetts B,
tes do sexo feminino com sobrepeso e obesidade. Simmonds SJ. Weight in infancy and death from
Rev Paul Pediatr. 2012;30:51-6. ischaemic heart disease. Lancet. 1989;2:577-80.
25. Carlone A, Venditti C, Cipolloni L, Zampetti S, 43. Barker DJ, Osmond C, Kajantie E, Eriksson JG. Growth
Spoletini M, Capizzi M, et al. [Childhhood obesity, and chronic disease: findings in the Helsinki Birth
insulin resistance and increased cardiovascular risk]. Cohort. Ann Hum Biol. 2009;36:445-58.
Recenti Prog Med. 2012;103:369-72. 44. Eriksson JG, Forsen T, Tuomilehto J, Jaddoe VW,
26. Wood P. Insulin Resistance: A Vicious Circle Of Ex- Osmond C, Barker DJ. Effects of size at birth and
cess Fat. Diabetes in control [Internet]. 2007 June childhood growth on the insulin resistance syndrome
9th, 2016. Available from: http:// in elderly individuals. Diabetologia. 2002;45:342-8.
www.diabetesincontrol.com/insulin-resistance-a-vi- 45. Roszkowska R, Taranta-Janusz K, Wasilewska A.
cious-circle-of-excess-fat/. [The role of early-life metabolic programming in the
27. Kendall D, Vail A, Amin R, Barrett T, Dimitri P, Ivison pathogenesis of lifestyle diseases]. Dev Period Med.
F, et al. Metformin in obese children and adoles- 2014;18:477-82.
cents: the MOCA trial. J Clin Endocrinol Metab. 46. Silveira PP, Portella AK, Goldani MZ, Barbieri MA.
2013;98:322-9. Origens desenvolvimentistas da saúde e da doen-
28. Li L, Perez A, Wu LT, Ranjit N, Brown HS, Kelder SH. ça (DOHaD). J Pediatr (Rio J). 2007;83:494-504.
Cardiometabolic Risk Factors among Severely Obese 47. Lane RH. Fetal programming, epigenetics, and adult
Children and Adolescents in the United States, 1999- onset disease. Clin Perinatol. 2014;41:815-31.
2012. Child Obes. 2016;12:12-9. 48. Segovia SA, Vickers MH, Gray C, Reynolds CM. Ma-
29. Bouchard C. Gene-environment interactions in the ternal obesity, inflammation, and developmental
etiology of obesity: defining the fundamentals. programming. Biomed Res Int. 2014;2014:418975.
Obesity (Silver Spring). 2008;16 Suppl 3:S5-S10. 49. Hofman PL, Regan F, Jackson WE, Jefferies C, Knight
30. Agurs-Collins T, Bouchard C. Gene-nutrition and DB, Robinson EM, et al. Premature birth and later
gene-physical activity interactions in the etiology of insulin resistance. N Engl J Med. 2004; 351:2179-
o b e s i ty. I n t r o d u c t i o n . O b e s i ty ( S i l ve r S p r i n g ) . 86.
2008;16 Suppl 3:S2-4. 50. Weber M, Grote V, Closa-Monasterolo R, Escribano
31. Wabitsch M, Funcke JB, Lennerz B, Kuhnle-Krahl U, J, Langhendries JP, Dain E, et al. Lower protein con-
Lahr G, Debatin KM, et al. Biologically inactive leptin tent in infant formula reduces BMI and obesity risk
and early-onset extreme obesity. N Engl J Med. at school age: follow-up of a randomized trial. Am J
2015;372:48-54. Clin Nutr. 2014;99:1041-51.
32. Loos RJ, Bouchard C. FTO: the first gene contribut- 51. Nogueira-de-Almeida CA, Pires LA, Miyasaka J,
ing to common forms of human obesity. Obes Rev. Bueno V, Khouri JM, Ramos ML, et al. Comparison
2008;9:246-50. of feeding habits and physical activity between eu-
33. Chung WK. An overview of mongenic and syndromic trophic and overweight/obese children and adoles-
obesities in humans. Pediatr Blood Cancer. 2012; cents: a cross sectional study. Rev Assoc Med Bras
58:122-8. (1992). 2015;61:227-33.
34. Milani D, Cerutti M, Pezzani L, Maffei P, Milan G, 52. Piccini RX, Facchini LA, Tomasi E, Thumé E, Silveira
Esposito S. Syndromic obesity: clinical implications DSd, Siqueira FV, et al. Efetividade da atenção pré-
of a correct diagnosis. Ital J Pediatr. 2014;40:33. natal e de puericultura em unidades básicas de saú-
de do Sul e do Nordeste do Brasil. Rev Bras Saúde
35. Lindgren AC, Barkeling B, Hagg A, Ritzen EM, Marcus Mater Infant. 2007;7:75-82.
C, Rossner S. Eating behavior in Prader-Willi syn-
drome, normal weight, and obese control groups. J 53. Del Ciampo LA, Ricco RG, Daneluzzi JC, Del Ciampo
Pediatr. 2000;137:50-5. IRL, Ferraz IS, Nogueira-de-Almeida CA. O Progra-
ma de Saúde da Família e a Puericultura. Ciênc
Saúde Coletiva (online). 2006;11:739-43.

54. Murphy EF, Clarke SF, Marques TM, Hill C, Stanton 72. Nezi M, Christopoulos P, Paltoglou G, Gryparis A,
C, Ross RP, et al. Antimicrobials: Strategies for tar- Bakoulas V, Deligeoroglou E, et al. Focus on BMI
geting obesity and metabolic health? Gut Microbes. and subclinical hypothyroidism in adolescent girls
2013;4:48-53. first examined for amenorrhea or oligomenorrhea.
55. Tremaroli V, Backhed F. Functional interactions be- The emerging role of polycystic ovary syndrome. J
tween the gut microbiota and host metabolism. Na- Pediatr Endocrinol Metab. 2016;29:693-702.
ture. 2012;489:242-9. 7 3 . S i n a i Ta l a u l i k a r V, Ta n g T, Ya s m i n E . Ro l e o f
56. Jess T. Microbiota, antibiotics, and obesity. N Engl J metformin in women’s health: review of its current
Med. 2014;371:2526-8. place in clinical practice and emerging indications
for future. Obstet Gynecol Surv. 2016;71:307-17.
57. Ajslev TA, Andersen CS, Gamborg M, Sorensen TI,
Jess T. Childhood overweight after establishment 74. Hochberg I, Hochberg Z. Expanding the definition
of the gut microbiota: the role of delivery mode, of hypothalamic obesity. Obes Rev. 2010;11:709-
pre-pregnancy weight and early administration of 21.
antibiotics. Int J Obes (Lond). 2011;35:522-9. 75. Hochberg I, Hochberg Z. Hypothalamic obesity.
58. Saari A, Virta LJ, Sankilampi U, Dunkel L, Saxen H. Endocr Dev. 2010;17:185-96.
Antibiotic exposure in infancy and risk of being over- 76. Liu J, Zhang A, Li L. Sleep duration and overweight/
weight in the first 24 months of life. Pediatrics. obesity in children: review and implications for
2015;135:617-26. pediatric nursing. J Spec Pediatr Nurs. 2012;17:193-
59. Dogra S, Sakwinska O, Soh SE, Ngom-Bru C, Bruck 204.
WM, Berger B, et al. Dynamics of infant gut microbiota 77. Woo Baidal JA, Locks LM, Cheng ER, Blake-Lamb
are influenced by delivery mode and gestational TL, Perkins ME, Taveras EM. Risk Factors for child-
duration and are associated with subsequent adi- hood obesity in the first 1,000 days: A Systematic
posity. MBio. 2015;6:e02419-14. Review. Am J Prev Med. 2016;50:761-79.
60. Schwartz BS, Pollak J, Bailey-Davis L, Hirsch AG, 78. Kim TW, Jeong JH, Hong SC. The impact of sleep
Cosgrove SE, Nau C, et al. Antibiotic use and child- and circadian disturbance on hormones and metabo-
hood body mass index trajectory. Int J Obes (Lond). lism. Int J Endocrinol. 2015;2015:591729.
2016;40:615-21. 79. Nogueira-de-Almeida CA, Mello E. Obesidade. In:
61. Gerber JS, Bryan M, Ross RK, Daymont C, Parks EP, Nogueira-de-Almeida CA, Mello E, editors. Nutrologia
Localio AR, et al. Antibiotic exposure during the first Pediátrica: Prática Baseada em Evidências. 1ª ed.
6 months of life and weight gain during childhood. São Paulo: Manole; 2016. p. 135-56.
JAMA. 2016;315:1258-65. 80. Vargas PA. The Link Between Inadequate Sleep and
62. Cho YM. A gut feeling to cure diabetes: potential Obesity in Young Adults. Curr Obes Rep. 2016;5:38-
mechanisms of diabetes remission after bariatric 50.
surgery. Diabetes Metab J. 2014;38:406-15. 81. Cooper SJ, Reynolds GP, With expert c-a, Barnes T,
63. Suarez-Zamorano N, Fabbiano S, Chevalier C, England E, Haddad PM, et al. BAP guidelines on the
Stojanovic O, Colin DJ, Stevanovic A, et al. Microbiota management of weight gain, metabolic disturbances
depletion promotes browning of white adipose tis- and cardiovascular risk associated with psychosis and
sue and reduces obesity. Nat Med. 2015;21:1497- antipsychotic drug treatment. J Psychopharmacol.
501. 2016;30:717-48.
64. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, 82. Reekie J, Hosking SP, Prakash C, Kao KT, Juonala
Mardis ER, Gordon JI. An obesity-associated gut M, Sabin MA. The effect of antidepressants and
microbiome with increased capacity for energy har- antipsychotics on weight gain in children and ado-
vest. Nature. 2006;444:1027-31. lescents. Obes Rev. 2015;16:566-80.
65. Smith SR. The endocrinology of obesity. Endocrinol 83. Tek C, Chwastiak L. Metformin for weight loss in
Metab Clin North Am. 1996;25:921-42. schizophrenia: safe but not a panacea. Evid Based
66. Han JC, Lawlor DA, Kimm SYS. Childhood obesity. Ment Health. 2014;17:51-2.
The Lancet.375:1737-48. 84. Malone M. Medications associated with weight gain.
67. Emokpae MA, Adeleke SI, Uwumarongie HO. Sub- Ann Pharmacother. 2005;39:2046-55.
clinical hypothyroidism in childhood obesity and its 85. Choi YJ. Efficacy of adjunctive treatments added to
correlation with lipoproteins. Afr J Med Med Sci. olanzapine or clozapine for weight control in patients
2011;40:361-5. with schizophrenia: a systematic review and meta-
68. Min L. Functional Hypercortisolism, Visceral obesity, analysis. The Scientific World Journal. 2015;
and metabolic syndrome. Endocr Pract. 2016;22:506- 2015:970730.
8. 86. Whigham LD, Israel BA, Atkinson RL. Adipogenic
69. Germain-Lee EL. Short stature, obesity, and growth potential of multiple human adenoviruses in vivo
hormone deficiency in pseudohypoparathyroidism and in vitro in animals. Am J Physiol Regul Integr
type 1a. Pediatr Endocrinol Rev. 2006;3 Suppl 2:318- Comp Physiol. 2006;290:R190-4.
27. 87. Atkinson RL, Dhurandhar NV, Allison DB, Bowen RL,
70. Berryman DE, Glad CA, List EO, Johannsson G. The Israel BA, Albu JB, et al. Human adenovirus-36 is
GH/IGF-1 axis in obesity: pathophysiology and thera- associated with increased body weight and paradoxi-
peutic considerations. Nat Rev Endocrinol. cal reduction of serum lipids. Int J Obes (Lond).
2013;9:346-56. 2005;29:281-6.
71. Lizneva D, Suturina L, Walker W, Brakta S, Gavrilova- 88. Broderick MP, Hansen CJ, Irvine M, Metzgar D,
Jordan L, Azziz R. Criteria, prevalence, and pheno- Campbell K, Baker C, et al. Adenovirus 36 serop-
types of polycystic ovary syndrome. Fertil Steril. ositivity is strongly associated with race and gender,
2016;106:6-15. but not obesity, among US military personnel. Int J
Obes (Lond). 2010;34:302-8.

89. Goossens VJ, deJager SA, Grauls GE, Gielen M, 98. Zavaroni DML. Amamentação, sintomas e consti-
Vlietinck RF, Derom CA, et al. Lack of evidence for tuição psíquica. In: Viana TCL, I., editor. Sintomas
the role of human adenovirus-36 in obesity in a alimentares, cultura, corpo e obesidade: questoes
European cohort. Obesity (Silver Spring). 2011; clínicas e de avaliação: Placebo; 2013.
19:220-1. 99. Klein M. Inveja e gratidão: e outros trabalhos 1946
90. Gabbert C, Donohue M, Arnold J, Schwimmer JB. - 1963. Rio de Janeiro: Imago; 1991.
Adenovirus 36 and obesity in children and adoles- 100. Klein M. Amor, culpa e reparação: e outros traba-
cents. Pediatrics. 2010;126:721-6. lhos 1921 - 1945. Rio de Janeiro: Imago; 1996.
91. Nguyen-Rodriguez ST, Unger JB, Spruijt-Metz D. Psy- 101. Araújo MFM, Beserra EP, Araújo TM, Chaves ES.
chological determinants of emotional eating in ado- Obesidade infantil: uma reflexão sobre dinâmica
lescence. Eat Disord. 2009;17:211-24. familiar numa visão etnográfica. Rev Rene. 2004;7.
92. Graziano PA, Calkins SD, Keane SP. Toddler self- 102. Bender SC. Influência dos fatores ambientais na
regulation skills predict risk for pediatric obesity. Int obesidade infantil Santa Maria: Centro Universitá-
J Obes (Lond). 2010;34:633-41. rio Franciscano; 2006.
93. Bowlby J. Apego e perda: apego, a natureza do 103. Cruvinel M, Borucho E. Sintomas de depressão in-
vínculo. 2 ed. São Paulo: Martins Fontes; 1990. fantil e ambiente familiar. Psicol Pesq. 2009;3:87-
94. Anderson SE, Whitaker RC. Attachment security and 100.
obesity in US preschool-aged children. Arch Pediatr 104. Small L, Aplasca A. Child Obesity and Mental Health:
Adolesc Med. 2011;165:235-42. A Complex Interaction. Child Adolesc Psychiatr Clin
95. Almeida CCJN, Mora PO, Oliveira VA, Joao CA, Joao N Am. 2016;25:269-82.
CR, Riccio AC, et al. Variables associated with fam- 105. Campbell MK. Biological, environmental, and so-
ily breakdown in healthy and obese/ overweigh ado- cial influences on childhood obesity. Pediatr Res.
lescents. Rev Paul Pediatr. 2014;32:8. 2016;79:205-11.
96. Nogueira-de-Almeida CA, Almeida CCJN, Barreto RF, 106. Kelly AS, Fox CK, Rudser KD, Gross AC, Ryder JR.
Oliveira VA, Ferrioli BHVM, João CA, et al. Atuação Pediatric obesity pharmacotherapy: current state
interdisciplinar em obesidade infanto-juvenil: a ex- of the field, review of the literature and clinical trial
periência do CESNI. Int J Nutrology. 2008;1:7. considerations. Int J Obes (Lond). 2016;40:1043-
97. Almeida CCJN. Psicologia da alimentação. In: No- 50.
gueira-de-Almeida CA, Mello E, editors. Nutrologia
Pediátrica: Prática Baseada em Evidências. 1ª ed.
São Paulo: Manole; 2016. p. 100-16.

Journal of Tropical Pediatrics, 2017, 0, 1–4
doi: 10.1093/tropej/fmx027
Case report
CASE REPORT
Obesity as a Presentation of Munchausen

Syndrome by Proxy
by Carlos Alberto Nogueira-de-Almeida,
Carla Cristina J. N. de Almeida, Nat!alia Inocêncio Pereira,
Nilton Antonio de Souza Filho, and Valmir Aparecido de Oliveira
University of Ribeir~ao Preto, S~ao Paulo 14027-150, Brazil
Correspondence: Carlos Alberto Nogueira-de-Almeida, University of Ribeir~ao Preto, Rua Eugênio Ferrante, 170, Jd. Nova Aliança Sul, Ribeir~ao
Preto, S~ao Paulo 14027-150, Brazil. Tel: þ55 16 992217498; E-mail <dr.nogueira@me.com>
ABSTRACT
Objective: To describe a case of an obese child whose weight gain was related to the Munchausen
Syndrome by proxy (MSP).
Methods: This is a case report including information regarding the child’s clinical history and the
mother’s behavior. The common features of the syndrome are confronted with the description of
the case, seeking to demonstrate the similarities.
Results: The description ratifies the diagnosis based on the signs and symptoms presented by the
child (<5 years old, frequent contacts with health system, symptoms witnessed only by the mother,
confusing findings, not helped by treatments, emotionally distant father) and the attitude of the
mother (concerned, interested in procedures, comfortable in the medical setting, higher medical
knowledge, hostile when thwarted).
Conclusion: The case presented points to a new etiology, the MSP, to be considered within the set
of factors currently known to cause and maintain obesity in childhood.
K E Y W O R D S : obesity, Munchausen syndrome by proxy, child, victimization, child abuse
INTRODUCTION and this leads professionals to seek unusual explana-

Obesity is a great challenge for pediatricians owing tions. The treatment usually depends on a good
to its high prevalence and difficulties in the definition diagnosis, which may be challenging, as new etiologi-
of causal factors. It is a disease that originates from a cal possibilities arise every day [5].
combination of genetic and environmental factors First described in 1977, Munchausen Syndrome
[1] and metabolic programming may influence the by proxy (MSP) is a psychiatric disorder listed in the
phenotypic expression [2]. Although the increase in DSM V as Factious Disorder Imposed on Another
fat storage is owing to positive energy balance [3], [6]. It appears when someone intentionally causes
sometimes the clinical history does not show an symptoms on another person, who will then be con-
excess of food intake or a sedentary behavior [4], sidered sick [7]. A lot of specific clinical findings
C The Author [2017]. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com
V " 1
2 " Case Report
have already been described, but, virtually, all sys- missed the appointments, but at every visit, V. brought
tems of the human body may be involved [8]. This new complaints. A total of 48 consultations took place
article aims to describe a case of an obese child and V. brought 174 complaints, 77 of different nature,
whose weight gain was related to MSP. with an average of 3.63 complaints/visit. Extensive
investigations of hormonal, genetic and neurological
causes were repeated, without any positive result.
CASE DESCRIPTION Two reports sent in writing by professionals from
L., male, aged 41=2 years, consulted for the first time in L.’s city revealed relevant aspects: a psychologist tes-
2011, at the nutrition outpatient clinic of the university, tified that ‘L.’s mother used the child’s disease to
brought by his mother V. They were coming from a demand attention and social benefits from the envi-
city about 100 km away. He had a previous history of ronment in which they lived’; L.’s teacher wrote that
severe obesity, having been investigated in several other L. ‘at the time of the school meal, since he enjoyed
health services. V. was extremely concerned about L.’s playing a lot, he often forgot to eat. On the other
obesity, stating several times that she would do any- hand, many times L. mentioned that, by mother’s
thing to help him, emphasizing the word ‘anything’, requirement, he should eat a lot. At this moments,
including bariatric surgery, if it would be necessary. he used to become anxious and to eat voraciously’.
The dietary questionnaire pointed to extremely low L.’s father betrayed the mother during pregnancy
caloric intake associated with intense physical activity. and they separated; the son had virtually no contact
This information, although incompatible with the pic- with his father. V. was a nursing assistant, fluent in
ture of obesity presented, was reported by the mother medical terminology, phrases and jargon, often con-
during the clinical interview. The physical examination fronting the team based on the medical knowledge
revealed no clinically relevant aspects in addition to she believed to have. She was always ready for any
excess adiposity and increased mass index (weight ¼ new interventions, procedures and tests ordered for
42.2 kg; stature ¼ 120 cm; body mass index ¼ the child, to the point of stimulating the team to
29.3 kg/m2, z-score ¼ þ8.01) (Fig. 1). Laboratory tests ‘unravel the mysteries of L.’s case’, according to her
were all normal, and interdisciplinary treatment for own words, registered several times in his record.
obesity was initiated without success (Fig. 1). L. never She described her son as ‘the case of a child who eats
Fig. 1. Body mass index evolution.

Case Report " 3
almost nothing and has very serious obesity’. As obesity is a disease of sub-acute progression, and
there were students enrolled, V. was often particu- therefore, separation would have to be relatively
larly interested in challenging them. She used to call long, and this was impossible considering that L.
members of the team by their names and praised depended on the mother as the only caregiver in the
everybody in an exaggerated way. Nevertheless, she city where they lived. We chose to insist on trying to
demanded more thorough and detailed investigation treat V., but after exhaustive attempts, we failed to
from the team and reacted aggressively when her enroll her in psychotherapy. In 2015, we began
statements were questioned or doubted. In the past, to consider hospitalizing the child to assess maternal
V. had been referred more than once for psychiatric behavior. However, the team demanded that the
treatment, but had always refused, saying she was mother remained with the child (as required by
not crazy and that the physicians said that because Brazilian law), under 24 h monitoring; she not only
they were unable to find out what L. had and how to refused hospitalization, becoming aggressive, but also
treat him. left our clinic, never returning to the unit. Many
Given the peculiarities of the case, especially attempts to contact the mother, the father and the
regarding maternal behavior, the team considered sister have been made since then, but they did not
the possibility of an obesity as a presentation of return the phone calls and the emails messages.
MSP. The search in scientific literature found no
similar reports, except for one case of secondary obe- CONCLUSION
sity consequent to excess prednisone intake [9]. The Obesity is an important issue in the whole world,
team psychologists ratified the diagnosis based on affecting 23.8% of boys and 22.6% of girls in devel-
the signs described by Criddle [10]: oped countries [12] and clinicians must be prepared
Characteristics of the child: to care for these patients. The case presents a new
etiologic possibility to be considered within the
• Less than 5 years old at the time of symp- already extensive set of factors currently known to
tom onset, cause and maintain obesity in childhood. An obese
• Frequent contacts with health care child affected by MSP needs to be addressed in a
providers, special way [13], focusing on the psychiatric treat-
• Symptoms that are witnessed only by the ment of the mother and, at the same time, on the
mother, recovery of the child. This may be a great challenge
• Multiple vague and confusing findings, and the success depends on the ability of the team
• Not helped by standard treatments, on approaching not only the health system but,
• Emotionally distant father. probably, the social service and even the police [14].
Characteristics of the mother:
REFERENCES
• Caring and concerned, 1. Kumar S, Kelly AS. Review of childhood obesity: from epi-
•
demiology, etiology, and comorbidities to clinical assess-
Consistently pushes for further tests, proce-
ment and treatment. Mayo Clin Proc 2017;92:251–65.
dures, surgeries, appointments and 2. Fall T, Mendelson M, Speliotes EK. Recent advances in
hospitalizations, human genetics and epigenetics of adiposity: pathway to
• Comfortable in the medical setting, precision medicine? Gastroenterology 2017, in press.
• Makes friends with staff members, 3. Crocker MK, Yanovski JA. Pediatric obesity: etiology and treat-
• Higher medical savvy, ment. Endocrinol Metab Clin North Am 2009;38:525–48.
• Ability to dichotomize staff members’ 4. Nogueira-de-Almeida CA, Pires LA, Miyasaka J, et al.
Comparison of feeding habits and physical activity between
opinions,
eutrophic and overweight/obese children and adolescents: a
• Hostile when thwarted. cross sectional study. Rev Assoc Med Bras 2015;61:227–33.
5. Romieu I, Dossus L, Barquera S, et al. Energy balance and
Definite confirmation could be established sepa- obesity: what are the main drivers? Cancer Causes
rating the child from the perpetrator [11]; however, Control. 2017;28:247–58.
4 " Case Report
6. American Psychological Association. Diagnostic and 11. Rosenberg DA. Munchausen Syndrome by Proxy: medical
Statistical Manual of Mental Disorders. 5th edn. diagnostic criteria. Child Abuse Negl 2003;27:421–30.
Wasnhington, DC: APA, 2013. 12. Ng M, Fleming T, Robinson M, et al. Global, regional, and
7. Dye MI, Rondeau D, Guido V, et al. Identification and national prevalence of overweight and obesity in children and
management of factitious disorder by proxy. J Nurse Pract adults during 1980-2013: a systematic analysis for the Global
2013;9:435–42. Burden of Disease Study 2013. Lancet 2014;384:766–81.
8. Petska HW, Gordon JB, Jablonski D, et al. The intersection 13. Chiczewski D, Kelly M. Munchausen syndrome by proxy.
of medical child abuse and medical complexity. Pediatr The importance of behavioral characteristics in recognition
Clin North Am 2017;64:253–64. and investigation. Emerg Med Serv 2002;31:117–9.
9. Witt ME, Ginsberg-Fellner F. Prednisone-induced 14. Heitzman J, Opio M, Ruzikowska A, et al. Munchausen
Munchausen syndrome. Am J Dis Child 1981;135:852–3. syndrome by proxy in a forensic psychiatric evaluation–the
10. Criddle L. Monsters in the closet: Munchausen syndrome description of a case and ethical controversy. Psychiatr Pol
by proxy. Crit Care Nurs 2010;30:46–55; quiz 6. 2012;46:677–89.
THIEME
Original Article | Artigo Original
Distorção da autopercepção de imagem

corporal em adolescentes
Body Image Self-perception Distortion in Teenagers
Carlos Alberto Nogueira-de-Almeida1 Rafael Cappello Garzella2 Camila da Costa Natera3
Ane Cristina Fayão Almeida4 Ivan Savioli Ferraz4 Luiz Antônio Del Ciampo4
1 Departamento de Medicina, Universidade Federal de São Carlos, Address for correspondence Carlos Alberto Nogueira-de-Almeida,
São Carlos, SP, Brasil MD, MSc, PhD, Departamento de Medicina, Universidade Federal de
2 Pediatria (Preceptor), Faculdade de Medicina da Universidade de São São Carlos, Rua São José, 2591, Ribeirão Preto, SP 14025-180, Brazil
Paulo, São Paulo, SP, Brasil (e-mail: dr.nogueira@me.com).
3 Hospital Sírio Libanês (Residente), São Paulo, SP, Brasil
4 Faculdade de Medicina de Ribeirão Preto da Universidade de São
Paulo, Ribeirão Preto, SP, Brasil
Int J Nutrol
Resumo Introdução Na adolescência, período de aceleração do crescimento e de mudanças

corporais, podem ocorrer comportamentos de contestação que tornam o indivíduo
vulnerável a preocupações ligadas ao corpo e à aparência.
Objetivo Verificar a presença de distorção da autopercepção da imagem corporal em
adolescentes da cidade de Ribeirão Preto, SP.
Métodos Estudo transversal, observacional e analítico. Foram avaliados 343 adoles-
centes entre 12 e 19 anos pertencentes ao Programa de Informação Profissional (PIP)
da Universidade de Ribeirão Preto, SP. Os adolescentes responderam como se
consideravam em relação ao seu peso corporal. Foram realizadas medidas antropomé-
tricas dos participantes (peso, estatura e índice de massa corporal [IMC]). A presença
de distorção da imagem corporal foi avaliada por meio da discrepância entre o IMC
diagnosticado pelo profissional e o IMC percebido pelo adolescente.
Resultados Houve prevalência de 41,7% de adolescentes com distorção da imagem
corporal, seja por superestimação ou subestimação do tamanho do corpo. Adoles-
centes do sexo feminino tiveram maiores distorções da percepção da autoimagem. A
superestimação da imagem corporal foi maior em adolescentes eutróficos, enquanto a
Palavras chave
subestimação foi maior em adolescentes obesos e com sobrepeso.
► Imagem Corporal
Conclusão Os resultados indicam a necessidade de implantação de políticas públicas
► adolescente
e de projetos dentro do âmbito escolar para a prevenção de distúrbios de imagem
► estado nutricional
corporal e de transtornos alimentares, inclusive nos adolescentes eutróficos.
Abstract Introduction During adolescence, a period of acceleration of growth and body

changes, there may be contending behaviors that make the individual vulnerable to
concerns about his or her body and appearance.
received DOI https://doi.org/ Copyright © by Thieme Revinter

June 11, 2018 10.1055/s-0038-1669407. Publicações Ltda, Rio de Janeiro, Brazil
accepted ISSN 1984-3011.
June 21, 2018
Distorção da Autopercepção de Imagem Corporal em Adolescentes Nogueira-de-Almeida et al.
Objective To verify the presence of body image self-perception distortion in adoles-

cents of the city of Ribeirão Preto, SP.
Methods The present work is a cross-sectional, observational and analytical study. A
total of 343 adolescents aged between 12 and 19 years old and belonging to the
Professional Information Program (PIP, in the Portuguese acronym) of the University of
Ribeirão Preto, state of São Paulo, Brazil, were evaluated. The adolescents responded
how they considered themselves in relation to their body weight. Anthropometric
measurements of the participants (weight, height, and body mass index [BMI]) were
performed. The presence of body image distortion was assessed through the discrep-
ancy between the BMI diagnosed by the professional and the BMI perceived by the
adolescent.
Results There was a prevalence of 41.7% of adolescents with body image distortion,
either due to overestimation or underestimation of the body size. Female adolescents
had greater distortions in the perception of self-image. The overestimation of body
image was higher in eutrophic adolescents, while the underestimation was greater in
Keywords obese and overweight adolescents.
► body image Conclusion The results indicate the need to implement public policies and projects
► adolescent within the school context for the prevention of body image and eating disorders,
► nutritional status including in eutrophic adolescents.
Introdução superestimação e a subestimação da imagem corporal não

constituem uma característica exclusiva de adolescentes
A imagem corporal é definida como uma imagem do corpo com TAs.11–13
formada na mente do indivíduo, ou seja, o modo como o Dessa forma, o presente trabalho teve como objetivo veri-
indivíduo percebe seu corpo, sendo esta construída desde a ficar a presença de distorção da autopercepção da imagem
infância até a puberdade.1–3 A autopercepção do peso é um corporal em adolescentes da cidade de Ribeirão Preto, SP.
aspecto importante da imagem corporal, pois reflete insatis-
fações e preocupações quanto ao tamanho e forma corporais.2
Metodologia
Na adolescência, por ser um período de aceleração do cresci-
mento e, portanto, de mudanças corporais, podem ocorrer O presente trabalho é um estudo transversal, observacional e
comportamentos de contestação que tornam o indivíduo analítico, realizado na cidade de Ribeirão Preto, SP. Foram
vulnerável a preocupações ligadas ao corpo e à aparência.4 convidados a participar do estudo 442 adolescentes entre 12
Ursoniu et al5 verificaram que adolescentes com autoper- e 19 anos pertencentes ao Programa de Informação Profissi-
cepção de sobrepeso foram mais propensos a se exercitar, a ter onal (PIP) da Universidade de Ribeirão Preto, o qual se destina
menor ingestão calórica e, ainda, a utilizar comportamentos a apresentar a universidade e suas atividades acadêmicas à
compensatórios como vômitos ou uso abusivo de laxativos. comunidade em geral, no ano de 2015. Destes, 343 aceitaram
Kimber et al6 observaram que adolescentes eutróficos que participar da pesquisa e assinaram o termo de consenti-
se consideraram desnutridos ou com excesso de peso expe- mento livre e esclarecido, no caso de maiores de 18 anos, ou
rimentam maiores sintomas de depressão. seus responsáveis o fizeram, no caso de menores de idade.
Entende-se como distorção da imagem corporal a discre- No momento da entrada no estudo, os adolescentes
pância entre o índice de massa corporal (IMC) percebido e o respondiam à seguinte pergunta: “Você se considera: muito
real.7 A distorção de imagem pode levar adolescentes a ado- magro (MM), magro (M), normal (N), sobrepeso (S) ou obeso
tarem hábitos de controle de peso não saudáveis, com conse- (O)?” Imediatamente após responderem a esta pergunta, os
quente ingestão inadequada de energia e nutrientes, além de adolescentes tiveram as suas medidas antropométricas (peso
distúrbios psíquicos como transtornos de ansiedade e de e estatura) obtidas. O peso foi aferido por meio de uma
humor.8,9 Um estudo epidemiológico recente verificou que balança portátil, eletrônica e digital, da marca Tanita (Tanita
de 17 a 43% dos adolescentes com IMC normal, principalmente Corporation, Tóquio, Japão), com capacidade de 150 kg e
do sexo feminino, apresentam distorção da imagem corporal.6 divisões de 100 g, estando o adolescente com roupas leves,
São poucos os estudos que avaliam a autopercepção corpo- sem calçados, em pé e com membros superiores estendidos
ral e fatores associados a ela, e a maioria aborda a distorção e a ao lado do corpo. A altura foi aferida em um estadiômetro
insatisfação com a imagem corporal especialmente em porta- vertical graduado em centímetros e milímetros, com escala
dores de transtornos alimentares (TAs) específicos (bulimia, de precisão de 0,1 cm. Os adolescentes foram posicionados
anorexia nervosa, obesidade mórbida).10 Porém, é sabido que a sem calçados, com os calcanhares unidos, em posição ereta,
International Journal of Nutrology

Tabela 1 Características clínicas dos adolescentes (n ¼ 343) Resultados

do Programa de Informação Profissional da Universidade de
Ribeirão Preto (Ribeirão Preto, SP), 2015 A idade média dos adolescentes foi de 17,02 " 1,00 anos, e a
média de IMC foi de 21,69 " 3,23.
Variáveis n (%) A ►Tabela 1 mostra as características clínicas dos ado-
Sexo masculino 84 (24,5) lescentes avaliados no estudo.
Sexo feminino 259 (75,5) Dos 276 adolescentes eutróficos, 81% eram do sexo femi-
nino e 79% eram do sexo masculino.
Diagnóstico nutricional
Em resposta à pergunta sobre a autopercepção de seu
Desnutrição 4 (1,2) estado nutricional, verificou-se que 55,1% (189/343) consi-
Eutrofia 276 (80,5) deravam-se eutróficos, independente de seu estado nutri-
Sobrepeso 52 (15,2) cional, sendo 25,4% (48/189) do sexo masculino e 74,6% (141/
189) do sexo feminino.
Obesidade 11 (3,2)
Observou-se uma correlação positiva entre excesso de
peso (sobrepeso e obesidade) e autopercepção corporal
olhando para a frente. A leitura foi feita no centímetro mais (r ¼ 0,34; p ¼ < 0,01). Também foi encontrada uma corre-
próximo, quando a haste horizontal da barra vertical da lação positiva entre eutrofia e autopercepção corporal
escala de estatura encostava-se à cabeça do adolescente. (r ¼ 0,45; p < 0,01).
A classificação antropométrica foi realizada de acordo com Observou-se que dos 276 adolescentes eutróficos, 15,6%
as curvas de crescimento recomendada pela Organização (43/276) consideravam-se com sobrepeso. Entre os adoles-
Mundial da Saúde (OMS),14 sendo utilizado o índice de massa centes eutróficos que se consideravam portadores de sobre-
corporal por idade (IMC/I). O software WHO Anthro Plus peso, 90,7% (39/43) eram do sexo feminino e 9,3% (4/43) do
(Organização Mundial de Saúde, Genebra, Suíça)15 foi utilizado sexo masculino. Dos 52 adolescentes classificados com
para auxiliar na identificação dos escores z dos adolescentes. A sobrepeso, 5,7% (3/52) consideravam-se portadores de obesi-
classificação do estado nutricional dos adolescentes obedeceu dade, sendo todos os indivíduos do sexo feminino. Dos quatro
aos seguintes pontos de corte: eutrófico (escore z entre - 2 desnutridos, apenas 1 (25%) se considerava eutrófico
e þ 1); desnutrido (escore z < - 2); sobrepeso (escore z entre (►Tabela 2).
þ 1 e þ 2); obesidade (escore z > þ 2).16 Entre os 276 adolescentes eutróficos, nenhum se consi-
A presença de distorção da imagem corporal foi avaliada derava desnutrido. Dos 52 adolescentes com sobrepeso,
por meio da discrepância entre o IMC diagnosticado pelo 40,4% (21/52) consideravam-se eutróficos. Entre os indi-
profissional e o IMC percebido pelo adolescente. víduos com sobrepeso que se consideravam eutróficos,
O estudo foi aprovado pelo comitê de ética da Universi- 61,9% (13/21) pertenciam ao sexo feminino e 38,1%
dade de Ribeirão Preto. (8/21) ao sexo masculino. Ainda, dos 11 adolescentes
As variáveis categóricas (idade, sexo, estado nutricional) classificados como obesos, 81,8% (9/11) consideravam-se
foram descritas por meio de distribuição de frequência para portadores de sobrepeso, sendo todos eles do sexo femi-
variáveis categóricas. Idade, sexo e estado nutricional foram nino (►Tabela 2).
expressos em médias e desvio-padrão. Para correlacionar Ao todo, houve prevalência de 41,7% (143/343) de ado-
estado nutricional e autopercepção corporal, foi utilizada a lescentes com distorção da imagem corporal, seja por supe-
correlação de Spearman. restimação ou subestimação do tamanho corporal.
Para avaliar a concordância entre o estado nutricional Na análise de concordância, o valor do teste Kappa foi de
percebido pelo adolescente e o estado nutricional diagnosti- 0,03 (p < 0,01), o que prediz baixa concordância entre os
cado, foi realizado o teste Kappa. O nível de significância dados. Os dados estão demonstrados na ►Tabela 2.
utilizado foi de 5%. Para as análises estatísticas, utilizou-se o A ►Tabela 3 ilustra a autopercepção corporal adequada
software SPSS versão 16.0 (SPSS Inc., Chicago, IL, EUA). segundo o sexo dos adolescentes.
Tabela 2 Relação entre estado nutricional percebido e diagnosticado em adolescentes do Programa de Informação Profissional da
Universidade de Ribeirão Preto (Ribeirão Preto, SP), 2015
Estado nutricional percebido

Estado nutricional diagnosticado Muito magro Magro Normal Sobrepeso Obeso Total
Desnutrido 0 3 1 0 0 4
Eutrófico 8 57 167 43 1 276
Sobrepeso 0 0 21 28 3 52
Obeso 0 0 0 9 2 11
Total 8 60 189 80 6 343

Tabela 3 Autopercepção corporal adequada segundo o sexo definição corporal sem se importar com eventuais conse-
dos adolescentes do Programa de Informação Profissional da quências prejudiciais à saúde. Os vigoréxicos se consideram
Universidade de Ribeirão Preto (Ribeirão Preto, SP), 2015 “fracos,” “raquíticos,” “frangos” ou “mirrados,” recorrendo
cada vez mais a anabolizantes e a exercícios intensos na
Autopercepção Estado nutricional tentativa de alcançar a silhueta “ideal”22.
corporal diagnosticado No presente estudo, mais de 80% dos adolescentes eram
adequada
eutróficos. Segundo Braga et al,23 a alta prevalência de
Magro Total de adolescentes adolescentes com IMC ideal pode ser explicada pelo fato
desnutridos: 4
do indivíduo buscar a imagem corporal idealizada pela
Sexo n (%) mídia, a qual consiste em um padrão estético de magreza.
Masculino 0 (0) Singh et al24 verificaram que adolescentes que estavam com
Feminino 3 (75%) sobrepeso tiveram quatro vezes mais chance de se considera-
rem obesos (odds ratio [OR] ¼ 4,65; intervalo de confiança [IC]
Normal Total de adolescentes
95%; 2,13–10,12). Também foi observado que 33% dos ado-
eutróficos: 276
lescentes com IMC normal estavam insatisfeitos com a imagem
Masculino 39 (23,3)
corporal, o que se assemelha ao resultado encontrado no
Feminino 128 (76,7) presente trabalho, visto que 39,5% dos adolescentes eutróficos
Sobrepeso Total de adolescentes apresentaram distorção da imagem corporal.
com sobrepeso: 52 Em um estudo recente,25 foi demonstrado que o excesso
Masculino 5 (17,8) de peso de adultos jovens apresentou associação positiva
significativa com a autopercepção de excesso ponderal, ou
Feminino 23 (82,1)
seja, a autopercepção do excesso ponderal sofre distorções
Obesidade Total de adolescentes
em relação ao diagnóstico nutricional real. Este fato também
com obesidade: 11
foi demonstrado no presente estudo.
Masculino 0 (0) Como foi observado, a superestimação da imagem corpo-
Feminino 2 (100) ral foi maior em adolescentes eutróficos, enquanto que a
subestimação da imagem corporal foi maior em adolescentes
obesos e com sobrepeso.
Discussão Resultados distintos têm sido relatados em diversos estu-
dos que mostraram maior subestimação do peso em ado-
Os dados mostram prevalência de 41,7% de adolescentes com lescentes do sexo masculino, enquanto adolescentes do sexo
distorção da imagem corporal, seja por superestimação ou feminino tendem a superestimar o tamanho corpo-
subestimação do tamanho corporal. No estudo de Glaner ral.2,3,5,11,26 Por outro lado, como no presente estudo, alguns
et al,17 realizado com 637 adolescentes, foi observado que autores observaram que a autopercepção corporal foi mais
60% estavam insatisfeitos com a imagem corporal. Os autores comprometida em adolescentes do sexo feminino, mesmo
argumentam que os avanços tecnológicos e os meios de sendo o grupo com maior prevalência de eutrofia.2,4
comunicação influenciam diretamente nos padrões de Além disso, a insatisfação com a imagem corporal esteve
beleza, levando a comportamentos inadequados de atividade associada a um maior risco de baixo peso. No presente
física e TAs. estudo, não foi possível realizar esta análise, diante do
Adolescentes do sexo feminino tiveram maiores distor- número pequeno de desnutridos, visto que dos quatro des-
ções da percepção da autoimagem, pois é sabido que indiví- nutridos, apenas um se considerava eutrófico.
duos do sexo feminino sofrem maiores pressões sociais para O presente trabalho apresenta algumas limitações. A não
a conquista de um “corpo perfeito”18. E, quanto mais o corpo utilização de uma escala de silhuetas padronizadas pode ter
real se distancia do corpo perfeito, maior será a probabili- dificultado a precisão da distorção da imagem corporal.
dade de conflito e de baixa autoestima, o que pode exacerbar Finalmente, a população estudada foi obtida por uma amos-
a insatisfação com o próprio corpo e ocasionar possíveis tra de conveniência e não pode ser considerada como repre-
TAs.19,20 Cheung-Lucchese et al21 comentaram que mulheres sentativa dos adolescentes de Ribeirão Preto.
se preocupam com o que os outros irão pensar ao olhar para A superestimação da imagem corporal em adolescentes
elas e, portanto, buscam se adequar aos modelos mais aceitos eutróficos, observada no presente estudo, é um fato preocu-
socialmente. pante, pois pode indicar o início de possíveis transtornos
Adolescentes do sexo masculino também apresentaram psíquicos e alimentares. Por outro lado, a subestimação da
distorções de autoimagem, porém em menor proporção. mesma encontrada em adolescentes com sobrepeso e obesos
Além disso, como foi observado, a maioria dos mesmos pode interferir no reconhecimento dos malefícios do excesso
subestimava seu estado nutricional. Meninos também de peso para a saúde.
podem apresentar obsessão pelo corpo perfeito, o que atual- Em conclusão, observou-se alta prevalência de distorção da
mente se enquadra em quadros de vigorexia nervosa, trans- imagem corporal nos adolescentes avaliados. Adolescentes
torno no qual o adolescente realiza práticas esportivas de eutróficos apresentaram maiores porcentagens de superesti-
forma intensa e contínua para ganhar massa muscular e mação, e adolescentes obesos apresentaram maior prevalência

de subestimação. Adolescentes do sexo feminino apresenta- 12 Kakeshita IS, de Sousa Almeida S. Relação entre índice de massa
ram maiores distorções de percepção da autoimagem. Os corporal e a percepção da auto-imagem em universitários. Rev
resultados indicam a necessidade de implantação de políticas Saude Publica 2006;40(03):497–504
13 Valença CN, Germano RM. Percepção da auto-imagem e satisfação
públicas e de projetos dentro do âmbito escolar para combater
corporal em adolescentes: perspectiva do cuidado integral na
o estereótipo de padrão de beleza e prevenir distúrbios de enfermagem. Revista da Rede de Enfermagem do Nordeste 2009;
imagem corporal e TAs, inclusive nos adolescentes eutróficos. 10(04):. Doi: http://dx.doi.org/10.15253/rev%20rene.v10i4.4877
14 de Onis M, Onyango AW, Borghi E, Siyam A, Nishida C, Siekmann J.
Development of a WHO growth reference for school-aged chil-
dren and adolescents. Bull World Health Organ 2007;85(09):
Referências 660–667
1 Graup S, Pereira ÉF, da Silva Lopes A, Araújo VC, Legnani RFS, 15 Organization WH. WHO Anthro for personal computers, version
Borgatto AF. Associação entre a percepção da imagem corporal e 3.2. 2, 2011: software for assessing growth and development of
indicadores antropométricos de escolares. Rev Bras Educ Fís the world’s children. Geneva: WHO; 2010
Esporte 2008;22(02):129–138 16 Growth WWGOI; WHO Working Group on Infant Growth. An
2 Pereira TA, Guimarães M, de Souza ECG, Pedro MAD. Percepção da evaluation of infant growth: the use and interpretation of anthro-
imagem corporal de adolescentes e sua relação com o índice de pometry in infants. Bull World Health Organ 1995;73(02):165–174
massa corporal. Revista Científica Da Faminas 2016;5(01) 17 Glaner MF, Pelegrini A, Cordoba CO, Pozzobon ME. Associação
3 Petroski EL, Pelegrini A, Glaner MF. Motivos e prevalência de entre insatisfação com a imagem corporal e indicadores antro-
insatisfação com a imagem corporal em adolescentes. Cien Saude pométricos em adolescentes. Rev Bras Educ Fís Esporte 2013;27
Colet 2012;17(04):1071–1077 (01):129–136
4 Branco LM, Hilário MOE, Cintra IDP. Percepção e satisfação 18 Corseuil MW, Pelegrini A, Beck C, Petroski EL. Prevalência de
corporal em adolescentes e a relação com seu estado nutricional. insatisfação com a imagem corporal e sua associação com a
Archives of Clinical Psychiatry (São Paulo) 2006;33(06):292–296 inadequação nutricional em adolescentes. J Phys Educ 2009;20
5 Ursoniu S, Putnoky S, Vlaicu B. Body weight perception among (01):25–31
high school students and its influence on weight management 19 Aerts D, Chinazzo H, Santos JAD, Oserow NR. Percepção da imagem
behaviors in normal weight students: a cross-sectional study. corporal de adolescentes escolares brancas e não brancas de escolas
Wien Klin Wochenschr 2011;123(11-12):327–333 públicas do Município de Gravataí, Estado do Rio Grande do Sul,
6 Kimber M, Georgiades K, Couturier J, Jack SM, Wahoush O. Brasil. Epidemiol Serv Saude 2011;20(03):363–372
Adolescent Body Image Distortion: A Consideration of Immigrant 20 Rocha M. Vigorexia: um distúrbio da imagem corporal. EFDe-
Generational Status, Immigrant Concentration, Sex and Body portes.com. Revista Digital Buenos Aires-Ano. 2013
Dissatisfaction. J Youth Adolesc 2015;44(11):2154–2171 21 Cheung-Lucchese T, Alves CS. Percepção do Corpo Feminino e os
7 Rosen JC. Body image disorder: Definition, development, and Comportamentos de Consumo de Serviços de Estética. Revista
contribution to eating disorders. The etiology of bulimia: The Organizações em Contexto. 2013;9(18):271–294
individual and familial context. 2013;1:157–77 22 Ferreira MEC, de Castro APA, Gomes G. A obsessão masculina pelo
8 Eisenberg ME, Neumark-Sztainer D, Story M, Perry C. The role of social corpo: malhado, forte e sarado. Rev Bras Ciênc Esporte 2005;27
norms and friends’ influences on unhealthy weight-control behaviors (01):167–182
among adolescent girls. Soc Sci Med 2005;60(06):1165–1173 23 Braga JGL, Facina VB. Perfil antropométrico de adolescentes do
9 Neutzling MB, Araújo CLP, Vieira MdeF, Hallal PC, Menezes AM. Recôncavo da Bahia. Revista Ciência em Extensão. 2013;9(03):
Freqüência de consumo de dietas ricas em gordura e pobres em 21–33
fibra entre adolescentes. Rev Saude Publica 2007;41(03):336–342 24 Singh MM, Ashok L, Binu VS, Parsekar SS, Bhumika TV. Adoles-
10 Kravchychyn ACP, Silva DFD, Machado FA. Relação entre estado cents and Body Image: A Cross Sectional Study. Indian J Pediatr
nutricional, adiposidade corporal, percepção de autoimagem 2015;82(12):1107–1111
corporal e risco para transtornos alimentares em atletas de 25 Florêncio RS, Moreira TMM, Silva MR, Almeida ÍL. Excesso ponderal
modalidades coletivas do gênero feminino. Rev Bras Educ Fís em adultos jovens escolares: a vulnerabilidade da autopercepção
Esporte 2013;27(03):459–466 corporal distorcida. Rev Bras Enferm 2016;69(02):258–265
11 Araújo CL, Dumith SC, Menezes AMB, Hallal PC. Peso medido, peso 26 Lee G, Ha Y, Vann JJ, Choi E. Weight perception and dieting
percebido e fatores associados em adolescentes. Rev Panam Salud behavior among Korean adolescents. J Sch Nurs 2009;25(06):
Publica 2010;27(05):360–367 427–435

pISSN: 2234-8646 eISSN: 2234-8840
https://doi.org/10.5223/pghn.2018.21.1.59
PGHN
Pediatr Gastroenterol Hepatol Nutr 2018 January 21(1):59-67
Original Article
Different Criteria for the Definition of Insulin Resistance and Its

Relation with Dyslipidemia in Overweight and Obese Children
and Adolescents
Carlos Alberto Nogueira-de-Almeida and Elza Daniel de Mello*
Department of Medical, Federal University of São Carlos (UFSCAR), São Carlos, *Department of Pediatric, Federal
University of Rio Grande do Sul (UFRGS), Porto Alegre, Brazil
Purpose: to compare cut off points corrected for age and gender (COOP) with fixed cut off points (FCOP) for fasting
plasma insulin and Homeostatic model assessment-insulin resistance (HOMA-IR) for the diagnosis of IR in obese
children and adolescents and their correlation with dyslipidemia.
Methods: A multicenter, cross-sectional study including 383 subjects aged 7 to 18 years, evaluating fasting blood
glucose, plasma insulin, and lipid profile. Subjects with high insulin levels and/or HOMA-IR were considered as having
IR, based on two defining criteria: FCOP or CCOP. The frequency of metabolic abnormalities, the presence of IR,
and the presence of dyslipidemia in relation to FCOP or CCOP were analyzed using Fisher and Mann-Whitney exact
tests.
Results: Using HOMA-IR, IR was diagnosed in 155 (40.5%) and 215 (56.1%) patients and, using fasting insulin,
150 (39.2%) and 221 (57.7%), respectively applying FCOP and CCOP. The use of CCOP resulted in lower insulin
and HOMA-IR values than FCOP. Dyslipidemia was not related to FCOP or CCOP. Blood glucose remained within
normal limits in all patients with IR. There was no difference in the frequency of IR identified by plasma insulin or
HOMA-IR, both for FCOP and CCOP.
Conclusion: The CCOP of plasma insulin or of HOMA-IR detected more cases of IR as compared to the FCOP, but
were not associated with the frequency of dyslipidemia. As blood glucose has almost no fluctuation in this age group,
even in the presence of IR, fasting plasma insulin detected the same cases of IR that would be detected by HOMA-IR.
Key Words: Obesity, Insulin, Child, Adolescent, Dyslipidemias
INTRODUCTION increased worldwide [1,2], with the consequent si-

multaneous increase of several comorbidities [3-7],
The prevalence of child and adolescent obesity has especially insulin resistance (IR) [8]. IR is consid-
Received：September 27, 2017, Revised：October 24, 2017, Accepted：October 26, 2017

Corresponding author: Carlos Alberto Nogueira-de-Almeida, Department of Medical, Federal University of S o Carlos (UFSCAR), Rua Eug nio
Ferrante 170, Ribeir o Preto, SP 14027-150, Brazil. Tel: +55-16-99221-7498, Fax: +55-16-38775034, E-mail: dr.nogueira@me.com
Copyright 2018 by The Korean Society of Pediatric Gastroenterology, Hepatology and Nutrition
This is an openaccess article distributed under the terms of the Creative Commons Attribution NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits
unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
PEDIATRIC GASTROENTEROLOGY, HEPATOLOGY & NUTRITION

Pediatr Gastroenterol Hepatol Nutr
ered the trigger for the onset of the many compo- Cuartero et al. [20], based on a survey that included
nents of metabolic syndrome (MS) [9-16], which is 372 subjects aged one month to 18 years, observed a
characterized by a series of comorbidities usually significant variation of fasting plasma insulin and
seen in clusters [17] (dyslipidemia, hypertension, HOMA-IR related to pubertal stage, age and gender.
diabetes, steatosis, subclinical inflammation, among Jeffery et al. [26] have demonstrated that this ele-
others), and that are risk factors for cardiovascular vation begins in childhood some years before pub-
disease. Studies have been conducted in order to de- erty, and that its onset depends more on age than pu-
fine the diagnostic criteria and cutoff points to de- bertal staging, questioning the relationship between
termine IR using Homeostatic model assessment sexual development and IR.
(HOMA)-IR, or fasting plasma insulin, although the There is no consensus regarding the reference val-
first is controversial [18]. The hyperinsulinemic- eu- ues of fasting plasma insulin or HOMA-IR for the di-
glycemic clamp, the gold standard for the diagnosis agnosis of IR in the pediatric age group and several
of IR, is not applicable in clinical practice due to its cutoff points have been reported in the literature
technical complexity, especially in the pediatric [18,28-34]. The most used are 15 μU/mL for fasting
age group [9,19-25]. According to Sinaiko [13], the plasma insulin [25] and 3.16 for HOMA-IR [21]. Due
values of fasting glucose and plasma insulin are the to the variability of plasma insulin in the pediatric
only ones required to calculate HOMA-IR, which in- age group, there is a proposal to use cutoff values for
tends to demonstrate the correlation between pan- HOMA-IR according to gender and pubertal staging
creatic capability of insulin production and the ca- [33]. It would be then necessary to add the Tanner
pacity of maintaining adequate glucose. criteria in order to identify IR, what limits the use in
Since in the pediatric age group there is rarely sig- population studies and adds subjectivity to it.
nificant variation in blood glucose, some authors Based on the study by Almeida [19], and consider-
suggest that fasting plasma insulin can be used alone ing the findings of Jeffery et al. [26], that IR depends
for the diagnosis of IR in children [14,22]. There are, more on age than on pubertal staging, it is possible to
however, several limitations to the use of these IR in- propose specific values of plasma insulin and HOMA-
dicators, such as the need to establish a cutoff point IR for each age group and gender. Therefore, this
related to any associated risk, which is usually ob- study intended to compare, in a sample of obese chil-
tained through longitudinal and long term studies, dren and adolescents, age-adjusted cutoff points,
and the significant variability of the values of fasting that we called “corrected cut off point” (CCOP) with
plasma insulin according to age group [19,20,23,26,27]. “fixed cut off point” (FCOP) for fasting plasma in-
Moran et al. [27] reported that puberty is a period sulin and for HOMA-IR for the identification of IR
in which a state of “physiological IR” occurs related using as outcome the presence of dyslipidemia.
to age advancement and independent of changes in
body composition. Aradillas-García et al. [28], when MATERIALS AND METHODS
evaluating Mexican children and adolescents 6 to 18
years of age, found that both fasting insulin and A multicenter cross-sectional study was con-
HOMA-IR, regardless of the presence of obesity, in- ducted at two outpatient clinics: the Centro de Estudos
crease gradually until the age of 12-13 years, and em Saúde e Nutrologia Infantojuvenil (Center for Studies
then reach a plateau. A study by Almeida et al. [19], on Child and Adolescent Nutrition and Health) at
conducted among eutrophic adolescents with mean the University of Ribeirão Preto (Cesni) and the
pubertal development, demonstrated that fasting Ambulatório de Obesidade Infantojuvenil do Serviço de
plasma insulin and HOMA-IR vary significantly ac- Nutrologia (Nutrology Service: outpatient clinic for
cording to age, increasing until around 13-15 years, Child and Adolescent Obesity) of the Hospital de
and then decreasing, both for boys and girls. García Clínicas of the Federal University of Rio Grande do
60 Vol. 21, No. 1, January 2018

Carlos Alberto Nogueira-de-Almeida and Elza Daniel de Mello：Insulin Resistance and Dyslipidemia
Sul (AmO). Both are academic services, where data sidered when the plasma insulin concentration was
collection follows rigorously standardized methodology. above the cutoff point according to two possibilities:
The work was approved by the ethics in research A) 15 μU/mL FCOP, as usually recommended [25];
committees of the University of Ribeirão Preto B) CCOP for age and gender, adding two standard
(number 94/2003) and of the Hospital de Clínicas de deviations to the mean values found in a previous
Porto Alegre (number 07/258). Written Informed study [19] for five age groups. As there is no study
Consent was obtained from the subjects. with clinical outcomes defining the cut off points ad-
Inclusion criteria were: all new cases of patients justed for age, we decided to use a statistical ap-
seen between January 2008 and December 2012, proach, considering as “normal,” values of insulin
aged 7 to 18 years, and with body mass index above between the average and 2 standards deviation
the z score +1 (n=489 eligible). The exclusion cri- above the average; and “hyperinsulinism” as values
teria were: refusal to sign the consent form (n=2), higher than this.
impossibility to do anthropometry (n=3) or to col- ㆍ7 to 8.9 years: 7.92 μU/mL (boys) and 6.70
lect laboratory tests (n=61), other diseases (diabetes μU/mL (girls)
mellitus type 1 [n=0], hypothyroidism [n=0], and ㆍ9 to 10.9 years: 8.69 μU/mL (boys) and 11.99
inborn errors of metabolism [n=1]) and incomplete μU/mL (girls)
data on medical record (n=39). After meeting the ㆍ11 to 12.9 years: 12.18 μU/mL (boys) and 13.26
above criteria, 383 subjects were included in the μU/mL (girls)
study, 190 of which were seen at Cesni and 193 at ㆍ13 to 14.9 years: 13.74 μU/mL (boys) and 14.85
AmO. μU/mL (girls)
All were instructed to fast for 12 hours; anthro- ㆍ15 to 17.9 years: 10.27 μU/mL (boys) and 13.13
pometric data and blood were collected at the time of μU/mL (girls)
the first visit. Weight and height measurements fol- HOMA-IR was the other diagnostic method for IR,
lowed the recommendations of the World Health considering the following cutoff points: A) FCOP of
Organization [35]. Two tubes of 4 mL of blood were 3.16 [21];B) CCOP for age and gender, adding two
collected in a recipient with no additive and sent to standard deviations to the mean values found in a
the laboratory within two hours for sample process- previous study [19] for five age groups. As there is no
ing and biochemical and hormonal analysis. The bio- study with clinical outcomes defining the cut off
logical material was separated in a Bio Eng cen- points adjusted for age, we decided to use a statistical
trifuge model BE 4000 (BIO-ENG, Curitiba, Brazil) approach, considering as “normal,” values of HOMA-
running for 5 minutes at 3,500 rpm between one and IR between the average and 2 standards deviation
two and a half hours after harvesting (sufficient time above the average; and “High HOMA-IR” as values
for blood clotting). Biochemical insulin dosage was higher than this.
carried out in one of the aliquots on the day the blood ㆍ7 to 8.9 years: 1.76 (boys) and 1.39 (girls)
was drawn, by automated chemiluminescence, in a ㆍ9 to 10.9 years: 1.97 (boys) and 2.62 (girls)
Immulitte DPC Medlab equipment (DPC MEDLAB, ㆍ11 to 12.9 years: 2.65 (boys) and 3.02 (girls)
Salvador, Brazil). Glucose and lipids were evaluated ㆍ13 to 14.9 years: 3.21 (boys) and 3.46 (girls)
by the automated enzymatic method with Cobas ㆍ15 to 17.9 years: 2.39 (boys) and 2.89 (girls)
Mira Plus Roche equipment (Roche Diagnostic The cutoff points used to define dyslipidemia were
Systems, Indianapolis, IN, USA). HOMA-IR was de- proposed in Brazil by the “I guidelines of prevention
termined applying the equation proposed by of atherosclerosis in childhood and adolescence”
Wallace and Matthews [36]: plasma glucose [37]: total cholesterol (TC) ＞150 mg/dL; low density
(mol/dL)×plasma insulin (μUI/mL)/22.5. lipoprotein cholesterol (LDL-C) ＞100 mg/dL; high
Hyperinsulinism, used as a marker of IR, was con- density lipoprotein cholesterol (HDL-C) ＜45 mg/dL;
www.pghn.org 61
triglycerides (TG) ＞100 mg/dL. For patients diagnosed with IR according to fast-
The variables studied were: 1) gender-related fre- ing plasma insulin, the use of CCOP resulted in sig-
quency of metabolic abnormalities; 2) presence or nificantly lower values of fasting plasma insulin and
absence of IR in relation to plasma insulin or HOMA-IR as compared to those obtained using
HOMA-IR FCOP or CCOP for age; and 3) the fre- FCOP, although still quite high in relation to the
quency of dyslipidemia in children with IR, also ac- whole sample. A similar result was found in the pa-
cording to FCOP and CCOP. tients diagnosed with IR by HOMA-IR as compared
The computer program Graphpad Prism 5 was to fasting plasma insulin values, but not when com-
used for statistical analysis. Fisher’s exact test (two- pared to HOMA-IR values. Table 1 also shows that
sided) was used to compare frequencies, and Mann- the mean values for TC, HDL-C, and TG were abnor-
Whitney test to compare non-parametric data, con- mal regardless of whether FCOP or CCOP of fasting
sidering statistical difference when p＜0.05. The re- plasma insulin or of HOMA-IR were considered.
sults were presented as mean±standard error of the Blood glucose remained within normal values in all
mean (SEM) or percentage. patients with IR, regardless of the type of cutoff val-
ues used for fasting plasma insulin or HOMA-IR.
RESULTS The frequency (%) of metabolic abnormalities
found in relation to gender is depicted in Table 2.
Table 1 depicts the demographic and laboratory Using insulin with FCOP, 33.1% of boys and 44.1% of
characteristics of the 383 children evaluated (mean± girls had IR and using HOMA with FCOP, the preva-
SEM). This sample consisted of 55% females, with a lence was 37.8% and 42.7%, respectively. Using in-
mean age of 11.3±0.1 year and body mass index z sulin with CCOP, 57.6% of boys and 57.8% of girls
score of +2.4. Among these, 221 (57.7%) and 217 had IR and using HOMA with CCOP, the prevalence
(56.7%) presented IR according to increased (fixed was 57.0% and 55.5%, respectively. There was no dif-
or corrected) values of fasting plasma insulin or ference between boys and girls in the frequency of IR
HOMA-IR, respectively. identified by FCOP or CCOP of fasting plasma insulin
Table 1. Demographic and Laboratory Characteristics of a Sample of Obese Children and Adolescents with Insulin Resistance
according to Fixed or Variable Cutoff Points of Fasting Plasma Insulin or of HOMA-IR
Increased plasma insulin Increased HOMA-IR

Characteristic All (n=383)
FCOP (n=150) CCOP (n=221) p-value FCOP (n=155) CCOP (n=215) p-value
Gender (male:female) 1:2 1:1.6 1:1.4 NS 1:2 1:2 NS

Age (y) 11.3±0.1 11.9±0.2 11.0±0.2 NS 11.7±0.2 10.9±0.2 NS
Z score (weight) 2.4±0.0 2.7±0.1 2.9±0.1 NS 2.8±0.1 2.9±0.1 NS
Total cholesterol (mg/dL) 164.1±1.6 163.3±2.5 164.4±2.1 NS 162.9±2.5 165.6±2.1 NS
LDL-C (mg/dL) 97.7±1.5 96.3±2.5 97.8±2.0 NS 96.3±2.4 99.5±1.9 NS
HDL-C (mg/dL) 46.0±0.6 44.1±0.9 44.6±0.7 NS 43.8±0.8 45.3±0.7 NS
Triglycerides (mg/dL) 105.1±2.8 122.8±5.3 117.4±4.1 NS 122.9±5.3 111.0±4.2 NS
Fasting glucose (mg/dL) 87.5±0.5 89.3±0.8 89.3±0.6 NS 90.3±0.8 89.5±0.6 NS
Plasma insulin (μU/mL) 16.0±0.7 27.0±1.3 22.1±1.0 0.003* 26.4±1.3 22.2±1.0 0.02*
HOMA-IR 3.5±0.2 6.1±0.4 4.9±0.4 0.002* 6.0±0.4 5.0±0.3 NS
Values are presented as number only or mean±standard error of the mean.

HOMA-IR: Homeostatic model assessment-insulin resistance, FCOP: fixed cut off point (fasting plasma insulin ＞15 μU/mL,
HOMA-IR ＞3.16), CCOP: corrected cut off point (according to age and gender), NS: not significant, LDL-C: low density lipoprotein
cholesterol, HDL-C: high density lipoprotein cholesterol.
*Exact Fisher’s test.
62 Vol. 21, No. 1, January 2018

Table 2. Gender-Related Frequency (%) of Metabolic Abnor- or of HOMA-IR.

malities in a Sample of Obese Children and Adolescents Table 3 depicts the distribution of patients with or
Male Female without IR, according to the use of FCOP or CCOP.
Variable
(%, n=172) (%, n=211) Using fasting plasma insulin or HOMA-IR CCOP, as
Fasting glucose ＞100 mg/dL 6.4 4.7 compared to FCOP, there was concordance in 150
Total cholesterol ＞150 mg/dL 65.7 64.9 (68.0%) and 153 (70.0%) subjects, respectively, and
LDL-C ＞100 mg/dL 44.8 46.4
HDL-C ＜45 mg/dL 44.8 52.6 discrepancy in 71 (32.1%) and 62 cases (28.6%) for
Triglycerides ＞100 mg/dL 44.8 46.0 the diagnosis of IR. On the other hand, for the diag-
Increased plasma insulin nosis of absence of IR, CCOP was consonant with
FCOP 33.1 44.1
FCOP in 162 (73.3%) and 166 (76.5%) for fasting
CCOP 57.6 57.8
Increased HOMA-IR plasma insulin and HOMA-IR, respectively, and dis-
FCOP 37.8 42.7 crepant in none for fasting plasma insulin and in 2
CCOP 57.0 55.5
for fasting HOMA-IR.
LDL-C: low density lipoprotein cholesterol, HDL-C: high The frequency (%) of lipid changes in the sample
density lipoprotein cholesterol; FCOP: fixed cut off point
of patients with IR according to the cutoff criteria for
(fasting plasma insulin ＞15 μU/mL, HOMA-IR ＞3.16), CCOP:
corrected cut off point (according to age and gender), fasting plasma insulin and HOMA-IR is depicted in
HOMA-IR: Homeostatic model assessment-insulin resistance. Table 4. The frequency of dyslipidemia was also high,
Exact Fisher’s test p＞0.05.
being above 50% for all indicators evaluated.
Table 3. Distribution of Children according to the Presence or Absence of Insulin Resistance Using Fixed or Variable Cutoff Points
of Fasting Plasma Insulin or of HOMA-IR
Increased fasting plasma insulin Increased HOMA-IR
FCOP Total FCOP Total
CCOP + CCOP +
+ 150 71 221 + 153 62 215
0 162 162 2 166 168
Total 150 233 383 Total 155 228 383
HOMA-IR ＞3.16), CCOP: corrected cut off point (according to age and gender).
Exact Fisher’s test p＜0.0001.
Table 4. Comparison of Dyslipidemia Frequencies in Children with Insulin Resistance Assessed by Fixed or Age-Adjusted Cutoff
Points of Insulin or of HOMA-IR
Increased plasma insulin (%) Increased HOMA-IR (%)

Alteration (mg/dL)
FCOP (n=150) CCOP (n=221) FCOP (n=155) CCOP (n=215)
Total cholesterol ≥150 60.7 62.9 60.0 63.3

LDL-C ≥100 44.7 45.2 45.1 45.1
HDL-C ≤45 54.7 52.9 56.7 53.5
Triglycerides ≥100 59.3 54.3 59.3 55.8
Fasting glucose ≥100 6.7 7.7 8.4 7.9
HOMA-IR ＞3.16), CCOP: corrected cut off point (according to age and gender), LDL-C: low density lipoprotein cholesterol, HDL-C:
high density lipoprotein cholesterol.
Mann-Whitney test p＞0.05.
www.pghn.org 63
DISCUSSION cents of different ethnicities [38,41-44]. In this

study, the frequency of metabolic alterations such as
The objective of this study was to compare, in a increased TC, LDL-C and TG, decreased HDL-C, and
sample of 383 children and adolescents with excess abnormal fasting glucose in cases of IR, identified ac-
weight, the criteria of age and gender CCOP with one cording to CCOP of fasting plasma insulin and of
of the criteria of FCOP for fasting plasma insulin and HOMA-IR, was similar to those found using FCOP
for HOMA-IR adopted in the literature, used to iden- (Table 3). Juárez-López et al. [38] demonstrated that
tify IR, and its correlation with dyslipidemia. The fre- in a sample of Mexican obese children, the most fre-
quency of IR identified by the use of the fasting plas- quent metabolic alteration was low HDL-C (69%),
ma insulin and HOMA-IR CCOP was 57.7% and followed by increased TG (29%), TC and LDL-C
56.1%, whereas the FCOP identified 39.2% and (11%), and glucose (4%). However, they used values
40.5% patients with IR, respectively (Tables 1 and 3). of HOMA-IR greater or equal to 3.4 for the diagnosis
This frequency is similar to that found in 466 of IR and different criteria for the definition of
Mexican obese adolescents aged 11 to 13 years, using dyslipidemia.
a HOMA-IR FCOP of 3.4 [38]. In this study, CCOP Corroborating with the findings by other authors
enabled the identification of more cases of IR than [8,22], this study found that fasting glucose values
FCOP. Nevertheless, fasting insulin and HOMA-IR were within normal limits regardless of the method
values in patients with IR identified by increased or cutoff point used for the diagnosis of IR (Table 1).
fasting plasma insulin were significantly lower when Since fasting glucose varies little in the pediatric age
CCOP was used as compared to FCOP (Table 1). group, many authors suggest that the use of HOMA-
When CCOP of fasting plasma insulin and of IR for the diagnosis of IR would be unnecessary,
HOMA-IR were used, as compared to FCOP, the au- since the component of the equation that effectively
thors found intense correlation both for the diag- varies is plasma insulin, therefore being sufficient
nosis of IR as for the absence of IR (Table 3). for the diagnosis [14,22]. In fact, in our cases, it was
In other studies, which used multivariate re- noted that the results of IR and metabolic abnormal-
gression analysis, a positive association was found ities, using fasting plasma insulin or HOMA-IR were
between the female gender and the presence of IR similar.
[39,40]. In our sample, however, no significant dif- Our study has limitations such as the small num-
ference was seen in the frequency of IR in relation to ber of patients, its cross-sectional design, unavail-
gender, corroborating previous results obtained in ability of a control group and of other clinical and
eutrophic children and adolescents [19] (Table 2). It laboratory outcomes related to IR (hypertension,
is important to note that, in the studies mentioned, waist circumference, steatosis, etc.), arbitrariness of
lower FCOPs were used than those employed in this the definitions for corrected cutoff points (two
study (HOMA-IR greater than or equal to 3.16). standard deviations above the mean), and the lack of
Another objective of our study was to evaluate the comparison with a validated diagnostic method of
frequency of some of the outcomes often found in IR. Ideally, it would be best if this definition came
MS, such as dyslipidemia and abnormal fasting glu- from longitudinal, risk association studies; however,
cose, in the presence of IR, identified by different these have not been published to this day. Nonetheless,
cutoff criteria for fasting plasma insulin and for it should be noted that this study was the first to
HOMA-IR. Many researchers have identified a corre- compare two criteria for the definition of cutoff
lation between markers of IR and the classic compo- points of fasting plasma insulin and of HOMA-IR for
nents of MS, especially hypertriglyceridemia, low the diagnosis of IR and the first to describe the fre-
HDL-C, hypertension, and increased waist circum- quency of metabolic alterations according to these
ference, both in adults and in children and adoles- criteria.
64 Vol. 21, No. 1, January 2018

For the clinician, this study shows the importance Comparação de indicadores de perfis glicêmico e lip-
of always evaluating values of fasting insulin and ídico entre crianças e adolescentes obesos egressos de
serviço público ou privado da cidade de Ribeirão Preto
HOMA-IR together with the age. Additionally, it is
(SP). Medicina 2016;49:504-10.
very important to remember that the hyperglycemia 7. Todendi PF, Valim AR, Reuter CP, Mello ED, Gaya AR,
is not common, but it is fundamental that some eval- Burgos MS. Metabolic risk in schoolchildren is asso-
uation of insulin resistance is used, because this phe- ciated with low levels of cardiorespiratory fitness, obe-
nomenon is the first step of a probable type 2 diabetes. sity, and parents' nutritional profile. J Pediatr (Rio J)
Based on this research, it can be concluded that, 2016;92:388-93.
8. Sekokotla MA, Goswami N, Sewani-Rusike CR, Iputo
among children and adolescents with excess weight:
JE, Nkeh-Chungag BN. Prevalence of metabolic syn-
1) fasting plasma insulin and/or HOMA-IR CCOP en- drome in adolescents living in Mthatha, South Africa.
abled more diagnosis of IR as compared to FCOP; 2) Ther Clin Risk Manag 2017;13:131-7.
the frequencies of metabolic abnormalities in the 9. Harrell JS, Jessup A, Greene N. Changing our future:
subjects with IR defined with CCOP were similar to obesity and the metabolic syndrome in children and
those found using FCOP; the frequency of detection adolescents. J Cardiovasc Nurs 2006;21:322-30.
10. Maffeis C, Banzato C, Brambilla P, Cerutti F, Corciulo
of IR by HOMA-IR was similar to that by fasting plas-
N, Cuccarolo G, et al. Insulin resistance is a risk factor
ma insulin, regardless of the cutoff point used; hy- for high blood pressure regardless of body size and fat
perglycemia was not prevalent. distribution in obese children. Nutr Metab Cardiovasc
Dis 2010;20:266-73.
ACKNOWLEDGEMENTS 11. Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH.
Long-term morbidity and mortality of overweight
adolescents. A follow-up of the Harvard Growth Study
The authors thanks to Dr. Ana Valeria B. Castro for
of 1922 to 1935. N Engl J Med 1992;327:1350-5.
her help on endocrinological concepts. 12. Sanches Pde L, Mello MT, Fonseca FA, Elias N, Piano
Ad, Carnier J, et al. Insulin resistance can impair reduc-
REFERENCES tion on carotid intima-media thickness in obese
adolescents. Arq Bras Cardiol 2012;99:892-8.
1. Ng M, Fleming T, Robinson M, Thomson B, Graetz N, 13. Sinaiko A. Obesity, insulin resistance and the metabol-
Margono C, et al. Global, regional, and national preva- ic syndrome. J Pediatr (Rio J) 2007;83:3-4.
lence of overweight and obesity in children and adults 14. Weiss R, Dziura J, Burgert TS, Tamborlane WV,
during 1980-2013: a systematic analysis for the Global Taksali SE, Yeckel CW, et al. Obesity and the metabolic
Burden of Disease Study 2013. Lancet 2014;384:766-81. syndrome in children and adolescents. N Engl J Med
2. de Onis M. Preventing childhood overweight and 2004;350:2362-74.
obesity. J Pediatr (Rio J) 2015;91:105-7. 15. Zachurzok-Buczyńska A, Klimek K, Firek-Pedras M,
3. Nogueira-de-Almeida CA, Benedeti ACGS, Garcia J, Małecka-Tendera E. Are metabolic syndrome and its
Caixe SH. Correlation between ultrasonographic meas- components in obese children influenced by the over-
ures of the abdominal adiposity and indicators of obe- weight status or the insulin resistance? Endokrynol Pol
sity in normal and overweight/obesity children. The 2011;62:102-8.
FASEB Journal 2016;30:1165.4. 16. Zimmet P, Alberti KG, Kaufman F, Tajima N, Silink M,
4. Nogueira-de-Almeida CA, Caixe SH, Benedeti ACGS, Arslanian S, et al. The metabolic syndrome in children
Garcia J. Echocardiography evaluation as a marker of and adolescents-an IDF consensus report. Pediatr
cardiovascular risk on obese children and adolescents. Diabetes 2007;8:299-306.
The FASEB Journal 2016;30:126.1. 17. Pinho AP, Brunetti IL, Pepato MT, de Almeida CAN.
5. Nogueira-de-Almeida CA, Garcia J, Caixe SH, Benedeti Metabolic syndrome in overweight/obese female
ACGS. Ultrasonographic assessment of the common adolescents. Rev Paul Pediatr 2012;30:51-6.
carotid intima-media complex in normal weight chil- 18. Levy-Marchal C, Arslanian S, Cutfield W, Sinaiko A,
dren and in overweight/obese children. The FASEB Druet C, Marcovecchio ML, et al. Insulin resistance in
Journal 2016;30:1165.3. children: consensus, perspective, and future directions.
6. Nogueira-de-Almeida CA, Pires LAF, dos Santos RG. J Clin Endocrinol Metab 2010;95:5189-98.
www.pghn.org 65
19. Almeida CA, Pinho AP, Ricco RG, Pepato MT, Brunetti obesidade: avaliação da reação inflamatória através da
IL. Determination of glycemia and insulinemia and the dosagem da proteína c-reativa ultra-sensível e preva-
homeostasis model assessment (HOMA) in school- lência de síndrome metabólica. Belo Horizonte: UFMG,
children and adolescents with normal body mass index. 2006.
J Pediatr (Rio J) 2008;84:136-40. 31. da Silva RC, Miranda WL, Chacra AR, Dib SA.
20. García Cuartero B, García Lacalle C, Jiménez Lobo C, Metabolic syndrome and insulin resistance in normal
González Vergaz A, Calvo Rey C, Alcázar Villar MJ, et glucose tolerant brazilian adolescents with family his-
al. The HOMA and QUICKI indexes, and insulin and tory of type 2 diabetes. Diabetes Care 2005;28:716-8.
C-peptide levels in healthy children. Cut off points to 32. DeFronzo RA. Lilly lecture 1987. The triumvirate: be-
identify metabolic syndrome in healthy children. An ta-cell, muscle, liver. A collusion responsible for
Pediatr (Barc) 2007;66:481-90. NIDDM. Diabetes 1988;37:667-87.
21. Keskin M, Kurtoglu S, Kendirci M, Atabek ME, Yazici 33. Kurtoğlu S, Hatipoğlu N, Mazıcıoğlu M, Kendirici M,
C. Homeostasis model assessment is more reliable than Keskin M, Kondolot M. Insulin resistance in obese chil-
the fasting glucose/insulin ratio and quantitative in- dren and adolescents: HOMA-IR cut-off levels in the
sulin sensitivity check index for assessing insulin re- prepubertal and pubertal periods. J Clin Res Pediatr
sistance among obese children and adolescents. Endocrinol 2010;2:100-6.
Pediatrics 2005;115:e500-3. 34. Salazar MR, Carbajal HA, Espeche WG, Dulbecco CA,
22. Mieldazis SF, Azzalis LA, Junqueira VB, Souza FI, Aizpurúa M, Marillet AG, et al. Relationships among
Sarni RO, Fonseca FL. Hyperinsulinism assessment in insulin resistance, obesity, diagnosis of the metabolic
a sample of prepubescent children. J Pediatr (Rio J) syndrome and cardio-metabolic risk. Diab Vasc Dis Res
2010;86:245-9. 2011;8:109-16.
23. Moran A, Jacobs DR Jr, Steinberger J, Hong CP, 35. de Onis M, Onyango AW, Borghi E, Siyam A, Nishida
Prineas R, Luepker R, et al. Insulin resistance during C, Siekmann J. Development of a WHO growth refer-
puberty: results from clamp studies in 357 children. ence for school-aged children and adolescents. Bull
Diabetes 1999;48:2039-44. World Health Organ 2007;85:660-7.
24. Pastucha D, Filipčíková R, Horáková D, Radová L, 36. Wallace TM, Matthews DR. The assessment of insulin
Marinov Z, Malinčíková J, et al. The incidence of meta- resistance in man. Diabet Med 2002;19:527-34.
bolic syndrome in obese Czech children: the importance 37. Back Giuliano Ide C, Caramelli B, Pellanda L, Duncan
of early detection of insulin resistance using homeo- B, Mattos S, Fonseca FH. I guidelines of prevention of
static indexes HOMA-IR and QUICKI. Physiol Res atherosclerosis in childhood and adolescence. Arq Bras
2013;62:277-83. Cardiol 2005;85 Suppl 6:4-36.
25. Ten S, Maclaren N. Insulin resistance syndrome in 38. Juárez-López C, Klünder-Klünder M, Medina-Bravo P,
children. J Clin Endocrinol Metab 2004;89:2526-39. Madrigal-Azcárate A, Mass-Díaz E, Flores-Huerta S.
26. Jeffery AN, Metcalf BS, Hosking J, Streeter AJ, Voss Insulin resistance and its association with the compo-
LD, Wilkin TJ. Age before stage: insulin resistance rises nents of the metabolic syndrome among obese children
before the onset of puberty: a 9-year longitudinal study and adolescents. BMC Public Health 2010;10:318.
(EarlyBird 26). Diabetes Care 2012;35:536-41. 39. Madeira IR, Bordallo MA, Carvalho CN, Gazolla FM,
27. Moran A, Jacobs DR Jr, Steinberger J, Steffen LM, de Souza FM, de Matos HJ, et al. The role of metabolic
Pankow JS, Hong CP, et al. Changes in insulin resist- syndrome components and adipokines in insulin resist-
ance and cardiovascular risk during adolescence: estab- ance in prepubertal children. J Pediatr Endocrinol
lishment of differential risk in males and females. Metab 2011;24:289-95.
Circulation 2008;117:2361-8. 40. Tester J, Sharma S, Jasik CB, Mietus-Snyder M,
28. Aradillas-García C, Rodríguez-Morán M, Garay-Sevilla Tinajero-Deck L. Gender differences in prediabetes and
ME, Malacara JM, Rascon-Pacheco RA, Guerrero-Romero insulin resistance among 1356 obese children in
F. Distribution of the homeostasis model assessment of Northern California. Diabetes Metab Syndr 2013;7:
insulin resistance in Mexican children and adolescents. 161-5.
Eur J Endocrinol 2012;166:301-6. 41. Angulo N, de Szarvas SB, Mathison Y, Hadad E,
29. Barja S, Arteaga A, Acosta AM, Hodgson MI. Insulin re- González D, Hernández A, et al. Diagnosis of insulin re-
sistance and other expressions of metabolic syndrome sistance by indirect methods in obese school children.
in obese Chilean children. Rev Med Chil 2003;131:259-68. Invest Clin 2013;54:149-60.
30. Brasil AR. Crianças e adolescentes com sobrepeso ou 42. Kim HA, Lee SY, Kwon HS, Lee SH, Jung MH, Han K,
66 Vol. 21, No. 1, January 2018

et al. Gender differences in the association of insulin re- (Rio J) 2014;90:600-7.

sistance with metabolic risk factors among Korean ado- 44. Tandon N, Garg MK, Singh Y, Marwaha RK.
lescents: Korea National Health and Nutrition Prevalence of metabolic syndrome among urban Indian
Examination Survey 2008-2010. Diabetes Res Clin adolescents and its relation with insulin resistance
Pract 2013;99:54-62. (HOMA-IR). J Pediatr Endocrinol Metab 2013;26:
43. Romualdo MC, Nóbrega FJ, Escrivão MA. Insulin re- 1123-30.
sistance in obese children and adolescents. J Pediatr
www.pghn.org 67
Volume 1- Issue 7 : 2017
DOI: 10.26717/BJSTR.2017.01.000586
Carlos Alberto Nogueira-de-Almeida. Biomed J Sci & Tech Res
ISSN: 2574-1241
Opinion Open Access
We Need To Look At the Comorbidities of Obesity during

Childhood and Adolescence
Carlos Alberto Nogueira-de-Almeida*
Medical Department, Federal University of São Carlos (UFSCAR), Brazil
Received: December 06, 2017; Published: December 13, 2017
*Corresponding author: Carlos Alberto Nogueira-de-Almeida, UFSCAR, Rua Eugênio Ferrante, 170 14027-150 Ribeirão Preto, SP, Brazil,
Tel: ; Email:
Opinion
Results from 59 children of both genders, between 7 and 10 years
Nowadays, almost 50% of boys and girls with ages between
old showed high correlation of fat deposits between each other
5 and 9 years old are overweight or obese. And these children
and the two compartments of abdominal fat deposition increased
frequently have one or more comorbidities. Unfortunately, there
together. And, even more important, both subcutaneous fat and
is a wrong belief that the great problem of obese children is the
visceral fat showed almost the same correlation with abdominal
risk of this child to be an obese adult. In fact, there are a lot of
circumference.
comorbidities that already appears during infancy and, if treated,
probably will not progress to adulthood. We have been studying This means that, at this age, when we measure the abdomen,
some of these comorbidities from the last 5 years. We studied we are measuring both visceral and subcutaneous fat and this two
dyslipidemia and insulin resistance and we found that 69.4% of measurements increase together with the increase of the abdominal
the children had high cholesterol, 45.2% high LDL, 54.8% low HDL circumference [8]. At this same study, we evaluated the liver and a
and 53.2% high triglycerides [1]. It is consensual that we have a hiperechoic image is an indicator of the presence of Non Alcoholic
vicious circle including obesity and insulin resistance [2] and we fat Liver Disease (NAFLD). Children with normal liver tend to have
evaluated 383 children with ages between 7 and 18 years using less subcutaneous fat then children with more echoic liver. And,
fasting insulinemia and Homa as indicators of insulin resistance. similarly, children with normal liver tend to have less visceral fat
The prevalence was very high, independently of the method: 33.1% then children with more echoic liver [8]. In conclusion, even among
using fasting insulin > 15 and 37.8% using HOMA> 3.5 [1]. We also school children, we could find a lot of obesity comorbidities, as:
looked at blood pressure and we showed high blood pressure values dyslipidemia, insulin resistance, high blood pressure, left ventricle
among obese children, when compared to eutrophic children [3-5]. hypertrophy, carotid intima hypertrophy, visceral fat accumulation
and NAFLD. And we need to treat these children early, to prevent
Regarding the heart, we investigated if obese children, with
the evolution to adult diseases and to give them a better quality of
ages between 6 and 9 years, has detectable modifications of the
life.
heart anatomy, especially regarding to the left ventricle, and we
found that, among 5 index evaluated, two of them (the LV mass References
and the LV3 index) showed differences, with greater thickness of
1. Nogueira-de-Almeida CA, Pires LA, dos Santos RG (2016) Comparação de
the ventricle among obese children [4]. The intima-media complex indicadores de perfis glicêmico e lipídico entre crianças e adolescentes
of common carotid artery can be accessed using ultrasonography. obesos egressos de serviço público ou privado da cidade de Ribeirão
This is a very safe and accurate method to evaluate the onset Preto (SP). Medicina (Ribeirao Preto Online) 49(6): 504-510.
appearance of atherosclerosis. We evaluated 59 children of both 2. De Almeida CAN, Pinho AP, Ricco RG, Pepato MT, Brunetti IL (2008)
genders, between 7 and 10 years old [5]. The average thickness Determination of glycemia and insulinemia and the homeostasis model
assessment (HOMA) in schoolchildren and adolescents with normal
of the intima-media complex in the group overweight / obese was body mass index. Jornal de pediatria 84(2): 136-140.
0.49mm; in the non-obese group, the measurement was 0.41mm.
3. Nogueira-de-Almeida CA, Caixe SH, Benedeti ACGS, Garcia J (2016)
There was a significant difference between groups (p <0.01).And, Echocardiography Evaluation as a Marker of Cardiovascular Risk on
also, we showed a correlation between the increase of the z-score Obese Children and Adolescents. The FASEB Journal 30(1): 126.1.
of BMI and the increase of the intima-media complex [6]. The waist 4. Caixe SH, Garcia Saab Benedeti AC, Garcia J, Martins WdP, Mauad
circumference is nowadays considered very important for children Filho F, et al. (2014) Evaluation of Echocardiography as a Marker of
health [7]. We evaluated the abdominal adiposity distribution [8]. Cardiovascular Risk in Obese Children and Adolescents 3(3): 72-78.
Cite this article: Carlos A N D A. We Need To Look At the Comorbidities of Obesity during Childhood and Adolescence. Biomed J Sci & Tech
Res 1(7)-2017. BJSTR. MS.ID.000586. DOI : 10.26717/BJSTR.2017.01.000586 1/2
Carlos Alberto Nogueira-de-Almeida. Biomed J Sci & Tech Res Volume 1- Issue 7 : 2017
5. Costa KCM, Lima JC, Almeida CANd, Ciampo LAD, Souza CSBd (2012) 7. De Almeida CA, Pinho AP, Ricco RG, Elias CP (2007) Abdominal
Variation of the brachial artery diameter in obese children: present and circumference as an indicator of clinical and laboratory parameters
future. Revista Paulista de Pediatria 30(3): 431-437. associated with obesity in children and adolescents: comparison
between two reference tables. J Pediatr (Rio J) 83(2): 181-185.
6. Nogueira-de-Almeida CA, Garcia J, Caixe SH, Benedeti ACGS (2016)
Ultrasonographic Assessment of the Common Carotid Intima-Media 8. Nogueira-de-Almeida CA, Benedeti ACGS, Garcia J, Caixe SH (2016)
Complex in Normal Weight Children and in Overweight/Obese Children. Correlation Between Ultrasonographic Measures of the Abdominal
The FASEB Journal 30(1): 1163-1165. Adiposity and Indicators of Obesity in Normal and Overweight/Obesity
Children. The FASEB Journal 30(1): 1165.4.
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ARTIGO ORIGINAL
Manejo da obesidade infanto-juvenil

1
2
1
Mestre e Doutora - Membro do Departamento de Nutrologia Pediátrica da Abran - Professora da UFRGS
2
Mestre em Saúde da Criança e Adolescente da Unicamp - Mestre e Doutor em Pediatria Pela USP
Diretor do Departamento de Nutrologia Pediátrica da Abran - Professor da Universidade de Ribeirão Preto
RESUMO
O assunto aqui abordado foi apresentado no Simpósio Paralelo: Manejo clínico da obesidade e da
doença hepática não gordurosa do fígado na criança“, coordenado por: Anil Dhawan (UK) e Mary
Fewtrell (UK). Estão sendo apresentados alguns aspectos salientados na apresentação de Cristina
Campoy (Granada, Espanha), com o título “Manejo não cirúrgico da obesidade infantil“.
Palavra chave: obesidade
ABSTRACT
The issue addressed here was presented at the Parallel Symposium: “Clinical management of obesity
and NAFLD in children “, coordinated by: Anil Dhawan (UK) and Mary Fewtrell (UK). Here are presented
some aspects highlighted in the presentation of Cristina Campoy (Granada, Spain), entitled “Nonsurgical
Management of childhood obesity.”
Keyword: obesity
INTRODUÇÃO das nos adultos; c) ter adequado desenvolvimento e

crescimento; d) manter, a longo prazo, o peso e um
Existem alguns momentos críticos de desen- estado de saúde saudáveis; e) otimizar o desenvol-
volvimento de obesidade (de crescimento do tecido vimento psico-afetivo e cognitivo.
adiposo) na infância. Observa-se que 14% das Para o tratamento da obesidade da criança e
crianças são obesas nos primeiros 5 anos de vida; do adolescente este grupo propôs o algorítimo que
40% entre 6-7 anos e 80% dos adolescentes. será apresentado a seguir. A presença e a gravidade
O impacto sócio econômico da obesidade das complicações constituem os determinantes
é muito grande. A obesidade infantil tem um custo primários para seleção da modalidade de trata-
estimado de 19.000 mil dólares por criança, quan- mento e a intensidade da terapia para perder
do se compara com os custos de manejo das peso: 1) intervenção do estilo de vida: modificação
morbidades em relação a crianças com peso normal. de comportamento, dieta e atividade física; 2)
Quando se multiplica pelo número de obesos aos farmacoterapia; 3) procedimento para perda de
10 anos de idade nos EUA, o custo com o manejo peso: cirurgia bariátrica, dispositivos envolvendo
dessas crianças, somente para esta idade, atinge 14 estimulação elétrica ou balão gástrico.
bilhões de dólares. 1. Intervenção do estilo de vida: modificação de
Os objetivos do tratamento da obesidade são: comportamento, realização de dieta e estímulo à
a) obter redução do IMC (índice de massa corporal); prática da atividade física.
b) prevenir a ocorrência das comorbidades observa-
322 S International Journal of Nutrology, a.10, n.1, p. 322 S - 324 S, Março 2017 - Suplemento
MANEJO DA OBESIDADE INFANTO-JUVENIL
a) Perda de peso: o objetivo da perda de peso sono que poderiam ser adequadas: 8-9 horas ou
depende da idade do paciente. Assim, crianças 14 horas; f) Crianças e adolescentes de 6 a 13
de 1 a 11 anos devem perder até 500g/mês; anos de idade: horas de sono ideal: 9 a 11 horas;
e,adolescentes, até 1 kg/mês; e, especialmente, horas de sono que poderiam seradequadas: 7-8
deve ocorrer melhora do índice de massa corporal horas ou 12 horas; g) Adolescentes de 14 a 17
(IMC) em 3 a 6 meses de tratamento. anos de idade: horas de sono ideal: 8 a 10 horas;
b) Restrição de calorias: em relação ao manejo horas de sono que poderiam ser adequadas: 7
dietético, deve-se fazer restrição da ingestão horas ou 11 horas;
calórica de acordo com a idade. Deve-se reduzir g) Participação de grupos de intervenção com-
15 a 18% da ingestão calórica naqueles com idade portamental, sendo especialmente importante
entre 9 e 13 anos e reduzir 20 a 25% naqueles para aquelas crianças e adolescentes que não
com idade entre 14 e 18 anos. têm controle dos pais ou vivem com a avó.
c) A distribuição das calorias no decorrer do
diadeveria ser a seguinte: 25% no café da manhã; O manejo dietético, a prática de atividade fí-
10% na merenda; 30% no almoço; 10% no lanche sica e o comportamento das crianças e dos ado-
tarde; e 25% nojantar. Sugeriu-se que o pré- lescentes são afetados por: comunidade, escolas,
escolar tivesse 4 refeições por dia; o escolar, 6 creches (child care sittings), faith-based institutions,
por dia e o adolescente, 5 por dia. agências governamentais, famílias, mídia eindústria
alimentícia.
d) A distribuição dos macronutrientes sugerida, As escolas têm importante papel em fornecer
seria de acordo com a idade. Crianças com idade ambiente para prática de hábitos de estilo de vida
entre 1 e 3 anos: 45 a 65% de carboidrato do valor saudável. Elas têm a oportunidade de educar
energético total (VET), 30 a 40% de gorduras do as crianças para estes comportamentose prover
VET e 5 a 20% de proteínas do VET. Crianças oportunidade para sua prática.
e adolescentes entre 4 a 18 anos: 45 a 65% de Deve-se estimular que as escolas aumentem
carboidrato do VET, 25 a 35% de gorduras do o número de frutas e verduras servidas na escola.
VET e 10 a 30% de proteínas do VET. O açúcar Exemplos de movimentos com este objetivo podem
deveria ser ofertado na quantidade máxima de ser citados: o “Let´s move salad to school“ (criado por
5% do VET. Michelle Obama) e o “The National Farm to School
e) Em relação à prática de atividade física, crianças Network“
e adolescentes de 5 a 17 anos de idade deveriam Para promoção de estilo de vida saudável
praticá-la diariamente, ou pelo menos 3 vezes por existe também o programa 5210:
semana, numa intensidade moderada a vigorosa, 5 - pelo menos 5 porções de frutas e verduras por
pelo menos 60 minutos por dia e de tipo aeróbico. dia.
f) A higiene do sono também é muito importante. 2 - menos de 2 horas por dia na frente de telas.
Assim, de acordo com a faixa etária recomendou 1 - pelo menos 1 hora por dia de prática de atividade
o seguinte: a) Lactente de 0 a 3 meses de idade: física moderada ou vigorosa, pelo menos 3
horas de sono ideal: 14-17 horas; horas de sono vezes por semana.
que poderiam ser adequadas: 11-13 horas ou 18-
0 - Não adicionar açúcar.
19 horas; b) Lactente de 0 a 3 meses de idade:
horas de sono ideal: 14-17 horas; horas de sono 2. Farmacoterapia: Em relação à farmacoterapia,
que poderiam ser adequadas: 11-13 horas ou refere que se poderiautilizar sibutramina e/ou
18-19 horas; c) Lactente de 4 a 11 meses de orlistat, embora os estudos demonstrem modesta
idade: horas de sono ideal: 12-15 horas; horas de perda de peso, de 3 a 8% comparado com
sono que poderiam seradequadas: 10-11 horas placebo.
ou 16-18 horas; d) Crianças de 1 a 3 anos de a) Sibutramina: promove a saciedade e aumenta
idade: horas de sono ideal: 11-14 horas; horas o gasto energético, inibindo a recaptação de no-
de sono que poderiam ser adequadas: 9-10 horas radrenalina e serotonina. Como efeitos adversos
ou 15-16horas; e) Crianças de 3 a 5 anos de apresenta: anorexia, palpitação, pressão arterial
idade: horas de sono ideal: 10-13 horas; horas de aumentada ecefaléia;
International Journal of Nutrology, a.10, n.1, p. 322 S - 324 S, Março 20176 - Suplemento 323 S
ELZA DANIEL DE MELLO
b) Orlistat: bloqueia a absorção de gordura no 6. Rondanelli M et al. Effects oft wo-months balanced diet in
intestino, por diminuir a ação da lipase, sendo metabolically healthy obesity:lipid correlations with gen-
der and BMI-related differences. Lipids in Health and Di-
o resultado um balanço energético negativo. Os
sease 2015;(14):139.DOI 10.1186/s12944-015-0131-1.
efeitos adversos possíveis são má absorção de
vitaminas lipossolúveis e presença de óleo nas 7. Van Jaarsveld CHM et al. Prospective associations be-
fezes. tween appetitive traits and weight gain in infancy. Am J
Clin Nutr. 2011;94:1562-7.
c) Outras drogas que poderiam ser utilizadas em
situações específicas seriam metformina (para ser 8. ESPGHAN Committee on Nutrition. Role of Dietary fac-
tors and food habits in the development of childhood
utilizada em adolescentes obesos com resistência
obesity: a commentary by the ESPGHAN Committee on
periférica à insulina e hiperinsulinemia), octreotide Nutrition. J Pediatr Gastroenterol Nutr. 2011; 52:662-9.
(como opção para o manejo da obesidade
hipotalâmica), hormônio de crescimento (indicado 9. Martinez-Gomez D et al. Design and evaluation of a treat-
ment programme for Spanish adolescents with overwei-
na Síndrome de Prader Willi) e leptina (indicada
ght and obesity. The EVASYON Study. BMC Public Heal-
no manejo da deficiência congênita de leptina). th 2009;9:414.
10. Martinez-Gomez D et al. Excessive TV viewing and cardio-

REFERÊNCIAS BIBLIOGRÁFICAS vascular disease risk factors in adolescents. The AVENA
cross-sectional study. BMC Public Health 2010;10:274.
1. Van Jaarsveld CHM et al. Appetite and growth. A longitu-
dinal sibling analysis. JAMA Pediatr. 2014;168(4):345-50. 11. Syrad H et al. Energy and nutrient intakes of young chil-
dren in the UK: findings from the Gemini twin cohort. Bri-
2. Llewellyn CH et al. Development and factors structure oft tish Journal of Nutrition 2016: 115:1843-50.
he baby eating behaviour questionnaire in the Gemini bir-
th cohort. Appetite 2011;57: 388-96. 12. Safdie M et al. Impact of a school-based intervention pro-
gram on obesity risk factors in Mexican children. Salud
3. Llewellyn C & Wardle J. Behavioral susceptibility to obe- Publica Mex 2013;55(S3):S374-S87.
sity: Gene-environment interplay in the development
of weight. Physiology & Behavior 2015. http://dx.doi.
org/10.1016/j.physbeh.2015.07.006.
Recebido em 30/08/2016
4. Lissner L et al. Differential outcome of the IDEFICS inter- Revisado em 20/09/2016
vention in overweight versus non-overweight children: did Aceito em 30/09/2016
we achieve “primary” or “secondary” prevention? Obesity
reviews. 2015;(16):119-26. Autor Correspondente:
Carlos Alberto Nogueira de Almeida
5. Kudlová E & Schneidrová D. Dietary patterns and their Rua São José, 2591 - Ribeirão Preto-SP - CEP 14025180
changes in early childhood. Cent Eur J Public Health Fone: 16 3877 5034
2012; 20(2):126-34. Email: dr.nogueira@me.com
324 S International Journal of Nutrology, a.10, n.1, p. 322 S - 324 S, Março 2017 - Suplemento
J Pediatr (Rio J). 2018;94(3):308---312
www.jped.com.br
ARTIGO ORIGINAL
Correlation of body mass index Z-scores with glucose

and lipid profiles among overweight and obese
children and adolescents!,!!
Carlos Alberto Nogueira-de-Almeida a,∗ e Elza Daniel de Mello b
a
Universidade Federal de São Carlos (UFSCAR), São Carlos, SP, Brasil
b
Universidade Federal do Rio Grande do Sul (UFRGS), Faculdade de Medicina, Porto Alegre, RS, Brasil
Recebido em 13 de janeiro de 2017; aceito em 4 de maio de 2017
KEYWORDS Abstract
Obesity; Objective: To evaluate the prevalence of abnormalities in plasma lipid and glucose profiles
Overweight; among overweight and obese children and adolescents, and to assess the presence of a cor-
Dyslipidemias; relation between body mass index Z-scores and indicators of comorbidities related to both
Insulin Resistance; profiles.
Child; Methods: This was a multicenter cross-sectional study conducted at two outpatient clinics.
Adolescent The study included all 417 comers for the first visit from 2008 to 2012, aged between 7 and
18 years, with BMI above the Z-score + 1. Anthropometry and blood sampling were obtained. The
prevalence of dyslipidemias, hyperglycemia, and insulin resistance were evaluated, together
with the correlations of these variables with the increase of Z-BMI.
Results: Dyslipidemia was observed in 43.4% of the boys and 66.1% of the girls, with no diffe-
rence between genders. High glucose levels were detected in 6.2% of the individuals. Insulin
resistance was present in 32.3% and 41.7% of the cases, with no statistical significance between
boys and girls. Correlations between the Z-BMI were noted for triglycerides in the entire group
and among girls; for HDL-c, only among girls; for glucose, a correlation was observed for the
entire group, but not when stratified by gender. The indicators of insulin resistance were all
correlated with Z-BMI, even when corrected for age.
Conclusions: Overweight and obesity give origin to a high prevalence of dyslipidemia and insulin
resistance. BMI Z-scores showed a weak positive correlation with glucose and triglyceride, and
negative with HDL-c. In turn, the strongest positive correlation was found with insulin resistance
indicators.
© 2017 Sociedade Brasileira de Pediatria. Published by Elsevier Editora Ltda. This is an open
access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/
4.0/).
DOI se refere ao artigo:
http://dx.doi.org/10.1016/j.jped.2017.06.012
! Como citar este artigo: Nogueira-de-Almeida CA, Mello ED. Correlation of body mass index Z-scores with glucose and lipid profiles among
overweight and obese children and adolescents. J Pediatr (Rio J). 2018;94:308---12.
!! Estudo feito na Universidade Federal de São Carlos (UFSCAR), São Carlos, SP; e na Universidade Federal do Rio Grande do Sul (UFRGS),
Porto Alegre, RS, Brasil.

∗ Autor para correspondência.
E-mail: dr.nogueira@me.com (C.A. Nogueira-de-Almeida).
2255-5536/© 2017 Sociedade Brasileira de Pediatria. Publicado por Elsevier Editora Ltda. Este é um artigo Open Access sob uma licença CC
BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/).
BMI and glucose and lipid profiles 309
PALAVRAS-CHAVE Correlação dos escores-z de IMC com os perfis glicêmico e lipídico entre crianças e
Obesidade; adolescentes com sobrepeso e obesidade
Sobrepeso;
Resumo
Dislipidemias;
Objetivo: Avaliar a prevalência de anormalidades nos perfis lipídico e glicêmico entre crianças
Resistência à Insulina;
e adolescentes com sobrepeso e obesidade e também verificar se existe correlação entre os
Criança;
escores-z de índice de massa corporal (z-IMC) e indicadores de comorbidades ligados a esses
Adolescente
perfis.
Métodos: Estudo de corte transversal multicêntrico, incluiu 417 pacientes entre 7 e 18 anos e
IMC acima do escore-z > + 1 que fizeram a consulta de caso novo entre 2008 e 2012. Antropo-
metria e coleta de sangue foram realizadas. As prevalências de dislipidemia, hiperglicemia e
resistência insulínica foram avaliadas, juntamente com as correlações entre essas variáveis e o
z-IMC.
Resultados: Dislipidemia foi encontrada em 43,4% dos meninos e 66,1% das meninas, sem
diferença entre os sexos. Hiperglicemia foi encontrada em 6,2% dos indivíduos. Resistência
insulínica esteve presente entre 32,3 e 41,7% dos casos, sem diferença estatística entre os
sexos. Foi observada correlação com z-IMC para triglicerídeos quando considerado o grupo todo
e entre as meninas; e para HDL-c apenas entre as meninas. A glicemia apresentou correlação
quando considerado o grupo todo, mas não quando separados por sexo. Os indicadores de resis-
tência insulínica estiveram todos correlacionados com IMC, mesmo quando se executou correção
para a idade.
Conclusões: Sobrepeso e obesidade levam a prevalências elevadas de dislipidemia e resistência
insulínica. Os escores-z de IMC mostraram discreta correlação positiva com glicose e triglicerí-
deos e negativa com HDL-c. Por outro lado, correlação positiva mais forte foi observada com
os indicadores de resistência insulínica.
© 2017 Sociedade Brasileira de Pediatria. Publicado por Elsevier Editora Ltda. Este é um artigo
Open Access sob uma licença CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.
0/).
Introdução continuum (avaliado por meio da elevação dos escores-

-z de IMC), os resultados foram diferentes. Bell et al.9
A prevalência cada vez maior de obesidade na infân- demonstraram uma correlação entre aumento da obesi-
cia e adolescência exige dos pesquisadores e interessados dade e acanthosis nigricans, depressão, ansiedade, dor de
em saúde pública o estabelecimento de critérios para cabeça, dor muscular e apneia do sono. Também foram
priorizar ações que visem a abordar esse problema.1 Dife- demonstradas as correlações com dislipidemia,10 resistência
rentes autores demonstraram a presença de fatores de à insulina11 e esteatose.12
risco cardiovascular associados a obesidade, principalmente Este estudo visou a avaliar a prevalência de anomalias nos
dislipidemia2 e resistência à insulina3 , porém os números perfis glicêmico e lipídico entre crianças e adolescentes com
variam muito e a prevalência ainda não é conhecida.4 Para sobrepeso e obesidade e também se é vista uma correlação
estudos populacionais, o índice de massa corporal (IMC) foi entre os escores-z de IMC e os indicadores de comorbidades
usado como indicador e ele consegue refletir a adiposidade com relação aos dois perfis.
corporal;5 a partir do escore-z de + 1, que define sobrepeso,
pode-se entender que quanto maior o valor, mais grave é Métodos
a situação.6 Nesse sentido, é relevante saber não somente
a prevalência, mas também como as comorbidades relaci- Estudo transversal multicêntrico feito em duas clínicas
onadas ao sobrepeso se comportam caso a situação piore ambulatoriais: o Centro de Estudos em Saúde e Nutrologia
e quais são as diferenças entre meninos e meninas. Alguns Infantojuvenil na Universidade de Ribeirão Preto (Cesni) e
autores avaliaram essa questão. Ricco et al.7 estudaram 34 o Ambulatório de Obesidade Infantojuvenil do Serviço de
indivíduos com sobrepeso e 50 com obesidade entre seis e Nutrologia do Hospital de Clínicas da Universidade Federal
18 anos para comparar pressão arterial, glicemia de jejum, do Rio Grande do Sul (AmO). Os dois são serviços acadê-
glicemia de duas horas, colesterol total, HDL-C, LDL-C e micos, nos quais a coleta de dados segue uma metodologia
triglicerídeos. Apenas a HDL-C foi ligeiramente maior em rigorosamente padronizada. O trabalho foi aprovado pelo
pacientes com sobrepeso (p = 0,048), demonstrou que, para comitê de ética em pesquisa da Universidade de Ribeirão
os parâmetros avaliados, o fato de ter IMC mais elevado não Preto (n◦ 94/2003) e do Hospital de Clínicas de Porto Alegre
substancialmente afeta as comorbidades. Lima et al.8 tam- (n◦ 07/258).
bém não encontraram impacto sobre o perfil lipídico em Os critérios de inclusão foram: todos os novos casos de
comparação com crianças e adolescentes com sobrepeso pacientes que passaram pelo local para consulta pela pri-
e obesidade. Por outro lado, quando analisado como um meira vez entre janeiro de 2008 e dezembro de 2012, idade
310 Nogueira-de-Almeida CA, Mello ED
entre sete e 18 anos e índice de massa corporal acima do comparar as frequências de valores normais/anormais entre
escore-z + 1 (n = 489 elegíveis). os gêneros. As correlações simples foram avaliadas pelo
Os critérios de exclusão foram: recusa a assinar o teste de Spearman e foi usada a regressão múltipla para ava-
consentimento informado (n = 2), impossibilidade de fazer liar a correlação entre o escore-z de IMC e insulina e HOMA
antropometria (n = 3), diabetes mellitus tipo 1 (n = 0), hipo- corrigida para a idade, pois esses dois indicadores variam
tireoidismo (n = 0), erros inatos do metabolismo (n = 1), de acordo com a faixa etária.14,15 Para todas as análises, foi
impossibilidade de coletar testes de laboratório (n = 41), considerado um nível de significância de 5%.
problemas médicos especiais, por exemplo, doença celíaca
(n = 0), uso de terapias médicas ou hormônios (n = 0) e dados
incompletos no prontuário médico (n = 25). Ao seguir os cri- Resultados
térios acima, 417 indivíduos foram incluídos no estudo, dos
quais 241 foram vistos no Cesni e 176 no AmO. Os valores médios para toda a população foram: idade
Todos os indivíduos foram orientados a jejuar por (anos): 11,3 (± 0,1); escore-z de IMC: + 2,4 (± 0,9); CT
12 horas e os dados antropométricos e sangue foram coleta- (mg/dL): 164,1 (± 1,6); LDL-c (mg/dL): 97,7 (± 1,5); HDL-c
dos no momento da primeira visita do paciente. Dois tubos (mg/dL): 46,0 (± 0,6); TG (mg/dL): 105,1 (± 2,8); glicemia
de 4 mL de sangue foram coletados em um recipiente sem (mg/dL): 87,5 (± 0,5); insulinemia (!U/mL): 16,0 (± 0,7);
aditivos e enviado para o laboratório até duas horas para HOMA-IR: 3,5 (± 0,2). Não houve diferenças entre meninos
processamento da amostra e análise bioquímica e hormo- e meninas.
nal. O material biológico foi separado em uma centrífuga A tabela 1 mostra a prevalência de valores anormais de
(Bio Eng® , modelo BR 4000, SP, Brasil) em funcionamento por acordo com os pontos de corte estabelecidos, bem como
cinco minutos a 3.500 rpm entre uma e duas horas e meia comparação entre sexos. Os diferentes tipos de dislipide-
após a coleta (tempo suficiente para coagulação do san- mia sempre foram muito prevalentes, com valores entre
gue). A insulina bioquímica foi dosada em uma das alíquotas 43,4 e 66,1%, sem diferença entre meninos e meninas. Os
no mesmo dia da coleta, pelo método quimioluminescên- altos níveis de glicose foram a alteração menos prevalente
cia automatizado no analisador Immulitte DPC (Medlab® , entre os indicadores estudados, atingiram um máximo de
SP, Brasil). A glicose foi medida pelo método enzimático 7,4%, encontrados entre meninos, também sem diferença
de hexoquinase com o equipamento de automação Cobas estatística entre os sexos. Deve-se observar que apenas um
Mira Plus (Roche® , SP, Brasil). A determinação da avaliação indivíduo, uma menina de 15 anos, apresentou níveis de
do modelo de homeostase --- resistência à insulina (HOMA- glicose acima de 125 mg/dL (160 mg/dL, não mostrado na
-IR) foi feita ao aplicar a equação proposta por Matthews tabela). Resistência à insulina, conforme avaliada pelos dois
et al.: glicose plasmática (mol/dL) x insulina plasmática indicadores, insulina plasmática e HOMA-IR estiveram pre-
(uUI/mL)/22,5.13 sentes em 32,3 e 41,7% dos casos, sem diferença estatística
Quando a concentração de insulina plasmática estava entre meninos e meninas.
acima de 15 !U/mL10 , considerou-se hiperinsulinismo, usado A tabela 2 mostra as correlações entre os escores-z de IMC
como um marcador para resistência à insulina. Outro método e os indicadores estudados. Em geral, as correlações estive-
de diagnóstico para resistência à insulina foi HOMA-IR, con- ram presentes, porém de forma branda. Com relação aos
siderado alto quando acima de 3,16.11 Os valores de corte lipídios, foi vista correlação para triglicerídeos, encontrada
usados para definir a presença de dislipidemia e hipergli- no grupo como um todo e entre as meninas; para HDL-C, ape-
cemia foram:13 colesterol total (CT) ≥ 150 mg/dL; LDL-C nas entre meninas. Foi encontrada correlação para glicose
≥ 100 mg/dL; HDL-C ≤ 45 mg/dL; triglicerídeos ≥ 100 em todo o grupo, porém não quando separada por sexo. Por
mg/dL; glicemia > 99 mg/dL. outro lado, os indicadores de resistência à insulina foram
Para a análise estatística, foi usado o programa de com- todos correlacionados com IMC, mesmo quando correlaci-
putador Graphpad Prism 5 (GraphPad Prism versão 7.00 para onados com idade. Não houve diferenças entre meninos e
Windows, CA, EUA). O teste exato de Fisher foi usado para meninas.
Tabela 1 Prevalência de anomalias nos indicadores estudados
Meninos + meninas (n = 417) Meninos (n = 189) Meninas (n = 228) Meninos versus meninas
n (%) n (% entre meninos) n (% entre meninas) pa
Colesterol total > 150 mg/dL 273 (65,5%) 125 (66,1%) 148 (64,9%) 0,8364
LDL-c > 100 mg/dL 189 (45,3%) 83 (43,9%) 106 (46,5%) 0,6221
HDL-c < 45 mg/dL 199 (47,7%) 82 (43,4%) 117 (51,3%) 0,1157
Triglicerídeos > 100 mg/dL 189 (45,3%) 84 (44,4%) 105 (46,1%) 0,7675
Glicose > 100 mg/dL 26 (6,2%) 14 (7,4%) 12 (5,3%) 0,4187
Insulina 156 (37,4%) 61 (32,3%) 95 (41,7%) 0,0537
plasmática > 15 !U/mL
HOMA > 3,16 161 (38,6%) 69 (36,5%) 92 (40,4%) 0,4795
HDL-C, Lipoproteína de Alta Densidade-Colesterol; HOMA, Avaliação do Modelo de Homeostase; LDL-C, Lipoproteína de Baixa Densidade-
-Colesterol.
a Teste exato de Fisher.
BMI and glucose and lipid profiles 311
Tabela 2 Correlações entre os escores Z de IMC e os indicadores estudados
Meninos + meninas R (p) Meninos R (p) Meninas R (p)

Colesterol total -0,01388 (0,7865) 0,05364 (0,4847) -0,1031 (0,1354)
LDL-c -0,01994 (0,6973) 0,05797 (0,4500) -0,08481 (0,2199)
HDL-c -0,08400 (0,1007) -0,04759 (0,5353) -0,1677 (0,0147)
Triglicerídeos 0,1184 (0,0204) 0,07521 (0,3268) 0,1592 (0,0207)
Glicose 0,1249 (0,0144) 0,1482 (0,0523) 0,06200 (0,3702)
Insulina plasmática 0,3228 (< 0,0001) 0,3076 (< 0,0001) 0,4297 (< 0,0001)
HOMA 0,3292 (< 0,0001) 0,3139 (< 0,0001) 0,4233 (< 0,0001)
Insulina ajustada para a idade 0,1578 (< 0,0001) 0,2627 (< 0,0001) 0,1078 (< 0,0001)
HOMA ajustada para a idade 0,1510 (< 0,0001) 0,2543 (< 0,0001) 0,0926 (< 0,0001)
HDL-C, Lipoproteína de Alta Densidade-Colesterol; HOMA, Avaliação do Modelo de Homeostase; IMC, Índice de Massa Corporal; LDL-C,
Lipoproteína de Baixa Densidade-Colesterol.
Teste de Spearman e regressão múltipla ajustada para a idade.
Discussão glicose. Sabe-se que a resistência periférica à insulina está

altamente correlacionada com a síndrome metabólica,2,3
A obesidade é uma doença multifatorial completa com com- é, possivelmente, o elemento causador dessa doença. Por-
ponentes genéticos, epigenéticos e ambientais. Portanto, tanto, entre as crianças estudadas, é possível considerar
espera-se que a forma como ela afeta a saúde das crianças que, além da dislipidemia demonstrada e do alto risco de
seja muito variável. É relevante saber em que medida o diabetes futura --- progressão natural da resistência à insulina
aumento do excesso de peso também implica o surgimento e --- outros aspectos, como hipertensão arterial, doença hepá-
pioria das comorbidades. Um estudo anterior7 já demonstrou tica gordurosa não alcoólica, síndrome do ovário policístico,
que, em comparação com crianças com sobrepeso ou obe- aterosclerose, hiperuricemia, dentre outros, também pode-
sidade, não havia praticamente diferença com relação aos rão estar presentes.19
parâmetros avaliados, ou seja, de certa forma, as comor- Estudos recentes mostraram que o IMC é o melhor
bidades já estavam presentes na fase de sobrepeso. Apesar indicador antropométrico para identificar fatores de risco
de o resultado ter sido importante, a simples divisão das cardiovascular em crianças.20 De Onis et al.21 demonstraram
crianças com sobrepeso em duas categorias, sobrepeso e que o aumento no IMC é acompanhado por redução da HDL-
obesidade, pode mascarar o aspecto contínuo da variável, ou -C e elevação de insulina plasmática, HOMA, triglicerídeos e
seja, o modelo usado não conseguiu mostrar uma correlação LDL-C. Bell et al.,11 com grupos de percentil, mostraram um
ocasional entre IMC e os parâmetros avaliados; esse foi exa- aumento em todos os grupos de percentil nos dois sexos. Foi
tamente o aspecto que tentamos avaliar neste estudo. encontrado um aumento para HDL-C, porém misturado, e,
Conforme mostrado na tabela 1, quando as crianças diferentemente de nosso estudo, foram encontrados resul-
com sobrepeso e obesidade são agrupadas, a prevalência tados não relacionados a sexo para triglicerídeos e glicose.
das comorbidades é bastante alta. Quase metade delas, Skinner et al.,10 que usaram grande número de dados do
independentemente do sexo, tem algum tipo de dislipide- Levantamento Nacional de Exames de Saúde e Nutrição
mia. LDL-C elevado, que afetou 45,3% dos indivíduos, é (NHANEs), também encontraram diferenças entre sexo, com
altamente preocupante devido ao risco associado a ate- valores mais elevados de colesterol total, triglicerídeos e
rosclerose. De fato, Garcia et al.16 demonstraram, em um glicose entre homens; com quatro classes de graus de sobre-
estudo recente que mesmo as crianças em idade escolar peso, eles encontraram também valores mais elevados de
já tinham espessamento médio-intimal da artéria carótida colesterol total, triglicerídeos e glicose e valores meno-
comum, o que indica processo aterosclerótico inicial; Caixe res de HDL-C entre as crianças mais obesas. No presente
et al.17 também demonstraram mudanças na geometria estudo, a avaliação das correlações entre IMC e os indi-
do coração nessa faixa etária, causadas pelo aumento do cadores estudados demonstrou diferentes resultados para
esforço no miocárdio para ultrapassar a alta resistência peri- perfis lipídicos e glicêmicos. Colesterol total e LDL-C não
férica devido ao espessamento das paredes arteriais. Graças mostraram correlação positiva com escore-z de IMC. Quando
à forte capacidade compensatória dos pâncreas jovens, esses dados são analisados em conjunto com a prevalência
mesmo entre crianças com importante resistência à insu- de colesterol total e LDL-C acima dos níveis de ponto de
lina, níveis elevados de glicemia não são frequentes.14,18 corte, pode-se entender que as crianças com sobrepeso e
Neste estudo, apenas 6,2% apresentaram níveis de glicose obesidade são gravemente afetadas. Com relação à HDL-C,
acima de 100 mg/dL e apenas um indivíduo apresentou nível a lógica é basicamente a mesma, com a exceção de que,
acima de 125 mg/dL. Por outro lado, a presença de resis- entre as meninas, foi observada uma fraca correlação nega-
tência à insulina foi alta, encontrada em mais de 1/3 dos tiva, mostrou que a HDL-C tende a ser ligeiramente menor
pacientes. Os dois indicadores usados, insulina plasmática e quanto maior o IMC. Em geral, considera-se que, no per-
HOMA-IR, ambos com pontos de corte fixos, levaram a resul- fil lipídico, triglicerídeo é o indicador que mais muda em
tados semelhantes, possivelmente devido ao fato, conforme crianças obesas. Apesar de isso não ter sido encontrado em
evidenciado pelos outros autores,18 de que a variável que termos de prevalência, foi encontrada uma fraca correlação
determina o valor da HOMA-IR em crianças é basicamente positiva entre o escore-z de IMC e triglicerídeo, particular-
insulina plasmática, pois há pouca variação nos níveis de mente evidente entre meninas.
312 Nogueira-de-Almeida CA, Mello ED
Não avaliamos o estado puberal, pois os valores do ponto 5. Ryder JR, Kaizer AM, Rudser KD, Daniels SR, Kelly AS. Utility of
de corte de lipídicos e glicose são os mesmos em todas as ida- body mass index in identifying excess adiposity in youth across
des incluídas e o perfil insulinêmico depende mais da idade the obesity spectrum. J Pediatr. 2006;177, 255---61.e2.
do que do estado puberal.22 Os valores de glicose apresenta- 6. de Onis M, Onyango AW, Borghi E, Siyam A, Nishida C, Siekmann
ram fraca correlação positiva com IMC, sem, contudo, atingir J. Development of a WHO growth reference for school-aged
children and adolescents. Bull WHO. 2007;85:660---7.
os valores do ponto de corte na maior parte dos pacientes.
7. Ricco RC, Ricco RG, Almeida CA, Ramos APP. Estudo comparativo
Por outro lado, os indicadores de resistência à insulina apre- de fatores de risco em crianças e adolescentes com diagnós-
sentaram as correlações mais fortes entre os indicadores tico antropométrico de sobrepeso ou obesidade. Rev Paul Ped.
estudados; os valores de insulina plasmática e HOMA-IR apre- 2010;28:320---5.
sentaram correlação positiva com os escores-z de IMC. Resul- 8. Lima SC, Arrais RF, Almeida MG, Souza ZM, Pedrosa LF. Plasma
tados semelhantes foram demonstrados por Mieldazis et al.18 lipid profile and lipid peroxidation in overweight or obese chil-
e Silva et al.23 Conforme demonstrado anteriormente,14,15 dren and adolescents. J Pediatr (Rio J). 2004;80:23---8.
os valores da insulina plasmática e HOMA-IR são influencia- 9. Bell LM, Byrne S, Thompson A, Ratnam N, Blair E, Bulsara M,
dos por idade, apresentam aumento significativo com pico et al. Increasing body mass index z-score is continuously associ-
ated with complications of overweight in children, even in the
próximo ao surto de crescimento. Por esse motivo, foi feita
healthy weight range. J Clin Endocrinol Metab. 2007;92:517---22.
regressão múltipla apenas para esse indicador, para con-
10. Skinner AC, Perrin EM, Moss LA, Skelton JA. Cardiometabolic
trolar os resultados para a idade, e, apesar de os valores risks and severity of obesity in children and young adults. N
da correlação terem reduzido, eles persistiram estatistica- Engl J Med. 2015;373:1307---17.
mente significativos. Deve-se observar que os valores da 11. Bell L, Hung J, Knuiman M, Divitini M, Beilby J, Hunter M, et al.
correlação para insulina plasmática e HOMA-IR são muito Body mass index and waist circumference: relationship to car-
semelhantes, independentemente do controle para a idade. diometabolic risk factors in children --- Busselton Health Study
Isso corrobora o fato de que, na infância e adolescência, 2005---2007. J Paediatr Child Health. 2013;49:955---62.
devido às limitações relacionadas à dificuldade de avaliar 12. Meng L, Luo N, Mi J. Impacts of types and degree of obesity on
a presença de resistência à insulina no laboratório, caso a non-alcoholic fatty liver disease and related dyslipidemia in Chi-
nese school-age children? Biomed Environ Sci. 2011;24:22---30.
opção seja usar um dos dois indicadores estudados, medir a
13. Back Giuliano Ide C, Caramelli B, Pellanda L, Duncan B, Mattos
insulina é suficiente e a variação da HOMA-IR basicamente
S, Fonseca FH. I guidelines of prevention of atherosclerosis in
reflete a variação na insulina plasmática. childhood and adolescence. Arq Bras Cardiol. 2005;85:4---36.
O estudo tem algumas limitações: trata-se de um estudo 14. Almeida CA, Pinho AP, Ricco RG, Pepato MT, Brunetti IL. Deter-
transversal, então, não é possível determinar a causa e o mination of glycemia and insulinemia and the homeostasis
efeito. As composições dietéticas e corporais não foram model assessment (HOMA) in schoolchildren and adolescents
avaliadas. A amostra foi obtida de todos os pacientes que with normal body mass index. J Pediatr (Rio J). 2008;84:136---40.
passaram pela primeira consulta nos dois centros durante 15. Cuartero BG, Lacalle CG, Lobo CJ, Vergaz AG, Rey CC, Vil-
o período do estudo, porém não é possível extrapolar os lar MJA, et al. Indice HOMA y QUICKI, insulina y peptido C en
resultados de toda a população de crianças e adolescentes niños sanos. Puntos de corte de riesgo cardiovascular. An Pediatr
(Barc). 2007;66:481---90.
com sobrepeso e obesidade, pois usamos uma amostra de
16. Nogueira-de-Almeida CA, Garcia J, Caixe SH, Benedeti
conveniência.
AC. Ultrasonographic assessment of the common carotid
Sobrepeso e obesidade levaram à alta prevalência de dis- intima-media complex in normal weight children and in
lipidemia e resistência à insulina em meninos e meninas. overweight/obese children. FASEB J. 2016;30, 1165.3.
Os escores-z de IMC mostraram fraca correlação positiva 17. Caixe SB, Saab AC, Garcia J, Martins WP, Mauad Filho F, Del
com glicose e triglicerídeos e correlação negativa com HDL- Ciampo LA, et al. Evaluation of echocardiography as a marker
-C. Por outro lado, foi encontrada forte correlação positiva of cardiovascular risk in obese children and adolescents. Int J
com os indicadores de resistência à insulina, mesmo quando Clin Pediatr. 2014;3:7.
ajustados para a idade. 18. Mieldazis SF, Azzalis LA, Junqueira VB, Souza FI, Sarni RO,
Fonseca FL. Hyperinsulinism assessment in a sample of prepu-
Conflitos de interesse bescent children. J Pediatr (Rio J). 2010;86:245---9.
19. Pinho AP, Brunetti IL, Pepato MT, Almeida CAN. Metabolic syn-
drome in overweight/obese female adolescents. Rev Paul Ped.
Os autores declaram não haver conflitos de interesse. 2012;30:51---6.
20. Zhu Y, Shao Z, Jing J, Ma J, Chen Y, Li X, et al. Body mass
Referências index is better than other anthropometric indices for iden-
tifying dyslipidemia in chinese children with obesity. PLOS ONE.
1. Keating C, Backholer K, Peeters A. Prevalence of overweight 2016;11:e0149392.
and obesity in children and adults. Lancet. 2014;384:2107---8. 21. de Onis M, Martínez-Costa C, Núñez F, Nguefack-Tsague G, Mon-
2. Mansour M, Nassef YE, Shady MA, Aziz AA, Malt HA. Metabolic tal A, Brines J. Association between WHO cut-offs for childhood
syndrome and cardiovascular risk factors in obese adolescent. overweight and obesity and cardiometabolic risk. Pub Health
Mac J Med Sci. 2016;4:118---21. Nut. 2013;16:625---30.
3. Romualdo MC, de Nóbrega FJ, Escrivão MA. Resistência à insu- 22. Jeffery AN, Metcalf BS, Hosking J, Streeter AJ, Voss LD, Wilkin
lina em crianças e adolescentes obesos. J Pediatr (Rio J). TJ. Age before stage: insulin resistance rises before the onset
2014;90:600---7. of puberty: a 9-year longitudinal study (EarlyBird 26). Diabetes
4. Martin L, Oepen J, Reinehr T, Wabitsch M, Claussnitzer G, Care. 2012;35:536---41.
Waldeck E, et al. Ethnicity and cardiovascular risk factors: eva- 23. Silva JL, Barbosa DS, Oliveira JA, Guedes DP. Centripetal dis-
luation of 40[thinsp]921 normal-weight, overweight or obese tribution of body fat, overweight and cardiorespiratory fitness:
children and adolescents living in Central Europe. Int J Obes. association with insulin sensitivity and metabolic alterations.
2015;39:45---51. Arq Bras Endocrinol Metabol. 2006;50:1034---40.
ARTIGO ORIGINAL
Comparação de indicadores de perfis glicêmico e

lipídico entre crianças e adolescentes obesos
egressos de serviço público ou privado da cidade
de Ribeirão Preto (SP)
Comparison of glycemic and lipid profiles indicators among obese children and
adolescents treated at public or private services from the city of Ribeirão Preto (SP)
Carlos A. Nogueira-de-Almeida1, Lara A. F. Pires2, Rafaela G. dos Santos2
RESUMO
Modelo: Observacional transversal. Objetivo: comparar os perfis lipídico e glicêmico de crianças e
adolescentes obesos atendidos em serviços de saúde público e privado. Metodologia: estudo transver-
sal, envolvendo 113 indivíduos obesos com idades entre 7 e 18 anos, conduzido em dois ambulatórios,
um público (n=51) e outro privado (n=62). Foram colhidos dados antropométricos e amostras de san-
gue, tendo-se comparado, entre os grupos, glicemia, insulinemia, HOMA e lipidograma. Resultados:
em relação às médias, apenas para o HDL houve diferença, sendo os valores inferiores para o serviço
público. Quanto à prevalência de indicadores fora da faixa de normalidade, esteve sempre acima de
45%, com exceção da hiperglicemia que se mostrou rara. Apenas a prevalência de indivíduos com HDL
baixo foi diferente entre os grupos, sendo inferior para o serviço privado. Conclusões: Não se observou
hiperglicemia, mas as prevalências de dislipidemia e resistência insulínica foram elevadas em ambos os
serviços. O HDL foi o único indicador que se mostrou diferente entre os dois grupos e, considerando-se
que ele é o mais sensível à qualidade da alimentação e à atividades física, pode-se sugerir que, tanto do
ponto de vista de saúde pública como individual, esses aspectos devam ser melhor cuidados nas popu-
lações de menor renda.
Palavras-chave: Obesidade., Criança. Adolescente. Insulina. Educação em Saúde.
ABSTRACT
Design: Observational cross-sectional. Objectives: To compare the lipid and glycemic profiles of obese
children and adolescents, followed at a public or a private health service. Methods: A cross-sectional
study involving 113 obese patients, aged 7 to 18 years, conducted at two clinics, one public (n = 51)
and the other private ( n = 62). Anthropometric data and blood samples were collected and glucose,
insulin, HOMA and lipid profile have been compared between groups. Results: regarding averages, it
1. Professor Titular, Universidade de Ribeirão Preto, Ribeirão CORRESPONDÊNCIA :

Preto, SP, Brasil Universidade de Ribeirão Preto
2. Acadêmica, Universidade de Ribeirão Preto, Ribeirão Preto, Seção de Pós Graduação Strito Senso
SP, Brasil Av. Costábile Romano, 2.201
CEP: 14096-900. Ribeirão Preto -SP - Brazil
dr.nogueira@me.com
Aprovado em 03/05/2016
Medicina (Ribeirão Preto. Online) 2016;49(6):504-510 DOI: http://dx.doi.org/10.11606/issn.2176-7262.v49i6p504-510

Medicina (Ribeirão Preto.Online) 2016;49(6):504-10 Nogueira-de-Almeida CA, Pires LAF, Santos RF.
Comparação de indicadores de perfis glicêmico e lipídico
was observed differences only for HDL, with lower values for public service. The prevalence of indicators
outside the normal range, has always been above 45%, with the exception of hyperglycemia witch was
rare. Only the prevalence of individuals with low HDL was different between groups, being lower at the
private service. Conclusions: there was almost no hyperglycemia, but the prevalence of dyslipidemia
and insulin resistance were high in both services. HDL was the only indicator that showed differences
between the two groups and, considering that it is the most sensitive to the quality of nutrition and
physical activity, it may be suggested that at the public health and on the individual management, these
aspects should be better managed in lower income populations.
Keywords: Obesity. Child. Adolescent. Insulin. Health Education.
Introdução Paralelamente, sabe-se que a qualidade da

alimentação influencia o metabolismo e, dietas de
A obesidade configura-se, nos dias atuais, má qualidade, podem levar a modificações nos per-
como relevante e crescente problema nutricional fis glicêmico e lipídico.8
acometendo crianças e adolescentes do mundo todo, O presente estudo visou comparar os perfis
inclusive brasileiros.1 Dentre as consequências à lipídico e glicêmico de dois grupos de crianças e
saúde, destacam-se as alterações no perfil glicêmi- adolescentes obesos atendidos em serviços de saúde
co, especialmente a resistência periférica à insuli- diferentes, sendo um deles público e, o outro, pri-
na, e as dislipidemias.2 Hoje, a preocupação com o vado.
excesso de peso e suas comorbidades tem se dis-
seminado entre profissionais de saúde e leigos, le- Metodologia
vando à procura, cada vez maior, pelos serviços de
assistência à saúde. Trata-se de estudo transversal retrospectivo
Atualmente, no Brasil, quando a família bus- com dados obtidos através de bancos de dados
ca atendimento para a criança obesa, dois tipos de construídos para realização de investigação cien-
serviços podem ser utilizados: público ou privado. tífica.
No primeiro, em geral são levados os pacientes pro- Dois serviços foram incluídos no levantamen-
venientes de famílias com baixa condição econômi- to, ambos sob responsabilidade do mesmo profissi-
ca, sem acesso aos planos de saúde.3 No segundo, onal, autor do presente trabalho, que supervisio-
encontram-se aquelas que possuem algum tipo nava a obtenção dos dados e seu registro. O pri-
de assistência de caráter privado, sejam seguros, meiro é um ambulatório de atendimento em
convênios ou mesmo remuneração direta ao profis- nutrologia pediátrica sediado dentro do campus da
sional.4 Universidade de Ribeirão Preto, e que atende crian-
É frequente a afirmação de que a obesidade ças e adolescentes por procura espontânea e/ou
apresenta, do ponto de vista nutricional, origens encaminhados por outras instâncias da rede públi-
diferentes de acordo com a classe social. Diz-se que, ca. Os atendimentos são gratuitos e a população
entre os mais pobres, ela é devida às menores opor- atendida pertence à Zona Leste de Ribeirão Preto
tunidades de atividade física, aos erros alimentares sendo constituída por famílias de baixa renda, usuá-
e ao consumo de alimentos de menor custo de aqui- rias do Sistema Único de Saúde e não possuidoras
sição, baixo valor nutricional e excessivamente de planos de saúde. O outro serviço é uma clínica
energéticos.5 Adicionalmente, segundo Sawaya, privada, localizada em área tradicional de consul-
populações em situações de carência podem apre- tórios médicos em Ribeirão Preto, e que atende cli-
sentar susceptibilidade genética para o desenvolvi- entela privada e/ou possuidora de plano de saúde
mento da obesidade, como fator protetor em pe- específico, voltado à classe alta.
ríodos de escassez de alimentos.6 Já entre os mais Os critérios de inclusão foram indivíduos com
ricos, a causa seria devida basicamente ao excesso idades entre 6 e 18 anos, com escore z de índice de
de consumo, de alimentos saudáveis ou não, mas massa corporal (IMC) maior que 2 (obesos), que
em quantidade acima das necessidades.7 tivessem sido admitidos em um dos ambulatórios
http://www.revistas.usp.br/rmrp / http://revista.fmrp.usp.br 505

Nogueira-de-Almeida CA, Pires LAF, Santos RF. Medicina (Ribeirão Preto.Online) 2016;49(6): 504-10
para tratamento no período entre janeiro de 1998 • Insulina corrigida para idade e sexo, com valores
e dezembro de 2008. obtidos através do estudo que avaliou a variação
Os critérios de exclusão foram impedimento da insulinemia de jejum em crianças eutróficas e
para realização de antropometria, exames labora- maturadoras médias,11 tendo-se acrescentado
toriais ausentes ou incompletos, dislipidemias fa- dois desvios-padrão aos valores médios encon-
miliares, hipotireoidismo e Diabetes. melito tipo 1. trados no estudo para cinco faixas de idade:
Durante esse período, foram atendidos na √ 6 a 8,9 anos: 7,92 µU/mL (meninos) e
instituição privada 821 indivíduos, sendo 698 den- 6,70 µU/mL (meninas)
tro da faixa etária proposta. Desses, 181 apresen- √ 9 a 10,9 anos: 8,69 µU/mL (meninos) e
taram obesidade e preencheram os critérios de in- 11,99 µU/mL (meninas)
clusão; 116 não completaram a avaliação laborato- √ 11 a 12,9 anos: 12,18 µU/mL (meninos) e
rial e 3 receberam diagnóstico de hipotireoidismo. 13,26 µU/mL (meninas)
O número final de indivíduos avaliados nesse grupo √ 13 a 14,9 anos: 13,74 µU/mL (meninos) e
foi de 62, sendo 30 entre 6 e 10 anos e 32 com 14,85 µU/mL (meninas)
mais de 10 anos. √ 15 a 17,9 anos: 10,27 µU/mL (meninos) e
Na clínica pública foram atendidos 760 indi- 13,13 µU/mL (meninas)
víduos, sendo 496 dentro da faixa etária proposta. • HOMA-IR corrigido para idade e sexo, com valo-
Desses, 198 apresentaram obesidade e preenche- res obtidos através de estudo que avaliou a vari-
ram os critérios de inclusão; 142 não completaram ação do HOMA-IR em crianças eutróficas e
a avaliação laboratorial, 2 receberam diagnóstico maturadoras médias,11 tendo-se acrescentado
de hipotireoidismo, 2 apresentaram dislipidemia dois desvios padrão aos valores médios encon-
familiar e 1 era diabético tipo 1. O número final de trados no estudo para cinco faixas de idade:
indivíduos avaliados nesse grupo foi de 51, sendo √ 6 a 8,9 anos: 1,76 (meninos) e 1,39 (meninas)
25 entre 6 e 10 anos e 26 com mais de 10 anos. √ 9 a 10,9 anos: 1,97 (meninos) e 2,62 (meni-
A avaliação antropométrica seguiu técnica nas)
padronizada 9. Os exames laboratoriais da clínica √ 11 a 12,9 anos: 2,65 (meninos) e 3,02 (meni-
pública foram realizados no ambulatório da univer- nas)
sidade e os da clínica privada em um de três labo- √ 13 a 14,9 anos: 3,21 (meninos) e 3,46 (meni-
ratórios da cidade que a família podia escolher. To- nas)
dos são instituições certificadas e as técnicas e kits √ 15 a 17,9 anos: 2,39 (meninos) e 2,89 (meni-
para os exames propostos foram os mesmos nos nas).
quatro serviços, a saber, centrifugação do material • Colesterol total ≥ 150 mg/dL12
biológico em centrífuga Bio Eng modelo BE 4000 • LDL ≥ 100 mg/dL12
por 5 minutos a 3.500 rpm entre uma e duas horas • HDL ≤ 45 mg/dL12
após a coleta. A seguir, a glicemia foi medida pelo • Triglicerídeos ≥ 100 mg/dL12
método enzimático da Hexoquinase com automação
Cobas Mira Plus Roche, a inculinemia pela método Os resultados estão apresentados como mé-
quimioluminescência, automação Immulitte DPC dias e desvios padrão e também de acordo com a
Medlab e o lipidograma por método enzimático COD- prevalência de valores alterados. Foram compara-
PAP, automação Cobas Mira Plus Roche. Todos os dos, em ambos os casos, os dados dos pacientes
pacientes fizeram avaliação antropométrica na pri- provenientes das duas clínicas. Para a comparação
meira consulta, momento em que foram solicitados de médias foram utilizados os testes Mann-Whitney
a colher exames laboratoriais com 12 horas de je- para as variáveis não paramétricas e T não pareado
jum, sendo tolerado intervalo de até 30 dias para o para aquelas com distribuição normal. As prevalên-
retorno com os exames solicitados. cias foram comparadas através do teste qui-qua-
Para a avaliação das prevalências de exames drado. O nível de significância definido foi de 5%.
alterados, foram definidos os seguintes pontos de O trabalho foi aprovado pelo Comitê de Ética
corte: da Universidade de Ribeirão Preto em 11 de março
• glicemia > 99 mg/Dl;10 de 2014 com parecer número 538.137.

Resultados Observou-se que a prevalência de indivíduos com

HDL baixo foi diferente entre os grupos, sendo in-
A tabela 1 mostra a comparação dos perfis ferior para o serviço privado.
glicêmico e lipídico entre os indivíduos dos grupos
de atendimento público e privado. Verifica-se que Discussão
apenas para o HDL houve diferença, sendo os valo-
res inferiores para o serviço público. Muitos estudos têm avaliado alterações nos
A tabela 2 mostra a comparação das preva- perfis lipídico e glicêmico entre crianças e adoles-
lências de alterações dos indicadores estudados centes obesos, sabendo-se que a obesidade é fator
entre os indivíduos dos dois grupos. Primeiramen- de risco para dislipidemia e resistência insulínica.
te, pode-se verificar que, de uma maneira geral, a Juarez e cols.13 mostraram que em uma amostra de
prevalência das comorbidades estudadas foi bas- crianças obesas mexicanas, a alteração metabólica
tante elevada, sempre acima de 45%, com exceção mais frequente foi HDL-C baixo (69%), seguida de
apenas da glicemia que apresentou valores baixos. hipertrigliceridemia (29%), aumento de CT e LDL-C
Tabela 1: Comparação dos perfis glicêmico e lipídico entre os indivíduos dos grupos de atendimento públi-
co e privado.
Público (média/dp) Privado (média/dp) p
Idade (meses) 146,2 (34,1) 147,11 (33,6) 0,8467*
Escore z de IMC 2,31 (0,21) 2,27 (0,19) 0,3387*
Glicemia 90,9 (13,0) 88,6 (12,9) 0,1439*
Insulinemia (mg/dL) 19,3 (12,1) 17,7 (12,8) 0,2438*
HOMA-IR 4,45 (3,59) 4,02 (3,68) 0,1532*
Colesterol total (mg/dL) 161,1 (30,6) 160,5 (29,5) 0,9152**
LDL colesterol (mg/dL) 99,5 (28,1) 95,1 (27,0) 0,3933**
HDL colesterol (mg/dL) 40,2 (8,2) 44,2 (9,9) 0,0231**
Triglicerídeos (mg/dL) 117,5 (45,2) 106,1 (39,0) 0,1541**
* Teste de Mann-Whitney. ** Teste T não pareado
Tabela 2: Comparação das prevalências de alterações dos indicadores estudados entre os indivíduos dos grupos de
atendimento público e privado.
Público Privado p
Hiperglicemia 5 (9,8%) 5 (8,0%) 0,7460
Hiperinsulinismo 31 (60,8%) 33 (53,2%) 0,5378
HOMA-IR elevado 31 (60,8%) 33 (53,2%) 0,5378
Hipercolesterolemia 32 (62,7%) 43 (69,4%) 0,6417
LDL colesterol elevado 28 (54,9%) 28 (45,2%) 0,7082
HDL colesterol baixo 38 (74,5%) 34 (54,8%) 0,0491
Hipertrigliceridemia 31 (60,8%) 33 (53,2%) 0,5378
Teste Qui-Quadrado

(11%) e glicemia de jejum alterada (4%). Wojcik e de 2,1% no primeiro quintil de renda familiar e de
col. 14 estudando 146 adolescentes obesos com ida- 9,2% no quinto. Entre as meninas, era de 2,7% no
des entre 10 e 17 anos verificaram que 23,29% primeiro quintil e de 4,3% no quinto. Esses dados
tinham hipercolesterolemia, 17,81% LDL elevado, mostram que, em nosso meio, à época do levanta-
37,67% hipertrigliceridemia e 15,07% HDL baixo. mento, a obesidade era mais prevalente entre a
Pires e col. 15 em estudo recente envolvendo 121 população mais rica. Esse padrão também foi apre-
crianças e adolescentes obesos com idades entre 6 sentado, em um primeiro momento, nos países de-
e 17 anos de Coimbra, Portugal, verificaram pre- senvolvidos, entretanto, com o passar dos anos, a
sença de resistência insulínica em 38,1%, tendo-se prevalência foi crescendo nas camadas sociais mais
utilizado o HOMA-IR com ponto de corte de 3; nes- baixas, tornando-se, inclusive, mais elevada.22 Acre-
se mesmo estudo, 12,5% dos indivíduos tinham dita-se que esse fenômeno deva-se a vários fato-
alguma dislipidemia. Rizzo e col. 16 estudaram 321 res, entre eles o fato de as camadas mais ricas te-
adolescentes obesos com idades entre 10 e 17 anos rem melhor conhecimento sobre os riscos da obesi-
e verificaram que 35,5% tinham HDL baixo, 18,5% dade, terem mais acesso à educação alimentar e
triglicerídeos elevados, 2% eram hiperglicêmicos e aos serviços de saúde, maiores oportunidades para
65% tinham resistência insulínica. Conforme se pode prática de atividade física, além de utilizarem ali-
verificar nos estudos acima, apesar de diferentes mentos de melhor qualidade nutricional e menor
autores observarem prevalências elevadas de alte- valor energético, tais como frutas, verduras e car-
rações nos perfis glicêmico e lipídico, os resultados nes,22 que apresentam custo mais elevado 23. De
são bastante variáveis. É provável que isso se deva fato, sabe-se, por exemplo, que a escolaridade
a diferentes metodologias ou pontos de corte dos materna baixa e a alimentação desequilibrada, tí-
exames laboratoriais mas, também, a diferentes picos de populações de baixa renda, elevam o risco
padrões de estilo de vida, incluindo-se a alimenta- de dislipidemia 24. Por outro lado, Fernandes e col.
ção e a prática de atividade física. Adicionalmente, 25
verificaram que crianças e adolescentes fisica-
reconhecendo-se a obesidade como sendo doença mente ativos, o que, no Brasil, é mais comum nas
de etiologia multifatorial,17 é esperado que estudos classes mais elevadas,26 apresentavam menor inci-
envolvendo crianças obesas mostrem diferentes dência de dislipidemia. Nossos dados mostraram que
padrões de comorbidades. No presente estudo, as tanto a concentração sérica como a prevalência de
prevalências elevadas de exames alterados, tanto valores baixos de HDL eram maiores entre os pa-
na clínica pública como na privada, apontam para cientes da clínica pública. Sabe-se que o HDL é o
um padrão de elevado risco de desenvolvimento indicador de perfil lipídico mais sensível à qualida-
futuro de doenças ligadas à síndrome metabólica. de da alimentação e à prática de atividade física.27
De fato, alguns estudos recentes, conduzidos entre Nobre e col.,28 estudando 227 crianças pré escola-
crianças originadas da mesma região, já mostra- res verificaram associação da dislipidemia com IMC
ram alterações de geometria cardíaca 18, de espes- elevado e com dieta inadequada. Afonso & Ariza29
sura da camada íntima carotídea 19 e de acúmulo elencam os principais fatores ambientais, associa-
de gordura hepática.20 dos à obesidade, que contribuem para redução do
Na comparação dos valores entre os dois gru- HDL: dietas ricas em carboidratos simples, seden-
pos, que eram homogêneos para idade e escore z tarismo, tabagismo e abuso de álcool. Pode-se ob-
de IMC, verificou-se que apenas o HDL se mostrou servar que, no Brasil, todos eles são mais prevalen-
diferente. No Brasil, segundo dados da última Pes- tes entre os mais pobres, o que pode explicar os
quisa de Orçamentos Familiares, referente aos anos achados do presente estudo.21,26 Também Magalhães
de 2008 e 2009,21 entre crianças de 5 a 9 anos de e col.30 estudando 185 crianças com idades entre 4
idade do sexo masculino, a prevalência de obesida- e 7 anos em Viçosa, MG, verificaram que a preva-
de era de 10,8% no primeiro quintil de renda fami- lência de HDL baixo mostrou valores decrescentes
liar (mais pobres) e de 23,6% no quinto (mais ri- com o aumento da renda per capita familiar.
cos). Entre as meninas, era de 8,8% no primeiro Apesar de ser, possivelmente, o primeiro es-
quintil e de 14,4% no quinto. Entre os adolescentes tudo que compara crianças e adolescentes obesos
do sexo masculino, a prevalência de obesidade era atendidos em diferentes tipos de serviço de saúde,

ele apresenta algumas limitações. A mais impor- Referências

tante delas, refere-se ao fato de que não foram efe-
1. Lobstein T, Jackson-Leach R, Moodie ML, Hall KD, Gortmaker
tivamente avaliados critérios socioeconômicos nos SL, Swinburn BA, et al. Child and adolescent obesity: part
dois grupos estudados. Conhecendo-se a realidade of a bigger picture. Lancet. 2015; 385(9986): 2510-20.
2. Gurnani M, Birken C, Hamilton J. Childhood Obesity: Causes,
de assistência à saúde do Brasil e, particularmente, Consequences, and Management. Pediatr Clin North
na região em que o levantamento foi conduzido, America.2015; 62: 821-40.
partiu-se da suposição de que os usuários do siste- 3. Silva ZPd, Ribeiro MCSdA, Barata RB, Almeida MFd. Perfil
sociodemográfico e padrão de utilização dos serviços de
ma privado são provenientes de classes mais ele- saúde do Sistema Único de Saúde (SUS), 2003-2008. Ciênc
vadas e os achados foram discutidos de acordo com Saúde Coletiva. 2011; 16: 3807-16.
essa premissa. Adicionalmente, não houve centra- 4. Leal RM, Matos JBBd. Planos de saúde: uma análise dos
custos assistenciais e seus componentes. Revista de Ad-
lização dos procedimentos de coleta e análise das ministração de Empresas 2009; 49: 447-58.
amostras de sangue utilizadas para os exames la- 5. Peña MB, J. La obesidad en la pobreza: un problema emer-
gente en las Ameìricas. In: PAHO, editor. Washinngton:
boratoriais, tendo-se tomado o cuidado de verificar
PAHO; 2000.
que os laboratórios envolvidos eram certificados e 6. Sawaya AL. Desnutric’ aÞo urbana no Brasil em um periìodo
que a metodologia de análise era a mesma em to- de transic’ aÞo. São Paulo: Cortez; 1997.
dos eles. Por fim, os dados obtidos não podem ser, 7. Hill JO, Peters JC. Environmental contributions to the obes-
ity epidemic. Science. 1998; 280(5368): 1371-4.
automaticamente, extrapolados para outras popu-
8. Romualdo MCS, de Nóbrega FJ, Escrivão MAMS. Resistên-
lações porque refletem a realidade observada lo- cia à insulina em crianças e adolescentes obesos. J Pediatr.
(Rio J.). 2014; 90): 600-7.
calmente.
9. Group WHOW. Use and interpretation of anthropometric
Em conclusão, o presente estudo mostrou indicators of nutritional status. Bulletin of the World Health
que, entre as crianças e adolescentes obesos estu- Organization. 1986; 64: 929-41.
dados, não se observou hiperglicemia, mas as pre- 10. Zimmet P, Alberti KG, Kaufman F, Tajima N, Silink M,
Arslanian S, et al. The metabolic syndrome in children
valências de dislipidemia e resistência insulínica fo- and adolescents - an IDF consensus report. Pediatr Dia-
ram bastante elevadas, sempre próximas ou supe- betes. 2007; 8: 299-306.
11. Nogueira-de-Almeida CA, Pinho AP, Ricco RG, Pepato MT,
riores a 50%, independente da origem, quando fo-
Brunetti IL. Determination of glycemia and insulinemia
ram comparadas a clínica pública e a privada. O and the homeostasis model assessment (HOMA) in school-
children and adolescents with normal body mass index. J
HDL foi o único indicador que se mostrou diferente
Pediatr. (Rio J.).2008; 84: 136-40.
entre os dois grupos, apresentado valores médios 12. I Diretriz de Prevenção da Aterosclerose na Infância e na
menores e maior prevalência de valores alterados Adolescência. Arq Bras Cardiol. 2005; 85: 3-36.
nos indivíduos provenientes da instituição pública. 13. Juarez-Lopez C, Klunder-Klunder M, Medina-Bravo P, Mad-
rigal-Azcarate A, Mass-Diaz E, Flores-Huerta S. Insulin
Considerando-se que o HDL é, dentre os indicado- resistance and its association with the components of the
res estudados, o mais sensível à qualidade da ali- metabolic syndrome among obese children and adoles-
cents. BMC public health 2010; 10: 318.
mentação e à atividades física, pode-se sugerir que,
14. Wojcik M, Janus D, Maslanka A, et al. [Disorders of lipid
tanto do ponto de vista de saúde pública como indi- metabolism in adolescents with simple obesity]. Prz. lek.
vidual, esses aspectos devem ser melhor cuidados 2010; 67: 1168-71.
15. Pires A, Martins P, Pereira AM, et al. Insulin Resistance,
nas populações de menor renda. Dyslipidemia and Cardiovascular Changes in a Group of
Obese Children. Arq Bras Cardiol. 2015; 104: 266-73.

16. Rizzo AC, Goldberg TB, Silva CC, Kurokawa CS, Nunes 23. Nogueira-de-Almeida CA, Almeida CCJN, João CA, João
HR, Corrente JE. Metabolic syndrome risk factors in over- CR. Custo da alimentação no Brasil: avaliação e implica-
weight, obese, and extremely obese Brazilian adolescents. ções. Revista de Nutrologia. 2008; 1(2): 53-6.
Nutr J. 2013; 12: 19. 24. Alcântara Neto ODd, Silva RdCR, Assis AMO, Pinto EdJ.
17. Nogueira-de-Almeida CA, Pires LA, Miyasaka J, et al. Com- Fatores associados à dislipidemia em crianças e adoles-
parison of feeding habits and physical activity between centes de escolas públicas de Salvador, Bahia. Rev Bras
eutrophic and overweight/obese children and adolescents: Epidemiol. 2012; 15: 335-45.
a cross sectional study. AMB. Rev Assoc Med Bras. 2015; 25. Fernandes RA, Christofaro DGD, Casonatto J, et al. Preva-
61: 227-33. lência de dislipidemia em indivíduos fisicamente ativos
18. Benedeti ACGS, Garcia J, Martins WP, Mauad Filho F, Del durante a infância, adolescência e idade adulta. Arq Bras
Ciampo LA, Nogueira-de-Almeida CA. Evaluation of Cardiol. 2011; 97: 317-23.
Echocardiography as a Marker of Cardiovascular Risk in 26. IBGE. Pesquisa Nacional de Saúde do Escolar. Rio de Ja-
Obese Children and Adolescents. Int J Clin Pediatr. neiro: Ministério do Planejamento, 2009.
2014;3:72-8.
27. Kelley GA, Kelley KS. Effects of diet, aerobic exercise, or
19. Garcia J. Avaliação ultrassonográfica do complexo médio- both on Non-HDL-C in adults: a meta-analysis of rand-
intimal das carótidas comuns em crianças eutróficas e omized controlled trials. Cholesterol. 2012; 2012: 5.
portadoras de sobrepeso/obesidade. Ribeirão Preto:
Unaerp; 2015. 28. Nobre LN, Lamounier JA, Franceschini SdCC. Determinan-
tes sociodemográficos, antropométricos e alimentares de
20. Benedetti ACGS. Correlação entre as medidas da adiposi- dislipidemia em pré-escolares. J Pediatr. (Rio J.).2013;
dade abdominal pela ultrassonografia e indicadores de 89: 462-9.
obesidade em crianças eutróficas e portadoras de sobre-
peso/obesidade. Ribeirão Preto: Unaerp; 2015. 29. Alfonso JEF, Ariza IDS. Elevando el colesterol HDL: ¿Cuál
es la mejor estrategia? AMB. Rev Assoc Med. Bras. 2008;
21. IBGE. Pesquisa de orçamentos familiares 2008-2009 - 54: 369-76.
Análise do consumo alimentar pessoal no Brasil. In: ren-
dimento Cdte, editor. Rio de Janeiro: IBGE; 2011. p. 150. 30. Magalhães TCA, Vieira SA, Priore SE, Ribeiro AQ,
Franceschini SdCC, Sant’ana LFdR. Fatores associados à
22. Levine JA. Poverty and obesity in the U.S. Diabetes. 2011; dislipidemia em crianças de 4 a 7 anos de idade. Rev
60: 2667-8. Nutr. 2015; 28: 17-28.

Artigo Original
Fatores de desagregação familiar em adolescentes eutróficos e nos

portadores de sobrepeso/obesidade
Variables associated with family breakdown in healthy and obese/overweigh adolescents
Carla Cristina J. N. de Almeida1, Paula de Oliveira Mora1, Valmir Aparecido de Oliveira2, Camila Aparecida João1,
Carolina Regina João1, Ana Carolina Riccio1, Carlos Alberto N. de Almeida1
RESUMO ABSTRACT
Objetivo: Investigar a existência de fatores de desagre- Objective: To evaluate the presence of family break-
gação familiar em adolescentes eutróficos e nos portadores down factors among eutrophic and overweight/obese
de sobrepeso/obesidade. adolescents.
Métodos: Estudo transversal de 242 alunos de uma escola Methods: Cross-sectional study of 242 students aged
pública, de 14 a 19 anos, que foram pesados, medidos e res- between 14 and 19 years old, from a public school.
ponderam a um questionário com questões fechadas, o qual Each student was weighed, measured and answered
investigou a presença de fatores de desagregação familiar. a questionnaire with closed questions addressing the
Em seguida, os adolescentes foram divididos em dois grupos, presence of family breakdown factors. The adolescents were
eutróficos e portadores de sobrepeso/obesidade, e as respostas divided in two groups: euthophic and overweight/obese.
foram confrontadas e analisadas por meio dos testes exato de The answers of both groups were compared by Fisher’s
Fisher e de Mann-Whitney. exact and Mann-Whitney tests.
Resultados: Não houve diferença significante para a Results: There was no statistically significant difference
prevalência dos fatores estudados entre os dois grupos. in the prevalence of the studied factors between the two
Comparando-se o número de respostas positivas (presença groups. Comparing the number of positive answers (pres-
do fator de desagregação familiar) e negativas (ausência do ence of family breakdown factors) and negative ones (absence
fator de desagregação familiar), não se observou diferença of family breakdown factors), no difference was observed
entre os dois grupos. between the groups.
Conclusões: A análise com a inclusão de um grupo controle Conclusions: The inclusion of a control group showed
mostrou que fatores ligados à desagregação familiar, habitual- that factors of family breakdown, usually identified as as-
mente apontados como associados à obesidade em adolescentes, sociated with obesity in adolescents, may also be present in
podem estar presentes também em adolescentes eutróficos. eutrophic adolescents.
Palavras-chave: obesidade; criança; adolescente; núcleo Key-words: obesity; child; adolescent; nuclear family;
familiar; relações familiares. family relations.
Instituição: Centro de Estudos em Saúde e Nutrição Infanto-Juvenil da Endereço para correspondência:

Universidade de Ribeirão Preto (Unaerp), Ribeirão Preto, SP, Brasil Carlos Alberto N. de Almeida
Rua Eugênio Ferrante, 170
1
Unaerp, Ribeirão Preto, SP, Brasil CEP 14027-150 – Ribeirão Preto/SP
2
Universidade de São Paulo (USP), Ribeirão Preto, SP, Brasil E-mail: dr.nogueira@me.com
Fonte financiadora: Universidade de Ribeirão Preto (Unaerp)

Conflito de interesse: nada a declarar
Recebido em: 15/8/2013

Aprovado em: 14/10/2013
Rev Paul Pediatr 2014;32(1):70-7.

Carla Cristina J. N. de Almeida et al
Introdução desenvolvimento humano, outras vão se agregando e am-

pliando o modelo de repostas futuras, como, por exemplo, as
A obesidade infantil tornou-se uma epidemia global. interações com o ambiente familiar e social(6). Por essa razão,
Nas últimas décadas, a prevalência aumentou nos países o núcleo familiar tem importância fundamental, tanto na
desenvolvidos e nas zonas urbanas dos países em desenvol- gênese quanto na manutenção da obesidade(7). A prática do
vimento(1). Países como Austrália, Brasil, Canadá, Chile, atendimento de crianças e adolescentes evidencia, quase sem-
Finlândia, França, Alemanha, Grécia, Japão e Reino Unido pre, um ambiente familiar alterado, no qual se identificam
constataram aumento expressivo da doença, no período características diversas, como superproteção, rigidez, mas,
compreendido entre os primeiros anos de 1970 e os últimos principalmente, falta de resolução de conflitos(8). Dentre os
anos de 1990(1). conflitos mais comumente encontrados, citam-se: separação
No Brasil, segundo o plano de ações estratégicas para o enfren- dos pais, morte de um ente querido, pessoa estranha ao núcleo
tamento das doenças crônicas não transmissíveis 2011–2022 familiar que vem momentânea ou permanentemente residir
do Ministério da Saúde, a prevalência de sobrepeso em com a família, alcoolismo, drogadição, pai ou mãe ausente e
crianças na faixa etária de cinco a nove anos atingiu 33,5%, um ou os dois genitores reclusos.
enquanto a obesidade, nessa mesma faixa etária, atingiu Dentro dessa lógica, parece que as transformações fami-
14,3%(2). Na faixa de dez a 19 anos, diagnosticou-se o sobre- liares da contemporaneidade possuem conexão com a cres-
peso em 20% dos adolescentes e a prevalência de obesidade cente frequência de obesidade(9). Estudos demonstram pouca
foi de 4,0% em meninas e de 5,9% em meninos. exposição de afetos como estratégia (inconsciente) adotada
A obesidade é considerada uma doença multifatorial, pelas famílias das crianças obesas a fim de enfrentarem a crise
caracterizada por excesso de tecido adiposo, com interações das transformações. Isso pode ser percebido, por exemplo,
complexas entre genética, atividade física e fatores culturais. pela falta de hábito de acariciar as crianças, que muitas ve-
Quanto aos fatores genéticos, a literatura ressalta que todos zes são consideradas culpadas e responsáveis pela doença(9).
os cromossomos humanos, exceto o cromossomo Y, podem Ainda sobre a questão alimentar, sabe-se que a família é a
apresentar pequenos defeitos que favorecem o ganho do responsável pela formação do comportamento alimentar da
peso. Essas alterações, chamadas de “predisposição genéti- criança por meio da aprendizagem social(8,10), o que equivale
ca”, seriam responsáveis por tornar os indivíduos suscetíveis a dizer que as famílias são dotadas de papel fundamental na
ao ganho excessivo de peso, desde que entrem em contato formação inicial dos hábitos alimentares da criança, sendo os
com fatores favoráveis do meio(3). Nessa mesma linha de pais o referencial de padrão para os filhos(11). É de se esperar
raciocínio, a influência dos pais resulta em determinante que famílias coesas, com elevado grau de vinculação entre
genético. Assim, quando apenas um dos pais é obeso, a seus componentes, possam atuar como fator de proteção ao
criança tem aproximadamente 40% de chance de se tornar surgimento da obesidade. Por outro lado, naquelas em que
obesa; por outro lado, quando os dois são obesos, esse índice se observa o contrário, é possível que o ganho excessivo de
chega a 80%(4). Distúrbios neurológicos também têm sido peso das crianças seja uma das consequências observadas(7).
considerados nas causas da obesidade, em especial aqueles A fim de colaborar com o conhecimento científico sobre
que acometem os núcleos hipotalâmicos cerebrais, onde se esse tema, o presente trabalho investigou a existência de
encontram os centros do apetite e da saciedade, favorecendo fatores de desagregação familiar em adolescentes eutróficos
a ingestão alimentar descontrolada(3). e naqueles com sobrepeso ou obesidade, estudantes de uma
Fatores psicológicos ou emocionais também podem levar escola pública do interior do Estado de São Paulo.
a criança a comer mais, como mecanismo de compensação
ou de defesa. Sem ignorar o lado constitucional, é possível Método
conceituar a obesidade como expressão sintomática dos
conflitos internos e externos que se realimentam como em Participaram da pesquisa 242 alunos, de ambos os sexos,
um mecanismo de feedback(5). Nesse contexto, sabe-se que as de 14 a 19 anos, estudantes do ensino médio no período ma-
primeiras trocas estabelecidas na díade mãe-filho são essen- tutino da Escola Estadual Professor Plínio Berardo, localizada
ciais para o estabelecimento do vínculo e a constituição da na cidade de Jardinópolis, São Paulo. Para ter acesso a esses
organização do funcionamento psíquico na criança. Porém, voluntários, divulgaram-se (coletivamente e em sala de aula)
ao lado das ditas experiências primitivas, no decorrer do os objetivos da pesquisa, convidando os alunos a participar.
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Fatores de desagregação familiar em adolescentes eutróficos e nos portadores de sobrepeso/obesidade
Apresentou-se a todos o termo de consentimento livre e Posteriormente, com o teste exato de Fischer, avaliou-se a
esclarecido, o qual, após ter sido lido e sanadas as possíveis significância estatística das diferenças observadas nessa dis-
dúvidas dos participantes, foi encaminhado aos responsá- tribuição. Realizou-se a análise das variáveis quantitativas
veis para que assinassem como forma de atestar sua ciência pela comparação entre as médias e as medianas. Como a dis-
e autorização para a participação. Do total de 326 alunos, tribuição não se apresentou normal, optou-se por empregar
84 recusaram-se a participar ou não trouxeram o termo de o teste de Mann-Whitney. Por fim, avaliaram-se os dados
consentimento assinado. em conjunto (cluster), comparando-se o número de respos-
Em um segundo momento, em uma sala de laboratório tas positivas (presença do fator de desagregação familiar) e
cedida pela escola, aplicou-se um questionário com ques- negativas (ausência do fator de desagregação familiar) entre
tões fechadas para se investigarem fatores de desagregação os dois grupos. Para os cálculos estatísticos, utilizou-se o
familiar habitualmente apontados na literatura como programa GraphPad(12).
potencialmente relacionados à obesidade infantil. As ques- O trabalho foi aprovado pelo Comitê de Ética da Universidade
tões abordadas distribuíram-se em dois grupos: variáveis de Ribeirão Preto (Unaerp).
qualitativas (presença no ambiente familiar de coabitantes
presos, drogaditos, alcoólatras, pessoas com necessidades Resultados
especiais, com doença grave, morte recente, desemprego,
fatos graves, desarmonia, intranquilidade, brigas, estra- As Tabelas 1 a 3 referem-se à analise das variáveis qualitati-
nhos que se agregaram à família, pais separados, pai ou vas e quantitativas aplicadas aos 242 participantes do estudo.
mãe adotivos e irmãos adotivos); variáveis quantitativas Verifica-se nas Tabelas 1 e 2 que, para todas as variáveis,
(número de irmãos e número de pessoas no domicílio). não houve diferenças com significância estatística ao se com-
Para cada questão, havia duas ou mais respostas possíveis, parar o grupo de adolescentes eutróficos com o grupo com
previamente determinadas, e o aluno marcava com um “x” sobrepeso/obesidade.
aquela que melhor representava sua opinião. Para construir Na análise da Tabela 3, observa-se que, mesmo quando
o questionário e o rol de respostas, além dos dados obtidos as variáveis foram analisadas em conjunto, comparando-se o
de outras pesquisas, realizou-se estudo-piloto prévio, na número de respostas positivas (presença do fator de desagre-
mesma instituição, com 20 voluntários, o que permitiu gação familiar) e negativas (ausência do fator de desagregação
aperfeiçoar o instrumento. Ato contínuo, na mesma sala, familiar), não houve diferença entre os dois grupos.
efetuou-se a antropometria dos participantes (pesagem e
medição de estatura) pelas nutricionistas da equipe, que Discussão
se valeram de técnicas padronizadas. O local ofereceu ade-
quada infraestrutura para a realização do trabalho, sendo a A origem deste estudo fundamenta-se na prática diária de
sala bem arejada, limpa e com instalações necessárias tanto atividade multidisciplinar do Centro de Estudos em Saúde
para acomodar uma balança antropométrica quanto para e Nutrologia Infanto-Juvenil da Unaerp(13). Para os pesqui-
atender aos aspectos de privacidade necessários. sadores desse serviço, médicos, psicólogos, nutricionistas e
Após a coleta, os dados (questionário e avaliação antro- assistentes sociais, durante as reuniões semanais da equipe,
pométrica) foram tabelados e analisados, dividindo-se os observava-se que determinados fatores, em especial aqueles
alunos em dois grupos: eutróficos (escore Z de índice de determinantes de desagregação familiar, apareciam com
massa corpórea entre -2 e +1) e portadores de sobrepeso/ elevada frequência entre as crianças portadoras de sobrepe-
obesidade (escore Z de índice de massa corpórea maior que so e obesidade atendidas pela equipe. Realizaram-se várias
+1). Confrontaram-se as respostas do questionário, a fim revisões da literatura científica para esclarecer se haveria,
de evidenciar possíveis diferenças na prevalência de fatores de efetivamente, maior prevalência desses fatores nas famílias
desagregação familiar entre os alunos eutróficos e os que de crianças obesas, mas a maioria dos trabalhos consultados
apresentaram sobrepeso/obesidade. não incluía um grupo controle. Por esse motivo, optou-se
Analisaram-se as variáveis qualitativas com a construção por realizar o presente estudo, cujos resultados são discutidos
de tabelas de contingência, nas quais foi possível verificar a seguir.
a distribuição da frequência de cada uma das variáveis de Quanto à presença de irmãos adotivos, Salim e Bicalho(14)
resposta entre os grupos “eutrofia” e “sobrepeso/obesidade”. entrevistaram famílias e professores para compreender a causa
72
Tabela 1 - Prevalência de indicadores qualitativos de desagregação familiar nos grupos de adolescentes eutróficos e portadores
de sobrepeso/obesidade
Sobrepeso/
Parâmetros Eutróficos (%) Valor p*
Obesidade (%)
Presença de irmãos adotivos 1,6 1,7 1,000
Presença de pai e/ou mãe adotivos 0,5 0,0 1,000
Presença de pais separados 24,7 14,2 0,141
Pessoa residindo junto com a família 20,4 25,0 0,462
Ocorrência de brigas no lar 13,4 16,0 0,618
Ocorrência de intranquilidade no lar 20,9 26,7 0,364
Ocorrência de desarmonia no lar 16,1 16,0 1,004
Ocorrência de fatos graves ou marcantes, nos últimos 10 anos 35,8 35,7 1,000
Ocorrência de desemprego na família 29,5 39,2 0,191
Ocorrência de morte na família, nos últimos 10 anos 27,4 33,9 0,400
Ocorrência de doença grave entre os membros da família 6,9 10,7 0,396
Presença de algum membro portador de necessidades especiais 4,3 1,7 0,688
Presença de alcoolismo 11,2 12,5 0,813
Presença de usuários de drogas 2,6 3,5 0,664
Presença de presidiários 12,9 16,0 0,513
*Teste exato de Fischer
Tabela 2 - Indicadores quantitativos de desagregação familiar nos adolescentes eutróficos e nos portadores de sobrepeso/obesidade
Eutróficos Sobrepeso/obesidade Eutróficos Sobrepeso/obesidade Valor
Parâmetros
Média (DP) Média (DP) Mediana (EP) Mediana (EP) p*
Número de pessoas
3,8 (1,2) 3,9 (1,5) 4,0 (0,1) 4,0 (0,2) 0,862
residentes no domicílio
Número de irmãos 1,8 (1,0) 1,6 (1,0) 2,0 (0,1) 2,0 (0,1) 0,304
*Mann-Whitney. DP: desvio padrão; EP: erro padrão
Tabela 3 - Quantidade de indicadores positivos de desagregação nos familiares adolescentes eutróficos e nos portadores de
sobrepeso/obesidade
Eutróficos Sobrepeso/Obesidade
Parâmetros Valor p*
Média (DP) Média (DP)
Quantidade de indicadores positivos 2,3 (1,9) 2,5 (1,9) 0,429
*Mann-Whitney; DP: desvio padrão
e a consequência da obesidade infantil. Concluíram que a avaliar a prevalência desses fatores na população não obesa,
adoção (assim como o nascimento de um irmão, a separação eles parecem estar igualmente presentes. Assim, a inclusão
dos pais, a mudança de cidade ou de estado, a perda de um de um grupo controle torna-se fundamental. Uma limita-
ente, a mudança de escola, a ausência de um dos pais e as ção importante dos nossos dados refere-se ao número muito
dificuldades financeira) era um fator que, aparentemente, pequeno de pais adotivos encontrados, o que torna difícil a
propiciava o ganho excessivo de peso. Ainda no referido análise estatística. Nesse particular, para uma análise mais
estudo, várias famílias citaram não apenas uma, mas duas adequada, seria fundamental o aumento da amostra.
ou mais causas para a obesidade, ou seja, a combinação de Conforme Wallerstein e Kelly(15), a separação física dos
alguns desses fatores concomitantemente. No entanto a me- pais é um dos fatores que mais perturba as crianças, pois
todologia do estudo conduzido por Salim e Bicalho(14) indica faz com que tenham de reformular a visão que tinham dos
não ter ocorrido comparação com um grupo de crianças eu- pais como uma unidade. A percepção de que existe algo se
tróficas. Os resultados por nós obtidos mostram que, ao se desfazendo dentro de sua própria família gera na criança a
73
preocupação com o que lhe vai acontecer, já que a família é obeso, mas a importância predominante do ambiente e de
percebida como sua fonte de apoio e proteção. O divórcio, outros fatores exógenos, na maioria dos casos de obesidade,
por sua vez, é visto como uma ameaça a essa estrutura. Ainda parece ser inquestionável.
segundo Wallerstein e Kelly(15), o estresse infantil pode estar Essa variação no padrão de resposta anteriormente descrita
envolvido na origem de vários distúrbios, tanto físicos quanto pode explicar a relação dos aspectos individuais que fazem
psicológicos, dentre os quais se pode citar a obesidade. Outra com que indivíduos que aparentemente compartilham de
questão, apontada por Viuniski(16) e que parece encontrar ambientes familiares similares não desenvolvam na sua
subsídios na experiência clínica, é a de que a perda de peso totalidade sobrepeso/obesidade. Quanto a esse aspecto, De
nas crianças de sete e 13 anos participantes de tratamentos Oliveira et al(20) referem que
ambulatoriais para emagrecimento é sensivelmente maior
nos filhos de pais casados do que nos filhos de pais separados. “a população infantil é, do ponto de vista psicológico,
Parece ser inquestionável o fato de que a separação dos pais socioeconômico e cultural, dependente do ambiente onde
é um fator de estresse para os filhos. Também é verdadeira vive, que na maioria das vezes é constituído pela família,
a observação de que o estado emocional influencia o ato de sendo suas atitudes, frequentemente, reflexo deste am-
comer(17), mas o resultado dessa interação é muitas vezes biente. Quando desfavorável, o ambiente poderá propiciar
imprevisível, havendo indivíduos que passam a comer em condições que levem ao desenvolvimento de distúrbios
demasia e outros que praticamente deixam de se alimentar. alimentares e, uma vez instalados, poderão permanecer
Dessa forma, parece ser correto afirmar que a separação dos caso não aconteçam mudanças neste contexto (p. 8).”
pais não é fator desencadeante do sobrepeso/obesidade, ao
menos no presente estudo. Todavia, essa condição pode ser Todavia, nossos dados reforçam o fato de que o padrão de
determinante no sucesso do tratamento. resposta que leva o indivíduo a se tornar obeso em um am-
Diversas situações efetivamente promovem algum grau de biente desarmônico é individual, pois vários jovens estudados
desestruturação na dinâmica familiar que poderia, por meio compartilham desse tipo de ambiente, sem, contudo, terem
do estresse gerado, se relacionar à obesidade da criança que se tornado portadores de sobrepeso/obesidade.
vive nesse ambiente. Algumas delas (pessoa estranha que Quanto a eventos desestabilizadores, como morte, doença
reside com a família, ocorrência de brigas, intranquilidade grave ou ser portador de necessidades especiais, sua inves-
e desarmonia no ambiente familiar) foram abordadas no pre- tigação deveu-se principalmente à experiência da equipe
sente estudo, mas a avaliação estatística mostrou que não se multidisciplinar. Uma análise dos questionários de história
relacionaram à presença de obesidade na população estudada. de vida dos pacientes do serviço permitiu observar que os
A literatura efetivamente aponta que o fator es- mesmos, frequentemente, relatavam tais ocorrências nas fa-
tresse leva o individuo a comer mais a fim de buscar mílias de crianças obesas. Pontin(21), ao analisar a influência
alívio, sendo, portanto, uma forma de compensação. do desemprego paterno (que pode ser entendido como evento
Bernardi et al(18) mencionam que os indivíduos obesos desestabilizador para a família) na ocorrência de sobrepeso,
consomem mais alimentos em situação de estresse e/ou observou razão de chances de 1,73 (IC95% 1,16-2,58) para os
condições emocionais adversas. Essa teoria, chamada de escolares cujos pais não haviam perdido o emprego. A variável
Modelo Psicossomático da Obesidade, afirma que as pessoas tempo de desemprego mostrou tendência de diminuição de
obesas, principalmente as do gênero feminino, comem ex- chance de sobrepeso entre os escolares cujos pais tiveram um
cessivamente como mecanismo compensatório em situações tempo maior de desemprego. Pode-se considerar o desem-
de ansiedade, depressão, tristeza ou raiva(18). Segundo De prego um evento polêmico. Por um lado, é fator de estresse,
Azevedo e Spadoto(19), “a constituição do corpo é herdada, já discutido anteriormente como possivelmente ligado à
mas a obesidade não” (p. 3). Assim, segundo esses autores, obesidade. Por outro, trata-se de uma situação de restrição
existiria uma predisposição constitucional genética, por meio da disponibilidade de renda para a família, hipoteticamente
da qual o excesso de peso tende a ocorrer em certos grupos levando a menor aquisição e consumo de alimento.
familiares e raciais, mas os hábitos ambientais e familiares Em estudo realizado por Rand e Stunkard(22,23) com 84
atuam modificando a tendência herdada(19). Os autores pacientes obesos e 63 com peso normal, concluiu-se que
mencionam ainda que a ascendência relativa do ambiente, o ganho de peso associa-se aos períodos de maior estresse
comparada à da hereditariedade, é variável em cada paciente durante casamento, divórcio, mudança de emprego ou
74
morte familiar, sendo relatado ganho de 4,5kg ou mais por dessa experiência em sua família. No grupo de participantes
79% dos pacientes obesos e por 9% dos pacientes com peso não obesos, essa situação foi relatada por apenas 18% da
normal nessas situações. Quando se busca entender como amostra. No presente estudo, quando comparadas as dife-
a obesidade se relaciona à perda de um ente querido pela renças entre os grupos de obesos e não obesos, essas foram
criança, Salim e Bicalho(14), em estudo com 41 sujeitos no estatisticamente significantes no que se refere ao abuso de
qual entrevistaram famílias e professores para compreender substâncias por um membro da família (p<0,001). Silva e
as causas e as consequências da obesidade infantil, concluíram Maia(28) também investigaram questões ligadas à prisão de
que a perda de um ente foi fator determinante da obesidade, um membro da família, demonstrando diferença significante
mas nossos dados não corroboram essa tese. Quanto à pre- entre os grupos de obesos e de não obesos (p=0,001). Tais
sença de doenças na família, segundo Góngora(24), naquelas dados reforçam a ideia de uma elevada comorbidade em
em que um de seus membros está doente, interagem três experiências de adversidade, sendo que a presença de deter-
subsistemas: o paciente e sua enfermidade, a família e sua minadas condições familiares (como a violência, o consumo
rede social e os serviços de saúde. Dessa forma, tomando-se de álcool ou a doença mental) podem ocasionar maior ad-
por base a teoria familiar sistêmica, é possível descrever um versidade individual. Assim, se na literatura encontram-se
modelo patológico que busca explicar o que ocorre nesses referências indicando que indivíduos obesos possuem, em
subsistemas quando um membro da família apresenta doença alguns casos, membros etilistas em suas famílias, é possível
crônica(25): nesse caso, algumas características, como falta de aludir que a relação inversa também pode ocorrer, ou seja,
limites interindividuais e entre os coabitantes, carência talvez o alcoolismo de algum familiar desencadeie ou man-
de habilidades de solução de problemas e padrões de intera- tenha o quadro de sobrepeso/obesidade.
ção rígidos seriam características predominantes. Por fim, Os dados obtidos nos dois grupos quanto ao número de
pode-se incluir a própria obesidade de um ou mais membros habitantes no domicílio aproximaram-se dos resultados do
no rol de doenças crônicas interferentes no ambiente fami- Censo Demográfico 2000, o qual revelou que, em média,
liar(25). Todos esses fatores poderiam exercer influência sobre cada família brasileira possuía 3,5 pessoas(29). Por outro lado,
o surgimento e a manutenção da obesidade nos adolescentes, nossos resultados quanto à questão da obesidade diferem de
mas o resultado deste estudo revelou que ter um membro outros trabalhos publicados. Estudo realizado por Magalhães
da família com alguma doença grave não pode ser apontado et al(30) no Nordeste constatou que as maiores prevalências
como fator desencadeante do sobrepeso/obesidade, já que a de sobrepeso/obesidade foram verificadas em moradores
diferença entre a prevalência nos dois grupos não foi estatis- de domicílios com até quatro pessoas, em comparação às
ticamente significante. casas com cinco ou mais pessoas. As meninas apresentaram
Fatores externos, tais como alcoolismo, drogadição e maior de risco de sobrepeso/obesidade do que os meninos
existência de familiar preso, têm sido apontados como ao residirem em domicílios com mais de cinco pessoas nessa
ligados à obesidade. Nesse paradigma, pesquisa realizada região [razão de prevalência (RP): 4,43; IC95% 2,15–9,09],
por Machado et al(26) com 322 pacientes e suas famílias no o que, no Sudeste, se apresentou de forma inversa (RP: 0,44;
Programa de Saúde da Família procurou relacionar o processo IC95% 0,23–0,85). Assim, os autores concluíram que morar
saúde-doença com a família, constatando-se que o uso do em domicílio com até quatro pessoas mostrou ter associação
álcool é um fator real de desagregação familiar. Igualmente, significante com sobrepeso/obesidade somente em meninos
conforme Spada(8,10), famílias que têm um membro com da Região Nordeste. Estudo de Bender(31) realizado com 208
transtorno alimentar costumam apresentar alguns traços crianças de ambos os sexos, estudantes de escolas públicas e
característicos, como dependência de álcool ou de drogas. particulares, mostrou que a maioria dos escolares portadores
Felitti et al(27), por sua vez, referem que, quanto às experiên- de sobrepeso/obesos possui apenas um irmão (47,9%) ou
cias de adversidade no ambiente familiar, estas são bastante não possui irmão (32,4%). A conclusão foi de que existe
frequentes nos sujeitos obesos e menos frequentes nos não correlação quanto ao número de irmãos que a criança possui e
obesos. E, ainda, em estudo realizado por Silva e Maia(28) com seu estado nutricional (p=0,01). Guedes et al(32) encontraram
144 pacientes obesos e não obesos, buscando-se investigar maior chance de obesidade em crianças com dois ou menos
aspectos de adversidade familiar relacionados à obesidade, irmãos (OR 1,74; IC95% 1,21–2,49). Guimarães et al(33)
constatou-se que, na categoria abuso de substâncias, pouco encontraram maior prevalência de sobrepeso em escolares que
mais da metade dos participantes obesos relatou a ocorrência possuíam apenas um irmão, com razão de chances ajustada
75
de 1,94, quando comparados com aqueles que tinham três como sendo os membros que coabitam um lar, estendendo suas
irmãos ou mais. Os autores discutem que a superproteção respostas a eventos como, por exemplo, morte de padrinhos.
materna e a maior oferta de alimentos sejam possíveis me- Dessa forma, por ser um questionário semiestruturado, não
canismos para a maior prevalência de obesidade nos filhos é possível mensurar se a resposta baseou-se na relevância que
únicos. Outra explicação possível, segundo esses autores, o fato teve para o jovem ou na compreensão que ele teve de
foi a de que quanto maior o número de crianças na família, família como sendo o macrogrupo a que pertence.
mais frequente seriam as brincadeiras e, por consequência, Outro aspecto que merece destaque refere-se à metodologia
a atividade física. Entretanto, nosso estudo não encontrou escolhida para a geração dos dados. Estudo português(28) que
diferença significante quanto ao número de pessoas que procurou associar a existência de adversidades familiares com
coabitam o lar, quando comparados os dois grupos. sobrepeso/obesidade encontrou resultados significantes para os
Na avaliação de cluster, consideraram-se os dados em itens violência, consumo de álcool, doença mental, abuso de
conjunto. Assim, para cada sujeito, somaram-se as respostas substâncias e prisão, entre outros. A possível explicação para
que indicavam a presença do fator de desagregação familiar que a referida pesquisa tenha encontrado resultados significantes
e realizou-se a quantificação do número de possíveis fatores encontra fundamento no fato de ter sido um estudo descritivo
que cada indivíduo apresentava. Estudo realizado por Silva e retrospectivo, ou seja, avaliou um efeito de uma causa passada.
Maia(28) com 144 pacientes obesos e não obesos observou que Assim, as adversidades mencionadas pelos participantes do
apenas 12% dos participantes obesos não relataram qualquer estudo tinham ocorrido na infância e gerado, por consequência,
tipo de adversidade na infância. Cerca de 47% desses parti- a obesidade na idade adulta. Por outro lado, nossa pesquisa
cipantes contaram cinco ou mais experiências de adversidade caracteriza-se por ser transversal, ou seja, a causa e o efeito são
durante a infância. Atendendo aos elementos que compõem buscados em um mesmo momento. Dessa forma, é imponde-
cada categoria de adversidade, os autores verificaram que 88% rável precisar se os fatores de desagregação familiar mensurados
dos sujeitos obesos e 69% dos não obesos relataram pelo menos dois grupos, eutróficos e sobrepeso/obesidade, não serão res-
nos uma dessas experiências, o que reforçaria a ideia de que a ponsáveis por gerar ou manter a obesidade futura nesses jovens.
obesidade é muito frequente em sujeitos com experiências de Deve-se também acrescentar como limitação o fato de se ter
adversidade. Ainda observaram que 68% dos participantes usado uma amostra de conveniência (sem cálculo amostral) e
obesos relataram pelo menos quatro experiências de adver- de o estudo ter sido conduzido em um local específico, o que
sidade ao longo da infância. No presente estudo, o resultado limita a extrapolação universal dos resultados encontrados.
das diferenças entre as médias e as medianas dos conjuntos de A interface entre problemas orgânicos e quadros psicológi-
respostas de adversidades não foi estatisticamente significante. cos muitas vezes apresenta esse tipo de dificuldade à análise.
Este trabalho mostra muitos resultados conflitantes com os Pode-se citar como exemplo o trabalho de Luiz et al, publicado
encontrados na literatura científica. Uma explicação razoável em 2010, que mostra maior prevalência de depressão em crian-
para essa diferença parece ter relação relevante com o fato de ças obesas, mas não consegue definir se existe relação de causa
se ter optado por incluir um grupo controle. Nenhum dos es- ou de consequência entre os eventos(34). O padrão individual
tudos citados neste artigo contou com a inclusão de um grupo de resposta não pode ser deixado de lado, posto que, como
controle para atestar os dados obtidos. É fato que vários fatores anteriormente citado, existem indivíduos que comem exa-
escolhidos para o estudo estão presentes nas crianças portado- geradamente frente a frustrações e estresse, enquanto outros,
ras de sobrepeso/obesidade, mas estão igualmente presentes pelos mesmos motivos, simplesmente deixam de se alimentar.
nas eutróficas e não poderiam, por esse motivo, ser indicadas Também não se pode descartar a questão genética, largamente
como variáveis da causalidade ou manutenção da obesidade. difundida e hoje entendida como de extrema importância na
Existem, contudo, limitações do estudo que devem ser desta- gênese e na manutenção do sobrepeso/obesidade(35). Por fim,
cadas. Uma das principais foi a distribuição de questionários conclui-se que o presente trabalho, que avaliou adolescentes
de autopreenchimento. Apesar do cuidado com as orientações com sobrepeso e obesidade, comprando-os a controles eutró-
prévias, existe sempre a possibilidade de os entrevistados não ficos, não encontrou diferença quanto à presença de fatores de
terem entendido os questionamentos e, consequentemente, desagregação familiar quando confrontados os grupos, apon-
terem respondido com base em compreensão errônea ou dis- tando que a ocorrência desses eventos, quando investigada,
torcida. Outro fator limitante é que, apesar de terem recebido possivelmente aparece de forma comum em adolescentes,
instruções para tanto, alguns jovens não entenderam “família” independentemente de seu estado nutricional.
76
Referências bibliográficas
1. Han JC, Lawlor DA, Kimm SY. Childhood obesity. Lancet 2010;375:1737-48. 20. De Oliveira AM, Cerqueira EM, Souza JS, Oliveira AC. Childhood overweight
2. Brasil - Instituto Brasileiro de Geografia e Estatística. Pesquisa de orçamentos and obesity: influence of biological and environmental factors in Feira de
familiares 2008-2009: análise do consumo alimentar pessoal no Brasil. Rio Santana, BA. Arq Bras Endocrinol Metab 2003;47:144-50.
de Janeiro: IBGE; 2011. 21. Pontin N. Prevalência de obesidade em adolescentes na faixa etária de 15
3. Vilar AP, Valverde MA, Lemes SO, Fisberg M. Uma medida de peso. São a 19 anos, nas escolas do ensino médio do município de Ouro, SC, Brasil.
Paulo: Celebris; 2002. Joaçaba: Unoesc; 2006.
4. Cunha LN. Dietbook. São Paulo: Mandarim; 1999. 22. Rand C, Stunkard AJ. Obesity and psychoanalysis. Am J Psychiatry
5. Mello Filho J. Psicossomática hoje. 2nd ed. Porto Alegre: Artmed; 1992. 1978;135:547-51.
6. Guimarães AC, Feijó I, Soares A, Fernandes S, Machado Z, Parcias 23. Rand CS. Psychodynamics of obesity. J Am Acad Psychoanal 1978;6:103-15.
SR. Overweight and obesity in school children: association between 24. Góngora JN. El impacto psicosocial de la enfermedad crónica en la família. In: Ríos
biopsychological, socioeconomic and behavioral factors. Arq Bras Endocrinol Gonzalez JA, editor. La família: realidad y mito. Madrid: Ramón Areces; 1998.
Metab 2012;56:142-8. 25. Castro EK, Piccinini CA. Implications of physical chronic disease in childhood to
7. Gupta N, Goel K, Shah P, Misra A. Childhood obesity in developing countries: family relationships: some theoretical questions. Psicol Refl Crit 2002;15:625-35.
epidemiology, determinants, and prevention. Endocr Rev 2012;33:48-70. 26. Machado HB, Soprano AT, Machado C, Lustosa AC, Lima MH, Mota AC.
8. Spada PV. Obesidade infantil: aspectos emocionais e vínculo mãe-filho. Rio Identification of risks in the family based on the genogram. Fam Saude Desenv
de Janeiro: Revinter; 2005. 2005;7:149-57.
9. Santos AM. O excesso de peso da família com obesidade infantil. Textos 27. Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V et al.
Contextos (Porto Alegre) [serial on the Internet]. 2003;(2):1-10 [cited 2013 Relationship of childhood abuse and household dysfunction to many of the
Sep 16]. Available from: http://revistaseletronicas.pucrs.br/ojs/index.php/fass/ leading causes of death in adults. The Adverse Childhood Experiences (ACE)
article/view/964/744 Study. Am J Prev Med 1998;14:245-58.
10. Spada PV. Aspectos psicológicos da alimentação. In: Nóbrega FJ, editor. 28. Silva SS, Maia AC. História de adversidade na família e queixas de saúde –
Vínculo mãe-filho. Rio de Janeiro: Revinter; 2005. um estudo comparativo entre obesos e não obesos. Actas do II Congresso
11. Araújo MF, Beserra EP, Araújo TM, Chaves ES. Childhood obesity: a reflection Família, Saúde e Doença; 2007, p. 1-13.
about familiar dynamics through an ethnographic point of view. Rev Rene 29. Brasil - Instituto Brasileiro de Geografia e Estatística. Censo Demográfico
2004;7:103-8. 2000 - famílias e municípios. Rio de Janeiro: IBGE; 2000.
12. Motulsky H. Grahpad 5.0. La Jolla (CA): Graphpad Software Inc; 2011. 30. Magalhães VC, Azevedo G, Mendonça S. Prevalence of overweight and obesity
13. De Almeida CA, De Almeida CC, Barreto RF, Oliveira VA, Ferrioli BH, João and associated factors among adolescents in the Northeast and Southeast
CA et al. Atuação interdisciplinar em obesidade infantojuvenil: a experiência regions of Brazil, 1996 to 1997. Cad Saude Publica 2003;19 (Suppl 1):S129-39.
do CESNI. Intern J Nutrol 2008;1:7. 31. Bender SC. Influência dos fatores ambientais na obesidade infantil
14. Salim CM, Bicalho RN. Infantile obesity-psychological aspects involved in the [monografia]. Santa Maria (RS): Unifra; 2006.
cause and their consequences. Univ Ci Saude 2004;2:23-37. 32. Guedes DP, Rocha GD, Silva AJ, Carvalhal IM, Coelho EM. Effects of
15. Wallerstein JS, Kelly JB. Sobrevivendo à separação. Porto Alegre: Artmed; 1998. social and environmental determinants on overweight and obesity among
16. Viuniski N. Obesidade Infantil: um guia prático para profissionais de saúde. Brazilian schoolchildren from a developing region. Rev Panam Salud Publica
Rio de Janeiro: Epub; 1999. 2011;30:295-302.
17. Mazur J, Dzielska A, Małkowska-Szkutnik A. Psychological determinants 33. Guimarães LV, Barros MB, Martins MS, Duarte EC. Factors associated with
of selected eating behaviours in adolescents. Med Wieku Rozwoj 2011; overweight in schoolchildren. Rev Nutr 2006;19:5-17.
15:240-9. 34. Luiz AM, Gorayeb R, Liberatore Júnior RD. Evaluation of depression,
18. Bernardi F, Cichelero C, Vitolo MR. Restrained eating behavior and obesity. behavioral problems and social skills in obese children. Estud Psicol
Rev Nutr 2005;18:85-93. (Campinas) 2010;27:41-8.
19. De Azevedo MA, Spadoto C. Psychological study of obesity: two clinical cases. 35. Loos RJ. Genetic determinants of common obesity and their value in prediction.
Temas Psicol 2004;12:127-44. Best Prac Res Clin Endocrinol Metab 2012;26:211-26.
77
ARTIGO ORIGINAL
Echocardiography for cardiovascular evaluation of overweight/obesity

children: a revision
Simone Helena Caixe1
Carlos Alberto Nogueira de Almeida2
2Doutor, Universidade de Ribeirão Preto

Instituição: Universidade de Ribeirão Preto
RESUMO
Palavras chave:
ABSTRACT
Keywords:
INTRODUÇÃO
108 International Journal of Nutrology, v.6, n.3, p. 108-113, Set / Dez 2013
ECOCARDIOGRAFIA PARA AVALIAÇÃO CARDIOVASCULAR DE
CRIANÇAS COM SOBREPESO/OBESIDADE: UMA REVISÃO
OBESIDADE E SUAS COMORBIDADES
SIMONE HELENA CAIXE
ECOCARDIOGRAFIA NA CRIANÇA OBESA
SIMONE HELENA CAIXE
CONSIDERAÇÕES FINAIS E RECOMENDAÇÕES
REFERENCES
1. Han JC, Lawlor DA, Kimm SY. Childhood obesity. Lancet. 2010.
375: 1737-48, 2010. Disponível em:http:// www.thelancet.com .
acesso em 16.08.2012.
2. Mattos AP, Brasil ALD, De Almeida CAN, Faria CDC, Gazal
CHA, Leone C et al. Obesidade na infância e adolescência: Ma-
nual de Orientação/ Sociedade Brasileira de Pediatria. Depar-
tamento de Nutrologia. – São Paulo: Sociedade Brasileira de
Pediatria. Departamento de Nutrologia, 2008.
3. Brasil. Ministério da Saúde. Secretaria de Vigilância em Saúde.
Departamento de Análise de Situação de Saúde. Plano de Ações
estratégicas para o enfrentamento das doenças crônicas não
transmissíveis (DCNT) no Brasil 2011-2022 – Brasília (DF), 2011.
4. De Oliveira CL, De Mello MT, Cintra IP, Fisberg M. Obesidade
e síndrome metabólica na infância e adolescência. Rev. Nutr.
2004. 17 (2): 237-245.
5. I Diretriz de Prevenção da Aterosclerose na infância e na ado-
lescência. Sociedade Brasileira de Cardiologia. Arq Bras Car-
diol. 2005; 85 Supl 6: S1-36.
6. Brasil. Ministério da Saúde. Secretaria de Atenção à Saúde. De-
partamento de Atenção Básica. Hipertensão Arterial Sistêmica
para o Sistema Único de Saúde – Cadernos de Atenção Básica
– 15. Brasília (DF), 2006.
7. VI Diretrizes Brasileiras de Hipertensão Arterial, Sociedade 23. Silva CES, Ortiz J. O Exame em Modo M. In: Ecocardiografia:
Brasileira de Cardiologia, Sociedade Brasileira de Hipertensão, princípios e aplicações clínicas. 2th Ed. Rio de Janeiro: Revinter,
Sociedade Brasileira de Nefrologia, Arq Bras Cardiol. 2010. 95 2012. v I. p. 85-92.
Supl 1: S1-51. 24. Feigenbaum H, Armstrong WF, Ryan T. Feigenbaum Ecocar-
8. Feedman DS, Dietz WH, Srinivasan SR, Berenson GS. The Rela- diografia. Trad. Do Couto LB. 6th Ed. Rio de Janeiro: Guanaba-
tion of Overweight to Cardiovascular Risk Factors Among Chil- ra Koogan, 2007. p.11-42.
dren and Adolescents: The Bogalusa Heart Study. Pediatrics. 25. Ghanem S, Mostafa M, Ayad S. Early echocardiography abnor-
1999; 103 (6): 1175-1182. malities in obese children and adolescent and reversibility of
9. Kavey REW, Daniels SR, Lauer RM, Atkins DL, Hayman LL, these abnormalities after significant weigth reduction. Journal
Taubert K. American Heart Association Guidelines for Primary of the Saudi Heart Association. 2010. 22: 13-18.
Prevention of Atherosclerotic Cardiovascular Disease Begin- 26. Dhuper S, Abdullah RA, Weichbrod L, Madhi E, Cohen HW.
ning in Childhood. Circulation. 2003; 107: 1562-1566. Association of Obesity and Hypertension With Left Ventricular
10. Srinivasan SR, Bao W, Wattigney WA, Berenson GS. Adolescent Geometry and Function in Children and Adolescents. Obesity.
overweights associated with adult overweight and related mul- 2011. 19 (1): 128-133.
tiple cardiovascular risk factors: The Bogalusa Study. Metabo- 27. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Fos-
lism. 1996; 45: 235-40. ter E, Pellikka PA et al. Recommendations for Chamber
11. Ribeiro RQC, Lotufo PA, Lamounier JA, Oliveira RG, Soares JF, Quantification: A Report from the American Society of
Botter DA. Additional Cardiovascular Risk Factors Associated Echocardiography`s Guidelines and Standards Committee and
with Excess Weight in Children and Adolescents. The Belo Ho- the Chamber Quantification Writing Group, Developed in Con-
rizonte Heart Study. Arquivos Brasileiros de Cardiologia. 2006; junction with the European Association of Echocardiography, a
86 (6): 408-18. Branch of the European Society of Cardiology. J Am Soc Echo-
12. Rosa EC, Zanella MT, Ribeiro AB, Kohlmann Junior O. Obe- cardiogr. 2005. 18 (12): 1440-1463.
sidade visceral, hipertensão arterial e risco cárdio-renal: uma 28. De Simone G, Devereux RB, Daniels SR, Koren MJ, Meyer RA,
revisão . Arq Bras Endocrinol Metab. 2005; 49 (2): 196-204. Laragh JH. Effect of Growth on Variability of Left Ventricular
13. Kershaw EE, Flier JS. Adipose Tissue as an Endocrine Organ . J Mass: Assessment of Allometric Signals in Adults and Children
Clin Endocrinol Metab. 2004. 89: 2548–2556. and Their Capacity to Predict Cardiovascular Risk. JACC. 1995.
25 (5): 1056-62.
14. Trayhurn P, Beattie JH. Physiological role of adipose tissue: whi-
te adipose tissue as an endocrine and secretory organ. Procee- 29. Lopez L, Colan CSD, Frommelt PC, Ensing GJ, Kendall K, You-
dings of the Nutrition Society. 2001. 60 (3): 329-339. noszai AK, et al. Recommendations for Quantification Methods
During the Performance of a Pediatric Echocardiogram: A Re-
15. Grundy SM. Obesity, metabolic Syndrome, and Cardiovascular
port From the Pediatric Measurements Writing Group of the
Disease. The journal of Clinical Endocrinology & metabolism.
American Society of Echocardiography Pediatric and Congeni-
2004. 89 (6): 2595-2600.
tal Heart Disease Council. J Am Soc Echocardiogr. 2010. 23 (5):
16. Nielsen S, Guo Z, Johnson CM, Hensrud DD, Jensen MD. 465-495.
Splanchnic lipolysis in human obesity. J Clin Invest. 2004. 113
30. Mawad W, Drolet C, Dahdah N, Dallaire F. A Review and Cri-
(11): 1582-1588.
tique of the Statistical Methods Used to Generate Reference
17. Bettmann MA. A Radiografia do Tórax na Doença Cardiovas- Values in Pediatric Echocardiography. J Am Soc Echocardiogr.
cular. In: Zipes DP, Libby P, Bonow RO, Braunwald E Braunwald 2013. 26: 29-37.
- tratado de doenças cardiovasculares. Trad. Varga VS. et al. 7th
Ed. Rio de Janeiro: Elsevier, 2013. I. p. 271-285.
18. Moreira VM. Ressonância Magnética e Tomografia Computa-
dorizada Cardiovascular. In: Crotti UA, Mattos SD, Pinto Júnior
VC, Aiello VD. Cardiologia e Cirurgia Cardiovascular Pediátri-
ca. São Paulo: Roca, 2008. p. 122-135.
19. Kozak MF, Guerra VC. Ecocardiografia. In: Crotti UA , Mattos
SD, Pinto Júnior VC, Aiello VD. Cardiologia e Cirurgia Cardio- Recebido em 29/07/2013
vascular Pediátrica. São Paulo: Roca, 2008. p. 104-119. Revisado em 20/08/2013
Aceito em 25/08/2013
20. Kolb Júnior JA. O Exame Bidimensional. In: Silva CES. Ecocar-
diografia: princípios e aplicações clínicas. 2th Ed. Rio de Janei-
ro: Revinter, 2012. I, p. 93-119. Autor correspondente:
21. Fraser AG. BIOGRAPHY Inge Edler and the Origins of Clini- Carlos Alberto Nogueira de Almeida
Clínica Nutre
cal Echocardiography. Eur J Echocardiography. 2 (1): 3-5, 2001.
Rua São José, 2591 - CEP 14025-180 - Ribeirão Preto - SP
22. Feigenbaum H. Evolution of Echocardiography. Circula- TELEFONE: 16 38775034
tion.1996. 93 (7): 1321-1327. Email: dr.nogueira@me.com
Review
Variation of the brachial artery diameter in obese children:

present and future
Variação do diâmetro da artéria braquial em crianças obesas: presente e futuro
Variación del diámetro de la arteria braquial en niños obesos: presente y futuro
Karla Cristina M. Costa1, Jailson Costa Lima2, Carlos Alberto N. de Almeida3, Luiz Antônio Del Ciampo4, Cristiane Simões B. de Souza5
ABSTRACT RESUMO
Objective: Literature review on the use of the vari- Objetivo: Revisão da literatura acerca do uso da medida
ation measure of the brachial artery diameter by high- da variação do diâmetro da artéria braquial por ultrassono-
resolution ultrasound (flow-mediated dilation) as a grafia de alta resolução (dilatação mediada por fluxo) como
predictor of cardiovascular disease risk in children and preditor de risco para doença cardiovascular em crianças e
adolescents. adolescentes obesos.
Data source: Survey of studies indexed in Medline/Pub- Fontes de dados: Levantamento de publicações indexadas
med, which were published between 2002 and 2011 using the no Medline/PubMed de trabalhos publicados entre 2002 e
following keywords in various combinations:“endothelium,” 2011, rastreadas com a combinação dos descritores: “endothe-
“child”, “ultrasonography” and “obesity”, as well as classic lium”, “child”, “ultrasonography” e “obesity”, além de estudos e
texts on the subject. We found 54 publications and 32 were textos clássicos sobre o tema. Foram encontradas 54 publi-
included in this review. cações e 32 delas foram incluídas na presente revisão do tema.
Synthesis of data: The study of endothelial dysfunc- Síntese dos dados: O estudo da disfunção endotelial
tion has been used as a predictor of risk for cardiovascular tem sido empregado como preditor de risco para doenças
diseases such as atherosclerosis and coronary heart disease, cardiovasculares, tais como aterosclerose e doença cardíaca
since endothelial injury is an important event in the physi- coronariana, visto que a lesão endotelial é um importante
opathology of these diseases. evento na fisiopatologia de tais doenças.
Conclusions: The flow-mediated dilation of the brachial Conclusões: A dilatação mediada por fluxo da artéria braquial
artery seems to be important as a diagnostic and prognostic mostra-se importante como ferramenta diagnóstica e prognóstica
tool to assess endothelial function in children and adolescents na avaliação da função endotelial de crianças e adolescentes com
who are overweight, because it is a noninvasive method with excesso de peso por ser um método não invasivo, com boa aplica-
good profile regarding cost, safety, and benefits. bilidade quanto ao custo, à inocuidade e ao benefício.
Key-words: endothelium; child; ultrasonography; Palavras-chave: endotélio; criança; ultrassonografia;

obesity. obesidade.
Instituição: Faculdade de Medicina de Ribeirão Preto da Universidade de Endereço para correspondência

São Paulo (USP), São Paulo, SP, Brasil Karla Cristina M. Costa
1
Doutoranda em Saúde da Criança e do Adolescente da Faculdade de Rua Quintino Bocaiuva, 51 – apto. 111 – Centro
Medicina de Ribeirão Preto da USP, Ribeirão Preto, SP, Brasil CEP 14015-160 – Ribeirão Preto/SP
2
Doutorando em Ginecologia-Obstetrícia da Faculdade de Medicina de E-mail: karlamaltavilanova@hotmail.com
Ribeirão Preto da USP, Ribeirão Preto, SP, Brasil
3
Doutor em Saúde da Criança e do Adolescente pela Faculdade de Conflito de interesses: nada a declarar
Medicina de Ribeirão Preto da USP; Docente da Universidade de Ribeirão
Preto (Unaerp), Ribeirão Preto, SP, Brasil Recebido em: 27/7/2011
4
Doutor em Saúde da Criança e do Adolescente pela Faculdade de Aprovado em: 22/11/2011
Medicina de Ribeirão Preto da USP; Docente da Faculdade de Medicina
de Ribeirão Preto da USP, Ribeirão Preto, SP, Brasil
5
Doutoranda em Saúde da Criança e do Adolescente da Faculdade de
Medicina de Ribeirão Preto da USP, Ribeirão Preto, SP, Brasil

Variation of the brachial artery diameter in obese children: present and future
RESUMEN Excessive weight in childhood can increase the likelihood of

developing coronary disease in adulthood as a result of the
Objetivo: Revisión de la literatura sobre el uso de la early effects of these risk factors(6). Damaged endothelium plays
medida de la variación del diámetro de la arteria braquial, and important role in the development of several CVDs(7),
por ultrasonografía de alta resolución (dilatación mediada such as atherosclerosis and coronary disease(7,8), and is used as
por flujo), como predictor de riesgo para enfermedad car- a predictor of the risk of these events(9,10).
diovascular en niños y adolescentes obesos. The endothelium performs its function through the
Fuentes de datos: Inventario de publicaciones indizadas action of a variety of different molecules in response to a
en Medline/Pubmed de trabajos publicados entre 2002 y range of physical and chemical stimuli, including hypoxia,
2011, buscadas mediante la combinación de los descriptores: acetylcholine, bradykinin, serotonin and increased blood
«endothelium», «child», «ultrasonography» y «obesity», además flow. Production and release of nitric oxide (NO) by endo-
de estudios y textos clásicos sobre el tema. Se encontraron thelial cells have been identified as the principal vasodilation
54 publicaciones y 32 de ésas fueron incluidas en la presente mediating mechanisms and this has been demonstrated in
revisión del tema. both in vitro and in vivo experiments(11,12). This means that
Síntesis de los datos: El estudio de la disfunción endo- poor regulation of NO production and release is one of the
telial viene siendo empleado como predictor de riesgo para principal factors in endothelial dysfunction. It is believed
enfermedades cardiovasculares, tales como aterosclerosis that endothelial dysfunction may be involved in the patho-
y enfermedad cardíaca coronariana, puesto que la lesión physiology of CVD and metabolic diseases in children(13-15)
endotelial es un importante evento en la fisiopatología de and adolescents(16-18) with severe obesity.
tales enfermedades. Several methods have been tested for analyzing endothelial
Conclusiones: La dilatación de la arteria braquial me- function, one of which, high resolution ultrasound measure-
diada por flujo se muestra importante como herramienta ment of variation in brachial artery diameter (flow-mediated
diagnóstica y pronóstica en la evaluación de la función en- dilation – FMD), is a noninvasive method that has been
dotelial de niños y adolescentes con exceso de peso, por ser widely used in research and correlated with clinical prac-
un método no invasivo, con buena aplicabilidad respecto al tice for the last two decades(19). The importance of studying
costo, a la inclusión y al beneficio. intermediate markers for analysis of endothelial function,
particularly in high risk groups, means that research into
Palabras clave: endotelio; niño; ultrasonografía; noninvasive ultrasound techniques such as brachial artery
obesidad. FMD has become a focus of efforts to correlate vascular
function with CVD and increased morbidity and mortality
Introduction in affected populations.
The objective of this study was to conduct an up to date
It is known that excess weight is currently the sixth most bibliographic review of the application of FMD for assess-
important risk factor for development of diseases(1). The ment of obese children, with emphasis on the technique’s
complex pathological process underlying obesity reflects envi- importance in nutrology and pediatric practice. This article
ronmental and genetic interactions(1,2). Environmental factors is based on the results of a literature search conducted on
that can contribute to reducing the impact of excess weight on Medline/Pubmed for studies published from 2002 to 2011,
children and adolescents include sociodemographic variables using the keywords “obesity and ultrasonography and child
and lifestyle factors that are potentially modifiable through and endothelium” in addition to classic studies and texts
healthy nutrition and engaging in physical activity(2,3). that address the subject. Fifty-four articles were identified,
The obesity epidemic has been growing since 1980, in of which 32 were chosen that fitted the study objectives.
both developed and developing countries, but it was only in
1997 the World Health Organization (WHO) classified it as Study of endothelial function
an important public health problem that should be monitored
from childhood(4,5). Overweight children exhibit risk fac- Atherosclerosis is a systemic arterial disease in which dam-
tors for cardiovascular diseases (CVD) such as hypertension, aged endothelium promotes the entry of circulatory inflam-
dyslipidemia, glucose intolerance and vascular disorders. matory cells, initiating a process of localized fibrosis and lipid
432
Rev Paul Pediatr 2012;30(3):431-7
Karla Cristina M. Costa et al
deposition(20). This is a diffuse process of the artery walls and Childhood Obesity and Cardiovascular Risk
its natural history of development includes an asymptomatic
stage that can have onset in childhood or adulthood and can Over the last few decades, childhood obesity has come to
lead to luminal stenosis or sudden occlusion of an artery by be considered a public health problem in both developed
unstable lesions, causing clinical events(21). countries and those in development. The consequences are
Endothelial dysfunction is the primary event in devel- similar to those observed in adults, including hypertension,
opment of atherosclerosis and can be detected long before dyslipidemia, chronic inflammation, hyperinsulinemia and
the appearance of structural atherosclerotic disease(19,21,22). endothelial dysfunction. Among adolescents and young
The endothelium used to be recognized only as a physical adults who had died of traumatic causes, risk factors for
barrier, part of the artery wall, but it is now known that it CVD were identified and correlated with asymptomatic
has countless autocrine, paracrine and endocrine properties atherosclerotic disease, and it was found that lesions were
and, since it takes part in vascular homeostasis, influences more advanced in obese individuals(29).
vascular tonus, cell growth, fibrinolysis, thrombolysis and The anthropometric-nutritional profile of the Brazilian popu-
inflammatory and immune responses(23,24). lation has changed over the last thirty years, with increasing
Under physiological conditions, the endothelium acts as overweight and obesity, which is a phenomenon known as epide-
a potent vasodilator and leukocyte adhesion inhibitor and is miological transition(4). Nutritional behavior during childhood
active in smooth muscle cell growth and platelet aggregation. has a direct influence on dietary habits in adulthood and, as a
Many different biologically active molecules take part in these result, obese children are more likely to become obese adults(30).
physiological mechanisms, such as NO produced by enzymes It is known that children and adolescents with excess weight
known as nitric oxide synthases, activated by increased blood are at increased risk of adverse health events over both the short
flow (shear stress), hypoxia, acetylcholine and bradykinin(23,25). term and long term. These include increased risk of early de-
Cardiovascular risk factors like atherosclerosis, arterial velopment of CVD and the metabolic abnormalities associated
hypertension, diabetes mellitus and smoking appear to with them, such as arterial hypertension, hypercholesterolemia,
be linked to a loss of endothelial functional integrity(19,26). hypertriglyceridemia, insulin resistance syndrome and vascular
Endothelial dysfunction is manifest in reduced NO produc- disorders, such as increased carotid thickness(5-6,14,30,31). All of
tion and can be exacerbated by constrictive factors, such as these factors increase the cost of healthcare to society(31).
endothelin. There is therefore an increase in vasoconstric- It has been suggested that prenatal exposure or exposure
tion responses, in vascular smooth muscle cell proliferation in early life confers an increased risk of excess weight in later
and migration and in expression of adhesion molecules and phases of life. In this context, excess weight, and particularly
platelets(27). Dysregulation of NO production and release is abdominal fat, is a recognized risk factor for CVD, adult on-
the primary factor in endothelial dysfunction. It is believed set diabetes mellitus, cerebral vascular accidents and death(32).
that endothelial dysfunction may be involved in the patho- As nutritional transition progresses, obesity affects people
physiology of vascular and metabolic diseases in hyperten- at ever younger ages and its effects appear ever earlier. This
sion and metabolism-related disorders and obesity(5,13,17,28), being so, it is important that high-risk populations be
including in obese children(13-15) and adolescents(16-18). monitored, preferably using noninvasive methods, so that
Countless methods for assessing endothelial function preventative measures and public health policies can be
have been investigated, both invasive, such as angiography, implemented as early as possible.
intravascular ultrasonography and intra-arterial infusion
of selective endothelial agonists, and noninvasive, such as Technical Aspects of Flow-mediated Dilation
measuring variation in brachial artery diameter (FMD) and
plethysmography. From a practical point of view, noninva- The technique was first described by Anderson and Merck
sive techniques are of greater interest because they are less (1989) and has been used in clinical research since 1992(19).
expensive, harmless and offer potential benefits. Foremost It has since been widely adopted for assessment of endo-
among the noninvasive methods is measurement of brachial thelial function(21,26,33-35). As a result, it became necessary to
artery FMD using high-frequency echography, which was standardize the technique to provide uniform results that
described in 1989 by Anderson and Merck and has been would allow comparison of the results found at different
used in research applications since 1992(19). research centers(34).
433
Vascular reactivity means that countless factors affect techniques(36). The majority of the current studies preferred
FMD, including ambient temperature, foods, drugs, the to measure the brachial artery longitudinally, from the an-
menstrual cycle, sympathetic stimuli and physical and terior, above the antecubital fossa(37-42). Occlusion times of
emotional stress, among others. All of these factors must be approximately 5 minutes provoked significant variation in
controlled for before the test is run, and it should be per- vascular diameter(36). The post-occlusion measurement time
formed between seven and nine o’clock in the morning(34-35). that provoked the most significant increase in artery diam-
To correctly execute the technique, the operator must be eter was 60 seconds, which was the interval chosen in the
trained in two-dimensional and Doppler ultrasound and must majority of studies(42). A high-resolution linear transducer
be equipped with a high-resolution ultrasound machine cou- is used to view the brachial artery longitudinally and mea-
pled to an electrocardiogram (ECG). There is a steep learning surements are taken before and after compressive stimulus,
curve to surmount and observers should conduct at least 100 as shown in Figure 1.
procedures under supervision(34). This degree of rigor is neces-
sary because the low magnitude of the variation in brachial Brachial Artery Flow-Mediated Dilation,
artery diameter before and after compression of the forearm Children and Obesity
means that intraobserver and interobserver reproducibility is
experience-dependent and easily compromised(33). While the clinical complications of atherosclerosis do
In 2005, Bots et al conducted a meta-analysis of publica- not emerge until adulthood, or even old age, atheroscle-
tions on FMD from 1991 to 2002, covering 219 studies and rotic disease is a lifelong process that has its roots in child-
16,680 subjects, assessing details such as type of equipment, hood. Improvements in noninvasive imaging methods, in
location of compression and point of brachial artery measure- particular ultrasonography, have made it possible to assess
ment, duration of occlusion, post-occlusion measurement the endothelial health of asymptomatic children, with or
time and pressure exerted during compression with the without cardiovascular risk factors(43).
sphygmomanometer. They observed a great deal of variation Abnormal arterial compliance can suggest subclinical
between studies in terms of FMD results (ranging from -1.9 atherosclerosis since it indicates the presence of arterial ri-
to 19.2%), resulting from the different techniques employed gidity and calcification, compromised endothelial function
and highly differentiated study samples(36). and increased carotid intima-media thickness. In children
The measurement location (upper arm or forearm) did nor and adolescents, arterial compliance has been investigated
significantly affect FMD measurements taken with different using noninvasive methods and its link with the risk of
A B
Figure 1 - High resolution linear ultrasound measurement of brachial artery diameter before stimulus (A) and 60 seconds after
5 minutes with forearm compressed (B). Observe the measurement coinciding with the electrocardiogram QRS complex. Flow-
mediated dilation (%) = diameter A – diameter B / diameter A x 100
434
developing CVD has been explored. Invasive techniques, Table 1 - Pediatric indications for investigating endothelial func-
such as coronary angiography, used to diagnose diagnosis
coronary artery stenosis, cannot assess arterial functional Indications
reactivity(44-45). 1. Dyslipidemia
Countless methods have been tested for assessing endo- 2. Familial hypercholesterolemia
thelial function in the pediatric population with a view to 3. Diabetes mellitus
defining prognosis and cardiovascular risk, but FMD and 4. Obesity
studies of the carotid intima-media thickness are the most 5. Chronic kidney diseases
widely used. Scientific publications have demonstrated cor- 6. Homocystinuria
relations between pediatric diseases and abnormalities of 7. Kawasaki disease
endothelial function detected by FMD(5,43,46-48). 8. Pediatric cardiac surgery
Woo et al studied 82 obese children aged between nine
and 12 to assess the degree of reversibility of early arterial
damage. The children were randomly assigned either to an and low density lipoprotein (LDL) levels(50). Reduced FMD has
intervention entirely based on diet or to one with a dietary also been observed in prepubescent children with high blood
component plus a structured program of physical exercises pressure and in obese children with insulin resistance(51). Obese
lasting initially for six weeks and then for one year, with children who are asymptomatic from a cardiovascular point
the objective of defining potentially effective strategies that of view, but have high body mass index (BMI), and abnormal
could improve obesity linked with vascular disorders. They glycemia, cholesterol and insulin levels have lower FMD than
assessed endothelial function using FMD and carotid artery healthy children(52). On the other hand, lifestyle changes,
intima-media thickness and analyzed a range of anthropo- such as routine physical exercise and diet, are correlated with
metric parameters and laboratory results. They concluded increases in FMD in both healthy and overweight children
that obesity linked with vascular dysfunction in healthy chil- and adolescents(53). Table 1 lists the principal indications for
dren was partially reversible with the dietary intervention investigating endothelial function using brachial artery FMD
alone or with the dietary intervention and physical training in school-aged children.
for six weeks and that the diet and physical exercise together Early identification of the cardiovascular risk factors
for one year led to sustained improvement(48). associated with excess weight in children and adolescents
Childhood obesity appears to contribute to development is important for development of educational interventions
and progression of premature atherosclerosis, particularly and prevention programs designed to target these factors, in
when combined with hypertension and dyslipidemia. Zhu et order to reduce excess weight among children and improve
al(5), demonstrated this in a study with obese and non-obese the health and quality of life of the population.
school-aged children, assessing carotid artery intima-media
thickness, FMD and biochemical markers of dyslipidemia. Final comments
They found that carotid thickness was significantly greater
(0.62 vs. 0.46 mm, p<0.001) and FMD was reduced (10.9 Brachial artery FMD is an important tool when inves-
vs. 18.8%) in the obese group, revealing the correlation with tigating endothelial function in people with cardiovas-
endothelial dysfunction(5). cular risk factors, since researchers and clinicians need an
Several situations in pediatric practice have a correla- intermediate marker to enable them to intervene in the
tion with reduced brachial artery FMD, including kidney natural history of CVDs, in order to reduce morbidity and
diseases, childhood cardiac surgery, Kawasaki disease, dys- mortality among children, adolescents and adults. There
lipidemia and homocystinuria(47). Flow-mediated dilation are certain technical limitations to the method, since it
results of less than 10 to 12% are linked with compromised requires a high-resolution ultrasound machine coupled
endothelial function in pediatric groups(5). to an ECG, mechanical apparatus and a properly trained
Adolescents with a family history of CVD and familial operator, but it can prove an essential instrument for pro-
hypercholesterolemia have lower FMD than healthy popula- viding the clinical evidence to support intervention in a
tions(49). A negative correlation has been shown between FMD patient’s lifestyle and health promotion.
435
References
S et al. The early origins of later obesity: pathways and mechanisms. Adv Exp mediated dilatation. Pharmacol Rep 2006;58 (Suppl 1):3-7.
Med Biol 2009;646:71-81.
endothelial dysfunction may occur in the absence of angiographic or ultrasound
adolescent obesity treatment interventions on physical activity: a systematic
review. Obes Rev 2010;11:516-30. Cardiol 1994;23:833-43.
factors associated with overweight in a representative sample of 11-15 year

olds in France: results from the WHO-Collaborative Health Behaviour in physiology: far beyond vessel tone control. Arch Med Res 2004;35:1-11.
School-aged Children (HBSC) cross-sectional study. BMC Public Health
2011;11:442.
2008;263:336-52.
2005;164:337-44. DS. Oestradiol improves arterial endothelial function in healthy men receiving
testosterone. Clin Endocrinol (Oxf) 2001;54:175-81.
et
al. Coronary vasomotor response to acetylcholine relates to risk factors for
coronary artery disease. Circulation 1990;81:491-7. 29. Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health crisis,
common sense cure. Lancet 2002;360:473-82.
acid reverses endothelial vasomotor dysfunction in patients with coronary
artery disease. Circulation 1996;93:1107-13. obese children become obese adults? A review of the literature. Prev Med
1993;22:167-77.
mediated dilation predicts incident cardiovascular events in older adults: the 31. Lobstein T, Baur L, Uauy R; IASO International Obesity Task Force. Obesity
Cardiovascular Health Study. Circulation 2007;115:2390-7. in children and young people: a crisis in public health. Obes Rev 2004;5
(Suppl 1):4-104.
32. Rasch R, Skriver E, Woods LL. The role of the RAS in programming of adult
status in an elderly cohort: the cardiovascular health study. Atherosclerosis hypertension. Acta Physiol Scand 2004;181:537-42.
2008;197:768-76.
Ultrasound Med Biol 2010;36:2036-41.

et al.
MA et al
et al.
Arterial rigidity and endothelial dysfunction in obese children. Arch Mal Coeur et al. Modulation
et al. sex and menstrual cycle. Circulation 1995;92:3431-5.
vasodilatation (FMD) of the brachial artery: effects of technical aspects of the

Biol 2006;26:2541-6.
et al et
endothelial and smooth muscle function relates to body mass index and glucose al. Both a combined oral contraceptive and depot medroxyprogesterone acetate
impair endothelial function in young women. Contraception 2009;79:35-40.
et al. Presence
of increased stiffness of the common carotid artery and endothelial dysfunction
in severely obese children: a prospective study. Lancet 2001;358:1400-4.
mediated vasodilation, carotid artery intima-media thickening, and elevated polycystic ovary syndrome women. Fertil Steril 2009;91:e23-4.
endothelial plasma markers in obese children: the impact of cardiovascular
risk factors. Pediatrics 2006;117:1560-7.
et al. Abnormal
MF et al. Increased arterial stiffness in nonobese women with polycystic ovary
2009;39:94-102. syndrome (PCOS) without comorbidities: one more characteristic inherent to
the syndrome? Clin Endocrinol (Oxf) 2009;71:406-11.
ID et al
at risk of atherosclerosis. Lancet 1992;340:1111-5.
20. Al-Qaisi M, Kharbanda RK, Mittal TK, Donald AE. Measurement of endothelial
2008;4:647-52.
436
44. Stout M. Flow-mediated dilatation: a review of techniques and applications.

Echocardiography 2009;26:832-41. history of cardiovascular events and endothelial dysfunction in children with
familial hypercholesterolemia. Atherosclerosis 2002;163:193-7.
Obes (Lond) 2005;29 (Suppl 2):S101-4.

et al. in children with familial hypercholesterolemia and is related to the lipoprotein(a)
and vascular function in children. Atherosclerosis 2009;204:244-9.

et al.
et al. Overweight in
children is associated with arterial endothelial dysfunction and intima-media
statement from the American Heart Association. Hypertension 2009;54:919-50.
et al. Effects of diet 53. Abbott RA, Harkness MA, Davies PS. Correlation of habitual physical activity
and exercise on obesity-related vascular dysfunction in children. Circulation
2004;109:1981-6. Atherosclerosis 2002;160:233-9.
437
0021-7557/08/84-02/136
Jornal de Pediatria
Copyright © 2008 by Sociedade Brasileira de Pediatria
ORIGINAL ARTICLE
Determination of glycemia and insulinemia and the

homeostasis model assessment (HOMA) in schoolchildren
and adolescents with normal body mass index
Carlos A. N. de Almeida,1 Adriana P. Pinho,2 Rubens G. Ricco,3
Maria Tereza Pepato,4 Iguatemy Lourenço Brunetti5
Abstract
Objective: To determine fasting glycemia and insulinemia levels and the HOMA index in a group of children and
adolescents with normal body mass index (BMI).
Methods: This was a cross-sectional study conducted at two public schools in Ribeirão Preto, SP, Brazil. A total of
447 children and adolescents of both sexes, with normal BMI, aged 7 to 17.9 years and of average maturity for their
age, underwent anthropometric measurements and provided personal data and a sample of venous blood so that
glycemia, insulinemia and HOMA index could be determined. The results obtained for boys and girls were compared for
each age range using the Mann-Whitney test. The results within each age band were then compared for boys and girls
using the Kruskal-Wallis test.
Results: Glycemia results varied from 7 to 8.9 years (p = 0.0005). Fasting insulinemia varied significantly with age
in both sexes (p < 0.001), with the highest values observed among children aged 13 to 14.9 years. HOMA indices varied
significantly with age in both boys and girls (p < 0.001), with values that increased progressively up to the age band of
13 and 14.9 years.
Conclusions: These data demonstrate the necessity of establishing reference curves for these three indicators.
J Pediatr (Rio J). 2008;84(2):136-140: Obesity, hyperinsulinism, insulin, metabolic syndrome X.
Introduction before they start school.4,5 Currently, the greatest difficulty

facing both scientific studies and clinicians is the identifica-
Prevalence rates of childhood obesity have reached alarm-
tion of adequate cutoff points for assessing indicators such
ing levels all over the world.1 In parallel, scientific evidence is
lipemia, arterial blood pressure, waist circumference, periph-
mounting up that suggests that the metabolic disorders that
eral insulin resistance (PIR), glycemia and insulinemia.5
habitually accompany excess body fat are already manifest
during childhood.2-5 The metabolic syndrome is defined as a The clamp test in particular, considered the gold standard
group of disorders that includes obesity, insulin resistance, for evaluating PIR, is difficult to carry out with pediatric
dyslipidemia, arterial hypertension and other metabolic patients because it demands that patients remain at a clinical
anomalies associated with cardiovascular disease,6,7 and it is research unit for several hours. For this reason, other indica-
possible that this syndrome is already affecting children even tors have been developed, and of these it is the homoeostasis
1. Doutor, Centro de Estudos de Saúde e Nutrição Infanto-Juvenil (CESNI), Universidade de Ribeirão Preto (UNAERP), Ribeirão Preto, SP, Brazil.
2. Doutora, CESNI, UNAERP, Ribeirão Preto, SP, Brazil.
3. Livre-docente, CESNI, UNAERP, Ribeirão Preto, SP, Brazil.
4. Doutora. Professora assistente, CESNI, UNAERP, Ribeirão Preto, SP, Brazil.
5. Doutor. Professor assistente, CESNI, UNAERP, Ribeirão Preto, SP, Brazil.
Financial support: Universidade de Ribeirão Preto (UNAERP), Ribeirão Preto, SP, Brazil.
No conflicts of interest declared concerning the publication of this article.
Suggested citation: de Almeida CA, Pinho AP, Ricco RG, Pepato MT, Brunetti IL. Determination of glycemia and insulinemia and the homeostasis model
assessment (HOMA) in schoolchildren and adolescents with normal body mass index. J Pediatr (Rio J). 2008;84(2):136-140.
Manuscript received Nov 14 2007, accepted for publication Jan 03 2008.

doi:10.2223/JPED.1767
136
Glycemia, insulinemia and HOMA in children – de Almeida CA et al. Jornal de Pediatria - Vol. 84, No. 2, 2008 137
model assessment (HOMA) that has attracted the most atten- Initially, all 1200 students enrolled at these schools were
tion since it only requires fasting glycemia and insulinemia considered for inclusion on the study, before the following
8
samples. The model is an attempt to demonstrate the rela- exclusion criteria were applied: body mass index below the
tionship between pancreatic insulin production capacity and fifth or above the 85th percentiles (n = 187); refusal to par-
the ability to maintain adequate glycemic levels. Within the ticipate (n = 218); failure to provide a consent form signed by
pediatric age group, however, HOMA provides less informa- parents or guardians (n = 306); puberty stage incompatible
tion because, during this phase, hyperglycemia rarely occurs. with age (n = 22); any active disease whatsoever under treat-
This being so, it appears that nowadays there is consensus ment (n = 18); or any condition that precluded anthropom-
that fasting insulinemia is a reliable parameter and adequate etry, such as prosthesis, plaster, physical disability, etc. (n =
for assessing PIR in children; however, the ideal cutoff points 2). This process resulted in the final sample size of 447
are not yet known.9-11 participants.
There are two relevant questions that have made it diffi- With the objective of evaluating the hypothesis that the
cult to define ideal insulinemia values: the first is related to values studied would vary according to age and sex and, at
the need to establish an adequate correlation between cutoff the same time, to guarantee an adequate number of individu-
points and associated risk, which will only be achieved by als in each group, it was decided to divide the 447 partici-
means of long-term studies.12 The second question is related pants in the following manner: boys and girls were separated
to the knowledge, still being consolidated, that fasting and subdivided into five age bands. Each of these age groups
insulinemia values vary significantly during childhood and covered a range of 2 years, with the exception of the oldest
adolescence, even under normal conditions.13 Therefore, fast- (15 to 17.9 years), where the interval was 3 years. These cri-
ing insulinemia itself and HOMA models, which depend on this teria made it possible to ensure that all groups contained more
value, become problematic as a result of this variation. than 25 individuals, which was proven to be adequate during
statistical analysis.
This study aimed to assess, within a group of children and
adolescents with normal body mass index (BMI), values for The research project was approved by the Ethics Commit-
glycemia, fasting insulinemia and HOMA index. tee at the Universidade de Ribeirão Preto on 20th October of
2003, as recorded in the minutes of hearing number 94/2003.
Methods
Before biological material was collected, participants and
The study was carried out at two public schools in the dis-
their parents or guardians received verbal explanations of the
trict of Bonfim Paulista, which is located around 6 km from
project and permission to participate was given by means of
the city of Ribeirão Preto (Southeast Brazil) and which is
a free and informed consent form. All of the participants were
administratively subordinate to it. The design was
instructed to fast for 12 hours, and anthropometry and blood
cross-sectional, in that the following data were all collected
sampling were carried out during the morning at the state
at a single point in time, from 447 children and adolescents
schools participating in the study. Weight and height were
with normal BMI and aged 7 to 17.9 years: anthropometric
measured according to World Health Organization recommen-
measurements, personal data and a venous blood sample. In
dations.15 Each subject provided two 4 mL blood samples
order to avoid that data from adolescents who were either
which were sent to the laboratory in tubes within 2 hours, for
maturing early or late could introduce errors, children were
processing and biochemical and hormone assays. Samples
only included if their Tanner puberty stage was normal for their
were transported in refrigerated thermal containers, and the
age.14 Puberty stage was assessed using a selection of dia-
biological material separated in a Bio Eng centrifuge, model
grams representing different stages of maturity from which
BE 4000, for 5 minutes at 3,500 rpm between 1 and 2.5 hours
each subject was requested to choose that which best repre-
after collection (long enough for the blood to have coagu-
sented their own stage of development. In order to avoid
lated). After centrifugation, serum was separated and divided
embarrassment and to guarantee consistency of the data, all
into three 500 µL samples. The biochemical insulin assay was
of these assessments were carried out by a professional of
performed on one of these samples on the same day as col-
the same sex as the interviewee, as part of the anthropom-
lection. Glycemia was assayed by the hexokinase enzymatic
etry procedure. Specifically, a male pediatrician interviewed
method using Cobas Mira Plus automation equipment
the boys and a female general nurse interviewed the girls.
(Roche). Insulinemia was assayed by chemiluminescence,
These two professionals had already been working at these
automated by Immulite apparatus (DPC, Medlab). The HOMA
schools for a long time, providing both education and care,
indices were calculated using the equation proposed by Mat-
which allowed for a relationship of mutual confidence between
teus et al.:16 glycemia (mol/dL) x insulinemia (µUI/mL) / 25.
interviewers and interviewees. In any case in which answers
appeared doubtful, a reevaluation was performed, by one of For analysis, subjects were grouped into subsets by sex
the two professionals mentioned, in the form of a physical and age group and two sets of comparisons were performed:
examination. the Mann-Whitney test was applied to each of the variables
138 Jornal de Pediatria - Vol. 84, No. 2, 2008 Glycemia, insulinemia and HOMA in children – de Almeida CA et al.
Table 1 - Means and standard deviations for fasting glycemia measured in boys and girls, by age group
Fasting glycemia (mg/dL)
Boys Girls
Age n Mean (SD) n Mean (SD) p*
7 to 8.9 years 30 89.40 (7.08) 39 83.72 (5.59) 0.0009
9 to 10.9 years 32 88.00 (6.75) 50 88.22 (6.08) 0.89
11 to 12.9 years 37 88.92 (7.46) 62 88.58 (6.83) 0.85
13 to 14.9 years 58 92.29 (9.46) 66 88.85 (8.96) 0.016
15 to 17.9 years 26 89.69 (8.65) 47 89.77 (6.52) 0.93
p† 0.067 0.0005
SD = standard deviation.
* Mann-Whitney test.
†
Kruskal-Wallis test for simultaneous comparisons between more than two groups.
fasting glycemia, fasting insulinemia and HOMA index to com- 12.9 years (p < 0.01) and between 15 and 17.9 years (p <
pare the boys with the girls in each age group and then the 0.01). Both sexes exhibited significant variation with age (p
Kruskal Wallis test for simultaneous comparisons between < 0.001), with peak levels observed in the 13 to 14.9 years
more than two groups was used to compare the results from subset.
each age group, for boys and girls.
The HOMA indices, given in Table 3, differed between sexes
Results for the age groups 11 to 12.9 years (p < 0.01) and 15 to 17.9
years (p < 0.01). For both boys and girls, HOMA indices exhib-
The results obtained are presented in Tables 1 to 3.
ited significant variation with age (p < 0.001), peaking
The fasting glycemia levels shown in Table 1 only differed between 13 and 14.9 years.
between boys and girls in the age bands 7 to 8.9 years (p <
0.001) and 13 to 14.9 years (p < 0.05); in both cases levels Discussion
were lower among the girls. In terms of progression accord- There is no doubt that the most correct manner of estab-
ing to age, the boys' glycemia levels exhibited no statistically lishing cutoff points for biological variables is to identify val-
significant variation; among the girls there was variation, due, ues which imply an associated risk. However, study designs
in particular, to the youngest age group, since, between 9 and capable of meeting this criterion demand long-term observa-
10.9 years, levels were practically uniform. tion and, often, it proves necessary to rely on cross-sectional
Fasting insulinemia levels, given in Table 2, revealed dif- studies, even if only provisionally, in order to observe the sta-
ferences between boys and girls at two ages: between 11 and tistical variation of those variables. A study published recently
Table 2 - Means and standard deviations for fasting insulinemia measured in boys and girls, by age group
Insulinemia (µUI/mL)
Boys Girls
7 to 8.9 years 30 3.08 (2.42) 39 3.14 (1.78) 0.51
9 to 10.9 years 32 4.21 (2.24) 50 5.49 (3.25) 0.081
11 to 12.9 years 37 4.64 (3.77) 62 6.50 (3.38) 0.0013
13 to 14.9 years 58 6.82 (3.46) 66 7.71 (3.57) 0.11
15 to 17.9 years 26 4.67 (2.80) 47 6.75 (3.19) 0.0015
p† 0.0001 0.0001
SD = standard deviation.
†
Glycemia, insulinemia and HOMA in children – de Almeida CA et al. Jornal de Pediatria - Vol. 84, No. 2, 2008 139
Table 3 - Means and standard deviations for HOMA indices calculated for boys and girls, by age group
HOMA
Boys Girls
7 to 8.9 years 30 0.68 (0.54) 39 0.65 (0.37) 0.91
9 to 10.9 years 32 0.93 (0.52) 50 1.20 (0.71) 0.086
11 to 12.9 years 37 1.03 (0.81) 62 1.44 (0.79) 0.0032
13 to 14.9 years 58 1.57 (0.82) 66 1.72 (0.87) 0.29
15 to 17.9 years 26 1.05 (0.67) 47 1.49 (0.70) 0.0035
p† 0.0001 0.0001
HOMA = homeostasis model assessment; SD = standard deviation.

†
by García Cuartero et al. did just that.17 They proposed a dis- resistance”.4,13,22 This being so, it is imperative that cutoff
tribution of insulin and HOMA values based on a survey of 372 points be defined that respect the biological variation of the
individuals aged between one month and 18 years, observ- indicator. Indeed, if the data obtained in this study are con-
ing, in common with this study, a significant variation in these sidered, summing the mean level with two standard devia-
indicators in relation to age and sex. tions, it will be observed that the maximum value would be
13.7 µUI/mL for boys and 14.8 µUI/mL for girls, both within
This study was carried out using a sample made up exclu- the 13 to 14.9 years age group, while other age groups exhib-
sively of individuals with normal BMI and average maturity ited much lower levels. Therefore, it is highly probable that
for their age and has demonstrated that mean fasting glyce- using 15 µUI/mL as a cutoff point for fasting insulinemia leads
mia levels, almost always considered constant in this age to under diagnosis of hyperinsulinism at ages prior to 13 years
18
group, varied at two of the five ages assessed; and that, for and at ages over 15 years.
the girls, levels were considered dissimilar when the different
age groups were compared simultaneously. If one considers Since HOMA indices are calculated based on glycemia and
the data from this study, summing the mean value to two stan- insulinemia levels, and since glycemia was unchanged in the
dard deviations, it will be observed that the maximum value two age groups, 11 to 12.9 years and 15 to 17.9 years, at
or pertaining would be 111.2 mg/dL for boys and 106.7 mg/dL which HOMA indices were different between sexes, it can be
for girls, both in the 13 to 14.9 years age group, with lower assumed that the variation observed in HOMA indices is due
values in all other groups. It is possible that using the 100 to their different insulinemia levels. In common with what has
mg/dL cutoff point that is currently recommended 19
for all been stated earlier, there is no consensus on cutoff points for
individuals in this group could lead to errors in the identifica- HOMA indices in childhood and adolescence. The figure that
tion of those who are truly hyperglycemic. is most widely stated as a cutoff point for HOMA index is
3.45;17 however, other authors have also suggested values
Internationally accepted cutoff levels for fasting insuline- such as 2.5,23 2.71,24 and 3.8,25 among others. One thing that
mia have not yet been defined. Since the studies published can be observed is that, in this case too, a fixed cutoff point
by Reaven et al.,20 the figure of 15 µUI/mL has been being appears to be highly inadequate, considering a significant
used, even though no studies have been undertaken in the variation between different age groups in at least two of the
pediatric age group designed to validate this cutoff point. five age bands studied. If the results of this study are consid-
Other cutoff points, such as 12, 27 and 30, have also been ered, summing the mean value to 2 standard deviations, it
suggested. 21 Our study has demonstrated that fasting will we observed that the maximum value obtained would be
insulinemia varies very significantly within the age range stud- 3.24 for boys and 3.4 for girls, both in the age group between
ied, to the extent that one could postulate the existence of a 13 and 14.9 years and it will also be observed that values in
curve on which values increase up to around 13 to 15 years, other age groups are much lower. Therefore, it is highly prob-
falling off after that. The shape is similar for both males and able that to use 3.45 as a cutoff point for HOMA indices lead to
females, differing only in terms of absolute values, which are underdiagnosis of PIR at ages lower than 13 and higher than
higher among the girls, in at least two of the age groups stud- 15 years; on the other hand, values in a range between 2.5
ied. Many studies have observed that during puberty events and 2.71 would only be appropriate for boys aged 11 to 12.9
take place that could be described as, “physiological insulin years and girls aged 9 to 10.9 years.
140 Jornal de Pediatria - Vol. 84, No. 2, 2008 Glycemia, insulinemia and HOMA in children – de Almeida CA et al.
This study aimed to assess how glycemia, insulinemia and 14. de Almeida C, Del Ciampo L, Ricco R, Crott G. Crescimento físico.
the HOMA index behave during school age childhood and ado- In: Ricco R, Del Ciampo L, De Almeida C, editores. Puericultura:
princípios e práticas. São Paulo: Atheneu; 2001. p. 9 19.
lescence and the data thus obtained has demonstrated that it
is necessary to take care when using fixed cutoff points for 15. WHO Working Group on Infant Growth. An evaluation of infant
growth: the use and interpretation of anthropometry in infants.
these indicators without taking into account sex or age. Our
Bull World Health Organ. 1995;73:165-74.
conclusions indicate the need to define reference curves for
16. Wallace TM, Matthews DR. The assessment of insulin resistance
these three indicators.
in man. Diabet Med. 2002;19:527-34.
17. García Cuartero B, García Lacalle C, Jiménez Lobo C, González

References Vergaz A, Calvo Rey C, Alcázar Villar MJ, et al. Índice HOMA y
QUICKI, insulina y péptido C en niños sanos. Puntos de corte de
1. Kimm SY, Obarzanek E. Childhood obesity: a new pandemic of
riesgo cardiovascular. An Pediatr (Barc). 2007;66:481-90.
the new millennium. Pediatrics. 2002;110:1003-7.
18. American Diabetes Association. Standards of medical care in
2. Berenson GS, Srinivasan SR, Nicklas TA. Atherosclerosis: a
diabetes-2007. Diabetes Care. 2007;30 Suppl 1:S4-S41.
nutritional disease of childhood. Am J Cardiol. 1998;82:22T-29T.
3. Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd, Tracy RE, 19. Expert Committee on the Diagnosis and Classification of Diabetes
Wattigney WA. Association between multiple cardiovascular risk Mellitus. Report of the Expert Committee on the Diagnosis and
factors and atherosclerosis in children and young adults. The Classification of Diabetes Mellitus. Diabetes Care. 2003;26 Suppl
Bogalusa Heart Study. N Engl J Med. 1998;338:1650-6. 1:S5-S20.
4. Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH. Prevalence 20. Reaven GM, Brand RJ, Chen YD, Mathur AK, Goldfine I. Insulin
of a metabolic syndrome phenotype in adolescents: findings from resistance and insulin secretion are determinants of oral glucose
the third National Health and Nutrition Examination Survey, tolerance in normal individuals. Diabetes. 1993;42:1324-32.
1988-1994. Arch Pediatr Adolesc Med. 2003;157:821-7. 21. Brasil AR. Crianças e adolescentes com sobrepeso ou obesidade:
5. Harrell JS, Jessup A, Greene N. Changing our future: obesity and avaliação da reação inflamatória através da dosagem da proteína
the metabolic syndrome in children and adolescents. J Cardiovasc c-reativa ultra-sensível e prevalência de síndrome metabólica
Nurs. 2006;21:322-30. [dissertação]. Belo Horizonte: Universidade Federal de Minas
Gerais; 2006.
6. Chen W, Berenson GS. Metabolic syndrome: definition and
prevalence in children. J Pediatr (Rio J). 2007;83:1-2. 22. Sinaiko AR, Steinberger J, Moran A, Prineas RJ, Vessby B,
Basu S, et al. Relation of body mass index and insulin resistance
7. Ferreira AP, Oliveira CE, França NM. Metabolic syndrome and risk to cardiovascular risk factors, inflammatory factors, and
factors for cardiovascular disease in obese children: the oxidative stress during adolescence. Circulation. 2005;111:
relationship with insulin resistance (HOMA-IR). J Pediatr (Rio J). 1985-91.
2007;83:21-6.
23. da Silva RC, Miranda WL, Chacra AR, Dib SA. Metabolic syndrome
8. Sinaiko A. Obesity, insulin resistance and the metabolic and insulin resistance in normal glucose tolerant Brazilian
syndrome. J Pediatr (Rio J). 2007;83:3-4. adolescents with family history of type 2 diabetes. Diabetes Care.
9. Sinaiko AR, Gomez-Marin O, Prineas RJ. Relation of fasting 2005;28:716-8.
insulin to blood pressure and lipids in adolescents and parents. 24. DeFronzo RA. Lilly lecture 1987. The triumvirate: beta-cell,
Hypertension. 1997;30:1554-9. muscle, liver. A collusion responsible for NIDDM. Diabetes. 1988;
10. Sinaiko AR, Jacobs DR Jr, Steinberger J, Moran A, Luepker R, 37:667-87.
Rocchini AP, et al. Insulin resistance syndrome in childhood: 25. Barja S, Arteaga A, Acosta AM, Hodgson MI. [Insulin resistance
associations of the euglycemic insulin clamp and fasting insulin and other expressions of metabolic syndrome in obese Chilean
with fatness and other risk factors. J Pediatr. 2001;139:700-7. children]. Rev Med Chil. 2003;131:259-68.
11. Valerio G, Licenziati MR, Iannuzzi A, Franzese A, Siani P,
Riccardi G, et al. Insulin resistance and impaired glucose
tolerance in obese children and adolescents from Southern Italy.
Nutr Metab Cardiovasc Dis. 2006;16:279-84.
12. Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH. Long-term Correspondence:
morbidity and mortality of overweight adolescents. A follow-up Carlos A. N. de Almeida
of the Harvard Growth Study of 1922 to 1935. N Engl J Med. 1992; Av. Portugal, 1620/73
327:1350-5. CEP 14020-380 – Ribeirão Preto, SP - Brazil
Tel.: +55 (16) 3916.3998, +55 (16) 3610.6176,
13. Moran A, Jacobs DR Jr, Steinberger J, Hong CP, Prineas R, +55 (16) 9221.7498
Luepker R, et al. Insulin resistance during puberty: results from Fax: +55 (16) 3610.6176
clamp studies in 357 children. Diabetes. 1999;48:2039-44. E-mail: calno@convex.com.br
0021-7557/07/83-02/181
Jornal de Pediatria
Copyright © 2007 by Sociedade Brasileira de Pediatria
ORIGINAL ARTICLE
Abdominal circumference as an indicator of clinical

and laboratory parameters associated with obesity
in children and adolescents: comparison
between two reference tables
Carlos A. N. de Almeida,1 Adriana P. Pinho,2 Rubens G. Ricco,3 Cecília P. Elias4
Abstract
Objective: To evaluate the sensitivity and specificity of two pediatric abdominal circumference reference tables to
detect abnormally high body mass index, total cholesterol, fasting blood insulin and leptin levels, and homeostasis
model assessment values.
Methods: A total of 624 male and female subjects, with ages ranging from 7 to 18 years, were evaluated. All
children were recruited from two public schools. Venous blood samples were collected for determination of fasting
plasma insulin, glucose, leptin, and total cholesterol levels. Weight, height and abdominal circumference were
assessed according to internationally accepted guidelines. Contingency tables were constructed, comparing the
presence or absence of increased abdominal circumference, according to cutoff points established by Taylor et al. and
Freedman et al., with the presence or absence of abnormal values in the laboratory tests.
Results: Sensitivity values were consistently higher for the table by Taylor et al., whereas the table by Freedman
et al. showed greater specificity. Positive predictive values were quite low in general, and were only relevant for body
mass index.
Conclusions: Results indicate that the table by Taylor et al. is best for screening purposes, as it identifies
individuals at higher risk of presenting abnormal test results. On the other hand, the reference table by Freedman et al.
is more suitable for clinical practice, as it could be used to replace laboratory measurements, such as blood insulin or
leptin levels, which may not be available at all sites.
J Pediatr (Rio J). 2007;83(2):181-185: Abdominal circumference, obesity, adolescent, dyslipidemias, insulin resistance,
leptin.
Introduction concern about the consequences of obesity during

childhood.2 Recent studies have demonstrated that problems
Child and adolescent obesity has reached epidemic
proportions worldwide.1 While in recent years the main such as atherosclerotic plaques, glucose intolerance,
concern associated with obesity in children has been the high non-insulin dependent diabetes mellitus, dyslipidemia,
risk of obesity during adulthood, there is currently growing hypertension, hyperleptinemia, among others, are also
1. Doutor. Universidade de Ribeirão Preto, Ribeirão Preto, SP, Brasil.

2. Doutora. Universidade de Ribeirão Preto, Ribeirão Preto, SP, Brasil.
3. Livre-docente. Universidade de Ribeirão Preto, Ribeirão Preto, SP, Brasil.
4. Interna em Medicina, Universidade de Ribeirão Preto, Ribeirão Preto, SP, Brasil.
Manuscript received Aug 30 2006, accepted for publication Nov 29 2006.

Suggested citation: de Almeida CA, Pinho AP, Ricco RG, Elias CP. Abdominal circumference as an indicator of clinical and laboratory parameters associated
with obesity in children and adolescents: comparison between two reference tables. J Pediatr (Rio J). 2007;83(2):181-185.
Financial support: Universidade de Ribeirão Preto, Ribeirão Preto, SP, Brazil.
doi 10.2223/JPED.1604
181
182 Jornal de Pediatria - Vol. 83, No. 2, 2007 Abdominal circumference and obesity – de Almeida CA et al.
present in children and adolescents, especially in those who such as use of prosthesis, cast, physical handicap, etc. (12).
are obese.3 Such information, however, is often disregarded The research was approved by the Research Ethics
in pediatric nutrition practice, especially because of the Committee of the Universidade de Ribeirão Preto, on October
difficulties associated with access to laboratory tests, which 20th, 2003, as described in the memorandum ComÉt/
are frequently expensive or even unavailable, and also no. 94/2003.
because of the lack of adequate international standards for
Prior to collecting biological material, participants and
establishing syndromic diagnosis, such as metabolic
their legal guardians were informed about the project, both
syndrome.4
orally and through an informed consent, by which permission
In adults, the measurement of abdominal circumference was granted for collecting blood samples. All participants
is accepted as an important tool for assessing the risk of were instructed to follow a 12-hour fasting; blood samples
underlying pathologic conditions, especially atherosclero- were taken in the morning, at the participating schools. Two 4
5
sis. For children and adolescents, however, the scarcity of mL tubes of blood, without additives, were collected; samples
long-term prospective studies does not allow the simple were taken to the laboratory within 2 hours, for processing
extrapolation of these findings.6 In addition, the fact that this and biochemical and hormonal analyses. Transportation was
measurement presents some degree of variation, due to made in insulated boxes. The biological material was
physical growth, demands that cutoff points, when existing, centrifuged in a Bio Eng BE 4000 centrifuge for 5 min at 3,500
be different for each age group.7 Two studies are important in rpm, between 1 and 2 h 30 min after blood collection (to allow
this respect. In 1999, with data from the Bogalusa Heart blood clotting). After centrifugation, the serum was
Study, Freedman et al.8 assessed the relationship between separated and divided into three aliquots of 500 µL.
abdominal circumference and blood insulin and lipid levels in Measurement of insulin was performed in one of the aliquots
2,996 subjects from 5 to 17 years. Considering the risk of on the same day of the collection. Blood glucose was assessed
abnormal blood test results, they produced a reference table enzymatically with the hexokinase method, using the
with cutoff points based on the 90th percentile of the sample automatic analyzer Cobas Mira Plus (Roche). Serum insulin
distribution. In 2000, Taylor et al.9 published a study with 580 levels were determined by chemiluminescence (Immulite,
children and adolescents with ages between 3 and 19 years DPC-Medlab). Leptin values were measured by a sandwich
aimed at validating the abdominal circumference measure- enzyme-linked immunosorbant assay, using an ELISA
ment as an indicator of central adiposity, using the dual Organon reader. Total cholesterol was measured with an
energy X-ray absorptiometry (DEXA) as the gold standard for enzymatic kit (CHOD-PAP), on a Cobas Mira Plus (Roche)
measuring adiposity. The authors developed a reference analyzer. HOMA was calculated using the equation proposed
table with cutoff points for abdominal circumference, defined by Wallace & Matthews10: blood glucose (mol/dL) x blood
as the 80th percentile of the sample. insulin (µUI/mL) / 25. Weight and height were measured
according to the recommendations by Cameron.11
The aim of the present study is to comparatively evaluate
Abdominal circumference was measured at the level of an
the sensitivity and specificity of two reference tables for
imaginary horizontal line at the midway region between the
detecting abnormally high body mass index (BMI), total
lowest rib margin and the iliac crest.12
cholesterol, blood insulin and leptin levels, and homeostasis
model assessment (HOMA) values. To evaluate the predictive value of the abdominal
circumference measurement as an indicator of obesity-
Methods associated metabolic abnormalities, contingency tables were
The study was carried out in two public schools in the constructed. In these, the presence or absence of an
district of Bonfim Paulista, located 6 kilometers from Ribeirão increased abdominal circumference – according to the
Preto (southeast Brazil) and administratively subordinated to criteria established by Taylor et al. and Freedman et al. – was
this city. In a cross sectional design, anthropometric compared against the presence or absence of high values of
measures, personal data and venous blood samples were BMI, total cholesterol, blood insulin and leptin, and HOMA.
taken at a single occasion. A total of 624 children and The cutoff point for fasting blood glucose level was set at 100
adolescents were evaluated, both male and female, with ages mg/dL.13 A high BMI was defined according to the guidelines
ranging from 7 to 18 years (84 to 215,9 months). Initially, all of the National Center for Health Statistics (NCHS) as a BMI
the 1,200 students enrolled at the two schools were above the 85th percentile.14 High total cholesterol was
considered for inclusion in the study. Exclusion criteria were defined as greater than 170 mg/dL, according to the III
the following: refusal to participate in the study (240); Brazilian Guidelines on Dyslipidemias and Guidelines for the
unsigned consent form from parents/guardians (306); Prevention of Atherosclerosis.15 The upper limit of normality
ongoing treatment for any medical condition (18); for blood insulin and leptin and HOMA was calculated based
inadequate conditions for anthropometric measurements, on the mean plus two standard deviations (SD) of the values
Abdominal circumference and obesity – de Almeida CA et al. Jornal de Pediatria - Vol. 83, No. 2, 2007 183
obtained for the 624 participants, grouped in 12 month age False-positive results were consistently low, especially for
groups, as these values present large variation according to the table by Freedman et al., which showed a maximal value
age group. of 8.1. False-positive results for Taylor et al. varied between
5.4 and 20.8. False-negative results were found more
Results frequently when using the values proposed by Freedman et
Cutoff points are presented in Table 1. Using the values al. (range 45.2-88).
proposed in this table, 143 (22.9%) individuals were
Global test coefficient values were similar for both
identified with BMI above the 85th percentile; 167 (26.8%)
reference tables, with slightly higher results for the table by
with high cholesterol levels; 27 (4.3%) with hyperinsuline-
Taylor et al. in regard to BMI, insulin, leptin and HOMA values.
mia; 21 (3.4%) with high HOMA index; and 31 (5.0%) with
hyperleptinemia.
Discussion
Comparative results are shown in Table 2. From the 30 The present study aimed at assessing if the measurement
pairs of results analyzed, sensitivity values were consistently of abdominal circumference, analyzed according to two
higher for the table by Taylor et al.; using this reference table, different reference tables, can indicate the presence of
BMI, insulin, HOMA and leptin values showed high sensitivity clinical and laboratory abnormalities associated with obesity,
(varying between 70.4 and 80.7); the same was not found for which generally require more complex methods. Taking into
total cholesterol, which presented very low sensitivity (24.6). consideration the technical advantages and feasibility of
Specificity values were consistently higher for the abdominal circumference measurement,16,17 this method
reference table by Freedman et al., varying from 91.9 to could constitute an alternative for screening patients at risk.
99.6; the lowest specificity was for total cholesterol. With this goal, as a screening method, higher sensitivity
Specificity results obtained with the values suggested by values are desirable.18 In this sense, the table by Taylor et al.
Taylor et al. were also high (ranging from 79.6 to 94.6), but showed marked superiority, reaching sensitivity levels above
did not surpass the results obtained with the values proposed 70 for all the parameters assessed, with the exception of total
by Freedman et al. cholesterol, for which sensitivity was low with both tables
tested. Accordingly, in other studies, total cholesterol levels
Positive predictive values were generally low, with the
were not associated with abdominal adiposity.6
exception of BMI. Negative predictive values were
consistently high, with slight advantage to the table by An important difference was noted for the sensitivity in
Taylor et al. detecting high BMI (above the 85th percentile). The chance of
Table 1 - Number of participants assessed in each age group and cutoff points used in this study
Cutoff points
Insulin HOMA Leptin
Age
(months) n (624) BMI Total cholesterol Boys Girls Boys Girls Boys Girls
84-119.9 155 P85 170 6.74 7.99 2.38 2.22 31.62 33.09
120-143.9 142 P85 170 14.5 15.06 3.39 3.43 40.87 42.41
144-167.9 155 P85 170 26.89 26.84 4.84 4.89 34.92 45.7
168-191.9 128 P85 170 14.53 16.11 4.28 4.59 33.58 52.43
192-216 44 P85 170 10.7 14.42 2.37 3.21 40.11 59.13
HOMA = homeostasis model assessment; BMI = body mass index.

184 Jornal de Pediatria - Vol. 83, No. 2, 2007 Abdominal circumference and obesity – de Almeida CA et al.
detecting individuals with high BMI among those who actually be more adequate for the individual evaluation of patients
have high BMI using the reference table by Taylor et al. is who present other indexes of peripheral insulin resistance
practically twice that of Freedman et al. Specificity values, on and in whom it is reasonable to suspect hyperleptinemia, as
the other hand, were relatively high for both methods, and well as in the absence of laboratory tests, which are still
therefore they were both capable of correctly identifying expansive and of limited availability.
individuals with BMI below the cutoff point. When observing
Some limitations of the present study must be
the global test coefficient, the reference table by Taylor et al.
recognized. The most important is surely the cutoff points
appears to be more able to identify true results.
used for insulin, HOMA and leptin values, which were based
This study shows that, for detecting peripheral insulin on a statistical calculation (means + 2 SD) and not on
resistance based on abdominal circumference measurement, “associated risk.” This was motivated by the inexistence, until
fasting blood insulin or HOMA values yield similar results. In the present moment, of internationally validated cutoff
both cases, sensitivity levels were considerably higher for the points for these variables. Another limitation refers to the
reference table by Taylor et al., reinforcing its role as a small number of variables investigated, as important
screening method. Specificity values, in this case, were markers – such as LDL-cholesterol, HDL-cholesterol,
different; the reference values suggested by Freedman et al. triglycerides, fibrinogen, polymerase chain reaction, uric
were more specific, and proved to be more effective in acid, blood pressure, etc. – were left out of the study.
identifying individuals without peripheral insulin resistance.
Despite these limitations, some important aspects must
Therefore, the global test coefficient was similar for both
be emphasized, such as the high number of study
references.
participants and the investigation of parameters such as
In terms of sensitivity, the numbers suggested by Taylor blood insulin and leptin levels in the whole sample. Generally,
et al. were markedly superior to those suggested by the study results indicate that the reference table by Taylor et
Freedman et al. for detecting hyperleptinemia, with less al. is best for screening purposes, since it indicates
false-negative results, supporting this reference as an individuals at higher risk of presenting laboratory
appropriate screening tool. The cutoff points suggested by abnormalities. On the other hand, the reference table by
Freedman et al. showed greater specificity, with less Freedman et al. is more adequate for clinical practice, and it
false-positive results; this profile suggests that this table may can replace laboratory test that may be unavailable for
Table 2 - Performance of abdominal circumference measurement according to the cutoff points suggested by Taylor et al. and
Freedman et al. for identifying laboratory abnormalities associated with abdominal adiposity in children and adolescents
BMI Total cholesterol Insulin HOMA Leptin

n = 624 n = 624 n = 624 n = 624 n = 624
Taylor Freedman Taylor Freedman Taylor Freedman Taylor Freedman Taylor Freedman
Sensitivity 76.9 38.5 24.6 12 70.4 48.2 71.4 42.9 80.7 54.8
Specificity 94.6 99.6 79.2 91.9 80.4 92.6 79.9 92 81.3 93.3
PPV 80.9 96.5 30.2 35.1 14 22.8 11 15.8 18.4 29.8
NPV 93.2 84.5 74.2 74.1 98.4 97.5 98.8 97.9 98.8 97.5
False + 5.4 0.4 20.8 8.1 19.6 7.4 20.1 8 18.7 6.8
False - 23.1 61.5 75.4 88 29.6 51.9 28.6 57.1 19.4 45.2
Test coefficient 85.9 74.5 52.0 53.2 69.6 67.0 69.3 63.6 75.5 71.0
BMI = body mass index; HOMA = homeostasis model assessment; NPV = negative predictive value; PPV = positive predictive value.
Abdominal circumference and obesity – de Almeida CA et al. Jornal de Pediatria - Vol. 83, No. 2, 2007 185
physicians at some locations. We suggest that such a 9. Taylor RW, Jones IE, Williams SM, Goulding A. Evaluation of waist
screening procedure, considering the magnitude of the circumference, waist-to-hip ratio, and the conicity index as
screening tools for high trunk fat mass, as measured by dual-
problem of child obesity, be always performed, reinforcing energy X-ray absorptiometry, in children aged 3-19 y. Am J Clin
the abdominal circumference measurement as a compulsory Nutr. 2000;72:490-5.
part of the pediatric examination. 10. Wallace TM, Matthews DR. The assessment of insulin resistance
in man. Diabet Med. 2002;19:527-34.
11. Cameron N. The measurement of human growth. London:
Croom-Helm; 1984.
12. Heyward VH, Stolarczyk LM. Applied body composition
References
assessment. Champaign, IL: Human Kinetics; 1996.
1. Kimm SY, Obarzanek E. Childhood obesity: a new pandemic of 13. Report of the Expert Committee on the Diagnosis and Classifica-
the new millennium. Pediatrics. 2002;110:1003-7. tion of Diabetes Mellitus. Diabetes Care. 1997;20:1183-97.
2. Batch JA, Baur LA. Management and prevention of obesity and 14. Dietz WH, Bellizzi MC. Introduction: the use of body mass index
its complications in children and adolescents. Med J Aust. to assess obesity in children. Am J Clin Nutr. 1999;70:123S-5S.
2005;182:130-5. 15. Santos RD. III Diretrizes brasileiras sobre dislipidemias e diretriz
de prevenção da aterosclerose do Departamento de
3. Iannuzzi A, Licenziati MR, Acampora C, Salvatore V, Auriemma
Aterosclerose da Sociedade Brasileira de Cardiologia. Arq Bras
L, Romano ML. Increased carotid intima-media thickness and
Cardiol. 2001;77:1-48.
stiffness in obese children. Diabetes Care. 2004;27:2506-8.
16. Lean ME, Han TS, Morrison CE. Waist circumference as a
4. Jessup A, Harrell JS. The metabolic syndrome: look for it in measure for indicating need for weight management. BMJ.
children and adolescents, too! Clin Diabetes. 2005;23:26-32. 1995;311:158-61.
17. McCarthy HD, Ellis SM, Cole TJ. Central overweight and obesity
5. Lakka HM, Lakka TA, Tuomilehto J, Salonen JT. Abdominal
in British youth aged 11-16 years: cross sectional surveys of
obesity is associated with increased risk of acute coronary
waist circumference. BMJ. 2003;326:624.
events in men. Eur Heart J. 2002;23:706-13.
18. Beck JR, Schultz EK. The use of relative operating characteristic
6. Maffeis C, Pietrobelli A, Grezzani A, Provera S, Tato L. Waist (ROC) curves in test performance evaluation. Arch Pathol Lab
circumference and cardiovascular risk factors in prepubertal Med. 1986;110:13-20.
children. Obes Res. 2001;9:179-87.
7. Wang J. Standardization of waist circumference reference data.

Correspondence:
Am J Clin Nutr. 2006;83:3-4. Carlos A. N. de Almeida
Av. Portugal, 1620/73
8. Freedman DS, Serdula MK, Srinivasan SR, Berenson GS. Rela- CEP 14020-380 – Ribeirão Preto, SP – Brazil
tion of circumferences and skinfold thicknesses to lipid and Tel.: +55 (16) 3916.3998, +55 (16) 9144.1213
insulin concentrations in children and adolescents: the Bogalusa Fax: +55 (16) 3610.6176
Heart Study. Am J Clin Nutr. 1999;69:308-17. E-mail: calno@convex.com.br
PALESTRAS
7. Ford E, Galuska D, Gillespie C, Will JC, Giles WH, Dietz WH. C-reac- 14. Libby, P. Atherosclerosis: The new view. Sci Am 2002, 286 (5):46-55.
tive protein and body mass in children: Findings from the Third 15. Misra A. Risk factors for atherosclerosis in Young individuals. J
National Health and Nutrition Examination Survey 1988-1994. J Cardiovasc Risk 2000, 7(3):215-29.
Pediatr 2001, 138:486-92.
16. Pellanda LC, Echenique L, Barcellos LMA, Maccari J, Borges FK, Zen
8. Goss F, Robertson R, Willians A, Sward K, Abt K, Ladewig M, Timmer BL. Doença cardíaca isquêmica: a prevenção inicia durante a infância.
J, Dixon C. A comparison of skin folds and leg-to-leg bioelectrical
J Pediatr (Rio J) 2002, 78(2):91-96.
impedance for the assessment of body composition in children. Dyn
Med 2003 26(2): 1-5. 17. Santos WB, Mesquita ET, Vieira RMR, Oley B, Coutinho M, Avezum
A. Proteína C-Reativa e doença cardiovascular. As bases da evidência
9. Iannoti, RJ, Zuckerman AE, Rifai N. Correlations of cardiovascular
Científica. Arq Bras Cardiol 2003, 80(4): 452—56.
disease risk factors between African American siblings. J Pediatr 2000,
136:511-19. 18. Saris WH, Blair SN, van Baak MA, Eaton SB, Davies PS, DiPietro L,
10. Isasi CR, Deckelbaum RJ, Tracy RP, Starc TJ, Berglund L, Shea S. Fogeholm M, Rissanen A, Swinbun B, Tremblay A, Westerterp KR,
Physical Fitness and C- Reactive Protein Level in Children and Young Wyatt H. How much physical activity is enough to prevent unwealthy
Adults: The Columbia University BioMarkers Study. Pediatrics 2003, weight gain: Outcome of the IASO 1st Stock Conference and
111:332-38. Consensus Statement. Obes Rev 2003, 4(2):101-14.
11. Katzmarzyk, PT, Tremblay A, Perusse L, Despres JP, Bouchard C. The 19. Smith JK, Dykes R, Douglas JE, Krishnaswamy G, Berk S. Long-term
utility of the international child and overweight guidelines for predic- exercise and atherogenic activity of blood mononuclear cells in persons at
ting coronary heart diseaserisk factors. J Clin Epidemiol 2003, 56 risk of developing ischemic heart disease. JAMA 1999, 281:1722-27.
(5):456-62. 20. Thomas NE, Baker JS, Davies B. Established and recently identified
12. Kiess W, Galler A, Reich A, Muller G, Kapellen T, Deutscher J, Raile coronary heart disease risk factors in young people and the influence of
K, Clinical aspects. Obesity in childhood and adolescence. Obes Rev physical activity and physical fitness. Sports Med 2003, 33(9):633-50.
2003, 4(2):29-36. 21. Tsolakis C, Vagena S, Dessypris A. Growth and anabolic hormones, leptin
13. Knehans AW. Childhood obesity: Why is this happening to our chil- and neuromuscular performance in moderately trained prepubescent ath-
dren? J Okla State Med Assoc 2003, 95 (8):539-44. letes and untrained boys. J Strength Cond Res 2003, 17(1): 40-46.
CONDUTAS TERAPÊUTICAS NA OBESIDADE INFANTO-JUVENIL

CARLOS A. N. DE ALMEIDA
A obesidade pode ser definida como a situação orgâ- a conscientização de pediatras e nutrólogos para a impor-
nica de excesso de tecido adiposo1 . Essa simplificação, tância de se atender a criança obesa de forma individual,
entretanto, não permite abordar as causas que podem buscando-se as peculiaridades de cada caso e o adequado
levar o ser humano a se tornar obeso, sendo fundamental direcionamento do tratamento.
que se abordem os aspectos etiológicos2 e não apenas clas- O primeiro parâmetro utilizado diz respeito à pre-
sificações como o CID 3 ou divisões entre primária e sença de resistência periférica à insulina (RPI). É
secundária 4 . Fatores importantes devem ser levados em conhecido o fato de que o indivíduo obeso quase sem-
conta, dentre eles a resistência periférica à insulina5 , os pre acaba apresentando algum grau de RPI, indepen-
genes ligados direta ou indiretamente ao aumento do teci- dentemente da causa que o tenha levado a desenvolver
do adiposo6,7 , o melhor entendimento da atuação dos a obesidade12 . A experiência clínica, entretanto, mos-
novos hormônios, especialmente a leptina8 e, principal- tra que os indicadores clínicos e laboratoriais, o prog-
mente, o grande insucesso que tem sido o tratamento tra- nóstico e, principalmente, os resultados do tratamento
dicional da obesidade na infância e adolescência 9 . são quase sempre muito diferentes entre os grupos com
Dessa forma, a proposta aqui apresentada é a de se e sem RPI13, 14 . Deve ficar claro que essa divisão ini-
conduzir o tratamento da obesidade buscando-se seus cial não tem por objetivo estabelecer uma idéia de hie-
aspectos etiológicos, através da classificação de cada caso, rarquia ou de relação causa-consequência, mas apenas
de forma a direcionar as condutas terapêuticas de forma alertar para o fato de que todo o esforço deve ser feito
individualizada. no sentido de investigar se, paralelamente à obesidade,
Hoje parece indiscutível que a obesidade se trata de está se desenvolvendo ou se manifestando também a
um quadro sindrômico, em que a manifestação comum é RPI o que, em caso afirmativo, implicará em aborda-
o acúmulo de tecido gorduroso10, sendo essencial o agru-
pamento dos casos semelhantes11 . A proposta de classi- 1
2
Fisioterapeuta, doutoranda em Pediatria, Faculdade de Medicina, UFMG.
Pediatra, mestranda em Pediatria.
ficação apresentada no presente texto pode ser verificada 3 Nutricionista do projeto
4 Psicóloga do projeto
na figura 1 e tem como objetivo principal contribuir com 5 Professores Departamento de Pediatria FM-UFMG
Rev Med Minas Gerais 2005; 15(2 Supl 3): S160-S233 226
PALESTRAS
gem diferenciada do tratamento. Para efeito de classifi- especial, deve respeitar as características peculiares de
cação, definiu-se como OBESIDADE METABÓLICA cada quadro e suas diferentes formas de apresentação,
aqueles casos em que se observa RPI. Para os outros resultado da interação de cada indivíduo com seu meio
casos, utilizaram-se as terminologias OBESIDADE ambiente. A detecção das informações presentes em
ALIMENTAR (somática e psicossomática), OBESIDA- uma anamnese completa, em um exame clínico minu-
DE INDUZIDA (neurológica, endocrinológica e far-
cioso e em uma avaliação laboratorial bem indicada,
macológica) e OBESIDADE SINDRÔMICA.
permitirá que o diagnóstico, muitas vezes restrito à
Por fim, a classificação apresentada não pretende
demonstração do excesso de peso, seja o mais completo
acrescentar fatos novos ao já extenso, apesar de incom-
pleto, conhecimento sobre a obesidade na infância. possível. Isso levará não apenas ao melhor tratamento
Objetiva apenas organizar os conhecimentos existentes, da obesidade em si, mas também das co-morbidades a
com a finalidade principal de facilitar a tomada de con- ela associadas as quais, freqüentemente, são as respon-
duta, reforçando a regra cada vez mais aceita de que o sáveis pelos maiores desconfortos e pelos maiores riscos
tratamento das doenças em geral, e da obesidade em de vida a que o indivíduo obeso está sujeito.
Sobrepeso e obesidade
(IMC > Percentil 85)
Sem Resistência Insulínica Com Resistência Insulínica
Obesidade Obesidade Obesidade Obesidade

Sindrômica Induzida Alimentar Metabólica
Prader-Willi
Cohen
Down, etc.
Endocrinológica Neurológica Por fármacos Somática Psicossomática
Hipotireoidismo Lesões do SNC: Corticóides Fraco vínculo

Hipercortisolismo Tumores Psicotrópicos, etc. Compesação
Deficiência de GH Hemorragias Compulsão, etc.
Hipoparatireoidismo, Traumas, etc.
etc.
Maus hábitos Sedentarismo

alimentares
227 Rev Med Minas Gerais 2005; 15(2 Supl 3): S160-S233
PALESTRAS
REFERÊNCIAS BIBLIOGRÁFICAS: 08. Wajchenberg BL. Tecido adiposo com glândula endócrina. Arquivos
Brasileiros de Endocrinologia e Metabologia 2001; 45(4): 266-8.
01. Damiani D, Carvalho DP, Oliveira RG. Obesidade. In: Setian N, editor.
Endocrinologia Pediátrica. 2a ed. São Paulo: Sarvier; 2002. p. 567-82. 09. Zlochevsky ERM. Obesidade na infância e adolescência. Rev Paul
Pediatria 1996; 14(3): 124-33.
02. Kopelman PG. Obesity as a medical problem. Nature 2000, 404: 635-43.
10. Klish WJ. Childhood obesity. Pediatr Rev 1998; 19(9): 312-15.
03. OMS CID-10 / Organização Mundial da Saúde; tradução Centro
Colaborador da OMS para a Classificação das Doenças em Português. 11. Fruhbeck G. Childhood obesity: time for action, not complacency:
6ª. ed. São Paulo: Editora da Universidade de São Paulo; 1998. definitions are unclear, but effective interventions exist. BMJ 2000,
04. Martinelli Jr CA, Sales DS. Obesidade. In: Ricco RG, Del Ciampo LA, 320: 328-329.
de Almeida CAN, editores. Puericultura Princípios e Práticas, Atenção 12. Jeffery ARGN, Voss LMA, Metcalf B, Wilkin T. Causes of insulin resis-
Integral à Saúde da Criança. 1 ed. Rio de Janeiro: Atheneu; 2000. p. tence in childhood. Nurs Stand 2002; 16(35): 33-7.
99-106. 13. Islam AH, Yamashita S, Kotani K, Nakamura T, Tokunaga K, Arai T, et
05. Arslanian S, Suprasongsin C. Insulin sensitivity, lipids and body com- al. Fasting plasma insulin level is an important risk factor for the deve-
position in childhood: is “syndrome X” present? J Clin Endocrinol lopment of complications in Japanise obese children – results from a
Metab 1996; 81(3): 1058-62. cross-sectional and a longitudinal study. Metabolism 1995, 44: 478-85.
06. Barsh G, Farooqi IS, O’Rahilly S. Genetics of body-weight regulation. 14. Jiang X, Srinivasan SR, Webber LS, Wattigney WA, Berenson GS.
Nature 2000; 404 (6778): 644-51. Association of fasting insulin level with serum lipid and lipoprotein
07. Shuldiner AR, Munir KM. Genetics of obesity: more complicated than levels in children, adolescents and young adults: the Bogalusa Heart
initially thought. Lipids 2003, 38: 97-101. Study. Arch Intern Me 1995, 155: 190-6.
ADESÃO AO TRATAMENTO DE OBESIDADE

MÁRCIA ROCHA PARIZZI*
A obesidade é um distúrbio nutricional de difícil trado na boca amplia as sensações bucais que determinam o
tamento, decorrente de múltiplas causas e responsável por paladar, tornando possível a sensação da saciedade (FON-
uma série de graves repercussões biológicas e psicossociais SECA, SILVA, FELIX, 2001).
(WHO, 1997). A baixa adesão e o abandono precoce ao A sociedade globalizada, cujo crescimento econômico
tratamento, freqüentemente observados nos serviços de depende do aumento da produção e da criação constante
atendimento ao obeso certamente contribuem para a de novos produtos, enfatiza o consumo, a pressa, a rapi-
manutenção da prevalência elevada da obesidade. A com- dez e a eficiência, características incompatíveis com o
preensão ampliada desse fenômeno, para adoção de medi- saborear detalhado (FONSECA, PEREIRA, 1997; FON-
das que possam minimizá-lo, é fundamental para redução SECA, SILVA, FELIX, 2001, FONSECA et al., 2001). O
desse grave problema médico-social. homem moderno, muito ocupado, desenvolve o hábito
Na literatura, a adesão ao tratamento de obesidade da de comer de forma apressada, diminuindo a capacidade
criança e do adolescente é considerada um fenômeno de degustar e de saciar-se. Por outro lado, consome com
complexo, determinado pelas interações de diversos fato- exagero os alimentos prontos e industrializados, ofereci-
res como: aspectos sócio-econômicos, aspectos psíquicos dos insistentemente pela mídia, que impõe novas modali-
e culturais do paciente e sua família, os fundamentos da dades na maneira de comer e do que comer: nota-se cada
abordagem terapêutica e a qualidade da interação com o vez mais uma expansão do consumo de alimentos com
profissional. Nesta seção, apresentamos uma breve discus- grandes densidades energéticas, ricos em gordura e em
são sobre esses fatores. açúcar refinado simples, e uma diminuição no consumo
de carboidratos complexos e de fibras alimentares (-
ASPECTOS SOCIOECONÔMICOS QUE TONIAL, 2001; PARIZZI, TASSARA, 2001; GARCIA,
INFLUENCIAM A ADESÃO
2003). As indústrias alimentícias, amparadas pela mídia,
Os fatores socioeconômicos, característicos da socie- definem não só a qualidade, mas também a quantidade de
dade contemporânea, exercem grande influência na con- alimento ingerido (KUMANYIKA, 2001).
duta alimentar, no apetite e, principalmente, na sacieda- Assim, as crianças e suas famílias inseridas neste con-
de do indivíduo. A capacidade de saciar-se está direta- texto sofrem a influência de duas forças antagônicas: por
mente relacionada com a maneira como a pessoa se ali- um lado a exigência do emagrecimento, por outro, os estí-
menta e saboreia o alimento; relaciona-se, portanto, com
o grau de atenção dedicado ao ato de comer. O hábito de *Médica pediatra da Prefeitura Municipal de Belo Horizonte
Mestre em pediatria pela Faculdade de Medicina da UFMG
saborear detalhadamente cada porção de alimento coloca- Membro do Comitê de Nutrição da Sociedade Mineira de Pediatria
Rev Med Minas Gerais 2005; 15(2 Supl 3): S160-S233 228
Artigo Original
leptineMia de jejuM eM CRianças e adOlesCentes eutRófiCOs

CaRlOs albeRtO nOgueiRa de alMeida1*, adRiana pelegRinO pinhO RaMOs2, iguateMy lOuRençO bRunetti3, MaRia teResa pepatO4, Rubens gaRCia RiCCO5
Trabalho realizado no Centro de Estudos em Saúde e Nutrição Infanto-Juvenil (CESNI) da Universidade de Ribeirão Preto, S. Paulo, SP
Resumo
ObjetivO. Determinar, em um grupo de crianças e adolescentes eutróficos, os valores de leptinemia
de jejum e sua correlação com idade e Índice de Massa Corporal (IMC).
MétOdOs. Estudo de corte transversal realizado em duas escolas públicas de Ribeirão Preto, Brasil.
Foram obtidos medidas antropométricas e amostra de sangue venoso em jejum para dosagem da
leptinemia de 448 crianças e adolescentes eutróficos, maturadores médios, de ambos os sexos, com
idades entre 7 e 17,9 anos. Utilizando-se o teste de Mann-Whitney foram realizadas comparações entre
as concentrações obtidas para meninos e meninas em cada faixa etária. Posteriormente, utilizando-
se o teste de Kruskal-Wallis, foram comparados os valores em cada faixa etária e, por meio do teste
de correlação de Spearman, foi avaliada a correlação entre a leptinemia de jejum e a idade e entre
leptinemia de jejum e o escore z do IMC.
ResultadOs. O valores de leptinemia de jejum diferiram entre meninos e meninas em todas as faixas
etárias sendo sempre mais elevados para as meninas. Entre os meninos, os valores de leptinemia não
apresentam variação estatisticamente significativa; entre as meninas, observou-se variabilidade, com
aumento progressivo de acordo com a faixa etária. O estudo de correlação, mostrou que a leptinemia
apresenta correlação positiva com o escore z do índice de massa corporal em ambos os sexos. Em
relação à idade, observou-se correlação apenas entre as meninas.
COnClusãO. Os dados apontam para a necessidade do estabelecimento de curvas de referência para
*Correspondência:
a leptinemia de jejum que levem em conta o sexo, a idade e o IMC.
Avenida Portugal, nº 1620
- Apto. 73
CEP: 14020-380 Unitermos: Leptina. Índice de Massa Corporal. Tecido adiposo. Criança. Adolescente. Valores de
Ribeirão Preto - SP referência.
intROduçãO central que o percentual mínimo de gordura foi atingido e que a

puberdade pode começar7.
A leptina é um hormônio codificado pelo gene ob presente Níveis plasmáticos elevados de leptina estão associados a
nos adipócitos que, por meio de sinalização ao sistema nervoso diversos fatores relacionados à síndrome metabólica8 como:
central, reduz o consumo cumulativo de alimentos por meio da o IMC, a insulinemia de jejum, a sensibilidade à insulina, a
supressão do apetite, promovendo a utilização das reservas de trigliceridemia, a pressão arterial e a circunferência abdominal9.
gordura1 e controlando a homeostase energética2. Exerce efeitos Dessa forma, acredita-se que a resistência à leptina também
em vários órgãos, nos sistemas reprodutor, renal e cardiovas- possa ser um componente importante da síndrome metabólica10
cular e apresenta, ainda, um papel metabólico, pois estimula e um provável marcador de risco de doença coronariana11. Na
a gliconeogênese e inibe a glicogenólise3,4, além de facilitar o infância, o aumento nos níveis de leptina é característica comum
consumo de glicose e de melhorar a sensibilidade à insulina(4). da obesidade.12.
Dentro do processo de maturação que caracteriza a adoles- Independentemente da composição corporal inicial, valores
cência, tem sido evidenciado que a leptina apresenta importante aumentados de leptina predispõe ao aumento progressivo do
papel como sinalizadora do momento de início da puberdade5 IMC e da porcentagem de gordura em crianças13. Entretanto,
cujo mecanismo seria, pelo menos entre as meninas, de origem uma das maiores dificuldades, tanto para estudos científicos
evolutiva, uma vez que se espera um percentual mínimo de quanto para a clínica médica, é encontrar os adequados pontos
gordura para que se possa assegurar uma gestação futura6. de corte para a avaliação da leptinemia. No sentido de contri-
Dessa forma, a sinalização da massa adiposa efetuada pela buir com essa questão, o presente estudo procurou avaliar, em
leptina teria, também, a função de informar ao sistema nervoso um grupo de crianças e adolescentes eutróficos, os valores das
1. Professor titular do Curso de Medicina da Universidade de Ribeirão Preto e Coordenador do CESNI, Ribeirão Preto, SP
2. Coordenadora do Laboratório de Análises Clínicas da Universidade de Ribeirão Preto, Ribeirão Preto, SP
3. Professor assistente doutor - Diretor da Faculdade de Ciências Farmacêuticas de Araraquara – UNESP, Araraquara, SP
4. Professora da Faculdade de Ciências Farmacêuticas de Araraquara – UNESP, Araraquara, SP
5. Professor associado da Faculdade de Medicina de Ribeirão Preto da USP, Ribeirão Preto, SP
Rev Assoc Med Bras 2009; 55(4): 463-7 463

AlmeidA CAn et Al.
concentrações de leptinemia de jejum e sua correlação com o e meia após a coleta (tempo suficiente para a coagulação do
sexo, a idade e o IMC. sangue). Após a centrifugação, o soro foi separado e foi realizado
ensaio imunoenzimático tipo sanduíche com resultado em leitora
MétOdOs de ELISA Organon para dosagem da leptinemia.
O estudo foi realizado nas duas únicas escolas públicas do Com finalidade de avaliar a hipótese da existência de variação
distrito de Bonfim Paulista, localizado a cerca de seis quilôme- nos valores do indicador estudado de acordo com a idade e o
tros de Ribeirão Preto (sudeste do Brasil) e administrativamente gênero e, ao mesmo tempo, garantir um número adequado de
subordinado a essa cidade. Foi desenhado como um estudo indivíduos em cada grupo, optou-se por dividir os 448 partici-
de corte transversal em que, em um mesmo momento, foram pantes da seguinte maneira: meninos e meninas e cinco faixas
obtidas medidas antropométricas e colhidas amostras de sangue de idade. Todas as faixas etárias obedeceram a intervalo de dois
venoso de 448 crianças e adolescentes eutróficos, de ambos os anos, à exceção da última (15 a 17,9 anos) que teve intervalo de
sexos, com idades entre 7 e 17,9 anos. Para se evitar que dados três anos. Com esses critérios, foi possível estudar grupos sempre
provenientes de adolescentes com maturação tardia ou precoce superiores a 25 indivíduos, o que se mostrou adequado durante a
pudessem produzir erros na avaliação, foram considerados para análise estatística. Utilizando-se o teste de Mann-Whitney foram
o estudo somente aqueles que se encontravam dentro do estadia- realizadas comparações entre os valores obtidos para meninos
mento esperado para sua idade, segundo critérios de Tanner14. e meninas em cada faixa etária. Posteriormente, utilizando-se o
O estadiamento puberal foi avaliado utilizando-se figuras teste de Kruskal-Wallis, foram comparados os valores em cada
representativas dos diferentes estágios, sendo solicitado ao faixa etária para meninos e meninas. Também foi avaliada, pelo
participante que apontasse as figuras que melhor refletissem teste de correlação de Spearman, a correlação entre o indicador
seu desenvolvimento. Para evitar constrangimento e garantir leptinemia de jejum e a idade e entre leptinemia de jejum e o
a consistência dos dados, essa avaliação foi sempre realizada escore z do IMC, separadamente para meninas e meninos.
por profissional do mesmo sexo que o entrevistado durante o O trabalho foi aprovado pelo comitê de ética da Universidade
procedimento de antropometria, sendo um médico pediatra para de Ribeirão Preto em 20 de outubro de 2003, conforme consta
os meninos e uma enfermeira padrão para as meninas. Esses no parecer do memorando ComÉt/n º 94/2003.
dois profissionais já atuavam nas escolas há bastante tempo, em
atividade docente-assistencial, o que permitia uma relação de ResultadOs
confiança mútua entre entrevistadores e entrevistados. Em todos Os resultados obtidos estão apresentados nas Tabelas 1 e 2.
os casos em que restou dúvida quanto à resposta, foi feita reava- O valores de leptinemia de jejum diferem entre meninos
liação, por um dos dois profissionais citados, por meio de exame e meninas em todas as faixas etárias estudadas e os valores
físico. A opção pela autoavaliação do estadiamento puberal foi crescentes das diferenças entre as médias apontam para um
feita devido à dificuldade de se realizar exame clínico de genitais incremento dessa diferença com o passar da idade. Observa-
em um ambiente escolar, o que poderia provocar menor adesão se, também, que as concentrações de leptina são sempre mais
dos adolescentes ao estudo. Sendo assim, inicialmente todos os elevadas para as meninas.
1200 estudantes matriculados nas escolas foram considerados Em relação à evolução por faixa etária, nos meninos, os
para a inclusão no estudo, tendo-se como critério de exclusão valores de leptinemia não apresentam variação estatisticamente
aqueles que: apresentavam percentil de IMC abaixo de 5 ou significativa; contudo, nas meninas, aparece variabilidade com
acima de 85 (n=187), não concordaram em participar (n=218), aumento progressivo de acordo com a faixa etária.
não apresentaram o termo de consentimento assinado pelos O estudo de correlação mostrou que a leptinemia apresenta
responsáveis (n=305), apresentavam estadiamento puberal correlação positiva com o escore z do IMC em ambos os sexos,
incompatível com a idade (n=22), apresentavam qualquer
podendo ser considerada fraca entre meninos e moderada entre
doença ativa em tratamento (n=18) ou apresentavam condições
meninas. Em relação à idade, não se observou correlação entre
inadequadas para antropometria como uso de próteses, gesso,
meninos, mas, entre as meninas, a correlação mostrou-se posi-
deficiências físicas, etc (n=2), chegando-se ao número final de
tiva e de moderada intensidade.
448 participantes.
Antes da coleta de materiais biológicos, os participantes
e seus responsáveis foram esclarecidos a respeito do projeto
disCussãO
verbalmente e por meio do termo de consentimento livre e escla- Apesar de ser atualmente reconhecido o fato de que indiví-
recido, tendo-se obtido autorização para a participação. Todos duos obesos apresentem valores elevados de leptina circulante,
foram orientados a fazer jejum de 12 horas, realizando-se antro- tem crescido o interesse científico para se conhecer como esse
pometria e coleta de sangue pela manhã nas escolas estaduais hormônio se comporta entre os eutróficos. Isso se deve ao fato
participantes do estudo. As aferições de peso e estatura seguiram de que, aparentemente, valores elevados determinam maior risco
as recomendações da Organização Mundial de Saúde15. De de resistência insulínica16 e obesidade futura13,17,18, o que pode
cada sujeito, foram coletados 4 mL de sangue em frasco sem ser clinicamente bastante útil sob o aspecto preventivo, espe-
aditivo e encaminhado em até duas horas ao laboratório para o cialmente em famílias geneticamente predispostas à obesidade.
processamento da amostra e a realização da análise hormonal. Wallace et al. demonstraram, em extenso estudo prospectivo,
O transporte foi realizado em caixas térmicas refrigeradas e o que a leptinemia é um fator de risco independente para doença
material biológico separado em centrífuga Bio Eng modelo BE coronariana19, o que tem sido confirmado em outros estudos
4000 por cinco minutos a 3.500 rpm entre uma e duas horas recentes11,20. Mesmo entre crianças e adolescentes obesos tem
464 Rev Assoc Med Bras 2009; 55(4): 463-7

leptinemiA de jejUm em CriAnçAs e AdolesCentes eUtrófiCos
Tabela 1 - Média e desvio padrão dos valores de leptinemia de jejum de meninos e meninas eutróficos de acordo com a faixa etária
leptinemia de jejum (ng/dL)
meninas meninos p**
Idade n média (dp) n média (dp)
7 a 8,9 anos 38 3,67 (2,61) 30 2,53 (2,66) 0,0347
9 a 10,9 anos 50 9,26 (8,17) 32 3,94 (3,61) 0,0003
11 a 12,9 anos 60 11,23 (7,62) 37 3,84 (5,63) < 0,0001
13 a 14,9 anos 69 16,41 (11,88) 58 4,04 (6,59) < 0,0001
15 a 17,9 anos 48 20,39 (10,46) 26 2,97 (4,50) < 0,0001
p* < 0,0001 0,4724
* Teste de Kruskal-Wallis para comparação simultânea de mais de dois grupos
** Teste de Mann-Whitney
Tabela 2 - Correlação entre leptinemia de jejum e idade e leptinemia de jejum e escore z de IMC entre meninos e meninas eutróficos
IDADe esCoRe Z De ImC
meninas meninos meninas meninos
n 265 183 265 183
r* 0,600 0,014 0,476 0,393
Intervalo de confiança de 95% 0,51 a 0,67 -0,14 a 0,16 0,37 a 0,57 0,26 a 0,51
p bicaudal < 0,0001 0,8476 < 0,0001 < 0,0001
* Coeficiente de correlação de Spearman
sido demonstrado que nem todos apresentam-se hiperleptinê- estudos também demonstram essa tendência7;21. No presente
micos e, entre aqueles que o são, é comum a associação com estudo, de fato os dados mostram tendência semelhante, com
outros fatores de risco, como hiperinsulinismo, dislipidemia e valores de leptina entre meninos apresentando valores máximos
hipertensão arterial10. na faixa entre 13 e 14,9 anos, caindo em seguida, mas essa
Para se estabelecer intervalos de referência para parâmetros dinâmica não se mostrou estatisticamente significativa. Por outro
biológicos, é fundamental que a investigação seja realizada lado, Brandão et al.22, avaliando 175 adolescentes saudáveis,
obtendo-se valores que impliquem em risco associado. Entre- com idades entre 10 e 18 anos e não obesos, verificaram corre-
tanto, o desenho de estudos para cumprir esse quesito exige lação negativa entre idade e leptinemia entre os meninos. Essas
longo tempo de observação e, frequentemente, é preciso recorrer, diferenças entre os estudos refletem basicamente a ausência de
mesmo que provisoriamente, a estudos de corte transversal para padronização metodológica, o que leva a resultados distintos já
se observar a variação estatística desse parâmetro. O presente que a leptinemia sofre influência marcante de indicadores como
estudo buscou descrever, por meio de avaliação transversal com estadiamento puberal, porcentagem de gordura corporal, entre
crianças e adolescentes eutróficos de diferentes faixas etárias, outros, o que dificulta a comparação entre os estudos. Deve-se
o comportamento da leptinemia de jejum. Pôde-se observar, enfatizar que, no presente estudo, observou-se dispersão acen-
primeiramente, que existe diferença entre os sexos, de modo tuada nos valores de leptinemia, com desvio padrão próximo,
que uma eventual curva de referência deverá, necessariamente, ou até superior a média em algumas faixas etárias. Também
ser sexo-específica. Essa diferença para leptinemia também têm é fato que, mesmo que a finalidade tenha sido de descrever o
sido descrita em outros estudos: Poveda et al.21, em estudo que comportamento da leptinemia em um grupo com características
avaliou transversalmente 545 crianças colombianas de 5 a 15 tão próximas quanto possível da normalidade, tendo-se incluído
anos e Garcia-Mayor et al.7, avaliando 789 crianças espanholas apenas indivíduos saudáveis, eutróficos e maturadores médios,
na mesma faixa etária, verificaram que havia diferença entre os mesmo entre os maturadores médios é possível que existam
sexos e, de modo semelhante ao presente estudo, que as meninas diferenças entre o estadiamento puberal que a avaliação por faixa
apresentavam valores mais elevados. etária possa ter escondido. Por esse motivo, novos estudos podem
Também se verificou que, entre os meninos, a leptinemia não ser necessários para avaliar a correlação entre a leptinemia e o
apresentou variação significativa com as diferentes faixas etárias, estadiamento puberal.
ao contrário das meninas em que os valores tendem a crescer. Outro aspecto verificado diz respeito à correlação positiva
Esse resultado difere ligeiramente em relação a outros estudos observada, ainda que fraca, para ambos os sexos, entre a
no que diz respeito aos meninos. Em estudo longitudinal, que leptinemia e o escore z de IMC, mesmo considerando-se que o
acompanhou 40 crianças dos 8 aos 16 anos, Ahmed et al.18 grupo estudado era de indivíduos eutróficos. Isso significa que,
verificaram que a leptinemia aumentava com a idade entre as para crianças e adolescentes, mesmo antes de atingir valores
meninas, mas, entre os meninos, aumentava até o início da puber- indicativos de sobrepeso, apresentar maior massa corporal
dade e, após esse período, passava a apresentar redução. Outros implica em, também, apresentar concentrações mais elevadas

AlmeidA CAn et Al.
de leptina plasmática. Essa observação deve ser levada em girls in each age group. Subsequently, using the Kruskal-Wallis
conta para o estabelecimento de curvas de referência, já que é test, values were compared in each age group and, using the
bastante provável que, fisiologicamente, sejam esperados valores Spearman correlation test, the correlations between fasting
maiores de leptinemia em indivíduos mais pesados, sem que leptinemia and age and between fasting leptinemia and the
isso represente qualquer problema. Por outro lado, o presente z-scores of body mass index were assessed.
estudo apresenta a limitação de não ter avaliado a composição Results. Fasting leptinemia values differed between boys and
corporal dos sujeitos envolvidos, o que pemitiria correlacionar a girls in all age groups and it was higher for girls. Among boys, the
leptinemia diretamente com a adiposidade. values of leptinemia did not show statistically significant varia-
Outros estudos que avaliaram a correlação entre IMC e tion; among girls, there was variability, with gradual increase
leptinemia, independentemente da inclusão7 ou exclusão 22 de according to age group. The correlation study showed positive
indivíduos obesos na análise, também demonstraram correlação correlation between leptinemia and z-scores of body mass index
positiva entre esses indicadores. Esse resultado corrobora com o in both genders and between leptinemia and age only for girls.
modelo da leptina, um dos principais sinalizadores para o início cOnclusiOn. The data show the necessity of establishing
da puberdade5. De fato, a observação clínica tem demonstrado reference curves for fasting leptinemia taking into account
de forma inequívoca que crianças obesas tendem a iniciar gender age and body mass index. [Rev Assoc Med Bras 2009;
mais precocemente a puberdade6, mas pouco tem se estudado 55(4): 463-7]
essa correlação entre as eutróficas. No presente estudo, foram
envolvidas apenas as maturadoras médias, ou seja, aquelas em Key words: Leptin. Body Mass Index. Adipose tissue. Child.
que os eventos puberais estavam compatíveis com o esperado Adolescent. Reference values.
para as diferentes faixas de idade cronológica. Mesmo assim, a
leptinemia não se apresentou constante, o que pode coadunar RefeRênCias
com a grande variabilidade biológica, em relação ao início e à 1. Halaas JL, Friedman JM. Leptin and its receptor. J Endocrinol.
1997;155(2):215-6.
duração da puberdade, já exaustivamente descrita entre os indi- 2. Gao Q, Horvath TL. Cross-talk between estrogen and leptin signaling in the
víduos normais, indicando que a massa corporal deva contribuir hypothalamus. Am J Physiol Endocrinol Metab. 2008;294(5):E817-E26.
com essa variabilidade. 3. Friedman JM. The function of leptin in nutrition, weight, and physiology. Nutr
Rev. 2002;60(10 Pt 2):S1-14.
Os dados do presente estudo apontam para a necessidade da 4. Havel PJ. Role of adipose tissue in body-weight regulation: mecha-
construção de curvas de referência para a leptinemia de jejum nisms regulating leptin production and energy balance. Proc Nutr Soc.
2000;59(3):359-71.
que respeitem, pelo menos, para os meninos, o IMC e, para as 5. Clayton PE, Trueman JA. Leptin and puberty. Arch Dis Child. 2000;83(1):1-4.
meninas, o IMC e a faixa etária. A evolução do conhecimento 6. Kaplowitz PB. Link between body fat and the timing of puberty. Pediatric.
sobre a leptina tem demosntrado, cada vez mais, a impor- 2008;121(Suppl 3):S208-S17.
7. Garcia-Mayor RV, Andrade MA, Rios M, Lage M, Dieguez C, Casanueva FF.
tância de se classificar os indivíduos como portadores ou não Serum leptin levels in normal children: relationship to age, gender, body mass
de hiperleptinemia. Por outro lado, a variação apresentada na index, pituitary-gonadal hormones, and pubertal stage. J Clin Endocrinol
Metab. 1997;82(9):2849-55.
concentração desse hormônio em relação a variáveis estudadas 8. Haffner SM, Mykkanen L, Rainwater DL, Karhapaa P, Laakso M. Is leptin
nesse e em outros estudos, como sexo, idade, estadiamento concentration associated with the insulin resistance syndrome in nondiabetic
puberal, adiposidade, etc, faz com que essa definição passe, men? Obes Res. 1999;7(2):164-9.
9. De Almeida CA, Pinho AP, Ricco RG, Elias CP. Abdominal circumference as
necessariamente, na faixa etária pediátrica, pela avaliação por an indicator of clinical and laboratory parameters associated with obesity in
meio de curvas que representem as faixas de variação fisiológicas children and adolescents: comparison between two reference tables. J Pediatr
e as distingam das situações de risco. (Rio J). 2007;83(2):181-5.
10. Valle M, Gascon F, Martos R, Bermudo F, Ceballos P, Suanes A. Relationship
between high plasma leptin concentrations and metabolic syndrome in obese
supORte finanCeiRO: pre-pubertal children. Int J Obes Relat Metab Disord. 2003;27(1):13-8.
11. Dubey L, Zeng HS, Wang HJ, Liu RY. Potential role of adipocytokine
Universidade de Ribeirão Preto e Faculdade de Ciências Farmacêuticas da leptin in acute coronary syndrome. Asian Cardiovasc Thorac Ann.
2008;16(2):124-8.
UNESP de Araraquara
12. Caprio S, Tamborlane WV, Silver D, Robinson C, Leibel R, McCarthy S, et al.
Hyperleptinemia: an early sign of juvenile obesity. Relations to body fat depots
Conflito de interesse: não há and insulin concentrations. Am J Physiol. 1996;271(3):E626-E30.
13. Fleisch AF, Agarwal N, Roberts MD, Han JC, Theim KR, Vexler A, et al. Influ-
ence of serum leptin on weight and body fat growth in children at high risk
suMMaRy for adult obesity. J Clin Endocrinol Metab. 2007;92(3):948-54.
14. De Almeida C, Del Ciampo L, Ricco R, Crott G. Crescimento físico. In: Ricco
fasting leptineMia in eutROphiC ChildRen and adOlesCents R, Del Ciampo L, De Almeida C, editores. Puericultura princípios e práticas.
2a ed. São Paulo: Editora Atheneu: 2008. p.43-54.
Objective. To determine, in a group of eutrophic children and 15. WHO Working Group On Infant Growth. An evaluation of infant growth:
adolescents, the values of fasting leptinemia and its correlation the use and interpretation of anthropometry in infants. Bull WHO.
with age and body mass index. 1995;73(2):165-74.
16. Slinger JD, Van BE, Keizer H, Rump P, Hornstra G, Kuipers H. Insulin resis-
MethOds. A cross-sectional study conducted in two public tance, physical fitness, body composition and leptin concentration in 7-8
schools in Ribeirao Preto, Brazil. Anthropometric measurements year-old children. J Sci Med Sport 2008;11(2):132-8.
and venous blood samples were obtained for determination 17. Butte NF, Cai G, Cole SA, Wilson TA, Fisher JO, Zakeri IF, et al. Metabolic and
behavioral predictors of weight gain in Hispanic children: the Viva la Familia
of fasting leptinemia of 448 eutrophic and medium maturers Study. Am J Clin Nutr. 2007;85(6):1478-85.
children and adolescents, of both genders, aged between 7 18. Ahmed ML, Ong KKL, Morrell DJ, Cox L, Drayer N, Perry L, et al. Longi-
tudinal study of leptin concentrations during puberty: sex differences and
and 17.9 years. Using the Mann-Whitney test, comparisons relationship to changes in body composition. J Clin Endocrinol Metab
were made between the concentrations obtained for boys and 1999;84(3):899-905.
466 Rev Assoc Med Bras 2009; 55(4): 463-7

leptinemiA de jejUm em CriAnçAs e AdolesCentes eUtrófiCos
19. Wallace AM, McMahon AD, Packard CJ, Kelly A, Shepherd J, Gaw A, et al. 22. Brandao CM, Lombardi MT, Nishida SK, Hauache OM, Vieira JG. Serum leptin
Plasma Leptin and the Risk of Cardiovascular Disease in the West of Scotland concentration during puberty in healthy nonobese adolescents. Braz J Med
Coronary Prevention Study (WOSCOPS). Circulation. 2001;104(25):3052-6. Biol Res. 2003;36(10):1293-6.
20. Romero-Corral A, Sierra-Johnson J, Lopez-Jimenez F, Thomas RJ, Singh P,
Hoffmann M, et al. Relationships between leptin and C-reactive protein
with cardiovascular disease in the adult general population. Natl Clin Pract
Cardiovasc Med. 2008;5(7):418-25.
Artigo recebido: 12/09/08
21. Poveda E, Callas NE, Baracaldo CM, Castillo C, Hernandez P. Leptin levels in
school age children associated with anthropometric measurements and lipid Aceito para publicação: 16/02/09
profiles. Biomedica. 2007;27(4):505-14.

Artigo Original
Estudo'comparativo'de'fatores'de'risco'em'crianças'e'adolescentes'
com'diagnóstico'antropométrico'de'sobrepeso'ou'obesidade
Comparative+study+of+risk+factors+among+children+and+adolescents+with+an+anthropometric+diagnosis+of+
overweight+or+obesity
Rafaela+Cristina+Ricco1,+Rubens+Garcia+Ricco2,+Carlos+Alberto+N.+de+Almeida3,+Adriana+Pelegrino+P.+Ramos4
RESUMO' de jejum, com maiores frequências de valores alterados

entre os obesos.
Objetivo: O excesso de peso é um grande problema de Conclusões: Os portadores de sobrepeso apresentaram
saúde pública em todo o mundo, atingindo crianças e ado- alterações indicativas de prejuízos à sua saúde, semelhante-
lescentes. O presente estudo teve por objetivo verificar se a mente aos obesos, sendo necessário também incluí-los nos
condição de portador de sobrepeso se associa à presença de programas de prevenção e tratamento.
fatores de risco à saúde.
Métodos: Foram estudados 84 sujeitos entre seis e 17 Palavras-chave: obesidade; sobrepeso; criança; adoles-
anos, constituindo-se um grupo de 34 pacientes porta- cente; fatores de risco.
dores de sobrepeso e outro de 50 obesos, atendidos em
ambulatório de Nutrologia Pediátrica da Universidade de ABSTRACT
Ribeirão Preto (Unaerp), durante o período de outubro de
2004 a outubro de 2005. Foram obtidas as variáveis: pres- Objective: Excess weight is a serious public health prob-
são arterial, circunferência abdominal, glicemia de jejum, lem all over the world, affecting children and adolescents.
glicemia de segunda hora, colesterol total, HDL-c, LDL-c The objective of the present study was to determine whether
e triglicérides. Comparam-se os dois grupos por meio de the condition of being overweight is associated to changes
duas abordagens estatísticas: comparação entre as distri- in health parameters.
buições dos valores absolutos (teste de Mann-Whitney) e Methods: 84 subjects aged 6-17 years old were studied
entre as frequências de valores considerados alterados (teste (34 overweight and 50 obese patients), all of them assisted
exato de Fisher). at the Pediatric Nutrology outpatient clinic of the Uni-
Resultados: Quanto à primeira abordagem, verificou-se versity of Ribeirão Preto (Unaerp) from October/2004 to
diferença estatística apenas para o HDL-c, com maiores October/2005. Arterial pressure, abdominal circumference,
valores para o subgrupo de portadores de sobrepeso de fast glycemia, second hour glycemia, total cholesterol and
seis a dez anos. Quanto à segunda comparação, verificou- its fractions (HDL-c and LDL-c) and triglycerides were de-
se diferença estatística para a circunferência abdominal termined. The two groups were compared by two statistical
(segundo os critérios de Freedman), HDL-c e glicemia approaches: comparison of absolute values by Mann-Whitney
Instituição: Universidade de Ribeirão Preto (Unaerp) e Faculdade de Endereço para correspondência:

Medicina de Ribeirão Preto da Universidade de São Paulo (USP), Ribeirão Rafaela Cristina Ricco
Preto, SP, Brasil Rua Amador Bueno, 1.155, apto. 73 – Centro
1
Mestre em Saúde da Criança e do Adolescente pela Faculdade de Medici- CEP 14010-070 – Ribeirão Preto/SP
na de Ribeirão Preto da USP; Professora Assistente do Curso de Medicina E-mail: rafaela.ricco@terra.com.br
da Unaerp, Ribeirão Preto, SP, Brasil
2
Livre Docente; Professor Associado do Departamento de Puericultura e Fonte financiadora: Unaerp
Pediatria da Faculdade de Medicina de Ribeirão Preto da USP, Ribeirão Conflitos de interesse: nada a declarar
Preto, SP, Brasil
3
Doutor em Saúde da Criança e do Adolescente pela Faculdade de Medi- Recebido em: 12/10/2009
cina de Ribeirão Preto da USP; Professor Titular do Curso de Medicina da Aprovado em: 31/5/2010
Unaerp, Ribeirão Preto, SP, Brasil
4
Doutora em Biociências e Biotecnologia Aplicadas à Farmácia pela Uni-
versidade Estadual Paulista “Júlio de Mesquita Filho”; Professora Assistente
do Curso de Farmácia e Bioquímica da Unaerp, Ribeirão Preto, SP, Brasil
Rev+Paul+Pediatr+2010E28(4):320J5.
Rafaela+Cristina+Ricco+et+al
test, and between frequencies of altered values by Fisher Para contribuir na elucidação dessa questão, delineou-se
exact test. o presente estudo, que teve como objetivo geral descrever e
Results: There was a statistical difference only for HDL-c, comparar dois grupos de crianças e adolescentes – um com
with higher concentrations in the overweight group when diagnóstico antropométrico de sobrepeso e outro, de obesi-
the subgroup of patients with 6-10 years old was considered. dade. Essa comparação foi feita por meio das distribuições
Regarding the second approach, there were statistical differ- dos valores absolutos e da prevalência de alterações em cada
ences in the abdominal circumference by Freedman criteria, grupo de variáveis antropométricas, clínicas e laboratoriais
HDL-c and fast glycemia, with higher frequencies of altered associadas a fatores de risco para agravos à saúde humana,
values among obese subjects. procurando-se verificar se a condição de sobrepeso já se as-
Conclusions: Overweight patients presented alterations sociava a tais fatores.
harmful to their health, similarly to obese individuals. It
is necessary to enroll overweight children and adolescents Métodos'
in programs dedicated to the prevention and treatment of
nutritional problems. Trata-se de um estudo descritivo, transversal em sua análise
estatística, que avaliou crianças e adolescentes com diagnósti-
Key-words: obesity; overweight; child; adolescent; risk cos antropométricos de sobrepeso e de obesidade, de ambos os
factors. sexos, na faixa etária de seis a 17 anos, que procuraram espon-
taneamente ou foram encaminhados por unidades de saúde ao
Introdução' Ambulatório de Nutrologia Pediátrica e Centro de Estudos em
Nutrição Infanto-Juvenil da Universidade de Ribeirão Preto
Sobrepeso e obesidade são definidos como acúmulo de (Unaerp). O trabalho foi aprovado pelo Comitê de Ética em
gordura anormal ou excessivo que pode prejudicar a saúde(1). Pesquisa do Hospital das Clínicas da Faculdade de Medicina
O excesso de peso é uma condição complexa, com sérias al- de Ribeirão Preto da Universidade de São Paulo.
terações biopsicossociais no ser humano, atingindo todas as O diagnóstico do estado nutricional foi estabelecido por
idades e condições socioeconômicas. Existem consideráveis meio do IMC – definido pelo peso, em quilogramas, dividido
danos à saúde das pessoas obesas, individualmente conside- pela altura, em metros, elevada ao quadrado –, sendo o valor
radas, e das populações de modo geral, sobrecarregando a encontrado para cada paciente levado à distribuição percenti-
atenção à sua saúde, que já é insuficiente em muitos países, lar do IMC. Considerou-se sobrepeso IMC com valores maio-
inclusive no Brasil. res ou iguais ao percentil 85 e menores que o percentil 95, e
Os obesos não são frequentemente identificados em ser- obesidade, IMC igual ou maior que o valor correspondente
viços de cuidados primários, salvo aqueles com altos valores ao percentil 95, conforme os critérios internacionalmente
de índice de massa corpórea (IMC)(2). Pode-se inferir que aceitos(3). O valor percentilar do IMC, segundo as curvas do
é ainda menos frequente a identificação dos portadores de Centers for Disease Control and Prevention(3), foi calculado pelo
sobrepeso, tanto nos serviços de Saúde quanto nas suas famí- programa Epi-Info Nutrition, Access 97, versão 3.2.2.
lias. Ainda são esparsos os conhecimentos sobre os diferentes A coleta de dados foi realizada no período de outubro de
riscos inerentes às condições de sobrepeso e obesidade na 2004 a outubro de 2005. O universo de elegíveis para o estu-
infância e adolescência e se os portadores de sobrepeso estão do era de 112 pacientes. Foram incluídos no estudo crianças
também sujeitos aos mesmos problemas de saúde presentes e adolescentes cujos responsáveis legais e o próprio paciente
na obesidade, tais como hipertensão arterial, hiperglicemia, consentiram em participar. Excluíram-se aqueles em uso de
dislipidemia e aumento da gordura visceral, entre outros. medicações que pudessem alterar os exames, os previamente
Esclarecer essa questão é fundamental para orientar políticas submetidos a dietas específicas e os portadores de doenças
de atenção à saúde de crianças e adolescentes com excesso de que levam ao comprometimento do estado nutricional, o
peso, podendo indicar que o foco das ações, que hoje privi- que totalizou 21 pacientes. Durante o desenvolvimento
legia a obesidade, deva também contemplar os portadores do trabalho, outros sete pacientes foram excluídos por não
de sobrepeso. Para estes, as medidas preventivas e curativas terem colhido os exames no período estipulado ou por falta
poderiam apresentar melhores resultados e maior efetividade de retorno para a avaliação ou, ainda, pelo fato de os exames
do que para os portadores de obesidade. laboratoriais indicarem que o excesso de peso era de origem
321
Estudo+comparativo+de+fatores+de+risco+em+crianças+e+adolescentes+com+diagnóstico+antropométrico+de+sobrepeso+ou+obesidade
secundária a doenças. Assim, excluíram-se 28 pacientes, os com os fatores de risco e morbidades associadas ao peso
quais continuaram seu seguimento clínico no serviço, sem excessivo. Os exames laboratoriais sanguíneos colhidos fo-
qualquer prejuízo para os mesmos. ram: hormônio estimulador da tireoide (TSH), glicemia de
Dessa forma, foram incluídos 84 pacientes, sendo 34 jejum, OGTT, triglicérides, colesterol total, LDL-colesterol
com diagnóstico de sobrepeso e 50, de obesidade. Entre os e HDL-colesterol. Os valores encontrados foram comparados
obesos, a idade variou entre seis anos e três meses e 16 anos a pontos de corte internacionalmente recomendados para as
e sete meses, sendo 20 do sexo feminino e 30 do masculino. dosagens de lípides(9) e para dosagens de glicemia de jejum
Entre os portadores de sobrepeso, a idade variou de sete a e de duas horas(10).
17 anos e três meses, sendo 26 do sexo feminino e oito do Para executar os testes de Mann Whitney e exato de
masculino. Os 50 obesos e os 34 portadores de sobrepeso, Fisher, utilizou-se o software do GraphPad Instat, 1998,
em algumas análises, foram considerados conjuntamente versão 3.05 para Windows 95. Foram realizadas duas abor-
e, em outras, separados em crianças (seis a nove anos) e dagens estatísticas. Na primeira, compararam-se os dados
adolescentes (dez a 17 anos), quando os pontos de corte absolutos obtidos entre os dois grupos (com sobrepeso e
indicativos para a variável considerada eram diferentes para obesidade). Uma vez que as variáveis não apresentaram
as duas faixas etárias. distribuição normal, optou-se pela aplicação do teste
Compararam-se as variáveis antropométricas (IMC e não-paramétrico de Mann-Whitney, sendo significante
circunferência abdominal), clínicas (pressão arterial) e as p<0,05. Na outra abordagem analítica, foram estimadas
seguintes dosagens laboratoriais sanguíneas: glicemia de as prevalências das alterações clínico-laboratoriais nas duas
jejum, teste de tolerância oral à glicose (OGTT do inglês amostras, permitindo comparar por meio do teste exato
oral glucose tolerance test – glicemia de duas horas após a in- de Fisher se os dois grupos eram diferentes ou não, sendo
gestão de 1,75g de glicose/kg de peso e máximo de 75g), significante p<0,05.
colesterol total, lipoproteína de alta densidade (HDL-c),
lipoproteína de baixa densidade (LDL-c) e triglicérides. Resultados'
As crianças e os adolescentes foram medidos descalços e
vestindo roupas íntimas e, sobre estas, um avental descar- A Tabela 1 mostra os valores encontrados para a dis-
tável de peso desprezível. Mediu-se o peso com balança tribuição dos resultados das dosagens laboratoriais dos
da marca Filizola®. A medida da estatura foi realizada por 84 sujeitos, agrupados em duas amostras independentes,
meio de um antropômetro vertical da marca Sanny®, de segundo o diagnóstico de sobrepeso ou obesidade. Para os
régua e fita métrica em metal, com escala em milímetros. quatro primeiros exames, agruparam-se crianças e adoles-
A medida da circunferência abdominal foi realizada com centes, pois o ponto de corte é o mesmo para a definição
fita metálica inextensível, seguindo-se recomendações de dosagem alterada, o que não acontece com as dosagens
técnicas rigorosas(4). Os valores obtidos foram comparados de HDL-c e triglicérides, que apresentam pontos de cortes
com as tabelas percentilares de referência propostas por diferentes para crianças e adolescentes. Não houve diferença
Freedman(5) e Taylor(6). Foram considerados como pontos estatisticamente significante entre os dois grupos quanto
de cortes, os valores de circunferência abdominal sugeri- aos valores de glicemia de jejum, OGTT, colesterol total,
dos pela distribuição percentilar de Freedman(5) (acima do LDL-colesterol, HDL-colesterol (nos adolescentes) e trigli-
percentil 90) e os sugeridos pela distribuição percentilar de cérides. Os valores de HDL-c apresentaram diferença esta-
Taylor(6) (acima do percentil 80). Foram utilizados os dois tística, com os maiores valores para o grupo de sobrepeso
métodos, pois subsidiam de maneiras diferentes o fator de entre os menores de dez anos.
risco associado(7). A Tabela 2 mostra os valores encontrados para as frequên-
A aferição da pressão arterial (PA) foi realizada com es- cias dos valores considerados alterados, com suas respectivas
figmomanômetro portátil de coluna de mercúrio calibrado percentagens, dos 84 sujeitos agrupados em duas amostras
e conjunto de manguitos adequados, seguindo-se as reco- independentes, segundo o diagnóstico de sobrepeso ou obesi-
mendações da força-tarefa norte-americana(8). Para todos os dade. Não houve diferença estatisticamente significante entre
pacientes, solicitaram-se exames laboratoriais sanguíneos, os dois grupos quanto aos valores comparados, exceto para
conforme a rotina do serviço, importantes para elucidação os valores de circunferência abdominal, segundo critérios de
diagnóstica e seguimento clínico, também relacionados Freedman, glicemia de jejum e HDL-c.
322
Discussão' Acredita-se que houve aumento da incidência da hiper-

tensão arterial paralelamente à epidemia de obesidade na
A obesidade é considerada como a maior epidemia em infância(19,20) e que o aumento mundial da prevalência de
Saúde Pública no mundo(11,12). Ela determina várias compli- crianças e adolescentes com hipertensão arterial primária
cações na infância e na vida adulta, associadas a importantes está diretamente relacionado ao aumento da prevalência da
problemas de saúde na população pediátrica(13,14). Acredita-se obesidade(17). Estudos indicam que há uma relação direta
que crianças e adolescentes obesos tornam-se adultos obe- entre o grau da obesidade e o risco de hipertensão arterial
sos(15), com relação direta entre a gravidade da obesidade na sistêmica na infância(21,22). No presente estudo, a prevalência
infância e o risco de se manter o sobrepeso ou a obesidade de hipertensão arterial nos grupos de crianças e adolescentes
na vida adulta(16). O IMC aumentado é indicativo de risco com sobrepeso e obesidade estudados não apresentou dife-
precoce para morbidade e mortalidade(13,17). A elevada pre- rença estatisticamente significante, como se proviessem de
valência da obesidade infantil, concomitante à hipertensão uma mesma população sujeita aos mesmos fatores de risco
arterial, hiperlipidemia e síndrome metabólica, está associada para hipertensão arterial, portanto, já aparecendo a doença
à doença cardiovascular na vida adulta(18). entre os portadores de sobrepeso. Sabendo-se que os fatores
Diante da gravidade e extensão do problema da obesi- de risco para o aparecimento da hipertensão arterial na vida
dade, há intensa produção de trabalhos sobre o tema em adulta provavelmente se iniciam antes dos cinco anos(23,24),
geral, embora ainda sejam escassos aqueles que comparam é necessário considerá-los para crianças de qualquer estado
crianças e adolescentes portadores de sobrepeso e obesidade, nutricional como parte integrante do exame semiológico,
procurando verificar os agravos à sua saúde, em especial, no durante as consultas pediátricas.
que diz respeito aos portadores de sobrepeso. Realizou-se o A circunferência abdominal nos adultos é usada para defi-
presente estudo nesse contexto. nir a obesidade central e, nas crianças, é um bom preditor de
adiposidade visceral, relacionada como fator de risco para o
Tabela' 1' G' Distribuições+ das+ dosagens+ laboratoriais+ dos+ 84+ diabetes melito tipo 2 e outras desordens metabólicas(7). No
sujeitos,+segundo+o+diagnóstico+de+sobrepeso+ou+obesidade+ presente estudo, quando os valores de corte foram baseados
Sobrepeso' na referência de Taylor(6) para considerar a circunferência
Exames'laboratoriais versus& abdominal alterada, observou-se não haver diferença esta-
obesidade tística entre os grupos de obesos e portadores de sobrepeso,
Glicemia+de+jejum+ p=0,858 encontrando-se 100% de alterações em ambos os grupos.
OGTT p=0,392
Ao aplicar os critérios de Freedman(5), observou-se, entre os
Colesterol+total p=0,339
LDLEcolesterol p=0,321
sujeitos com sobrepeso e obesos, respectivamente 14 e 50%
HDLEcolesterol+(<10+anos) p=0,048 com circunferência abdominal alterada. A análise estatística
HDLEcolesterol+( 10+anos) p=0,189 mostrou diferença significante entre os grupos, com maior
Triglicérides+(<10+anos) p=0,067 prevalência para os obesos. Os resultados obtidos neste estudo
Triglicérides+( 10+anos) p=0,189 corroboram os obtidos por Almeida(7), o qual – na referên-
p:+nível+descritivoP+OGTT:+teste+de+tolerância+oral+à+glicose. cia de Taylor para os valores de corte para a circunferência
Tabela'2'G'Frequências+dos+valores+considerados+alterados+e+suas+respectivas+percentagens+nos+84+sujeitos,+segundo+o+diagE
nóstico+de+sobrepeso+ou+obesidade
Variáveis'clínicoGlaboratoriais Sobrepeso'(%) Obesidade'(%) Valor'de'p
Pressão+arterial 3+(8,8) 13+(26) 0,087
Circunferência+abdominal+(Freedman) 12+(35) 42+(84) <0,001
Circunferência+abdominal+(Taylor) 34+(100) 50+(100) 0,082
Glicemia+de+jejum 0 9+(18) 0,009
OGTT+(glicemia+2h) 0 3+(6) 0,268
Colesterol+total 12+(35) 22+(44) 0,500
LDLEcolesterol 13+(38) 23+(46) 0,509
HDLEcolesterol 10+(29) 26+(52) 0,046
Triglicérides 6+(17) 18+(36) 0,087
323
Estudo+comparativo+de+fatores+de+risco+em+crianças+e+adolescentes+com+diagnóstico+antropométrico+de+sobrepeso+ou+obesidade
abdominal – selecionou com maior probabilidade os indi- dez anos revelou haver diferença entre os dois grupos, com
víduos para adiposidade abdominal excessiva, sendo mais valores maiores no grupo portador de sobrepeso do que no
sensível e adequado para estudos epidemiológicos de triagem. de obesos. A comparação análoga entre os pacientes entre
Por outro lado, a tabela de Freedman(5) mostrou-se mais ade- dez e 17 anos, categorizados em dois grupos, segundo o
quada para uso clínico, por apresentar maior especificidade. diagnóstico de sobrepeso ou obesidade, mostrou não haver
Dessa forma, também essa medida deveria fazer parte do diferença entre ambos. Quanto à distribuição dos valores
exame semiológico da criança e do adolescente. de HDL-c alterados e não-alterados para os dois grupos,
A associação entre obesidade, doença cardiovascular ate- incluindo-se todos os 84 sujeitos, encontrou-se diferença
rosclerótica (DCVA) e diabetes melito tipo 2 em adultos estatisticamente significante entre eles, com maior proporção
aumentou consideravelmente(25). Embora as crianças e adoles- de valores alterados entre os obesos.
centes não apresentem DCVA franca, aquelas com obesidade Quando os resultados são globalmente considerados,
apresentam perfil de risco cardiovascular compatível com o pode-se observar que apenas os níveis de HDL-c nos grupos
seu desenvolvimento precoce, isto é, hipertensão arterial, de seis a dez anos, a frequência de portadores de alteração da
triglicérides e glicemia de jejum aumentados e HDL-c circunferência abdominal segundo os critérios de Freedman(5)
diminuído. e a frequência de pacientes com HDL-c e glicemia de jejum
Neste estudo, a comparação entre as distribuições da apresentaram diferença significante, com indicadores mais
glicemia de jejum para os grupos de portadores de sobrepeso favoráveis nos portadores de sobrepeso. Em todas as outras
e obesidade revelou não haver diferença estatisticamente comparações, não houve diferença entre esses grupos, como
significante entre os dois. Por outro lado, para a distri- se ambos fossem provenientes da mesma população, ou seja,
buição dos valores considerados alterados e não-alterados expostos aos mesmos fatores de risco, o que torna relevante a
de glicemia de jejum, encontrou-se diferença estatística, exposição dos portadores de sobrepeso a esses fatores. Confir-
indicando que os dois grupos são diferentes: no grupo dos mando essas observações, para as variáveis PA, circunferência
portadores de sobrepeso, nenhum paciente tinha glicemia abdominal pelos critérios de Freedman(5) e Taylor(6), colesterol
de jejum alterada, enquanto, entre os obesos, nove pacien- total, LDL-c, HDL-c e triglicérides, houve uma proporção
tes apresentaram tal alteração. Quanto ao OGTT neste considerável de sujeitos com valores alterados entre os por-
estudo, as distribuições dos resultados de suas dosagens tadores de sobrepeso, mostrando novamente a importância
mostraram não haver diferença estatisticamente significante da exposição dos portadores de sobrepeso a esses fatores de
entre portadores de sobrepeso e obesidade. A comparação risco para a saúde global.
entre as distribuições de valores considerados alterados e A dificuldade de estudar crianças e adolescentes portadores
não-alterados de OGTT também não apresentou diferen- de sobrepeso é grande, seja pela falta de procura espontânea
ça estatística significante entre os grupos, como mostra a ou pela falta de encaminhamento para serviços de saúde,
Tabela 2, na qual se pode observar que nenhum paciente surgindo daí uma limitação do estudo, que não pretendeu
com sobrepeso mostrou valores alterados, enquanto três do representar nenhuma população específica. No entanto, os
grupo de obesos tinham OGTT alterada. dados são indicadores úteis para a atuação clínica e podem
Estudos prospectivos indicam que as dislipidemias presen- ajudar a orientar políticas de saúde, focalizando a condição
tes na infância e na adolescência persistem na vida adulta(26). do portador de sobrepeso, pois ainda são escassos os trabalhos
Os níveis elevados de LDL-c e de IMC são preditivos para com esse enfoque. A procura espontânea pelos serviços de
alterações nas carótidas em adolescentes e essas são fortemente saúde esbarra na falta de percepção sobre a condição daque-
relacionadas com aterosclerose coronariana e risco cardiovas- les que não são flagrantemente obesos e eufemisticamente
cular(27). O desfecho na vida adulta é a elevada incidência de considerados “fortes”, “robustos” ou outros adjetivos, não
mortalidade prematura por doença cardiovascular e geral, em havendo preocupação da própria criança ou adolescente ou
indivíduos obesos na adolescência(18). Neste estudo, a com- de seus familiares(28). O baixo encaminhamento pelos serviços
paração dos níveis de colesterol total, LDL-c e triglicérides de saúde, por sua vez, esbarra na falta de um diagnóstico
entre os portadores de sobrepeso e de obesidade não revelou seguro do estado nutricional(29,30) por meio do cálculo do
diferença significante. Quanto ao HDL-c, considerado fator IMC do paciente e sua situação nos gráficos de IMC, que
protetor contra as doenças cardiovasculares, a distribuição ainda são raros nesses serviços, ficando tais encaminhamentos
dos resultados de sua dosagem para as crianças menores de restritos aos casos de obesidade mais grave ou com alterações
324
importantes com relação às comorbidades que frequentemen- clínico de crianças e adolescentes pode ajudar a promover
te acompanham a obesidade. a educação nutricional e a educação em saúde e facilitar a
É importante considerar que os portadores de sobrepeso, detecção precoce do início do processo de aumento excessivo
na faixa etária e na população estudadas, já podem apresentar de peso, facilitando a atuação na prevenção de riscos e na
alterações indicativas de prejuízos à sua saúde, à semelhança promoção da saúde.
dos obesos, sendo, portanto, necessária a sua inclusão nos
programas de prevenção e tratamento, tanto no atendimento Agradecimentos
individual, quanto nas políticas públicas. O correto diagnós-
tico do estado nutricional e a monitorização do crescimento, Ao Professor Doutor Gerson Muccillo, pela análise e
incluindo as medidas de IMC nos serviços de seguimento supervisão estatísticas.
1.+ World+ Health+ Organization+ (WHO)+ [homepage+ on+ the+ Internet].+ Obesity+ and+ 16.+Must+A,+Dallal+GE,+Dietz+WH.+Reference+data+for+obesity:+85th+and+95th+percentiles+
overweight+ [cited+ 2007+ May+ 20].+Available+ from:+ http://who.int/mediacentre/ of+ body+ mass+ index+ (wt/ht²)+ and+ triceps+ skinfold+ thickness.+Am+ J+ Clin+ Nutr+
factsheets/fs311/en/print.html+ 1991P53:839E46.
2.+ Dilley+KJ,+Martin+LA,+Sullivan+C,+Seshadri+R,+Binns+HJP+Pediatric+Practice+Research+ 17.+Groner+JA,+Joshi+M,+Bauer+JA.+Pediatric+precursors+of+adult+cardiovascular+disease:+
noninvasive+assessment+of+early+vascular+changes+in+children+and+adolescents.+
screening+ for+ comorbidities+ of+ overweight+ in+ pediatric+ primary+ care+ practice.+ Pediatrics+2006P118:1683E91.
Pediatrics+2007P119:e148E55.+ 18.+Weiss+R,+Dziura+J,+Burgert+TS,+Tamborlane+WV,+Taksali+SE,+Yeckel+CW+et+al.+
3.+ Centers+for+Disease+Control+and+Prevention+[homepage+on+the+Internet].+Growth+ Obesity+and+the+metabolic+syndrome+in+children+and+adolescents.+N+Engl+J+Med+
charts+[cited+2007+May+20].+Available+from:+http://www.cdc.gov/growthcharts/+ 2004P350:2362E74.
4.+ Cameron+N.+Anthropometric+measurements.+In:+Cameron+N..+The+measurement+ 19.+Chiolero+A,+Bovet+P,+Paradis+G,+Paccaud+F.+Has+blood+pressure+increased+in+
of+human+growth.+London:+Croom+HelmP+1984.+p.+57E99. children+in+response+to+the+obesity+epidemic?+Pediatrics+2007P119:544E53.
5.+ Freedman+ DS,+ Serdula+ MK,+ Srinivasan+ SR,+ Berenson+ GS.+ Relation+ of+ 20.+Freedman+DS.+Clustering+of+coronary+heart+disease+risk+factors+among+obese+
circumferences+and+skinfold+thicknesses+to+lipid+and+insulin+concentrations+in+children+ children.+J+Pediatr+Endocrinol+Metab+2002P15:1099E108.
and+adolescents:+the+Bogalusa+Heart+Study.+Am+J+Clin+Nutr+1999P69:308E17. 21.+Garcia+FD,+Terra+AF,+Queiroz+AM,+Correia+CA,+Ramos+PS,+Ferreira+QT+et+al.+
6.+ Taylor+RW,+Jones+IE,+Williams+SM,+Goulding+A.+Evaluation+of+waist+circumference,+ Evaluation+of+risk+factors+associated+with+increased+blood+pressure+in+children.+J+
waistEtoEhip+ratio,+and+the+conicity+index+as+screening+tools+for+high+trunk+fat+mass,+ Pediatr+(Rio+J)+2004P80:29E34.
as+measured+by+dualEenergy+XEray+absorptiometry,+in+children+aged+3E19+y.+Am+ 22.+Kuschnir+MC,+Mendonça+GA.+Risk+factors+associated+with+arterial+hypertension+
J+Clin+Nutr+2000P72:490E5. in+adolescents.+J+Pediatr+(Rio+J)+2007P83:335E42.
7.+ de+Almeida+CA,+Pinho+AP,+Ricco+RG,+Elias+CP.+Abdominal+circumference+as+an+ 23.+Sun+SS,+Grave+GD,+Siervogel+RM,+Pickoff+AA,+Arslanian+SS,+Daniels+SR.+Systolic+
indicator+of+clinical+and+laboratory+parameters+associated+with+obesity+in+children+ blood+pressure+in+childhood+predicts+hypertension+and+metabolic+syndrome+later+
and+adolescents:+comparison+between+two+reference+tables.+J+Pediatr+(Rio+J)+ in+life.+Pediatrics+2007P119:237E46.
2007P83:181E5. 24.+Morrison+JA,+Friedman+LA,+GrayEMcGuire+C.+Metabolic+syndrome+in+childhood+
8.+ National+ High+ Blood+ Pressure+ Education+ Program+ Working+ Group+ on+ High+ predicts+adult+cardiovascular+disease+25+years+later:+the+Princeton+Lipid+Research+
Blood+Pressure+in+Children+and+Adolescents.+The+fourth+report+on+the+diagnosis,+ Clinics+FollowEup+Study.+Pediatrics+2007P120:340E5.
evaluation,+and+treatment+of+high+blood+pressure+in+children+and+adolescents.+ 25.+Sinaiko+AR,+ Steinberger+ J,+ Moran+A,+ Prineas+ RJ,+ Vessby+ B,+ Basu+ S+ et+ al.+
Pediatrics+2004P114+(2+Suppl+4th+Report):555E76. Relation+of+body+mass+index+and+insulin+resistance+to+cardiovascular+risk+factors,+
9.+ Kwiterovich+Junior+PO.+Beyond+cholesterol:+the+Johns+Hopkins+complete+guide+ Circulation+
for+avoiding+heart+disease.+Baltimore:+Johns+Hopkins+University+PressP+1989. 2005P111:1985E91.
10.+FollowEup+Report+on+the+Diagnosis+of+Diabetes+Mellitus.+The+Expert+Committee+ 26.+Santos+Junior+A,+Duarte+LF,+Taddei+JA.+Dosage+of+cholesterol+and+risk+factors+for+
on+ the+ Diagnosis+ and+ Classification+ of+ Diabetes+ Mellitus.+ Diabetes+ Care+ hyperlipidemia+in+adolescents+from+a+public+school+of+São+Paulo,+Brazil.+Rev+Paul+
2003P26:3160E7. Pediatr+2006P24:239E43.
11.+Cintra+Ide+P,+Passos+MA,+Fisberg+M,+Machado+HC.+Evolution+of+body+mass+index+ 27.+Boyd+GS,+Koenigsberg+J,+Falkner+B,+Gidding+S,+Hassink+S.+Effect+of+obesity+and+
in+two+historical+series+of+adolescents.+J+Pediatr+(Rio+J)+2007P83:157E62. high+blood+pressure+on+plasma+lipid+levels+in+children+and+adolescents.+Pediatrics+
12.+Mello+ED,+Luft+VC,+Meyer+F.+Childhood+obesity+EE+towards+effectiveness.+J+Pediatr+ 2005P116:442E6.
(Rio+J)+2004P80:173E82. 28.+Parry+LL,+Netuveli+G,+Parry+J,+Saxena+S.+A+systematic+review+of+parental+perception+
13.+Barros+Filho+AA.+Obesity:+a+puzzling+disorder.+J+Pediatr+(Rio+J)+2004P80:1E2. of+overweight+status+in+children.+J+Ambul+Care+Manage+2008P31:253E68.
14.+James+WPT.+Tendências+globais+da+obesidade+infantil+E+conseqüências+a+longo+ 29.'Benson+L,+Baer+HJ,+Kaelber+DC.+Trends+in+the+diagnosis+of+overweight+and+obesity+
prazo.+Anais+Nestlé+2002P62:1E11. in+children+and+adolescents:+1999E2007.+Pediatrics+2009P123:e153E8.
15.+Back+Giuliano+Ide+C,+Caramelli+B,+Pellanda+L,+Duncan+B,+Mattos+S,+Fonseca+FHP+ 30.++Bethell+C,+Read+D,+Goodman+E,+Johnson+J,+Besl+J,+Cooper+J+et+al.+Consistently+
Sociedade+Brasileira+de+Cardiologia.+I+guidelines+of+prevention+of+atherosclerosis+ inconsistent:+a+snapshot+of+acrossE+and+withinEstate+disparities+in+the+prevalence+
in+childhood+and+adolescence.+Arq+Bras+Cardiol+2005P85+(Suppl+6):4E36. of+childhood+overweight+and+obesity.+Pediatrics+2009P123+(Suppl+5):S277E86.
325
UPDATE ON THE TASK FORCE
REPORT (1987) ON HIGH BLOOD
PRESSURE IN CHILDREN AND
A DOLESCENTS: A W ORKING
GROUP REPORT FROM THE
NATIONAL HIGH BLOOD PRESSURE
EDUCATION PROGRAM
N IH PUBLICAT ION
N O . 96-3790
SEPT EMBER 1996
N AT ION AL I N ST IT UT ES
OF H EALT H
National Heart, Lung,
and Blood Institute

NATIONAL HIGH BLOOD PRESSURE EDUCATION PROGRAM
W ORKING GROUP ON HYPERTENSION CONTROL
IN CHILDREN AND A DOLESCENTS
Working Group Members Bernard Rosner, Ph.D.

Professor of Medicine (Biostatistics)
Bonita Falkner, M.D., Chair
Channing Laboratory
Professor of Medicine and Pediatrics
Harvard Medical School
Allegheny University of the Health Sciences
Boston, Massachusetts
Philadelphia, Pennsylvania
Alan R. Sinaiko, M.D.
Stephen R. Daniels, M.D., Ph.D.
Professor of Pediatrics
Professor of Pediatrics and Cardiology
Department of Pediatrics
University of Cincinnati
University of Minnesota Medical School
Children’s Hospital Medical Center
Minneapolis, Minnesota
Cincinnati, Ohio
Michael J. Horan, M.D., Sc.M. NHLBI Resource Staff
Director, Division of Heart and
Edward J. Roccella, Ph.D., M.P.H.
Vascular Diseases
Coordinator
National Heart, Lung, and Blood Institute
National High Blood Pressure
Bethesda, Maryland
Education Program
Jennifer M.H. Loggie, M.D. National Heart, Lung, and Blood Institute
Professor of Pediatrics Bethesda, Maryland
University of Cincinnati
Darrell E. Anderson, M.S.
Children’s Hospital Medical Center
Program Manager
Cincinnati, Ohio
National High Blood Pressure
Ronald J. Prineas, M.D., Ph.D. Education Program
Professor and Chair of Epidemiology and R.O.W. Sciences, Inc.
Public Health Rockville, Maryland
University of Miami School of Medicine
Miami, Florida
ii
A CKNOWLEDGM ENTS
The NHBPEP would like to acknowledge the Bruce Z. Morgenstern, M.D.

following reviewers: Pediatric Nephrology Consultant
Section of Pediatric Nephrology
Barry L. Carter, Pharm.D.
Mayo Clinic Rochester
Professor and Chair
Rochester, Minnesota
Department of Pharmacy Practice
School of Pharmacy, UCHSC Marvin Moser, M.D.
University of Colorado Clinical Professor of Medicine
Denver, Colorado Yale University School of Medicine
New Haven, Connecticut
Rae-Ellen W. Kavey, M.D.
Professor of Pediatrics and Preventive Medicine Sheldon G. Sheps, M.D.
Division of Pediatric Cardiology Professor of Medicine
State University of New York Mayo Medical School and Clinic
Health Science Center Rochester, Minnesota
College of Medicine
Douglas W. Teske, M.D.
Syracuse, New York
Pediatric Cardiology
Lindsey Lane, M.D. Children’s Hospital
Assistant Professor of Pediatrics Columbus, Ohio
Director of Pediatric Clerkship, East Falls
Mary C. Winston, Ed.D., R.D.
Allegheny University of the Health Sciences
Senior Science Consultant
Hanemann School of Medicine
Science and Medicine Division
Philadelphia, Pennsylvania
Office of Scientific Affairs
Gerald R. Marx, M.D. American Heart Association
Associate Chief Dallas, Texas
Division of Pediatric Cardiology
Director, Non-Invasive Laboratory
Tuffs University School of Medicine
Associate Professor
New England Medical Center
Boston, Massachusetts
We wish to acknowledge the contributions of the Centers for Disease Control and Prevention, National
Center for Health Statistics.
iii
NATIONAL HIGH BLOOD PRESSURE EDUCATION PROGRAM
COORDINATING COM M ITTEE M EM BER ORGANIZATIONS
Agency for Health Care Policy and Research American Red Cross
American Academy of Family Physicians American Society of Health-System Pharmacists
American Academy of Insurance Medicine American Society of Hypertension
American Academy of Neurology Association of Black Cardiologists
American Academy of Ophthalmology Citizens for Public Action on High Blood
American Academy of Physician Assistants Pressure and Cholesterol, Inc.
American Association of Occupational Health Council on Geriatric Cardiology
Nurses Department of Veterans Affairs
American College of Cardiology Health Care Financing Administration
American College of Chest Physicians Health Resources and Services Administration
American College of Occupational and International Society on Hypertension in Blacks
Environmental Medicine National Black Nurses’ Association, Inc.
American College of Physicians National Center for Health Statistics, Centers for
American College of Preventive Medicine Disease Control
American Dental Association National Heart, Lung, and Blood Institute
American Diabetes Association, Inc. National Heart, Lung, and Blood Institute
American Dietetic Association Ad Hoc Committee on Minority Populations
American Heart Association National Hypertension Association, Inc.
American Hospital Association National Institute of Diabetes and Digestive and
American Medical Association Kidney Diseases
American Nurses’ Association, Inc. National Kidney Foundation, Inc.
American Optometric Association National Medical Association
American Osteopathic Association National Optometric Association
American Pharmaceutical Association National Stroke Association
American Podiatric Medical Association Society for Nutrition Education
American Public Health Association
iv
FOREWORD
Since the publication of the Report of the Second • The normative blood pressure tables use the
Task Force on Blood Pressure Control in Chil- fifth Korotkoff sound for the definition of
dren—1987 (Pediatrics. 1987;79:1-25), new diastolic blood pressure for all age groups
information has become available to assist except infants younger than 1 year of age.
pediatricians in identifying, preventing, and • New charts have been developed to guide
treating high blood pressure in children. Al- practicing clinicians in selecting antihyper-
though hypertension generally was treated as an tensive drug therapy. These include newer
indication of a secondary medical problem in the classes of drugs not available at the time of the
past, it is now known that elevated blood pres- last report.
sure in many young persons may be the first sign
of future adult essential hypertension. • A public health statement encourages health
professionals to promote healthy lifestyles in
This report was produced by a working group all children and adolescents.
appointed by the National High Blood Pressure
Education Program (NHBPEP) under the • Easy-to-use physician education charts provide
capable leadership of Dr. Bonita Falkner. The a quick reference tool for clinicians.
report drew upon the combined knowledge and Dr. Falkner and the members of the working
experience of pediatricians, pediatric cardiolo- group are to be congratulated for developing this
gists, clinicians, epidemiologists, and public important document. Pediatric care must be a
health specialists. priority if our efforts to solve important public
This report updates the 1987 report and includes health problems through prevention and treat-
the following new information. ment of hypertension are to be successful.
• New data, such as results from the 1988-91
National Health and Nutrition Examination
Survey, have been included to develop revised
normative blood pressure tables, which now
include height percentiles, age, and gender. Claude Lenfant, M.D.
Director
National Heart, Lung, and Blood Institute
National Institutes of Health
and
Chair
NHBPEP Coordinating Committee
v
TABLE OF CONTENTS
Int roduct ion ..................................................................................................................................................... 1

Def init ion of Hypert ension ............................................................................................................................. 2
M easurement of Blood Pressure in Children ................................................................................................. 3
New Blood Pressure Tables Adjust ed f or Height ........................................................................................... 6
Treat ment of Hypert ension in Children and Adolescent s............................................................................. 10
Nonpharmacologic Therapy ...................................................................................................................... 10
Pharmacologic Therapy ............................................................................................................................. 11
Public Healt h Considerat ions..................................................................................................................... 12
Ref erences ........................................................................................................................................................ 14
Appendix 1: Demographic Dat a on Height /Blood Pressure Dist ribut ion Curves of St udy Populat ion ...... 19
Appendix 2: Quick-Ref erence Diagnost ic Chart s.......................................................................................... 20
FIGURES
Figure 1: Dimensions of Bladder and Cuff in Relat ion t o Arm Circumf erence ........................................... 3
Figure 2: Det erminat ion of Proper Cuf f Size, St ep 1 .................................................................................... 4
Figure 3: Det erminat ion of Proper Cuf f Size, St ep 2 .................................................................................... 4
Figure 4: Blood Pressure M easurement ......................................................................................................... 4
TABLES
Table 1: Blood Pressure Levels f or t he 90t h and 95t h Percent iles of Blood Pressure f or Boys
Age 1 t o 17 Years by Percent iles of Height .................................................................................................... 7
Table 2: Blood Pressure Levels f or t he 90t h and 95t h Percent iles of Blood Pressure f or Girls
Age 1 t o 17 Years by Percent iles of Height .................................................................................................... 8
Table 3: Ant ihypert ensive Drug Therapy f or Hypert ensive Emergencies in Children ................................ 12
Table 4: Ant ihypert ensive Drug Therapy f or Chronic Hypert ension in Children ........................................ 13
vi
INTRODUCTION
whereas in other cases the elevated BP may

The relevance of childhood blood pressure
represent the early onset of essential hyperten-
(BP) measurement to pediatric health care and sion.
the development of adult essential hyperten-
sion has undergone substantial conceptual Since publication of the 1977 task force
change during the past 2 decades. The original report,2 new and more extensive epidemiologic
orientation of physicians with regard to BP in data on normal BP distributions and the natural
children and adolescents was toward identifi- history of BP throughout the pediatric age
cation and treatment of secondary forms of range have been published. These data, as
hypertension, such as renal parenchymal well as advances in diagnosis of and therapy
disease and renal artery stenosis. The incorpo- for hypertension, prompted publication of the
ration of BP measurement into the routine Report of the Second Task Force on Blood
pediatric examination as well as the publica- Pressure Control in Children—1987.3 From
tion of national norms for BP in children1-3 not the expanded body of knowledge on hyperten-
only enabled detection of significant asymp- sion in the young, several sources are now
tomatic hypertension secondary to a previously available that provide detailed guidelines for
undetected disorder but also confirmed that clinical evaluation and treatment of children
mild elevations in BP during childhood were and adolescents with hypertension.4-6 The
more common than previously recognized, purpose of this report is to update practitioners
particularly in adolescents. It is now under- on new data on BP in children and to call
stood that hypertension detected in some attention to modifications that are recom-
children may be a sign of an underlying mended for the diagnosis, treatment, and
disease such as renal parenchymal disease, prevention of hypertension in children.
DEFINITION OF HYPERTENSION
Although clinical hypertension occurs less BP varies widely throughout the day in chil-
frequently in children than in adults,7-9 ample dren, as well as in adults, due to normal
evidence now supports the concept that the diurnal fluctuation and changes in physical
roots of essential hypertension extend back to activity, emotional stress, or other factors.
childhood. Familial patterns for BP have been This variability can make the diagnosis of
established from early infancy,10,11 and chil- hypertension in children a difficult task. The
dren with BP in the higher distributional second National Heart, Lung, and Blood
percentiles are more likely to come from Institute (NHLBI) task force developed defini-
families with a history of hypertension.12,13 tions based on the distribution of BP in normal
Although it is generally agreed that early children as well as clinical experience and
essential hypertension poses little immediate consensus.3 Normal BP is defined as systolic
risk to most children, evidence from prelimi- and diastolic BP below the 90th percentile for
nary studies of children and adolescents has age and sex. High-normal BP is defined as
shown cardiac ventricular and hemodynamic average systolic or diastolic BP greater than or
changes consistent with an adverse effect of equal to the 90th percentile but less than the
mild hypertension prior to the third decade of 95th percentile. Hypertension is defined as
life.14-19 Of particular importance is the average systolic or diastolic BP greater than or
documentation that elevated BP in childhood equal to the 95th percentile for age and sex
often correlates with hypertension in early measured on at least three separate occasions.
adulthood, thereby supporting the need to track
BP in children.20
2
MEASUREMENT OF BLOOD
PRESSURE IN CHILDREN
Methods of BP measurement in children must two cuffs may be needed for use in obese
be standardized.21,22 BP in children is most adolescents. A technique to establish an
conveniently measured with a standard clinical appropriate cuff size is to choose a cuff having
sphygmomanometer, using the stethoscope a bladder width that is approximately 40
placed over the brachial artery pulse, proximal percent of the arm circumference midway
and medial to the cubital fossa, and below the between the olecranon and the acromion. This
bottom edge of the cuff (i.e., about 2 cm above will usually be a cuff bladder that will cover 80
the cubital fossa). Correct measurement of BP to 100 percent of the circumference of the arm
in children requires use of a cuff that is appro- (see figures 1, 2, 3, and 4). Use of the
priate to the size of the child’s upper right arm. manufacturer’s lines on the cuff facilitates
The right arm is preferred for consistency and choice of the correct cuff size for a given child.
comparison to the standard tables. The equip- BP should be measured in a controlled envi-
ment necessary to measure BP in children age ronment and after 3 to 5 minutes of rest in the
3 years through adolescence includes three seated position with the cubital fossa supported
pediatric cuffs of different sizes as well as a at heart level. BP should be recorded at least
standard adult cuff, an oversized cuff, and a twice on each occasion, and the average of
thigh cuff for leg BP measurement. The latter each of the systolic and diastolic BP measure-
Figure 1: Dimensions of Bladder and Cuff in Relation to Arm Circumference
D E F
B C
A: Ideal arm circumference; B: Range of acceptable arm circumferences;

C: Bladder length; D: Midline of bladder; E: Bladder width; F: Cuff width
Source: Perloff D et al. Human blood pressure determination by sphygmomanometry. Circulation.

1993;88:2460-2467. Copyright© 1993 American Heart Association. Reproduced with permission.
3
Figure 2: Determination of Proper Cuff Size, Step 1 Figure 3: Determination of Proper Cuff Size, Step 2
Acromion
Acromion
40% of circumference
at midpoint
Olecranon
Olecranon
The cuff bladder width should be approximately Cuff bladder length should cover 80% to 100%
40% of the circumference of the arm measured at a of the circumference of the arm.
point midway between the olecranon and acromion.
ments should be used to estimate BP level. Figure 4: Blood Pressure Measurement
Systolic BP is determined by the onset of the

“tapping” Korotkoff sounds. The phase of the
Korotkoff sounds that defines diastolic BP has
been somewhat controversial. The American
Heart Association has established the fifth
Korotkoff sound (K5), or the disappearance of Cubital fossa
Korotkoff sounds, as the definition of diastolic

BP. In children, particularly preadolescents, a
difference of several mm Hg is frequently
present between K4, the muffling of Korotkoff
sounds, and K5.23 In some children, Korotkoff Blood pressure should be measured with cubital fossa at
sounds can be heard to 0 mm Hg. When this heart level. The arm should be supported. The stethoscope
bell is placed over the brachial artery pulse, proximal and
occurs, it excludes diastolic hypertension. medial to the cubital fossa, and below the bottom edge of
the cuff.
When the second task force report was pub-
lished, the BP distribution curves were devel-
oped from the body of data available, which
indicated that K5 was a reliable measure of
diastolic BP for children age 13 years and diastolic BP for all ages. The BP tables
provided in this report use K5 as the diastolic
older. The addition of more childhood BP
data, with reanalysis of the entire database, BP.
now indicates that K5 can be used to define In recent years, there has been increasing use
diastolic BP in children as well as adolescents of automated devices to measure BP in chil-
and adults. This change to a K5 definition of dren. The most commonly used devices utilize
diastolic BP enables a uniform designation of oscillometric methodology to measure systolic
4
and mean arterial BP. Diastolic BP is then Once a diagnosis of hypertension is confirmed
calculated from these values. One advantage by repeated BP measurements exceeding the
of these devices is their ease of use. Instances 95th percentile, decisions must be made on
in which use of the automated devices is further evaluation and treatment. Most chil-
acceptable include BP measurement in new- dren and adolescents with BP levels at or just
borns and young infants in whom auscultation above the 95th percentile for their age and sex
is difficult as well as in the intensive care are overweight and have a family history of
setting where frequent BP measurement is hypertension.3 For them, a careful history and
needed. However, the reliability of these physical examination are most important.
instruments in a more standard clinical setting They require few diagnostic tests other than a
is less clear due to the need for frequent urinalysis and blood profiles to examine blood
calibration of the instruments and the current urea nitrogen and serum creatinine levels. A
lack of established reference standards. Under cardiovascular risk factor that may be associ-
most circumstances, the recommended method ated with hypertension in children is abnormal
of BP measurement in children is auscultation. lipids. A lipid profile may provide useful
Ambulatory BP monitoring refers to portable information because many overweight children
and adolescents with hypertension have
BP devices worn by the patient that record BP
over a specified period, usually 24 hours. elevated triglycerides and low-density lipopro-
Standards for ambulatory BP recording in tein cholesterol levels with low high-density
lipoprotein cholesterol.
children currently are not available, although
some data have been published.24,25 Ambula- Children and adolescents with both diastolic
tory BP monitoring is becoming increasingly and systolic BP well above the 95th percentile
popular in the management of hypertension in frequently have an underlying cause of hyper-
adults. However, more data are needed before tension, usually some form of renal-related
this procedure can be recommended for routine disease. In children with hypertension, femo-
clinical use in children. ral pulses should be palpated and BP also
Elevated BP must be confirmed on repeated should be measured in the legs to rule out
coarctation of the aorta. Previous reports have
visits before characterizing an individual as
having hypertension. This is because BP at the reviewed the type and expression of secondary
high levels tends to fall on subsequent mea- hypertension during childhood and the diag-
nostic approach recommended to exclude
surement as the result of (1) an accommodation
effect (i.e., reduction of anxiety by the patient causes of secondary hypertension.3 Some
from one visit to the next), and (2) regression genetic types of hypertension, such as gluco-
corticoid remediable aldosteronism, can now
to the mean, a nonbiological phenomenon that
derives, in part, from mathematical consider- be identified by sending a blood sample to
ations. BP level is not static but varies even centers capable of performing the genetic
under standard resting conditions. Therefore, a testing. Although genetic testing for most
children is unnecessary at this time, it is
more precise characterization of an individual’s
BP level is an average of multiple BP measure- appropriate to consult with a physician experi-
ments taken over weeks to months. With enced in the field of childhood hypertension
for those children in whom further testing for
repeated measurement of BP using measure-
ment techniques standardized for children, underlying causes of hypertension is indicated
only about 1 percent of children and adoles- to determine the type and extent of diagnostic
testing necessary for a given child.
cents will be found to have hypertension.
5
NEW BLOOD PRESSURE
TABLES ADJUSTED FOR HEIGHT
Body size is the most important determinant of The BP data in this report on children and
BP in childhood and adolescence. The concept adolescents have been updated and reanalyzed
that the differential growth rates present in to include height percentiles. The report now
children would require some adjustments in includes the data presented in the second task
interpretation of the BP percentile for indi- force report,3 the data added in the report by
vidual children was suggested in the second Rosner et al.,26 and newly obtained data from
task force report. That report included tables the 1988-91 National Health and Nutrition
for the 90th percentile of height and weight Examination Survey (NHANES III).27 These
with the sex and age BP distribution curves and normative tables are based on the first BP
indicated that tall children with pressures that measured during screening on 61,206 children,
seem to be elevated may actually be normoten- including 31,158 boys and 30,048 girls.
sive if their height for a given age is beyond Demographic data for the study population are
the 90th height percentile.3 In a recent report given in appendix 1.
that reanalyzed the national childhood BP data,
The 90th and 95th percentiles of systolic and
the BP percentiles were refined and based not diastolic BP (using the fifth Korotkoff phase)
only on sex and age but also on height to for the 5th through 95th percentiles for height
determine age-, sex-, and height-specific
by sex and age are given for children in tables
systolic and diastolic BP percentiles.26 This 1 and 2, respectively. The difference in the
approach provides information that allows for 90th and 95th percentiles for BP for children
consideration of different levels of growth in of the same age and sex but of different height
evaluating BP and demonstrates that BP
is apparent in these tables.
standards that are based on sex, age, and height
permit a more precise classification of BP The BP tables adjusted for height and age in
according to body size.26 More importantly, this report, as compared with the tables using
this approach avoids misclassifying children at only age, alter the BP percentile estimates of
the extremes of normal growth. For example, boys and girls at all ages and particularly for
very tall children will not be misclassified as very young children. In general, BPs in the
hyper-tensive, and very short children with 90th and 95th percentiles for sex, height, and
high normal BP or even hypertension will not age are lower for shorter children than BPs in
be missed. Although BP clearly is also associ- the 90th and 95th percentiles given for chil-
ated with obesity, this association is believed to dren by age alone. Conversely, tall children
be a causal one, wherein the obesity contrib- are allowed higher normal BPs when their
utes to higher BP and to increased risk for height is taken into consideration than when
cardiovascular disease. age alone is used.
6
Table 1
PRESSURE FOR BOYS AGE 1 TO 17 YEARS BY PERCENTILES OF HEIGHT
Systolic BP (mm Hg) Diastolic BP (mm Hg)
Height
Age Percentiles* ➞5% 10% 25% 50% 75% 90% 95% 5% 10% 25% 50% 75% 90% 95%
BP†
➞
1 90th 94 95 97 98 100 102 102 50 51 52 53 54 54 55

95th 98 99 101 102 104 106 106 55 55 56 57 58 59 59
2 90th 98 99 100 102 104 105 106 55 55 56 57 58 59 59
95th 101 102 104 106 108 109 110 59 59 60 61 62 63 63
3 90th 100 101 103 105 107 108 109 59 59 60 61 62 63 63
95th 104 105 107 109 111 112 113 63 63 64 65 66 67 67
4 90th 102 103 105 107 109 110 111 62 62 63 64 65 66 66
95th 106 107 109 111 113 114 115 66 67 67 68 69 70 71
5 90th 104 105 106 108 110 112 112 65 65 66 67 68 69 69
95th 108 109 110 112 114 115 116 69 70 70 71 72 73 74
6 90th 105 106 108 110 111 113 114 67 68 69 70 70 71 72
95th 109 110 112 114 115 117 117 72 72 73 74 75 76 76
7 90th 106 107 109 111 113 114 115 69 70 71 72 72 73 74
95th 110 111 113 115 116 118 119 74 74 75 76 77 78 78
8 90th 107 108 110 112 114 115 116 71 71 72 73 74 75 75
95th 111 112 114 116 118 119 120 75 76 76 77 78 79 80
9 90th 109 110 112 113 115 117 117 72 73 73 74 75 76 77
95th 113 114 116 117 119 121 121 76 77 78 79 80 80 81
10 90th 110 112 113 115 117 118 119 73 74 74 75 76 77 78
95th 114 115 117 119 121 122 123 77 78 79 80 80 81 82
11 90th 112 113 115 117 119 120 121 74 74 75 76 77 78 78
95th 116 117 119 121 123 124 125 78 79 79 80 81 82 83
12 90th 115 116 117 119 121 123 123 75 75 76 77 78 78 79
95th 119 120 121 123 125 126 127 79 79 80 81 82 83 83
13 90th 117 118 120 122 124 125 126 75 76 76 77 78 79 80
95th 121 122 124 126 128 129 130 79 80 81 82 83 83 84
14 90th 120 121 123 125 126 128 128 76 76 77 78 79 80 80
95th 124 125 127 128 130 132 132 80 81 81 82 83 84 85
15 90th 123 124 125 127 129 131 131 77 77 78 79 80 81 81
95th 127 128 129 131 133 134 135 81 82 83 83 84 85 86
16 90th 125 126 128 130 132 133 134 79 79 80 81 82 82 83
95th 129 130 132 134 136 137 138 83 83 84 85 86 87 87
17 90th 128 129 131 133 134 136 136 81 81 82 83 84 85 85
95th 132 133 135 136 138 140 140 85 85 86 87 88 89 89
*Height percentile determined by standard growth curves.
†Blood pressure percentile determined by a single measurement.
7
Table 2
PRESSURE FOR GIRLS AGE 1 TO 17 YEARS BY PERCENTILES OF HEIGHT
Systolic BP (mm Hg) Diastolic BP (mm Hg)
Height
Age Percentiles* ➞5% 10% 25% 50% 75% 90% 95% 5% 10% 25% 50% 75% 90% 95%
BP†
➞
1 90th 97 98 99 100 102 103 104 53 53 53 54 55 56 56

95th 101 102 103 104 105 107 107 57 57 57 58 59 60 60
2 90th 99 99 100 102 103 104 105 57 57 58 58 59 60 61
95th 102 103 104 105 107 108 109 61 61 62 62 63 64 65
3 90th 100 100 102 103 104 105 106 61 61 61 62 63 63 64
95th 104 104 105 107 108 109 110 65 65 65 66 67 67 68
4 90th 101 102 103 104 106 107 108 63 63 64 65 65 66 67
95th 105 106 107 108 109 111 111 67 67 68 69 69 70 71
5 90th 103 103 104 106 107 108 109 65 66 66 67 68 68 69
95th 107 107 108 110 111 112 113 69 70 70 71 72 72 73
6 90th 104 105 106 107 109 110 111 67 67 68 69 69 70 71
95th 108 109 110 111 112 114 114 71 71 72 73 73 74 75
7 90th 106 107 108 109 110 112 112 69 69 69 70 71 72 72
95th 110 110 112 113 114 115 116 73 73 73 74 75 76 76
8 90th 108 109 110 111 112 113 114 70 70 71 71 72 73 74
95th 112 112 113 115 116 117 118 74 74 75 75 76 77 78
9 90th 110 110 112 113 114 115 116 71 72 72 73 74 74 75
95th 114 114 115 117 118 119 120 75 76 76 77 78 78 79
10 90th 112 112 114 115 116 117 118 73 73 73 74 75 76 76
95th 116 116 117 119 120 121 122 77 77 77 78 79 80 80
11 90th 114 114 116 117 118 119 120 74 74 75 75 76 77 77
95th 118 118 119 121 122 123 124 78 78 79 79 80 81 81
12 90th 116 116 118 119 120 121 122 75 75 76 76 77 78 78
95th 120 120 121 123 124 125 126 79 79 80 80 81 82 82
13 90th 118 118 119 121 122 123 124 76 76 77 78 78 79 80
95th 121 122 123 125 126 127 128 80 80 81 82 82 83 84
14 90th 119 120 121 122 124 125 126 77 77 78 79 79 80 81
95th 123 124 125 126 128 129 130 81 81 82 83 83 84 85
15 90th 121 121 122 124 125 126 127 78 78 79 79 80 81 82
95th 124 125 126 128 129 130 131 82 82 83 83 84 85 86
16 90th 122 122 123 125 126 127 128 79 79 79 80 81 82 82
95th 125 126 127 128 130 131 132 83 83 83 84 85 86 86
17 90th 122 123 124 125 126 128 128 79 79 79 80 81 82 82
95th 126 126 127 129 130 131 132 83 83 83 84 85 86 86
*Height percentile determined by standard growth curves.
†Blood pressure percentile determined by a single measurement.
8
To use the tables in a clinical setting, the are indicated. BP measurements between the
height percentile is determined from the 90th and 95th percentiles are high-normal and
standard growth charts. The child’s measured warrant further observation and consideration
systolic and diastolic BP is compared with the of other risk factors.
numbers provided in the table (boys or girls) Standards for systolic and diastolic BP for
for age and height percentile. The child is infants younger than 1 year are available in the
normotensive if BP is below the 90th percen-
second task force report.3 Additional data
tile. If the child’s BP (systolic or diastolic) is recently have been published.28,29 In children
at or above the 95th percentile, the child may younger than 1 year, systolic BP has been used
be hypertensive and repeated measurements
to define hypertension.
9
TREATMENT OF HYPERTENSION
IN CHILDREN AND ADOLESCENTS
NONPHARMACOLOGIC THERAPY BP also is directly related to degree of physical

fitness. The benefit of the increased physical
Nonpharmacologic therapy comprises weight
activity occurs gradually over months.40 When
reduction, exercise, and dietary intervention.
increases in physical activity are combined
Nonpharmacologic therapy should be intro-
with weight loss, the reduction in BP is supe-
duced not only in the care of patients with
rior to the effect resulting from weight reduc-
hypertension but also in children with high-
tion alone.30 Hypertension usually is not a
normal BP (90th to 95th percentile BP distribu-
contraindication to participation in sports and
tion) and to complement drug therapy for
strenuous activity, particularly because exercise
patients with severe hypertension.
has a beneficial effect on BP and other risk
Body size is the major determinant for BP factors. Sudden death during sporting events
among children. In obese children, both has not been reported in athletes with hyperten-
systolic and diastolic BP may decrease in sion as it has in athletes with hypertrophic
response to weight loss.30 In addition, weight cardiomyopathy or cardiac arrhythmias.
loss offers other benefits. The adverse effect of
Although dietary interventions to control or
obesity on cardiovascular function31 is com-
reduce obesity in childhood have demonstrated
pounded in the presence of hypertension, and
benefit to BP, limited data support the benefit
overweight adolescents are at increased risk for
to BP of other dietary interventions in the
cardiovascular disease as adults.32 Weight loss
young. The preponderance of evidence from
also has a positive effect on serum lipid pro-
published clinical trials suggests that dietary
files, and, in obese children, weight loss
sodium restriction reduces BP in adults with
diminishes the effect of dietary salt on BP.33
hypertension.41,42 Most studies to determine
The prevention of obesity in childhood would
whether sodium reduction lowers BP in chil-
convey significant benefits in reducing risks for
dren have been very short term.43-45 As yet, no
cardiovascular disease as well as other benefits.
clear evidence supports sodium reduction as
When elevated BP is associated with obesity,
beneficial in children or adolescents with mild
efforts should be directed at reducing obesity
hypertension. However, because sodium intake
with strategies to lower excessive calorie intake
is generally well in excess of needs and mild
and to increase physical exercise. Correction
BP elevation often is associated with obesity, a
of obesity is difficult to achieve in children as
moderate reduction in dietary sodium can be
well as adults. Because of the known benefits
beneficial. Sodium restriction is also of benefit
of weight control, efforts both to prevent and to
in some types of secondary hypertension such
control childhood obesity should be pursued.
as chronic glomerulonephritis. Practical
More effective weight loss strategies for
dietary considerations include an increase in
children are developing, which should facilitate
fresh fruits and vegetables, elimination of
more effective treatment.34-39
10
added salt to home-cooked foods in preparation history. Diuretics and beta-blockers have been
and at the table, and a reduction in foods with used in treating hypertension in children and
high sodium content. adolescents, and these medications continue to
These strategies for nonpharmacologic therapy be useful. Since publication of the second task
should be employed as initial treatment maneu- force report, a number of newer antihyperten-
vers for children with BP above the 90th per- sive agents have become available and are
described below.
centile for age, gender, and height. Similarly,
these nonpharmacologic methods are appropri- Angiotensin-converting enzyme (ACE) inhibi-
ate for children and adolescents with other risk tors have become one of the primary agents for
factors for hypertension, particularly a strong antihypertensive therapy not only because of
family history of hypertension. Some child- their effectiveness in reducing BP but also
hood data sets46 indicate that African American because of their positive benefits on cardiac
children have BP levels that are somewhat function, peripheral vasculature, and renal
higher than those of white children, suggesting function.48 ACE inhibitors are effective in
that the prevalence of high BP may be greater in children and can be useful in young infants and
African American children than white children. newborns.49 Both the potency and the duration
Recent data from California regarding Asian of action seem greater in this age group than in
American children show that they also tend to older children.50
have higher BP than white children.47 With the A significant adverse effect of ACE inhibitors
known excess prevalence, morbidity, and on the kidneys is severe reduction in glomeru-
mortality of essential hypertension among adult
lar filtration in patients with bilateral renal
African Americans in the United States, it is artery stenosis or renal artery stenosis in a
advisable to be vigilant in monitoring BP and to solitary or transplanted kidney.51 A more recent
encourage healthy diet, exercise, and weight
observation is the adverse effect of ACE
control behaviors in African American children, inhibitors on the developing fetus. The use of
especially in the presence of a family history of ACE inhibitors during the second and third
hypertension. This approach seems to be trimesters of pregnancy is associated with
prudent for other groups with a higher preva-
oligohydramnios and fetal effects of pulmonary
lence of hypertension or individuals with a hypoplasia, renal tubular dysplasia, and
family history of high BP. hypocalvaria as well as with hypotension and
PHARMACOLOGIC THERAPY anuria after birth.52 Because of the teratogenic
risk with fetal exposure, ACE inhibitors should
When drug therapy is used, the goal is to reduce be used with extreme caution in adolescent
BP to below the 95th percentile. The second girls who may be sexually active.
task force report provided guidelines for the use
of antihypertensive drugs in childhood, which Calcium channel blockers constitute a class of
compounds that inhibit intracellular flux of
continue to be endorsed.3 These drugs and their
dosing recommendations are provided in table calcium. At the present time, nifedipine is the
3, which contains the drugs recommended for calcium channel blocker used most often for
acute antihypertensive therapy, and in table 4, treatment of childhood hypertension. The
usefulness of nifedipine in treating chronic
which lists the drugs used for chronic antihyper-
tensive therapy. Antihypertensive drug therapy hypertension is limited by a short duration of
should be individualized, depending on the action. Long-acting preparations have im-
proved the effectiveness of nifedipine, but the
level of BP, the degree of response, the occur-
rence of side effects, and the patient’s medical tablet strength makes it impractical for use in
small children. Because of recent concerns
11
Table 3
Antihypertensive Drug Therapy for Hypertensive Emergencies

in Children
Drug Dose
Nifedipine 0.25-0.5 mg/kg oral prn. May be repeated two times, if no response.
Sodium Nitroprusside 0.5-1 mcg/kg/min IV initially. May be increased stepwise to
8 mcg/kg/min maximum.
Labetalol 0.2-1 mg/kg/dose IV. May be increased incrementally to 1 mg/kg/dose
until response achieved.
0.25-2 mg/kg/hr maintenance, either bolus or IV infusion.
Esmolol 500-600 mcg/kg IV load dose over 1-2 min then 200 mcg/kg/min.
May be increased by 50-100 mcg/kg q 5-10 min to max of 1,000 mcg/kg.
Diazoxide 1-5 mg/kg/dose IV bolus up to max of 150 mg/dose.
Hydralazine 0.2-0.4 mg/kg IV prn. May be repeated two times if no response.
Minoxidil 0.1-0.2 mg/kg oral.
about possible adverse effects of short-term those who have a strong family history of
calcium channel blockers used in adults, it has hypertension, are at greater risk for develop-
been recommended that physicians exercise ment of diabetic nephropathy.55 Children, as
caution in their use.53,54 Presently there are no well as adults, with diabetes are likely to
long-term data available on children using achieve renal protective benefits from therapy
calcium channel blockers or any classes of to maintain BP below the 90th percentile.56
antihypertensive agents. Most adverse effects Extensive clinical trials have not been con-
are limited to a brief period of time after initial
ducted to examine the benefits and risks of
drug administration. The heart rate and cardiac antihyper-tensive therapy in children and
output increase but usually return to pretreat- adolescents. Because of the limited data
ment levels within a few weeks. Newer cal-
available on therapy outcomes, the guidelines
cium channel blocking agents seem to have for treatment of children with hypertension are
fewer side effects, although their use in chil- conservative. Treatment of children with mild
dren has been limited. hypertension should focus on lifestyle- or
Benefit may be achieved with pharmacologic health-related behavioral changes including
intervention at less severe levels of hyperten- weight reduction and increased physical
sion in some clinical situations. Children with activity. Children with secondary hyperten-
confirmed chronic renal disease such as chronic sion, which may or may not be curable, should
glomerulonephritis should have therapy to have therapy directed at the underlying cause
reduce BP to below the 95th percentile to of the hypertension.
preserve renal function. Children with diabetes
constitute another group of patients warranting PUBLIC HEALTH CONSIDERATIONS
very careful BP surveillance. There is evidence In the general population, it is estimated that
that some children with diabetes, especially more than 70 percent of premature morbidity
12
Table 4
Antihypertensive Drug Therapy for Chronic Hypertension

in Children
Listed in alphabetical order by drug class*
Dose (mg/kg/day) Dosing
Drug Initial Maximum Interval
Adrenergic-Blocking Agents
Alpha-/Beta-Blocker
Labetalol 1 3 q 6-12 hr
Alpha-Blocker
Prazosin 0.05-0.1 0.5 q 6-8 hr
Beta-Adrenergic Blockers
Atenolol 1 8 q 12-24 hr
Propranolol 1 8 q 6-12 hr
Alpha-Agonist
Clonidine 0.05-0.1** 0.5-.6† q 6 hr
Calcium Antagonists
Nifedipine 0.25 3 q 4-6 hr
Nifedipine XL 0.25 3 q 12-24 hr
Converting Enzyme Inhibitors

Captopril
Children 1.5 6 q 8 hr
Neonates 0.03-0.15 2 q 8-24 hr
Enalapril 0.15 not established q 12-24 hr
Diuretics
Bumetanide 0.02-0.05 0.3 q 4-12 hr
Furosemide 1 12 q 4-12 hr
Hydrochlorothiazide 1 2-3 q 12 hr
Metolazone 0.1 3 q 12-24 hr
Spironolactone 1 3 q 6-12 hr
Triamterene 2 3 q 6-12 hr
Vasodilators
Hydralazine 0.75 7.5 q 6 hr
Minoxidil 0.1-0.2 1 q 12 hr
*Other drugs are available in some classes, but data on dosage in children have not been published.
**Total initial dose in mg.
†Total daily dose in mg.
can be attributed to tobacco use, undertreatment be encouraged for all children and their fami-
of hypertension, and obesity.57,58 From a public lies. In addition to monitoring BP, appropriate
health perspective, health-related behaviors that nutrition and exercise should be encouraged
reduce the risk of cardiovascular disease should and smoking should be strongly discouraged
during childhood.
13
REFERENCES
1. National Health and Nutrition Examination 8. Sinaiko AR, Gomez-Marin O, Prineas RJ.
Survey: blood pressure levels of persons 6-74 Prevalence of “significant” hypertension in
years, U.S., 1971-74. Hyattsville, MD: junior high school-aged children: the
National Center of Health Statistics, 1977; Children and Adolescent Blood Pressure
DHEW publication no. (HRA) 78-1648 Program. J Pediatr. 1989;114:664-669.
(Vital and Health Statistics; series 11; no.
9. Sinaiko AR, Gillum RF, Jacobs DR Jr, Sopko
203):37-44. G, Prineas RJ. Renin-angiotensin and
2. National Heart, Lung, and Blood Institute. sympathetic nervous system activity in grade
Report of the Task Force on Blood Pressure school children. Hypertension. 1982;4:299-
Control in Children. Pediatrics. 1977;59:797- 306.
820.
10. Zinner SH, Rosner B, Oh W, Kass EH.
3. National Heart, Lung, and Blood Institute. Significance of blood pressure in infancy:
Report of the Second Task Force on Blood familial aggregation and predictive effect on
Pressure Control in Children—1987. later blood pressure. Hypertension. 1985;7:
Pediatrics. 1987;79(1):1-25. 411-416.
4. Loggie J. Pediatric Hypertension. Boston: 11. Zinner SH, Levy PS, Kass EH. Familial
Blackwell Scientific Publications, 1992. aggregation of blood pressure in childhood.
5. Falkner B. Evaluation of the child and N Engl J Med. 1971;284:401-404.
adolescent with hypertension. In: Izzo JL, 12. Shear CL, Burke GL, Freedman DS,
Black HR, eds. Hypertension Primer. Dallas: Berenson GS. Value of childhood blood
American Heart Association, 1993;239-242. pressure measurements and family history in
6. Rocchini AP. Treatment of childhood hyper- predicting future blood pressure status:
tension. In: Izzo JL, Black HR, eds. Hyper- results from 8 years of follow-up in the
tension Primer. Dallas: American Heart Bogalusa Heart Study. Pediatrics. 1986;77:
862-869.
Association, 1993;320-321.
13. Prineas RJ, Gomez-Marin O, Gillum RF.
7. Joint National Committee. The fifth report
of the Joint National Committee on Detec- Tracking of blood pressure in children and
tion, Evaluation, and Treatment of High nonpharmacological approaches to the
prevention of hypertension. Ann Behav Med.
Blood Pressure. Arch Intern Med. 1993;153:
154-183. 1985;7:25-29.
14
14. Shieken RM, Clarke WR, Lauer RM. Left 22. Prineas RJ, Sinaiko AR. Hypertension in
ventricular hypertrophy in children with children. In: Swales JD, ed. Textbook of
blood pressures in the upper quintile of the Hypertension. Boston: Blackwell Scientific
distribution: the Muscatine Study. Hyperten- Publications, 1994;750-766.
sion. 1981;3:669-675. 23. Sinaiko AR, Gomez-Marin O, Prineas RJ.
15. Zahka KG, Neill CA, Kidd L, Cutilletta Diastolic fourth and fifth phase blood
MA, Cutilletta AF. Cardiac involvement in pressure in 10-15-year-old children: the
adolescent hypertension: echocardiographic Children and Adolescent Blood Pressure
determination of myocardial hypertrophy. Program. Am J Epidemiol. 1990;132:647-
Hypertension. 1981;3:664-668. 655.
16. Culpepper WS, Sodt PC, Messerli FH, 24. Reusz GS, Hóbor M, Tulassay T, Sallay P,
Ruschhaupt DG, Arcilla RA. Cardiac status Miltényi M. 24 hour blood pressure moni-
in juvenile borderline hypertension. Ann toring in healthy and hypertensive children.
Intern Med. 1983;98:1-7. Arch Dis Child. 1994;70:90-94.
17. Sinaiko AR, Bass J, Gomez-Marin O, Prineas 25. Harshfield GA, Alpert BS, Pulliam DA,
RJ. Cardiac status of adolescents tracking Somes GW, Wilson DK. Ambulatory blood
with high and low blood pressure since early pressure recordings in children and adoles-
childhood. J Hypertens. 1985;4(suppl cents. Pediatrics. 1994;94:180-184.
5):S378-S380. 26. Rosner B, Prineas RJ, Loggie JMH, Daniels
18. Daniels SD, Meyer RA, Loggie JMH. SR. Blood pressure nomograms for children
Determinants of cardiac involvement in and adolescents, by height, sex, and age, in
children and adolescents with essential the United States. J Pediatr. 1993;123:871-
hypertension. Circulation. 1990;82:1243- 886.
1248. 27. Centers for Disease Control and Prevention,
19. Burke GL, Arcilla RA, Culpepper WS, National Center for Health Statistics.
Webber LS, Chiang Y-K, Berenson GS. National Health and Nutrition Examination
Blood pressure and echocardiographic Survey (NHANES III), 1988-1991, data
measures in children: the Bogulusa Heart computed for the National Heart, Lung, and
Study. Circulation. 1987;75:106-114. Blood Institute. Atlanta, GA: Centers for
Disease Control and Prevention.
20. Lauer RM, Clarke WR. Childhood risk
factors for high adult blood pressure: the 28. Hulman S, Edwards R, Chen YQ, Polansky
Muscatine Study. Pediatrics. 1984;84:633- M, Falkner B. Blood pressure patterns in the
641. first three days of life. J Perinatol. 1991;11:
231-234.
21. Prineas RJ, Elkwiry ZM. Epidemiology and
measurement of high blood pressure in 29. Zubrow A, Hulman S, Kushner H, Falkner
children and adolescents. In: Loggie JMH, B. Determinants of blood pressure in infants
ed. Pediatric and Adolescent Hypertension. admitted to neonatal intensive care units: a
Boston: Blackwell Scientific Publications, prospective, multicenter study. J Perinatol.
1992;91-103. 1995;15:470-479.
15
30. Rocchini AP, Katch V, Anderson J, 40. Hansen HS, Froberg K, Hyldebrandt N,
Hinderliter J, Becque D, Martin M, Marks Nielsen JR. A controlled study of eight
C. Blood pressure in obese adolescents: effect months of physical training and reduction of
of weight loss. Pediatrics. 1988;82:16-23. blood pressure in children: the Odense
School-Child Study. Br Med J.
31. Messerli FH, Sundgaard-Riise K, Reisin E,
Dreslinski G, Dunn FG, Frohlich E. Dispar- 1991;303:682-685.
ate cardiovascular effects of obesity and 41. Law MR, Frost CD, Wald NJ. By how much
arterial hypertension. Am J Med. does dietary salt reduction lower blood
1983;74(5):808-812. pressure? III. Analysis of data from trials of
salt reduction. Br Med J. 1991;302:819-824.
32. Must A, Jacques PF, Dallal GE, Bajema CJ,
Dietz WH. Long-term morbidity and 42. Cutler JA, Follmann D, Elliott P, Suh I. An
mortality of overweight adolescents. N Engl overview of randomized trials of sodium
J Med. 1992;327:1350-1355. reduction and blood pressure. Hypertension.
1991;17(suppl I):I27-I33.
33. Rocchini AP, Key J, Bondie D, Chico R,
Moorehead C, Katch V, Martin M. The effect 43. Cooper R, Van Horn L, Liu K, Trevisan M,
of weight loss on the sensitivity of blood Nanas S, Ueshima H, Larbi E, Yu C-S,
pressure to sodium in obese adolescents. N Sempos C, LeGrady D, Stamlar J. A ran-
Engl J Med. 1989;321:580-585. domized trial on the effect of decreased
dietary sodium intake on blood pressure in
34. Epstein LH, Valoski A, McCurley J. Effect of
weight loss by obese children on long-term adolescents. J Hypertens. 1984;2:361-366.
growth. Am J Dis Child. 1993;147:1076- 44. Howe PRC, Cobiac L, Smith RM. Lack of
1080. effect of short-term changes in sodium
35. Himes JH, Dietz WH. Guidelines for intake on blood pressure in adolescent
schoolchildren. J Hypertens. 1991;9:181-186.
overweight in adolescent preventive services:
recommendations from an expert commit- 45. Prineas RJ. Salt intake and blood pressure in
tee. Am J Clin Nutr. 1994;59:307-316. childhood: implications for clinical practice
36. Brownell KD, Kelman J, Stunkard J. and public health. In: Filer LJ, Lauer RM,
Treatment of obese children with and Luepker RV, eds. Prevention of Atherosclerosis
and Hypertension Beginning in Youth. Philadel-
without their mothers: change in weight and
blood pressure. Pediatrics. 1983;71:515-523. phia: Lea & Febiger, 1994;120-128.
37. Epstein LH, Valoski A, Wing RR, McCurley 46. Berenson GS, Voors AW, Webber LS,
J. Ten-year follow-up of behavioral, family- Dalferes ER Jr, Harsha DW. Racial differ-
ence of parameters associated with blood
based treatment for obese children. JAMA.
1990;264:2519-2523. pressure levels in children: the Bogalusa
Heart Study. Metabolism. 1979;28:1218-
38. Mellin LM, Frost L. Child and adolescent 1228.
obesity: the nurse practitioner’s use of the
SHAPEDOWN Method. J Pediatr Health 47. Hohn AR, Dwyer KM, Dwyer JH. Blood
pressure in youth from four ethnic groups:
Care. 1992;6:187-193.
the Pasadena Prevention Project. J Pediatr.
39. Mellin LM. To: President Clinton, Re: 1994;125:368-373.
Combating childhood obesity. J Am Diet
Assoc. 1993;93:265-266.
16
48. Doyle AE. Angiotensin-converting enzyme 57. Lawrence M, Arbeit M, Johnson CC,
(ACE) inhibition: benefits beyond blood Berenson GS. Prevention of adult heart
pressure control. Am J Med. 1992;92(4B): disease beginning in childhood: intervention
1S-107S. programs. Cardiovasc Clin. 1991;21:249-
262.
49. Mirkin BL, Newman TJ. Efficacy and safety
of captopril in the treatment of severe 58. Konner, M. Medicine at the Crossroads: The
childhood hypertension: report of the Crisis in Health Care. New York: Pantheon
International Collaborative Study Group. Books, 1993;220.
Pediatrics. 1985;75:1091-1100. 59. Harlan WR, Cornoni-Huntley J, Leaverton
50. O’Dea RF, Mirkin BL, Alward CT, Sinaiko PE. Blood pressure in childhood: the Na-
AR. Treatment of neonatal hypertension tional Health Examination Survey. Hyperten-
with captopril. J Pediatr. 1988;113:403-406. sion. 1979;1:559-565.
51. Hricik DE, Dunn MJ. Angiotensin-convert- 60. Schachter J, Kuller LH, Perfetti C. Blood
ing enzyme inhibitor-induced renal failure: pressure during the first five years of life:
causes, consequences, and diagnostic uses. J relation to ethnic group (black or white) and
Am Soc Nephrol. 1990;1:845-858. to parental hypertension. Am J Epidemiol.
52. Pryde PG, Sedman AB, Nugent CE, Barr M. 1984;119:541-553.
Angiotensin-converting enzyme inhibitor 61. Fixler DE, Laird WP. Validity of mass blood
fetopathy. J Am Soc Nephrol. 1993;3:1575- pressure screening in children. Pediatrics.
1582. 1983;72:459-463.
53. Furberg CD, Psaty BM, Meyer JV. 62. Baron AE, Freyer B, Fixler DE. Longitudinal
Nifedipine: dose-related increase in mortal- blood pressure in blacks, whites and Mexican
ity in patients with coronary heart disease. Americans during adolescence and early
Circulation. 1995;92:1326-1331. adulthood. Am J Epidemiol. 1986;123:809-
817.
54. National Heart, Lung, and Blood Institute.
New Analyses Regarding the Safety of Calcium- 63. Voors AW, Foster TA, Frerichs RR, Webber
Channel Blockers: A Statement for Health LS, Berenson GS. Studies of blood pressure
Professionals From the National Heart, Lung, in children, ages 5-14 years in a total biracial
and Blood Institute. Bethesda, MD: National community: the Bogalusa Heart Study.
Institutes of Health, 1995. Circulation. 1976;54:319-327.
55. Krolewski AS, Canessa M, Warram JH, 64. Berenson GS, McMahan CA, Voors AW, et
Laffel LMB, Christlieb AR, Knowler WC, al. Cardiovascular Risk Factors in Children: The
Rand LI. Predisposition to hypertension and Early Natural History of Atherosclerosis and
susceptibility to renal disease in insulin- Essential Hypertension. New York: Oxford
dependent diabetes mellitus. N Engl J Med. University Press, 1980.
1988;318:140-145. 65. Berenson GS. Causation of Cardiovascular Risk
56. National High Blood Pressure Education Factors in Children: Perspectives on Cardiovascu-
Program. Working group report on hyper- lar Risk in Early Life. New York: Raven
tension and diabetes. Hypertension. 1994;23: Press, 1986.
145-158.
17
66. Gutgesell M, Terrell G, Labarthe D. Pediat- 68. Clarke WR, Schrott HG, Leaverton PE,
ric blood pressure: ethnic comparison in a Connor WE, Lauer RM. Tracking of blood
primary care center. Hypertension. 1981;3:39- lipids and blood pressures in school-age
49. children: the Muscatine study. Circulation.
1978;58:626-634.
67. Lackland DT, Riopel DA, Shepard DM,
Wheller FC. Blood pressure and anthro- 69. Lauer RM, Clarke WR, Beaglehole R. Level,
pometric measurement results of the South trend, and variability of blood pressure
Carolina Dental Health and Pediatric Blood during childhood: the Muscatine study.
Pressure Study. Columbia: South Carolina Circulation. 1984;69:242-249.
Department of Health and Environmental
70. Gomez O, Prineas RJ, Sinaiko AR. The
Control, 1985. sodium-potassium blood pressure trial in
children. Controlled Clin Trials. 1991;12:408-
423.
18
APPENDIX 1. DEMOGRAPHIC DATA ON HEIGHT/BLOOD PRESSURE
DISTRIBUTION CURVES OF STUDY POPULATION
Personsa Personsb Total

Ethnic Group (Visits) (Visits) No. of
Age Gender Native SBP DBP (K5) Personsc
Source (year) Boys Girls Black Hispanic White Asian American Other Missing Available Available (Visits)
NIH59 6-17 1,901 1,751 600 0 2,968 0 0 84 0 3,647 3,614 3,652

(3,647) (3,614) (3,652)
Pittsburgh60 1-5 150 137 109 0 177 0 0 0 1 287 0 287
(899) (0) (899)
Dallas61,62 13-17 5,916 5,649 5,266 1,570 4,729 0 0 0 0 11,565 11,565 11,565
(21,860) (21,852) (21,860)
Bogalusa63-65 1-17 3,752 3,611 2,483 0 4,880 0 0 0 0 7,363 0 7,363
(15,922) (0) (15,922)
Houston66 3-17 1,457 1,378 638 1,341 748 23 0 0 85 2,835 0 2,835
(2,835) (0) (2,835)
South Carolina67 4-17 3,167 3,264 3,110 0 3,321 0 0 0 0 6,431 6,369 6,431
(6,431) (6,369) (6,431)
Iowa68,69 5-17 2,100 1,993 0 0 4,093 0 0 0 0 4,093 0 4,093
(4,093) (0) (4,093)
Providence10 1-3 231 231 24 4 432 0 0 2 0 462 371 462
(906) (566) (906)
Minnesota70 9-17 9,995 9,425 3,422 556 11,320 1,678 644 1,800d 0 19,420 19,217e 19,420
(19,420) (19,217) (19,420)
NHANES III27 5-17 2,489 2,609 1,793 1,851 1,334 64 10 12 34 5,027 4,291e 5,098
(5,027) (4,291) (5,098)
Total 1-17 31,158 30,048 17,445 5,322 34,002 1,765 654 1,898 120 61,130 45,427 61,206
(81,040) (55,909) (81,116)
Percent of Total
Number of People (51) (49) (29) (9) (56) (3) (1) (3) (0)
SBP = systolic blood pressure; DBP = diastolic blood pressure; K5 = fifth Korotkoff sound; NIH = National Institutes of Health.
a
Number of persons (visits) at which SBP was available.
b
Number of persons (visits) at which DBP (K5) was available.
c
Number of persons (visits) at which either SBP or DBP (K5) was available.
d
These children were mostly of mixed ancestry, with the predominant categories white/black or white/Hispanic.
e
Excludes subjects with a value of 0 for the fifth Korotkoff sound.
19
APPENDIX 2. QUICK-REFERENCE DIAGNOSTIC CHARTS
QUICK-REFERENCE DIAGNOSTIC CHARTS 4. Find the child’s age on the right side of the
chart. Follow the age line horizontally
The quick-reference diagnostic charts are for across the chart to the intersection of the
use in the clinical setting. By following the line for the height percentile (vertical line).
steps listed below, clinicians can make a quick
assessment for classification of blood pressure. 5. Move UP or DOWN the height percentile
line to the intersection of measured blood
pressure.
CLASSIFICATION OF BLOOD PRESSURE
INCHILDREN AND ADOLESCENTS* Result on 90th Percentile Chart:
• If you move DOWN on the height
SBP and DBP < 90th percentile Normal percentile line, blood pressure is
SBP or DBP > 90th percentile High- NORMAL. Repeat steps 3 through 5 on
and < 95th percentile Normal** the chart for 90th percentile SBP.
SBP or DBP > 95th percentile Hypertension** • If you move UP on the height percentile
* for age and sex line, you must repeat steps 3 through 5 on
** for age and sex measured on at least three the chart for 95th percentile DBP.
separate occasions
Result on 95th Percentile Chart:
SBP = systolic blood pressure
DBP = diastolic blood pressure • If you move DOWN on the height
percentile line, blood pressure is HIGH-
NORMAL. Repeat steps 3 through 5 on
USING THE CHARTS the chart for 95th percentile SBP.
1. Use the standard height charts to determine • If you move UP on the height percentile
the height percentile. line, HYPERTENSION* is indicated.
2. Measure the child’s blood pressure. Repeat steps 3 through 5 on the chart for
Record SBP and DBP. 95th percentile SBP.
3. Use the correct gender chart for 90th
percentile of DBP.
Data points for the Quick-Reference Diagnostic Charts are found in tables 1 and 2.
*Note that hypertension is diagnosed after three consecutive BP readings above the 95th percentile
on three separate occasions.
20
90TH PERCENTILE OF SYSTOLIC AND DIASTOLIC BLOOD PRESSURE
BY HEIGHT AND AGE, GIRLS
Systolic (mm Hg) Age Diastolic (mm Hg) Age

140 90
135
85
15,16 and 17
130
14
16,17
15 80 13
14
125 12
13 11
12 10
75 9
120 11 8
10
7
9 6
115 70
8 5
7
6 4
110
5 65
4 3
3
105 2
1 2
60
100
1
55
95
90 50
5 10 25 50 75 90 95 5 10 25 50 75 90 95
Height Percentile Height Percentile
21
BY HEIGHT AND AGE, GIRLS

140 90
135 15,16 and 17

85 14
16,17 13
15
130 14 12
13 11
80 10
12 9
125 8
11
10 7
75 6
120 9
5
8
7 4
115 70
6
5
3
4
110 3
2 65 2
1
105
60 1
100
55
95
90 50
5 10 25 50 75 90 95 5 10 25 50 75 90 95
22
BY HEIGHT AND AGE, BOYS

140 90
17
135
16 85 17
15 16
130
15
14
80 13,14
13 12
125 10,11
9
12
11 75 8
120 7
10
9 6
8
115 7 70
6 5
5
4
110 4
3 65
2 3
105
1 60
2
100
55 1
95
90 50
5 10 25 50 75 90 95 5 10 25 50 75 90 95
23
BY HEIGHT AND AGE, BOYS

140 17 90
17
16
16
135 15 15
85 14
14 13
11,12
130 13 10
9
12 80 8
125 11 7
10
6
9 75
120 8 5
7
6
5 4
115 4 70
3
3
110 2
65
1 2
105
60
1
100
55
95
90 50
5 10 25 50 75 90 95 5 10 25 50 75 90 95
24
Seminar
Childhood obesity
Joan C Han, Debbie A Lawlor, Sue Y S Kimm
Worldwide prevalence of childhood obesity has increased greatly during the past three decades. The increasing Lancet 2010; 375: 1737–48
occurrence in children of disorders such as type 2 diabetes is believed to be a consequence of this obesity epidemic. Published Online
Much progress has been made in understanding of the genetics and physiology of appetite control and from these May 6, 2010
DOI:10.1016/ S0140-
advances, elucidation of the causes of some rare obesity syndromes. However, these rare disorders have so far taught 6736(10)60171-7
us few lessons about prevention or reversal of obesity in most children. Calorie intake and activity recommendations
Unit on Growth and Obesity,
need reassessment and improved quantification at a population level because of sedentary lifestyles of children Program on Developmental
nowadays. For individual treatment, currently recommended calorie prescriptions might be too conservative in view Endocrinology and Genetics,
of evolving insight into the so-called energy gap. Although quality of research into both prevention and treatment has Eunice Kennedy Shriver
National Institute of Child
improved, high-quality multicentre trials with long-term follow-up are needed. Meanwhile, prevention and treatment Health and Human
approaches to increase energy expenditure and decrease intake should continue. Recent data suggest that the Development, National
spiralling increase in childhood obesity prevalence might be abating; increased efforts should be made on all fronts to Institutes of Health, DHHS,
continue this potentially exciting trend. Bethesda, MD, USA
(J C Han MD); MRC Centre for
Causal Analyses in Translational
Epidemiology to age and sex that, on average, correspond to adult Epidemiology, Department of
8 years have passed since the last Seminar on childhood thresholds. The IOTF classification has high specificity, Social Medicine, University of
obesity in The Lancet.1 Our goal is to review new but low sensitivity.8 Bristol, Bristol, UK
(Prof D A Lawlor PhD); and
information and outline some of the remaining Department of Internal
challenges. A review of secular trends in the number of Determinants and risk factors Medicine/Epidemiology,
overweight or obese children concluded that prevalence A historical convergence of forces, biological and University of New Mexico
had increased during the past two to three decades in technological, has led to the obesity epidemic. During School of Medicine,
Albuquerque, NM, USA
most industrialised countries, apart from Russia and millennia of frequent food scarcities, natural selection (S Y S Kimm MD)
Poland, and in several low-income countries, especially probably favoured people with parsimonious energy Correspondence to:
in urban areas.2 Prevalence doubled or trebled between metabolism, known as the thrifty gene hypothesis.9 Dr Sue Y S Kimm, University of
the early 1970s and late 1990s in Australia, Brazil, Canada, Although the advent of agriculture about 14 000 years New Mexico Health Sciences
Chile, Finland, France, Germany, Greece, Japan, the UK, ago ensured more stable food supplies, activities of daily Center, Department of Internal
Medicine/Epidemiology,
and the USA.2 By 2010, more than 40% of children in the living still needed substantial energy expenditure until University of New Mexico,
North American and eastern Mediterranean WHO about 50 years ago, when radical changes occurred in MSC 10 5550 Albuquerque,
regions, 38% in Europe, 27% in the western Pacific, and food availability and energy expenditure. The obesity NM 87131-0001, USA
22% in southeast Asia were predicted to be overweight or epidemic is probably the result of evolutionary legacy kimm@pitt.edu
obese. However, that 2006 review pre-dates recent data, interacting with our technologically advanced and
which, although still too soon to be certain, suggest that consumerist society. Population groups in North America
the increase in childhood obesity in the USA, the UK, who have preserved traditional lifestyles with substantial
and Sweden might be abating.3–5 embedded physical activity have reduced prevalences of
Internationally agreed thresholds of body-mass index obesity.10 Likewise, in countries with low and middle
(BMI) define underweight, normal weight, overweight, incomes, the obesity epidemic is largely occurring in
and obesity in adults, but in children, effects of age, sex, urban areas that have easy access to energy-dense cheap
puberty, and race or ethnicity on growth make foods and low energy requirements in daily life.2
classification difficult. Definition of a standard age- Obesity is a complex disorder that is affected by many
related growth chart and clinically meaningful thresholds interacting genetic and non-genetic factors. We focus
for overweight and obesity present challenges. The mainly on prevention and treatment. The table summarises
International Obesity Taskforce (IOTF) international
standard growth chart enables global comparison of
prevalence.6 However, many countries continue to use Search strategy and selection criteria
their own country-specific charts, including the USA, We identified original research, reviews, and commentaries by
where standards are based on a national survey from the searching PubMed using the search terms "paediatric obesity",
early 1960s, before the present epidemic.7 "childhood obesity", "paediatric overweight", "childhood
Widely used thresholds for being overweight or obese overweight", and "body mass index in children". All dates and
in childhood are: 110% or 120% of ideal weight for height; languages were considered. Articles published between 1962
weight-for-height Z scores of higher than 1 or higher and 2010 were included, but we directed special attention to
than 2, and BMI at the 85th, 90th, 95th, and 97th reports published since 2002. Research developments and
percentiles (on the basis of international or country- published work were also identified by discussions with
specific reference populations).2 The IOTF recommend specialists in paediatric obesity, nutrition, and public health.
using their international growth charts and limits specific
www.thelancet.com Vol 375 May 15, 2010 1737

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Association potentially modifiable Type of evidence*

Genetic variation
Rare single gene defects in which obesity is the specific abnormality—eg, those related to the leptin No, apart from leptin replacement in the few leptin- Basic science studies, case series,
signalling pathway (figure 1) deficient individuals family linkage, and genetic
association studies11
Obesity is a manifestation of several genetic syndromes (figure 2); Prader-Willi syndrome is associated No Genetic association studies11
with hyperghrelinaemia, but the mechanism of hyperphagia remains unclear;12,13 animal models of
ciliopathies (Bardet-Biedl and Alström syndromes) have defects in leptin pathway signalling;14,15
haploinsufficiency of BDNF, a downstream mediator of leptin action, is associated with hyperphagia and
obesity in children with WAGR syndrome16
Genome-wide association studies have identified several common genetic variants associated with high No Genome-wide association
adiposity and obesity, each with weak effects studies17
Epigenetics
The mechanism whereby in-utero factors can produce heritable changes in adiposity has been suggested Possibly; in animals, maternal consumption of folate, Non-systematic review of
to be due to DNA methylation or histone modification of DNA in gene regulatory regions; however, methionine, and vitamin B12 during pregnancy can evidence (largely from basic
evidence in man is scarce affect DNA methylation in offspring science and animal studies)18
Endocrine disease
Classically, hypothyroidism, growth hormone deficiency or resistance, and cortisol excess; PCOS is a Some—eg, thyroxine and growth-hormone Non-systematic review of
consequence of but also possible contributor to obesity; obesity associated with replacement, surgical treatment of Cushing syndrome; evidence (basic science,
pseudohypoparathyroidism (caused by Gαs inactivating mutation) might be due to defective signalling for PCOS, oral contraceptives, anti-androgens, and epidemiology, clinical)21
at G-protein coupled receptors, including the melanocortin receptor of the leptin pathway19 insulin sensitisers have been used, but long-term large
RCTs in adolescents are scarce20
CNS pathology
Congenital or acquired hypothalamic abnormalities have been associated with a severe form of obesity in Possibly, but still under investigation; hyperinsulinaemia Non-systematic review of
children and adolescents due to increased vagal tone has been postulated as a evidence (basic science,
contributing factor, prompting studies using octreotide, epidemiology, clinical)23
which prevented further weight gain in a small RCT, but
long-term large RCTs are needed22
Intrauterine exposure to gestational diabetes
In populations at high risk of obesity and diabetes (eg, Pima Indians), exposure to gestational diabetes is Yes Review of observational studies
associated with increased risk of childhood and early adult obesity in offspring; evidence for similar in Pima Indians;24 prospective
associations in other populations is poor cohorts in other populations25
(and other studies cited in this
reference)
Intrauterine exposure to high maternal adiposity
Investigators comparing obesity in children whose mothers had undergone bariatric surgery for extreme Yes Within sibling comparisons,26
morbid obesity showed that siblings born before surgery (when mother was very obese) were more prospective cohort studies,24,27
obese than were siblings born after weight loss in response to surgery; evidence that less extreme and mendelian randomisation
variation in maternal adiposity affects offspring obesity is scarce study27
Birthweight
High birthweight is associated with increased offspring fat and lean mass; small-for-gestational age Safe means of modification of birthweight to improve Prospective cohort studies28,29
babies who show catch-up growth might be at risk of childhood obesity, but this finding could simply health are unknown
show increased growth resulting in larger size
BMI rebound
Early age at BMI rebound is associated with greater risk of obesity, but this finding could be a statistical No, since can only be established retrospectively in Non-systematic review of
artifact individuals largely prospective cohort
studies30
(Continues on next page)
determinants or risk factors that are associated with regulate energy homoeostasis. Ghrelin, which is secreted
childhood obesity or variation in adiposity, and figure 1 by the stomach and duodenum, serves as a hunger signal
shows a simplified model of leptin signalling, which is the at the hypothalamus and brainstem, whereas other
key biological pathway controlling energy balance.2,4,11–45 peptides secreted by the gastrointestinal tract, including
Since the discovery of leptin, understanding of the peptide YY, act as satiation signals. The ligands leptin,46
mechanisms controlling energy balance has rapidly pro-opiomelanocortin,47,48 cocaine-amphetamine related
advanced. Apart from leptin replacement therapy in a few transcript,49 and brain-derived neurotrophic factor
leptin-deficient individuals, interventions that effectively (BDNF),16,50 the receptors for leptin,51,52 melanocortins,53–56
prevent or treat obesity in the general population are yet to and BDNF,57 and the enzyme prohormone convertase 158,59
emerge. Both insulin and leptin are secreted in proportion have function-changing mutations that are associated
to body fat and serve as adiposity signals, acting on the with obesity in children. Mutations in the ligands and
same neurons of the hypothalamic arcuate nucleus to receptors for neuropeptide Y,60 agouti-related protein,61
1738 www.thelancet.com Vol 375 May 15, 2010

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Association potentially modifiable Type of evidence*

(Continued from previous page)
Diet
Breastfeeding is unlikely to be causally protective against childhood obesity Yes Systematic review of
prospective cohort studies,31
RCT32
High-quality prospective evidence is sparse; available evidence suggests that high energy intake in early Yes Non-systematic review of
infancy and high consumption of sweetened drinks in childhood are prospectively associated with raised observational studies33
childhood obesity risk; absence of evidence for other dietary characteristics could be attributable to poor
study design and difficulties of accurate assessment of diet in children
Energy expenditure
Low levels of physical activity are associated with high childhood obesity risk Yes Systematic review of
observational studies34
Television viewing
Large number of hours spent viewing are associated with raised childhood obesity risk Yes Systematic review of
observational and experimental
studies35
Sleep
Short sleep duration in infancy and childhood is associated with raised childhood obesity risk Possibly Prospective cohort study36
Microbial infection
Potential role of microbial infection (eg, adenovirus Ad-36) and composition of gut flora (eg, ratio of Yes Cross-sectional studies37,38
Firmicutes to Bacteroidetes spp) in the pathogenesis of obesity; however, epidemiological evidence in the
non-selected general population is scarce
Iatrogenic
Cranial irradiation or surgery causing hypothalamic damage; psychotropic drugs (eg, olanzapine and Depends on disease or treatment and risk-benefit Non-systematic review of
risperidone), chemotherapeutics (eg, treatment of acute lymphocytic leukaemia even without cranial considerations evidence (basic science,
irradiation), and hormonal contraception (eg, depot medroxyprogesterone acetate) have been epidemiology, clinical)23 and
associated with increased weight gain in children and adolescents prospective cohort studies39–41
Ethnic origin
Some ethnic groups—eg, Hispanic and south Asian—seem to be more likely to become obese; at a No Cross-sectional studies42,43
specific BMI, children and infants of south Asian origin have higher adiposity than do their counterparts
Country of birth
Children from countries with low and middle incomes tend to be stunted and underweight, but with No Cross-sectional and ecological
sufficient nutrition gain healthy weight, and with overnutrition are prone to obesity studies44
Urban versus rural residence
Children in urban areas are more likely to be obese than are those in rural areas in many countries, Unlikely to be able to change where families live, but Cross-sectional studies2
including those with high and low-middle incomes might be able to modify underlying reasons for
association
Socioeconomic position
In high-income countries, generations born before the 1950s and 1960s did not show socioeconomic Yes, with major political and cultural changes; might be Prospective two-generational
differentials in adiposity or obesity in childhood (though do as adults); some evidence exists that in able to modify underlying reasons for association cohort study45
contemporary populations, children in lowest socioeconomic groups in high-income countries have
raised obesity rates
This table has been modified and updated from reference 4. *We cite the most recent systematic review of the highest level of evidence for most risk factors, rather than providing a comprehensive list of all
papers for every risk factor, which would be beyond the scope of this Seminar. BDNF=brain-derived neurotrophic factor. WAGR=Wilms tumour, aniridia, genitourinary anomalies, mental retardation.
PCOS=polycystic ovary syndrome. RCT=randomised controlled trial. BMI=body-mass index.
Table: Determinants or risk factors for development of childhood obesity or increased adiposity
carboxypeptidase E,62,63 and melanin-concentrating hor- affecting appetite should be considered during
mome64 change energy balance in rodents, but have not assessment of paediatric patients with obesity (figure 2).
been convincingly associated with human obesity. For Clinical history and examination should guide differential
several risk factors, evidence is weak and, although diagnosis. Onset of obesity during early infancy raises
important advances have been made, how to incorporate suspicion of function-changing genetic mutations
the information effectively and cost-effectively into affecting the leptin signalling pathway, but these
prevention programmes for children is unclear. disorders are very rare, with the most common,
melanocortin-4-receptor defects, affecting less than
Differential diagnosis and complications 5% of children with early-onset obesity.56 During
Endocrine diseases, congenital and acquired hypo- assessment of new-onset excessive weight gain, potential
thalamic defects, genetic syndromes, and use of drugs side-effects from a recently initiated drug should be

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Hypothalamus
Adipocytes Leptin
(+) LR POMC PC1 (+)
α-MSH Melanocortin
IR CART CPE receptors
Insulin (–)
(–)
LR AgRP
Pancreas (+)
IR NPY (+)
(+)
(+) BDNF
Ghrelin (–)
(+)
Y2 receptor
CRH, TRH, oxytocin,
histamine, others TrkB
receptor
PYY,
others MCH, orexin, galanin,
GABA, others
Hindbrain
GI tract (+) (+) (+)
(+)
(+) (+)
Catabolic effects
Anabolic effects
Food and/or Energy Food and/or Energy

intake expenditure intake expenditure
Figure 1: A simplified model of the leptin signalling pathway

Lines with arrowheads show stimulatory action. Lines with perpendicular endblocks show inhibitory action. AgRP=agouti-related protein. BDNF=brain-derived neurotrophic
factor. CART=cocaine-amphetamine related transcript. CPE=carboxypeptidase E. CRH=corticotropin-releasing hormone. GABA=gamma amino butyric acid.
GI=gastrointestinal. IR=insulin receptor. LR=leptin receptor. MCH=melanin-concentrating hormone. MSH=melanocyte-stimulating hormone. NPY=neuropeptide Y.
PC1=prohormone convertase 1. POMC=pro-opiomelanocortin. PYY=peptide YY. TRH=thyrotropin-releasing hormone. TrkB=tropomyosin receptor kinase B.
taken into consideration, because weight gain can be lipid and glucose concentrations after overnight fasting,
associated with administration of insulin or insulin and alanine aminotransferase. If fasting glucose
secretagogues, glucocorticoids, hormonal contraceptives concentration is 5·6–6·9 mmol/L, an oral glucose
(eg, depot medroxyprogesterone acetate), psychotropic tolerance test is recommended. Screening for vitamin D
drugs (including atypical antipsychotics [eg, clozapine, and iron deficiency should also be considered.
olanzapine, risperidone], mood stabilisers [eg, lithium], Childhood obesity can adversely affect almost every
tricyclic antidepressants [eg, amitriptyline, imipramine, organ system (figure 3) and often has serious
and nortriptyline], and anticonvulsants [eg, valproic acid, consequences, including hypertension, dyslipidaemia,
gabapentin, and carbamazepine]), antihypertensive insulin resistance or diabetes, fatty liver disease, and
drugs (eg, propranolol and clonidine), and anti- psychosocial complications.66 Results of one study
histamines.65 In patients with decreased growth velocity showed that being overweight or obese between ages
despite continued weight gain, an endocrinopathy 14 and 19 years was associated with increased adult
should be considered; measurement of thyroid- mortality (from age 30 years) from various systemic
stimulating hormone and free thyroxine and referral to a diseases.67 The atherosclerotic process68 seems to be
paediatric endocrinologist are recommended. accelerated in obese children and almost half of children
Almost all patients, however, do not have any of these with BMI higher than the 97th percentile have one or
identifiable disorders. All patients, irrespective of cause more of the disorders that make up the metabolic
of obesity, should be assessed for modifiable lifestyle syndrome.69 High childhood and adolescent BMI is
factors, including physical activity and diet, and screened associated with increased risk of cardiovascular disease
for complications of obesity, including measurement of in adulthood.70 Pulmonary disorders, including

Seminar
obstructive sleep apnoea and reactive airway disease,71 are

Onset of obesity in early Yes Possible genetic defect of
reported more frequently in obese children than in their See figure 1
infancy leptin signalling pathway
normal-weight counterparts. Asthma severity, however,
No
does not seem to be affected by obesity;72 weight-related
but non-asthmatic airflow limitations are perhaps being Drug-associated weight Yes
Consider change of drug
misdiagnosed as asthma in some obese children.73 gain
Specific nutritional deficiencies often accompany No
childhood obesity. High BMI and adiposity have been Hypothyroidism
associated with low vitamin D concentrations in children.74 Poor linear growth despite Yes Consider endocrine Growth hormone deficiency
weight gain disorders Cushing syndrome
The mechanism underlying low vitamin D concentrations Pseudohypoparathyroidism 1a
in obesity is unclear, but increased storage of vitamin D in No
adipose tissue has been proposed.75 Overweight or obese Imaging and neuroendocrine
Congenital midline defect Yes screening for structural or
children are also at least twice as likely to be iron-deficient or history of intracranial functional hypothalamic
irradiation or surgery
than children of normal weight.76 Obesity leads to increased dysfunction
Prader-Willi syndrome
production of proinflammatory cytokines that in turn No Bardet-Biedl syndrome
promote release of hepcidin, which is a peptide hormone Alström syndrome
Developmental delay or Yes Consider genetic Cohen syndrome
produced by the liver and adipocytes that decreases iron dysmorphic features syndromes Smith-Magenis syndrome
absorption from the gut.77 Fragile X syndrome
SIM1 mutation
Complications of childhood obesity include acceleration No WAGR syndrome
in timing of thelarche and menarche in girls,78,79 pubertal
advancement in boys80 and adverse effects on maturation81 Assess modifiable lifestyle
Normal examination, Yes Screen for comorbidities of
and alignment82 of developing bones in both sexes. normal or increased stature factors (diet and physical
obesity
activity)
Advanced skeletal maturation has been attributed to
increased adipose tissue aromatisation of weak andro-
Figure 2: Recommended assessment of childhood-onset obesity
gens into more potent oestrogens. Obesity might also Y=yes. N=no. WAGR=Wilms tumour, aniridia, genitourinary anomalies, mental retardation.
affect pubertal timing through nutrition-related signals
(eg, insulin and leptin) on the reproductive axis.83 further weight gain in 90% of overweight children; this
Orthopaedic complaints, including fractures, musculo- deficit is equivalent to a child walking an additional 1–2 h
skeletal discomfort, impaired mobility, and lower-limb per day at 1·9 km/h, or consuming roughly a fifth fewer
malalignment seem to be more common in obese children calories than usual per day.
than in those who are not overweight.82 Serious orthopaedic Prevention measures can be instituted at individual,
complications of childhood obesity are tibia vara (Blount’s household, institutional, community, and health-care
disease or adolescent bowing of the legs)84 and slipped levels. At the individual level, carers should be targeted
capital femoral epiphyses.85 By contrast, however, obesity rather than young children themselves, and focus on
might have some beneficial effect on bone mineral density. mothers seems reasonable. First, developmental or fetal
Results of a recent study, using variation in the FTO gene overnutrition as a result of gestational diabetes or
as an instrumental variable, suggested that high fat mass maternal obesity might have contributed to the obesity
in children was causally associated with increased total, epidemic (table).1 So far, no intervention studies have
spinal, and limb bone mineral content.86 examined the long-term effect of reduction of gestational
diabetes or maternal adiposity on future obesity risk in
Prevention offspring. Second, breastfeeding might prevent
Prevention, especially in young people, is universally childhood obesity. However, results of systematic
viewed as the best approach to reverse the rising global reviews suggest that observational associations could
prevalence of obesity. However, evidence about the most be accounted for largely by residual confounding or
effective means of prevention of obesity development in publication bias, and in a large randomised trial of a
children is scarce. Many prevention trials have had breastfeeding promotion intervention, no causal effect
sample sizes too small for expected effect size or of breastfeeding on obesity risk was reported.91 Third,
insufficient length of follow-up. Some trials have also mothers might influence diets of offspring more than
been criticised for not being based on sound theories of do fathers;92 however, no intervention trials of maternal-
behavioural change and for having inadequate feasibility only interventions to prevent childhood obesity have
and pilot work.87 been done.
Trials of prevention interventions might also have At a household or family level, encouragement of parents
failed to show notable effects because they did not to offer appropriate food portions, foster physical activity,
adequately address the energy gap88 separating children increase activities of daily living, and keep sedentary
who remain lean from those who gain weight throughout behaviours to a minimum are viewed as basic measures of
childhood.89 Butte and Ellis90 calculated that an energy prevention.93 Most government guidelines have traditionally
deficit of more than 250 kcal per day is needed to prevent focused on ensuring that nutritional intake is adequate.94

Seminar
CNS/psychosocial might be effective. Gonzalez-Suarez and colleagues96

Pseudotumour cerebri identified 19 high-quality trials of school-based inter-
Decreased quality of life ventions and reported reduced odds of overweight or
Pulmonary
obesity in intervention compared with control groups
Obstructive sleep apnoea (pooled odds ratio 0·74 [95% CI 0·60–0·92]). The key
Asthma effective characteristics of such programmes remain to be
Exercise intolerance Cardiovascular
Raised blood pressure
established, and, since most studies were done in the
Dyslipidaemia USA, whether they are effective elsewhere. Although
Atherosclerosis initiatives have also been aimed at children in kindergarten
Endocrine
Chronic inflammation
Insulin resistance
Coagulopathy or nurseries,97 the few controlled trials in this setting have
PCOS
Pubertal advancement not yet been systematically reviewed. One area to be
addressed is the built environment of schools or nurseries.
Renal
Hyperfiltration Architectural designs of school buildings and their
Glomerulopathy environment can be re-examined for opportunities to
Gastrointestinal/nutrition impose increased energy expenditure. A multi-storey
Fatty liver disease
Gastro-oesophageal reflux
building with purposefully designed class schedules could
Cholelithiasis Orthopaedic
lead to substantial stair (or ramp) climbing during the
Iron deficiency Lower-limb malalignment school day.
Vitamin D deficiency SCFE Prevention in the community includes public policies
Osteoarthritis
and mass-media campaigns.98,99 For the past decade,
pressure has been increasing for labelling of caloric
contents on menus, especially at fast-food restaurants.
However, data for the effects of such labelling on
prevention of childhood obesity are scarce.100 In 2002, the
US Centers for Disease Control and Prevention launched
a 2-year marketing campaign via media advertisements
to promote physical activity in children aged 9–13 years.101
Children’s physical activity (assessed by self-report)
increased,98,99 but effects on BMI were not assessed. In
several countries, governments are being urged to
address the toxic environment by levying taxes on sugared
Figure 3: Complications associated with childhood obesity beverages and fast foods, though the effectiveness of
Image obtained by dual energy x-ray absorptiometry from a teenage girl with BMI 38 kg/m². Disorders that are of such measures is unknown.102
high prevalence and are well established in their association with childhood obesity are shown in red.
PCOS=polycystic ovary syndrome. SCFE=slipped capital femoral epiphysis.
Popular media in several countries have given much
attention to the topic of obesity, but no objective
However, these guidelines might not be useful to ensure information is available about the effect of these
energy intakes that are appropriate for contemporary messages on the public. Public health surveillance and
sedentary lifestyles. We are unaware of any randomised screening for childhood obesity have been implemented
controlled trials focusing solely on household or family- in some communities. In 2003, Arkansas was the first
based interventions to prevent childhood obesity. US state to pass legislation for mandatory BMI
Most randomised prevention trials have taken place in assessments of children in public schools, with yearly
schools since they are viewed as a universal catchment reporting to parents. This approach has since been
setting for children. The core features of most prevention followed in 13 other states.103,104 In 2005, a National Child
programmes are to change the caloric content of school Measurement Programme was introduced in the UK
meals and encourage physical activity. One policy that is for yearly surveillance of two school year groups. In
debated in the USA is removal of vending machines from 2007, the British Government introduced legislation to
schools to curb availability of energy-dense snack foods. give parents the results of their child’s measurements.
However, a US national survey showed that snack foods Existing evidence is unclear as to whether surveillance
from vending machines contributed only 1·3% of total or screening of childhood obesity will be valuable
daily calories from snacks, whereas snacks at or from for prevention.
home contributed 69·1%.95 At least nine systematic Infants and young children are seen frequently in
reviews have examined randomised controlled trials of medical settings for well-child and acute care. These
school-based childhood obesity prevention program- visits present an opportunity to detect upward deviations
mes87,96 (see also citations of other systematic reviews in a child’s growth rate, thus placing the primary-care
within these reports). Early reviews noted scarce evidence provider at the strategic first line of defence before BMI
of effectiveness and poor quality of studies, whereas more exceeds recommended values. However, data for the
recent reviews suggested that school-based interventions effectiveness of such counselling for obesity prevention

Seminar
are scarce. Some crucial periods during childhood with a behavioural program aimed at changing diet and
present both challenges and windows of opportunity for physical activity and thinking patterns provide significant
obesity prevention because they are associated with and clinically meaningful decreases in overweight in both
notable changes in adiposity accrual or obesity-related children and adolescents...in the short- and the long-
behaviour. These periods are the first year of life,28 during term”. These findings are encouraging and provide useful
adiposity rebound (age 3–7 years), and menarche.105 The guidance for treatment of obese children, but they also
transition from childhood to adolescence is a time of emphasise the need for additional large randomised
striking behavioural changes, including an abrupt controlled trials with long-term follow-up.
reduction in physical activity.106 Although whether A catabolic state of stored energy is needed to induce
preventive measures instituted during these times will weight loss. Guidelines from the American Academy of
prevent excessive growth is unclear, these opportunities Pediatrics recommend that weight-reducing diets contain
should be investigated further. “less energy than that required to maintain weight but not
Common sense supports a key role for decreased less than 1200 kilocalories a day.”110 Equivalent UK
energy intake and increased energy expenditure in guidance emphasises energy balance between intake and
human beings, who have adapted through evolutionary expenditure, but does not specify amounts of intake.111
processes to parsimonious energy metabolism. Thus, Another recommended approach is to construct a diet that
prevention programmes should decrease energy intake, is 300–400 kcal per day lower than weight-maintenance
increase activity, and reduce sedentary behaviour. To requirements as assessed by dietary history or as calculated
balance the need for more definitive research into which on the basis of a formula relating anthropometry to energy
interventions best achieve changes in these behaviours expenditure, such as the Harris-Benedict equation. In
against the pressure to act now to halt and reverse the view of the magnitude of the energy gap, a sizeable energy
obesity epidemic, we need to continue with both deficit would be needed to induce appreciable weight
prevention activities and research to better understand reduction in an obese child, and many weight-loss diets
the means of induction of behavioural changes and their might be energy neutral in young children or even lead to
effect on childhood obesity. weight gain in sedentary female adolescents.88,90
For prevention, one might recall the words of Some guidelines (eg, in the UK) and commentators
Rudolph Virchow, a 19th century German pathologist, emphasise behavioural strategies that do not specify
who wrote that ‘‘epidemics appear, and often disappear actual caloric intake. Results of a randomised trial of
without traces, when a new culture period has started” behavioural treatment without specified calorie limits
and that mass diseases are “due to...disturbances of showed no effect on BMI.112,113 A protein-sparing modified
human culture”.107 Geoffrey Rose promulgated the notion fast has a very low calorie regimen (600–800 kcal per day)
further that whole populations can be sick (such as the and seems to be promising, but this notion has not
case of obesity), and that political action might be needed progressed since it was first reported.114 Transient growth
to improve population health.108 Thus, we should continue deceleration was recorded, but growth returned to normal
to seek opportunities for prevention at all levels of society, by 14 months.115 However, this trial was not randomised
including having responsible public policies to modify and had few follow-up data.
our manner of living, since there remain many untapped Promotion of increased energy expenditure for weight
resources and untried venues. reduction has not received the same attention as have
dietary prescriptions. We found only one randomised
Non-pharmacological treatment controlled trial of 6–11-year-old obese children that
We recommend that children with BMI higher than the compared hypocaloric diet, 90 min of moderate exercise
95th percentile, or higher than the 85th percentile when 3 days per week, or both. Weight loss was greater in the
accompanied by comorbidities, such as hyperten- diet or diet-plus-exercise group (being similar in these
sion, hyperlipidaemia, or impaired glucose tolerance, be two) than in the exercise-only group, but there was no
considered for treatment. Non-pharmacological control group and follow-up lasted only 9 months.116
approaches should be the foundation of all obesity treat- Interventions to decrease sedentary activity, such as
ments, especially in children, and should always be restriction of television viewing, have been examined and
considered as first-line therapy. In a systematic review109 are promising.117
of randomised controlled trials of treatments for The macronutrient composition of diets has been
childhood obesity, investigators identified 64 trials, 54 of examined for differential weight-loss benefits. Several
which assessed non-pharmacological lifestyle inter- popular diets, including Atkin’s, have emphasised
ventions. These trials were generally of small sample size increasing protein intake, but not changing energy
(16 to 218 participants), with 70% including fewer than content. Although some results show increased weight
30 participants. Most trials had substantial methodological loss with this diet in adults,118–120 data from long-term
limitations and short-term follow-up. Despite these studies generally show no difference in weight loss
limitations, the investigators concluded that “…this between diets of varying macronutrient contents that do
review shows that family-based, lifestyle interventions not change total energy intake.121,122 Demol and

Seminar
Better research into non-pharmacological treatment is

A B
urgently needed, especially into extent of caloric restric-
tion and effectiveness of increasing energy expenditure.
Consensus guidelines for age-appropriate safety
monitoring of weight-reducing regimens are also needed
to ensure appropriate height growth and biological and
social development. Since randomised clinical trials are
costly, multicentre collaborative research with common
protocols might be the most cost-effective and
generalisable approach. In view of ageing populations
worldwide and increasing use of technology-intensive
medical treatments, allocation of increasingly scarce
medical resources will demand more evidence-based
information for treatment of childhood obesity. Questions
such as how often an obese child should have dietary
Figure 4: Operations undertaken for weight loss counselling will not be readily answered unless improved
(A) Roux-en-Y gastric bypass. (B) Adjustable gastric band. Reproduced from evidence is made available.
reference 138, by permission of Elsevier Ltd.
Pharmacological and surgical treatment
colleagues121 reported no differences in BMI decrease in A Cochrane review109 identified ten randomised controlled
obese adolescents on different macronutrient diets. trials of pharmacological treatments for obese children.
Dietary glycaemic index has also been implicated in Most of these trials had small sample sizes (range
weight reduction.123 Two small, short-term studies of 24–539 participants, with 60% including fewer than
obese adolescents reported increased weight loss on a 30 participants), but most were high quality. With one
diet with reduced glycaemic load, but the numbers were exception, all the pharmacological treatment trials were in
small and long-term effects are unknown.124,125 older children or adolescents (minimum age 12 years); the
Strategies to change dietary habits to a more calorie- exception enrolled individuals aged 9–18 years. Trials
reduced intake are based on behavioural principles, of meeting criteria for pooled meta-analysis included only
which Bandura’s social cognitive model126 is the most two drugs: orlistat (a lipase inhibitor that prevents
widely used. The model is based on the notion that lifestyle absorption of dietary fat from the gut) and sibutramine
changes succeed through cognitively driven, intentional (an inhibitor of serotonin, norepinephrine, and dopamine
behaviours such as self-monitoring, goal setting, and reuptake). The additional effect of orlistat compared with
rewarding of successful change. A widely adopted placebo when given in combination with a lifestyle
approach in children uses the traffic light system, which intervention was a difference in BMI of –0·76 kg/m²
was developed by Epstein and colleagues.127 Motivational (95% CI –1·07 to –0·44) at 6 months. The additional effect
interviewing has been advocated as an especially useful of sibutramine compared with placebo when given in
technique for patients who might not feel ready for combination with a lifestyle intervention was a difference
change.128 It is a so-called empathetic way of being, in BMI of –1·66 kg/m² (95% CI –1·89 to –1·43) at
including reflective listening, shared decision making, 6 months. For long-term outcomes, there has been only
and agenda setting.129 American Heart Association one randomised trial of orlistat, which showed a change in
guidelines recommend motivational interviewing for BMI of –0·55 kg/m² with orlistat versus 0·31 kg/m² with
paediatric weight management.130 However, the effective- placebo at 12 months (p=0·001),136 and only one randomised
ness of this approach versus other behavioural approaches trial of sibutramine, in which investigators reported a
is not known. change in BMI of –2·9 kg/m² with sibutramine versus
Most weight reduction programmes are provided by –0·3 kg/m² with placebo at 12 months (p<0·001).137 Side-
outpatient clinics. In one study, investigators examined effects (reported as prevalence in excess of that reported
an inpatient intervention and showed some evidence of for placebo) of orlistat were oily stool (42%), abdominal
effectiveness.131,132 Although the school setting has not pain (11%), faecal incontinence (9%), and new cholelithiasis
been regarded as a site for treatment of childhood obesity (2%).136 Side-effects of sibutramine were tachycardia (6%),
(as opposed to prevention), promising results from a dry mouth (5%), constipation (4%), dizziness (4%),
randomised trial of classroom-based weight reduction in insomnia (3%), and hypertension (2%).137 Thus, although
obese Mexican-American children suggest that this evidence exists for slight effectiveness of orlistat and
venue needs further examination.133 Residential summer sibutramine when combined with lifestyle intervention,
camps for obese adolescents have short-term treatment with these drugs is associated with more adverse
effectiveness,134 but long-term effects remain unknown. effects than is lifestyle intervention alone.
Internet intervention for obese adolescents has been No randomised controlled trials of bariatric surgery
examined, without promising results.135 have been done in children or adolescents.109 In a

Seminar
systematic review of observational studies reporting chronic disorder needing continuing management, long-
outcome data in patients aged 21 years or younger term clinical trials are needed to show safety and efficacy
(range 9–21 years, mean 16·8 years) with a minimum of treatments, not only for a few months, but also during
follow-up of 12 months, investigators identified four the crucial period of active growth and maturation. In
studies of Roux-en-Y gastric bypass (a restrictive and children, safety of treatment needs to be examined as an
malabsorptive procedure)138 and six of laparoscopic equal outcome to efficacy.
adjustable gastric banding (LAGB; a purely restrictive Despite remaining challenges, glimmers of hope can be
procedure) that met inclusion criteria for meta-analysis seen. Recent statistics suggest that prevalence of child-
(figure 4).139 For gastric bypass, the 95% CI for change hood obesity might be stabilising in developed countries.
in BMI from baseline was –17·8 to –22·3 kg/m² at All past efforts made towards prevention and treatment of
1–6·3 years, and for gastric banding, –13·7 to obesity, though not of notable individual effect in trials,
–10·6 kg/m² at 1–3 years.139 Complications of gastric might still have contributed collectively to this trend.108
bypass were pulmonary embolism, shock, intestinal The increased attention that has been directed to obesity
obstruction, postoperative bleeding, staple-line leak, by the media might have helped to raise public awareness
and severe malnutrition;139 those of gastric banding of energy balance. Expansion of food-product availability
were band slippage or erosion, micronutrient deficiency, and more informative food labelling by the private sector
port or tube dysfunction, hiatal hernia, wound infection, might have helped the consumer to make better choices.
and pouch dilatation.139 Long-term prospective studies We cannot wait to delineate the complex causal web of the
are needed to establish safety and efficacy of restrictive obesity epidemic. Unravelling of even one thread might
and malabsorptive procedures and to establish whether allow an important degree of prevention.140 Efforts to
reductions in morbidity and mortality outweigh the prevent obesity should continue at all levels, with the goal
risks of serious surgical complications and life-long of an outcome that is greater than the sum of its parts.
nutritional deficiencies. These efforts should be made in tandem with an increased
Large trials that are sufficiently powered to examine commitment to more robust research. We expect that the
long-term effects and that allow direct comparisons of next 10 years will be a time of new discoveries and collective
non-pharmacological, pharmacological, and surgical societal actions that will help to eliminate this scourge of
treatments are needed. In view of the paucity of data, the new millennium.
poor effectiveness, and unknown risks for long-term Contributors
drug use, we recommend a conservative approach— All authors participated in deciding content, reviewing evidence, and
namely, to use pharmacotherapy only in patients with writing of this Seminar.
BMI higher than the 95th percentile who have substan- Conflicts of interest
tial medical complications of obesity and after a SYSK serves as a member of the Medical Advisory Board of the
Aspartame Resource Center, from which she received no support for her
reasonable period of behavioural intervention. The risks research or her effort in this Seminar. JCH and DAL declare that they
of bariatric surgery are substantial, and long-term safety have no conflicts of interest.
and effectiveness in children remain largely unknown. Acknowledgments
Therefore, surgery should be reserved for only the most JCH receives research support from the Intramural Research Program of
severely obese (BMI ≥50 kg/m², or ≥40 kg/m² with the Eunice Kennedy Shriver National Institute of Child Health and
important comorbidities), and even then, considered Human Development, and is a commissioned officer in the US Public
Health Service, Department of Health and Human Services. The funding
with extreme caution. source had no direct role in writing of this Seminar. DAL receives
funding from the US National Institutes of Health (R01 DK077659), UK
Conclusion Medical Research Council (G0600705 and G0801456), and National
Institute for Health Research (RP-PG-0407-10044) for her work in the area
Much progress has been made in understanding of the
of childhood obesity and determining causality from observational
genetics and physiology of appetite control and, from research. The opinions and assertions expressed in this report are those
this, the elucidation of the causes of some very rare of the authors and are not to be construed as reflecting the views of the
obesity syndromes. Much work remains to be done, US Public Health Service or any other funding body.
however, since these rare disorders have so far taught us References
few lessons about how to prevent or reverse obesity in 1 Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-
health crisis, common sense cure. Lancet 2002; 360: 473–82.
most children. No evidence-based, clinically meaningful 2 Wang Y, Lobstein T. Worldwide trends in childhood overweight and
definition of childhood obesity has been established. obesity. Int J Pediatr Obes 2006; 1: 11–25.
Calorie intake and activity recommendations need to be 3 Ogden CL, Carroll MD, Flegal KM. High body mass index for age
among US children and adolescents, 2003–2006. JAMA 2008;
reassessed and better quantified at a population level 299: 2401–05.
because of the modern sedentary lifestyles of children. 4 Kipping RR, Jago R, Lawlor DA. Obesity in children. Part 1:
For individual treatment, the currently recommended epidemiology, measurement, risk factors, and screening. BMJ 2008;
calorie prescriptions might be too conservative in view of 337: a1824.
5 Sundblom E, Petzold M, Rasmussen F, Callmer E, Lissner L.
evolving insight into the energy gap. Quality of scientific Childhood overweight and obesity prevalences levelling off in
reports needs to improve to allow comparisons between Stockholm but socioeconomic differences persist. Int J Obes (Lond)
interventions and pooling of studies. Because obesity is a 2008; 32: 1525–30.

Seminar
6 Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard 31 Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG. Effect of
definition for child overweight and obesity worldwide: international infant feeding on the risk of obesity across the life course:
survey. BMJ 2000; 320: 1240–43. a quantitative review of published evidence. Pediatrics 2005;
7 Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. 115: 1367–77.
Overweight prevalence and trends for children and adolescents. The 32 Kramer MS, Matush L, Vanilovich I, et al. Effects of prolonged and
national health and nutrition examination surveys, 1963 to 1991. exclusive breastfeeding on child height, weight, adiposity, and blood
Arch Pediatr Adolesc Med 1995; 149: 1085–91. pressure at age 6·5 y: evidence from a large randomized trial.
8 Neovius MG, Linne YM, Barkeling BS, Rossner SO. Sensitivity and Am J Clin Nutr 2007; 86: 1717–21.
specificity of classification systems for fatness in adolescents. 33 Moreno LA, Rodriguez G. Dietary risk factors for development of
Am J Clin Nutr 2004; 80: 597–603. childhood obesity. Curr Opin Clin Nutr Metab Care 2007; 10: 336–41.
9 Neel JV. Diabetes mellitus: a “thrifty” genotype rendered 34 Jimenez-Pavon D, Kelly J, Reilly JJ. Associations between objectively
detrimental by “progress”? Am J Hum Genet 1962; 14: 353–62. measured habitual physical activity and adiposity in children and
10 Bassett DR. Physical activity of Canadian and American children: adolescents: systematic review. Int J Pediatr Obes 2010; 10: 3–18.
a focus on youth in Amish, Mennonite, and modern cultures. 35 Marshall SJ, Biddle SJ, Gorely T, Cameron N, Murdey I.
Appl Physiol Nutr Metab 2008; 33: 831–35. Relationships between media use, body fatness and physical activity
11 Farooqi S, O’Rahilly S. Genetics of obesity in humans. Endocr Rev in children and youth: a meta-analysis. Int J Obes Relat Metab Disord
2006; 27: 710–18. 2004; 28: 1238–46.
12 Feigerlova E, Diene G, Conte-Auriol F, et al. Hyperghrelinemia 36 Al Mamun A, Lawlor DA, Cramb S, O’Callaghan M, Williams G,
precedes obesity in Prader-Willi syndrome. J Clin Endocrinol Metab Najman J. Do childhood sleeping problems predict obesity in young
2008; 93: 2800–05. adulthood? Evidence from a prospective birth cohort study.
13 Cummings DE, Clement K, Purnell JQ, et al. Elevated plasma Am J Epidemiol 2007; 166: 1368–73.
ghrelin levels in Prader Willi syndrome. Nat Med 2002; 8: 643–44. 37 Atkinson RL, Dhurandhar NV, Allison DB, et al. Human
14 Seo S, Guo DF, Bugge K, Morgan DA, Rahmouni K, Sheffield VC. adenovirus-36 is associated with increased body weight and
Requirement of Bardet-Biedl syndrome proteins for leptin receptor paradoxical reduction of serum lipids. Int J Obes (Lond) 2005;
signaling. Hum Mol Genet 2009; 18: 1323–31. 29: 281–86.
15 Davenport JR, Watts AJ, Roper VC, et al. Disruption of intraflagellar 38 Turnbaugh PJ, Hamady M, Yatsunenko T, et al. A core gut
transport in adult mice leads to obesity and slow-onset cystic kidney microbiome in obese and lean twins. Nature 2009; 457: 480–84.
disease. Curr Biol 2007; 17: 1586–94. 39 Correll CU, Manu P, Olshanskiy V, Napolitano B, Kane JM,
16 Han JC, Liu QR, Jones M, et al. Brain-derived neurotrophic factor Malhotra AK. Cardiometabolic risk of second-generation
and obesity in the WAGR syndrome. N Engl J Med 2008; 359: 918–27. antipsychotic medications during first-time use in children and
adolescents. JAMA 2009; 302: 1765–73.
17 Willer CJ, Speliotes EK, Loos RJ, et al. Six new loci associated with
body mass index highlight a neuronal influence on body weight 40 Mayer EI, Reuter M, Dopfer RE, Ranke MB. Energy expenditure,
regulation. Nat Genet 2009; 41: 25–34. energy intake and prevalence of obesity after therapy for acute
lymphoblastic leukemia during childhood. Horm Res 2000;
18 Campion J, Milagro FI, Martinez JA. Individuality and epigenetics
53: 193–99.
in obesity. Obes Rev 2009; 10: 383–92.
41 Bonny AE, Ziegler J, Harvey R, Debanne SM, Secic M, Cromer BA.
19 Long DN, McGuire S, Levine MA, Weinstein LS, Germain-Lee EL.
Weight gain in obese and nonobese adolescent girls initiating depot
Body mass index differences in pseudohypoparathyroidism type 1a
medroxyprogesterone, oral contraceptive pills, or no hormonal
versus pseudopseudohypoparathyroidism may implicate paternal
contraceptive method. Arch Pediatr Adolesc Med 2006; 160: 40–45.
imprinting of Galpha(s) in the development of human obesity.
J Clin Endocrinol Metab 2007; 92: 1073–79. 42 Freedman DS, Khan LK, Serdula MK, Ogden CL, Dietz WH. Racial
and ethnic differences in secular trends for childhood BMI, weight,
20 Pfeifer SM, Kives S. Polycystic ovary syndrome in the adolescent.
and height. Obesity (Silver Spring) 2006; 14: 301–08.
Obstet Gynecol Clin North Am 2009; 36: 129–52.
43 Yajnik CS, Lubree HG, Rege SS, et al. Adiposity and
21 Weaver JU. Classical endocrine diseases causing obesity.
hyperinsulinemia in Indians are present at birth.
Front Horm Res 2008; 36: 212–28.
J Clin Endocrinol Metab 2002; 87: 5575–80.
22 Lustig RH, Hinds PS, Ringwald-Smith K, et al. Octreotide therapy
44 de Onis M, Garza C, Victora CG, Onyango AW, Frongillo EA,
of pediatric hypothalamic obesity: a double-blind, placebo-controlled
Martines J. The WHO multicentre growth reference study:
trial. J Clin Endocrinol Metab 2003; 88: 2586–92.
planning, study design, and methodology. Food Nutr Bull 2004;
23 Lee M, Korner J. Review of physiology, clinical manifestations, and 25 (1 suppl): S15–26.
management of hypothalamic obesity in humans. Pituitary 2009;
45 Li L, Pinot de Moira A, Power C. Changing influences on childhood
12: 87–95.
obesity: a study of two generations of the 1958 British birth cohort.
24 Dabelea D. The predisposition to obesity and diabetes in offspring J Epidemiol Community Health 2009; 63 (suppl 2): A11.
of diabetic mothers. Diabetes Care 2007; 30 (suppl 2): S169–74.
46 Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin
25 Lawlor DA, Fraser A, Lindsay RS, et al. Association of existing deficiency is associated with severe early-onset obesity in humans.
diabetes, gestational diabetes and glycosuria in pregnancy with Nature 1997; 387: 903–08.
macrosomia and offspring body mass index, waist and fat mass in
47 Krude H, Biebermann H, Luck W, Horn R, Brabant G, Gruters A.
later childhood: findings from a prospective pregnancy cohort.
Severe early-onset obesity, adrenal insufficiency and red hair
Diabetologia 2010; 53: 89–97.
pigmentation caused by POMC mutations in humans. Nat Genet
26 Kral JG, Biron S, Simard S, et al. Large maternal weight loss from 1998; 19: 155–57.
obesity surgery prevents transmission of obesity to children who were
48 Creemers JW, Lee YS, Oliver RL, et al. Mutations in the amino-
followed for 2 to 18 years. Pediatrics 2006; 118: e1644–49.
terminal region of proopiomelanocortin (POMC) in patients with
27 Lawlor DA, Timpson NJ, Harbord RM, et al. Exploring the early-onset obesity impair POMC sorting to the regulated secretory
developmental overnutrition hypothesis using parental-offspring pathway. J Clin Endocrinol Metab 2008; 93: 4494–99.
associations and FTO as an instrumental variable. PLoS Med 2008;
49 Challis BG, Pritchard LE, Creemers JW, et al. A missense mutation
5: e33.
disrupting a dibasic prohormone processing site in pro-
28 Ong KK, Loos RJ. Rapid infancy weight gain and subsequent obesity: opiomelanocortin (POMC) increases susceptibility to early-onset
systematic reviews and hopeful suggestions. Acta Paediatr 2006; obesity through a novel molecular mechanism. Hum Mol Genet
95: 904–08. 2002; 11: 1997–2004.
29 Rogers IS, Ness AR, Steer CD, et al. Associations of size at birth and 50 Gray J, Yeo GS, Cox JJ, et al. Hyperphagia, severe obesity, impaired
dual-energy X-ray absorptiometry measures of lean and fat mass at cognitive function and hyperactivity associated with functional loss
9 to 10 y of age. Am J Clin Nutr 2006; 84: 739–47. of one copy of the BDNF gene. Diabetes 2006; 55: 3366–71.
30 Taylor RW, Grant AM, Goulding A, Williams SM. Early adiposity 51 Farooqi IS, Wangensteen T, Collins S, et al. Clinical and molecular
rebound: review of papers linking this to subsequent obesity in genetic spectrum of congenital deficiency of the leptin receptor.
children and adults. Curr Opin Clin Nutr Metab Care 2005; 8: 607–12. N Engl J Med 2007; 356: 237–47.

Seminar
52 Clement K, Vaisse C, Lahlou N, et al. A mutation in the human 76 Nead KG, Halterman JS, Kaczorowski JM, Auinger P, Weitzman M.
leptin receptor gene causes obesity and pituitary dysfunction. Overweight children and adolescents: a risk group for iron
Nature 1998; 392: 398–401. deficiency. Pediatrics 2004; 114: 104–08.
53 Yeo GS, Farooqi IS, Aminian S, Halsall DJ, Stanhope RG, 77 McClung JP, Karl JP. Iron deficiency and obesity: the contribution
O’Rahilly S. A frameshift mutation in MC4R associated with of inflammation and diminished iron absorption. Nutr Rev 2009;
dominantly inherited human obesity. Nat Genet 1998; 20: 111–12. 67: 100–04.
54 Lee YS, Poh LK, Loke KY. A novel melanocortin 3 receptor gene 78 Rosenfield RL, Lipton RB, Drum ML. Thelarche, pubarche, and
(MC3R) mutation associated with severe obesity. menarche attainment in children with normal and elevated body
J Clin Endocrinol Metab 2002; 87: 1423–26. mass index. Pediatrics 2009; 123: 84–88.
55 Feng N, Young SF, Aguilera G, et al. Co-occurrence of two partially 79 Bau AM, Ernert A, Schenk L, et al. Is there a further acceleration in
inactivating polymorphisms of MC3R is associated with pediatric- the age at onset of menarche? A cross-sectional study in 1840 school
onset obesity. Diabetes 2005; 54: 2663–67. children focusing on age and bodyweight at the onset of menarche.
56 Farooqi IS, Yeo GS, Keogh JM, et al. Dominant and recessive Eur J Endocrinol 2009; 160: 107–13.
inheritance of morbid obesity associated with melanocortin 4 80 Mamun AA, Hayatbakhsh MR, O’Callaghan M, Williams G,
receptor deficiency. J Clin Invest 2000; 106: 271–79. Najman J. Early overweight and pubertal maturation—pathways of
57 Yeo GS, Connie Hung CC, Rochford J, et al. A de novo mutation association with young adults’ overweight: a longitudinal study.
affecting human TrkB associated with severe obesity and Int J Obes (Lond) 2009; 33: 14–20.
developmental delay. Nat Neurosci 2004; 7: 1187–89. 81 Denzer C, Weibel A, Muche R, Karges B, Sorgo W, Wabitsch M.
58 Jackson RS, Creemers JW, Ohagi S, et al. Obesity and impaired Pubertal development in obese children and adolescents.
prohormone processing associated with mutations in the Int J Obes (Lond) 2007; 31: 1509–19.
human prohormone convertase 1 gene. Nat Genet 1997; 82 Taylor ED, Theim KR, Mirch MC, et al. Orthopedic complications of
16: 303–06. overweight in children and adolescents. Pediatrics 2006; 117: 2167–74.
59 Farooqi IS, Volders K, Stanhope R, et al. Hyperphagia and early- 83 DiVall SA, Radovick S. Endocrinology of female puberty.
onset obesity due to a novel homozygous missense mutation in Curr Opin Endocrinol Diabetes Obes 2009; 16: 1–4.
prohormone convertase 1/3. J Clin Endocrinol Metab 2007; 84 Gordon JE, Hughes MS, Shepherd K, et al. Obstructive sleep
92: 3369–73. apnoea syndrome in morbidly obese children with tibia vara.
60 Lin S, Boey D, Herzog H. NPY and Y receptors: lessons from J Bone Joint Surg Br 2006; 88: 100–03.
transgenic and knockout models. Neuropeptides 2004; 38: 189–200. 85 Murray AW, Wilson NI. Changing incidence of slipped capital
61 Moussa NM, Claycombe KJ. The yellow mouse obesity syndrome femoral epiphysis: a relationship with obesity? J Bone Joint Surg Br
and mechanisms of agouti-induced obesity. Obes Res 1999; 2008; 90: 92–94.
7: 506–14. 86 Timpson NJ, Sayers A, Davey-Smith G, Tobias JH. How does body
62 Naggert JK, Fricker LD, Varlamov O, et al. Hyperproinsulinaemia in fat influence bone mass in childhood? A Mendelian randomization
obese fat/fat mice associated with a carboxypeptidase E mutation approach. J Bone Miner Res 2009; 24: 522–33.
which reduces enzyme activity. Nat Genet 1995; 10: 135–42. 87 Summerbell CD, Waters E, Edmunds LD, Kelly S, Brown T,
63 Berman Y, Mzhavia N, Polonskaia A, Devi LA. Impaired Campbell KJ. Interventions for preventing obesity in children.
prohormone convertases in Cpe(fat)/Cpe(fat) mice. J Biol Chem Cochrane Database Syst Rev 2005; 3: CD001871.
2001; 276: 1466–73. 88 Hill JO, Wyatt HR, Reed GW, Peters JC. Obesity and the
64 Marsh DJ, Weingarth DT, Novi DE, et al. Melanin-concentrating environment: where do we go from here? Science 2003; 299: 853–55.
hormone 1 receptor-deficient mice are lean, hyperactive, and 89 Swinburn BA, Sacks G, Lo SK, et al. Estimating the changes in
hyperphagic and have altered metabolism. Proc Natl Acad Sci USA energy flux that characterize the rise in obesity prevalence.
2002; 9: 3240–45. Am J Clin Nutr 2009; 89: 1723–28.
65 Malone M. Medications associated with weight gain. 90 Butte NF, Ellis KJ. Comment on “Obesity and the environment:
Ann Pharmacother 2005; 39: 2046–55. where do we go from here?” Science 2003; 301: 598.
66 Daniels SR. Complications of obesity in children and adolescents. 91 Kramer MS, Matush L, Vanilovich I, et al. A randomized breast-
Int J Obes (Lond) 2009; 33 (suppl 1): S60–65. feeding promotion intervention did not reduce child obesity in
67 Bjorge T, Engeland A, Tverdal A, Smith GD. Body mass index in Belarus. J Nutr 2009; 139: 417–21S.
adolescence in relation to cause-specific mortality: a follow-up of 92 Brion M-J, Ness A, Rogers I, et al. Maternal macronutrient and
230,000 Norwegian adolescents. Am J Epidemiol 2008; 168: 30–37. energy intake in pregnancy and offspring intake at 10 y: exploring
68 Freedman DS, Patel DA, Srinivasan SR, et al. The contribution of parental comparisons and prenatal effects. Am J Clin Nutr 2010;
childhood obesity to adult carotid intima-media thickness: the 91: 748–56.
Bogalusa Heart Study. Int J Obes (Lond) 2008; 32: 749–56. 93 Hawkins SS, Cole TJ, Law C. An ecological systems approach to
69 Calcaterra V, Klersy C, Muratori T, et al. Prevalence of metabolic examining risk factors for early childhood overweight: findings
syndrome (MS) in children and adolescents with varying degrees of from the UK Millennium Cohort Study.
obesity. Clin Endocrinol (Oxf) 2008; 68: 868–72. J Epidemiol Community Health 2009; 63: 147–55.
70 Owen CG, Whincup PH, Orfei L, et al. Is body mass index before 94 Welsh SO, Davis C, Shaw A. USDA’s food guide: background and
middle age related to coronary heart disease risk in later life? development. Hyattsville, MD, USA: United States Department of
Evidence from observational studies. Int J Obes (Lond) 2009; Agriculture, Human Nutrition Information Service, 1993.
33: 866–77. 95 Nielsen SJ, Siega-Riz AM, Popkin BM. Trends in energy intake in
71 Gilliland FD, Berhane K, Islam T, et al. Obesity and the risk of U.S. between 1977 and 1996: similar shifts seen across age groups.
newly diagnosed asthma in school-age children. Am J Epidemiol Obes Res 2002; 10: 370–78.
2003; 158: 406–15. 96 Gonzalez-Suarez C, Worley A, Grimmer-Somers K, Dones V.
72 Santamaria F, Montella S, De Stefano S, et al. Asthma, atopy, and School-based interventions on childhood obesity: a meta-analysis.
airway inflammation in obese children. J Allergy Clin Immunol 2007; Am J Prev Med 2009; 37: 418–27.
120: 965–67. 97 Jouret B, Ahluwalia N, Dupuy M, et al. Prevention of overweight in
73 Sutherland ER. Obesity and asthma. Immunol Allergy Clin North Am preschool children: results of kindergarten-based interventions.
2008; 28: 589–602, ix. Int J Obes (Lond) 2009; 33: 1075–83.
74 Alemzadeh R, Kichler J, Babar G, Calhoun M. Hypovitaminosis D 98 Berkowitz JM, Huhman M, Nolin MJ. Did augmenting the VERB
in obese children and adolescents: relationship with adiposity, campaign advertising in select communities have an effect on
insulin sensitivity, ethnicity, and season. Metabolism 2008; awareness, attitudes, and physical activity? Am J Prev Med 2008;
57: 183–91. 34 (6 suppl): S257–66.
75 Yanoff LB, Parikh SJ, Spitalnik A, et al. The prevalence of 99 Huhman ME, Potter LD, Duke JC, Judkins DR, Heitzler CD,
hypovitaminosis D and secondary hyperparathyroidism in obese Wong FL. Evaluation of a national physical activity intervention for
Black Americans. Clin Endocrinol (Oxf) 2006; 64: 523–29. children: VERB campaign, 2002–2004. Am J Prev Med 2007; 32: 38–43.

Seminar
100 Yamamoto JA, Yamamoto JB, Yamamoto BE, Yamamoto LG. 120 Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-
Adolescent fast food and restaurant ordering behavior with and carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;
without calorie and fat content menu information. J Adolesc Health 359: 229–41.
2005; 37: 397–402. 121 Demol S, Yackobovitch-Gavan M, Shalitin S, Nagelberg N,
101 Wong F, Huhman M, Heitzler C, et al. VERB—a social marketing Gillon-Keren M, Phillip M. Low-carbohydrate (low & high-fat)
campaign to increase physical activity among youth. versus high-carbohydrate low-fat diets in the treatment of obesity in
Prev Chronic Dis 2004; 1: A10. adolescents. Acta Paediatr 2009; 98: 346–51.
102 Brownell KD, Frieden TR. Ounces of prevention—the public policy 122 Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets
case for taxes on sugared beverages. N Engl J Med 2009; with different compositions of fat, protein, and carbohydrates.
360: 1805–08. N Engl J Med 2009; 360: 859–73.
103 Justus MB, Ryan KW, Rockenbach J, Katterapalli C, 123 Ludwig DS. The glycemic index: physiological mechanisms relating
Card-Higginson P. Lessons learned while implementing a legislated to obesity, diabetes, and cardiovascular disease. JAMA 2002;
school policy: body mass index assessments among Arkansas’s 287: 2414–23.
public school students. J Sch Health 2007; 77: 706–13. 124 Sondike SB, Copperman N, Jacobson MS. Effects of a low-
104 Nihiser A, Lee S, Wechsler H, et al. BMI Measurement in School. carbohydrate diet on weight loss and cardiovascular risk factor in
Pediatrics 2009; 124: S89–97. overweight adolescents. J Pediatr 2003; 142: 253–58.
105 Cole TJ. Children grow and horses race: is the adiposity rebound a 125 Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS.
critical period for later obesity? BMC Pediatr 2004; 4: 6. A reduced-glycemic load diet in the treatment of adolescent obesity.
106 Kimm SY, Glynn NW, Kriska AM, et al. Decline in physical activity Arch Pediatr Adolesc Med 2003; 157: 773–79.
in black girls and white girls during adolescence. N Engl J Med 126 Bandura A. Social foundations of thought and action. Englewood
2002; 347: 709–15. Cliffs, NJ, USA: Prentice Prentice-Hall, 1986.
107 Stamler J. Population-wide adverse dietary patterns: a pivotal cause 127 Epstein LH, Valoski A, Wing RR, McCurley J. Ten-year follow-up of
of epidemic coronary heart disease/cardiovascular disease. behavioral, family-based treatment for obese children. JAMA 1990;
J Am Diet Assoc 2008; 108: 228–32. 264: 2519–23.
108 Rose G, Khaw K-T, Marmot M. Rose’s strategy of preventive 128 Miller W, Rollnick S. Motivational interviewing: preparing people
medicine. Oxford, UK: Oxford University Press, 2008. for change. New York, NY, USA: Guilford Press, 2002.
109 Oude Luttikhuis H, Baur L, Jansen H, et al. Interventions for 129 Resnicow K, Davis R, Rollnick S. Motivational interviewing for
treating obesity in children. Cochrane Database Syst Rev 2009; pediatric obesity: conceptual issues and evidence review.
1: CD001872. J Am Diet Assoc 2006; 106: 2024–33.
110 Spear BA, Barlow SE, Ervin C, et al. Recommendations for 130 Daniels SR, Jacobson MS, McCrindle BW, Eckel RH, Sanner BM.
treatment of child and adolescent overweight and obesity. Pediatrics American Heart Association childhood obesity research summit
2007; 120 (suppl 4): S254–88. report. Circulation 2009; 119: e489–517.
111 National Institute for Health and Clinical Excellence, 2006. Obesity: 131 Braet C. Patient characteristics as predictors of weight loss after an
the prevention, identification, assessment and management of obesity treatment for children. Obesity (Silver Spring) 2006;
overweight and obesity in adults and children. http://www.nice.org. 14: 148–55.
uk/guidance/index.jsp?action=byID&o=11000 (accessed Nov 2, 2009). 132 Braet C, Tanghe A, Bode PD, Franckx H, Winckel MV. Inpatient
112 Stewart L, Houghton J, Hughes AR, Pearson D, Reilly JJ. Dietetic treatment of obese children: a multicomponent programme without
management of pediatric overweight: development and description stringent calorie restriction. Eur J Pediatr 2003; 162: 391–96.
of a practical and evidence-based behavioral approach. 133 Johnston CA, Tyler C, McFarlin BK, et al. Weight loss in overweight
J Am Diet Assoc 2005; 105: 1810–15. Mexican American children: a randomized, controlled trial.
113 Hughes AR, Stewart L, Chapple J, et al. Randomized, controlled Pediatrics 2007; 120: e1450–57.
trial of a best-practice individualized behavioral program for 134 Gately PJ, Cooke CB, Barth JH, Bewick BM, Radley D, Hill AJ.
treatment of childhood overweight: Scottish Childhood Overweight Children’s residential weight-loss programs can work: a prospective
Treatment Trial (SCOTT). Pediatrics 2008; 121: e539–46. cohort study of short-term outcomes for overweight and obese
114 Figueroa-Colon R, von Almen TK, Franklin FA, Schuftan C, children. Pediatrics 2005; 116: 73–77.
Suskind RM. Comparison of two hypocaloric diets in obese 135 Doyle AC, Goldschmidt A, Huang C, Winzelberg AJ, Taylor CB,
children. Am J Dis Child 1993; 147: 160–66. Wilfley DE. Reduction of overweight and eating disorder symptoms
115 Sothern, Udall JN Jr, Suskind RM, Vargas A, Blecker U. Weight loss via the Internet in adolescents: a randomized controlled trial.
and growth velocity in obese children after very low calorie diet, J Adolesc Health 2008; 43: 172–79.
exercise, and behavior modification. Acta Paediatr 2000; 136 Chanoine JP, Hampl S, Jensen C, Boldrin M, Hauptman J. Effect of
89: 1036–43. orlistat on weight and body composition in obese adolescents:
116 Shalitin S, Ashkenazi-Hoffnung L, Yackobovitch-Gavan M, et al. a randomized controlled trial. JAMA 2005; 293: 2873–83.
Effects of a twelve-week randomized intervention of exercise and/or 137 Berkowitz RI, Fujioka K, Daniels SR, et al. Effects of sibutramine
diet on weight loss and weight maintenance, and other metabolic treatment in obese adolescents: a randomized trial. Ann Intern Med
parameters in obese preadolescent children. Horm Res 2009; 2006; 145: 81–90.
72: 287–301. 138 Inge TH, Zeller MH, Lawson ML, Daniels SR. A critical appraisal of
117 Robinson TN. Reducing children’s television viewing to prevent evidence supporting a bariatric surgical approach to weight
obesity: a randomized controlled trial. JAMA 1999; 282: 1561–67. management for adolescents. J Pediatr 2005; 147: 10–19.
118 Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low- 139 Treadwell JR, Sun F, Schoelles K. Systematic review and meta-
carbohydrate diet for obesity. N Engl J Med 2003; 348: 2082–90. analysis of bariatric surgery for pediatric obesity. Ann Surg 2008;
119 Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the 248: 763–76.
Atkins, Zone, Ornish, and LEARN diets for change in weight and 140 MacMahon B, Pugh TF. Chapter 2: concepts of cause. In:
related risk factors among overweight premenopausal women: the Epidemiology: principles and methods. Boston, MA, USA: Little,
A TO Z Weight Loss Study: a randomized trial. JAMA 2007; Brown and Company, 1970.
297: 969–77.

Artigo de Revisão
As p e c to s Dia g nó s tic o s e Te r a p ê u tic o s Atu a is d a Hip e r te ns ã o

Ar te r ia l na Cr ia nç a e no Ad o le s c e nte , c o m Ênfa s e no “Four th
Repor t on th e Diagn osis, Evaluation , an d Tr eatmen t of High
Blood Pr essur e in Ch ildr en an d Adolescen ts” d e 2004
Vera Hermina Koch RESUMO
O desenvolvimento da normatização da medida de pressão arterial na criança

e no adolescente tomou impulso na década de 70 e desde então tem sido
motivo de amplas modificações. Simultaneamente, o conhecimento sobre
diagnóstico, avaliação e tratamento da hipertensão arterial pediátrica desen-
volveu-se, principalmente após a instituição do Modernization Act pelo Food
and Drug Administration (FDA), que impulsionou a geração de dados
pediátricos de eficácia e segurança de medicamentos em geral, e espe-
cificamente de hipotensores. Esta publicação visa a apresentar uma atua-
lização sobre normatização, diagnóstico, avaliação e tratamento da hipertensão
arterial pediátrica com ênfase nas recomendações do Fourth Report on the
Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and
Adolescents, publicado em 2004, pelo National High Blood Pressure Education
Program Working Group on High Blood Pressure in Children and Adolescents.
(J Bras Nefrol 2005;27(2):84-92)
Descritores: Criança. Adolescente. Medida de pressão arterial. Hipertensão

arterial. Diagnóstico. Terapêutica não farmacológica. Terapêutica farmacológica.
ABSTRACT
Update on diagnosis and treatment of pediatric arterial hypertension

with emphasis on the recommendations of the "Fourth Report on the
Unidade de Nefrologia Pediátrica, Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children
Instituto da Criança, Hospital das and Adolescents", 2004.
Clínicas, Universidade de São
Paulo, SP. The pediatric blood pressure norms have been a focus of important change
since its initial development in the late 70s. Simultaneously the body of
knowledge about the diagnosis, evaluation and therapy of pediatric
hypertension has expanded, especially after the institution of the Modernization
Act by the Food and Drug Administration (FDA), which stimulated the
generation of pediatric efficacy and safety data on medications in general, anti-
hypertensive drugs included. This article presents an update on pediatric blood
pressure norms, diagnosis, evaluation and therapy of pediatric hypertension
with emphasis on the recommendations of the Fourth Report on the Diagnosis,
Evaluation, and Treatment of High Blood Pressure in Children and Adolescents,
published in 2004, by the National High Blood Pressure Education Program
Working Group on High Blood Pressure in Children and Adolescents. (J Bras
Nefrol 2005;27(2):84-92)
Keywords: Child adolescent. Blood pressure measurement. Arterial

Recebido em 31/01/2005 hypertension. Diagnosis. Non pharmacological therapy. Pharmacological
Aprovado em 10/05/2005 therapy.
J Bra s Nefrol Volum e XXVII - nº 2 - Junho d e 2005 85
Normatização de pressão arterial na faixa etária ciente apresenta valores de pressão arterial acima do per-
pediátrica centil 95 em ambulatório ou consultório médico, com
medidas normais em ambientes não relacionados à prática
Múltiplos estudos epidemiológicos têm demons- clínica; este diagnóstico requer a utilização da monito-
trado que os valores de pressão arterial (PA) na infância e rização ambulatorial de pressão arterial8.
na adolescência são os melhores preditores dos valores de Comparando valores de PA obtidos na população
PA no adulto 1-3. infantil americana, de 8 a 17 anos, em 1988-94 e em1999-
Os primeiros dados pediátricos normativos de PA 2000, verificou-se que a pressão sistólica elevou-se em
foram desenvolvidos em 19774, com revisões e impor- 1,4mmHg e a pressão diastólica, em 3,3mmHg. Este in-
tantes mudanças conceituais em 19875 e 1996 6. A partir cremento é parcialmente atribuível ao aumento na preva-
de 1996, a PA da criança e do adolescente não foi mais lência de sobrepeso e obesidade, da população infantil
relacionada somente à idade cronológica e ao sexo, mas neste período10. Dados normativos de PA para crianças
também à altura, utilizando-se dados antropométricos do abaixo de 1 ano de idade estão disponíveis no documento
estudo National Health and Nutrition Examination de 1987 5 e em dois estudos mais recentes11,12.
Survey, 1988-91, ou NHANES III 7. Esta normatização A tabela 1 demonstra as dimensões aceitáveis da
definiu também o quinto ruído auscultatório (K5), isto é, bolsa de borracha para braços de diferentes tamanhos, de
o desaparecimento dos sons, como equivalente à pressão acordo com o padrão preconizado nas diretrizes de 2004.
diastólica para toda criança de 1 a 17 anos de idade. Em A técnica sugerida de medida de pressão arterial
2004, foi publicada uma revisão mais recente8, baseada em membros superiores na criança e no adolescente segue
em dados antropométricos do relatório de 2000 do Centers a rotina apresentada na edição de 19967. A pressão sistó-
for Disease Control and Prevention e do National Center lica de membros inferiores deve ser avaliada sempre que
for Health Statistics 9. a pressão medida em membros superiores estiver elevada.
Define-se o valor normal de PA em Pediatria com Esta avaliação pode ser realizada com o paciente em posi-
base em percentis, o valor de PA sistólica e diastólica ção deitada, com o manguito colocado na região da pan-
encontra-se normal quando inferior ao valor do percentil turrilha cobrindo pelo menos 2/3 da distância entre o joe-
90 para idade, sexo e percentil de estatura. A partir de lho e o tornozelo. A pressão sistólica medida na perna po-
20048 incorporou-se o termo pré-hipertensão, definido a de ser mais elevada do que no braço devido ao fenômeno
partir de valores de PA iguais ou superiores ao percentil da amplificação do pulso distal, esta diferença pode variar
90 e inferiores ao percentil 95 para idade, sexo e percentil de alguns milímetros no lactente até 10-20mmHg na crian-
de estatura, ou para o adolescente, como valores ≥ ça maior ou no adulto, mas a PA medida no braço NUN-
120/80mmHg e < percentil 95 para idade, sexo e percentil CA deve exceder a medida da perna, pois esta variação, se
de estatura. Hipertensão arterial pediátrica é considerada confirmada, sugere o diagnóstico de coarctação da aorta.
a partir de valores de PA iguais ou superiores ao percentil As tabelas 2 e 3 demonstram os valores de pressão
95 para idade, sexo e percentil de estatura, confirmados arterial de acordo com a idade, sexo e percentil de estatura
em 3 ocasiões subseqüentes. Define-se também, a partir relacionados para os percentis 50, 90, 95 e 99, de acordo
de 20048, como hipertensão “estágio 1”, valores de medi- com as diretrizes de 20048, para crianças masculinas e fe-
da entre o percentil 95 e 5mmHg acima do percentil 99 e, mininas de 1 a 17 anos de idade. As curvas de crescimen-
como hipertensão “estágio 2”, para valores acima do to para meninos e meninas a partir das quais devem ser
limite superior do “estágio 1”. A hipertensão do avental obtidos os valores do percentil de estatura podem ser en-
branco é definida como a situação clínica na qual o pa- contradas na página eletrônica www.cdc.gov/growthcharts9.
As diretrizes de 2004 inovam na recomendação
para avaliação de PA de toda criança com idade superior
Tabela 1. Dimensões aceitáveis da bolsa de borracha para a 3 anos em todas as consultas médicas8, assim como de
braços de diferentes tamanhos 8. crianças abaixo de 3 anos de idade quando portadoras dos
Max. Denominação Largura do Comprimento seguintes antecedentes ou condições clínicas 8: prematuri-
circunferência do manquito manquito da bolsa dade, recém-nascido de muito baixo peso ao nascer, sobre-
do braço (cm) (cm) (cm)
10 recém nascido 4 8 vivente de Unidade de Terapia Intensiva Neonatal, cardio-
15 criança 6 12 patia congênita, infecção urinária de repetição, hematúria,
22 infantil 9 18 proteinúria, má-formação ou doença nefro-urológica,
26 adulto pequeno 10 24 história familiar de nefropatia congênita, transplante de
34 adulto 13 30 órgãos, problemas oncológicos ou transplante de medula
44 adulto grande 16 38
52 coxa 20 42 óssea, doenças sistêmicas reconhecidamente associadas à
86 Aspectos Atuais da Hipertensão Arterial Pediátrica
Tabela 2. Valores de pressão arterial para meninos de acordo com idade e percentil de estatura8.
PA SISTÓLICA (mmHg) PA DIASTÓLICA (mmHg)

Idade PA
Percentil de Altura Percentil de Altura
(Anos) Percentil
5 10 25 50 75 90 95 5 10 25 50 75 90 95
1 50 80 81 83 85 87 88 89 34 35 36 37 38 39 39
90 94 95 97 99 100 102 103 49 50 51 52 53 53 54
95 98 99 101 103 104 106 106 54 54 55 56 57 58 58
99 105 106 108 110 112 113 114 61 62 63 64 65 66 66
2 50 84 85 87 88 90 92 92 39 40 41 42 43 44 44
90 97 99 100 102 104 105 106 54 55 56 57 58 58 59
95 101 102 104 106 108 109 110 59 59 60 61 62 63 63
99 109 110 111 113 115 117 117 66 67 68 69 70 71 71
3 50 86 87 89 91 93 94 95 44 44 45 46 47 48 48
90 100 101 103 105 107 108 109 59 59 60 61 62 63 63
95 104 105 107 109 110 112 113 63 63 64 65 66 67 67
99 111 112 114 116 118 119 120 71 71 72 73 74 75 75
4 50 88 89 91 93 95 96 97 47 48 49 50 51 51 52
90 102 103 105 107 109 110 111 62 63 64 65 66 66 67
95 106 107 109 111 112 114 115 66 67 68 69 70 71 71
99 113 114 116 118 120 121 122 74 75 76 77 78 78 79
5 50 90 91 93 95 96 98 98 50 51 52 53 54 55 55
90 104 105 106 108 110 111 112 65 66 67 68 69 69 70
95 108 109 110 112 114 115 116 69 70 71 72 73 74 74
99 115 116 118 120 121 123 123 77 78 79 80 81 81 82
6 50 91 92 94 96 98 99 100 53 53 54 55 56 57 57
90 105 106 108 110 111 113 113 68 68 69 70 71 72 72
95 109 110 112 114 115 117 117 72 72 73 74 75 76 76
99 116 117 119 121 123 124 125 80 80 81 82 83 84 84
7 50 92 94 95 97 99 100 101 55 55 56 57 58 59 59
90 106 107 109 111 113 114 115 70 70 71 72 73 74 74
95 110 111 113 115 117 118 119 74 74 75 76 77 78 78
99 117 118 120 122 124 125 126 82 82 83 84 85 86 86
8 50 94 95 97 99 100 102 102 56 57 58 59 60 60 61
90 107 109 110 112 114 115 116 71 72 72 73 74 75 76
95 111 112 114 116 118 119 120 75 76 77 78 79 79 80
99 119 120 122 123 125 127 127 83 84 85 86 87 87 88
9 50 95 96 98 100 102 103 104 57 58 59 60 61 61 62
90 109 110 112 114 115 117 118 72 73 74 75 76 76 77
95 113 114 116 118 119 121 121 76 77 78 79 80 81 81
99 120 121 123 125 127 128 129 84 85 86 87 88 88 89
10 50 97 98 100 102 103 105 106 58 59 60 61 61 62 63
90 111 112 114 115 117 119 119 73 73 74 75 76 77 78
95 115 116 117 119 121 122 123 77 78 79 80 81 81 82
99 122 123 125 127 128 130 130 85 86 86 88 88 89 90
11 50 99 100 102 104 105 107 107 59 59 60 61 62 63 63
90 113 114 115 J17 119 120 121 74 74 75 76 77 78 78
95 117 118 119 121 123 124 125 78 78 79 80 81 82 82
99 124 125 127 129 130 132 132 86 86 87 88 89 90 90
12 50 101 102 104 106 108 109 110 59 60 61 62 63 63 64
90 115 116 118 120 121 123 123 74 75 75 76 77 78 79
95 119 120 122 123 125 127 127 78 79 80 81 82 82 83
99 126 127 129 131 133 134 135 86 87 88 89 90 90 91
13 50 104 105 106 108 110 111 112 60 60 61 62 63 64 64
90 117 118 120 122 124 125 126 75 75 76 77 78 79 79
95 121 122 124 126 128 129 130 79 79 80 81 82 83 83
99 128 130 131 133 135 136 137 87 87 88 89 90 91 91
14 50 106 107 109 111 113 114 115 60 61 62 63 64 65 65
90 120 121 123 125 126 128 128 75 76 77 78 79 79 80
95 124 125 127 128 130 132 132 80 80 81 82 83 84 84
99 131 132 134 136 138 139 140 87 88 89 90 91 92 92
15 50 109 110 112 113 115 117 117 61 62 63 64 65 66 66
90 122 124 125 127 129 130 131 76 77 78 79 80 80 81
95 126 127 129 131 133 134 135 81 81 82 83 84 85 85
99 134 135 136 138 140 142 142 88 89 90 91 92 93 93
16 50 111 112 114 116 118 119 120 63 63 64 65 66 67 67
90 125 126 128 130 131 133 134 78 78 79 80 81 82 82
95 129 130 132 134 135 137 137 82 83 83 84 85 86 87
99 136 137 139 141 143 144 145 90 90 91 92 93 94 94
17 50 114 115 116 118 120 121 122 65 66 66 67 68 69 70
90 127 128 130 132 134 135 136 80 80 81 82 83 84 84
95 131 132 134 136 138 139 140 84 85 86 87 87 88 89
99 139 140 141 143 145 146 147 92 93 93 94 95 96 97
Nota: Adolescentes com pressão arterial ≥ 120/80mmHg devem ser considerados pré-hipertensos, mesmo se o valor do percentil
90 for superior a esta marca. Esta situação pode ocorrer para pressão sistólica em maiores de 12 anos e para pressão diastólica
em maiores de 16 anos.
Tabela 3. Valores de pressão arterial para meninas de acordo com idade e percentil de estatura28.
PA SISTÓLICA (mmHg) PA DIASTÓLICA (mmHg)
Idade PA
Percentil de Altura Percentil de Altura
(Anos) Percentil
5 10 25 50 75 90 95 5 10 25 50 75 90 95
1 50 83 84 85 86 88 89 90 38 39 39 40 41 41 42
90 97 97 98 100 101 102 103 52 53 53 54 55 55 56
95 100 101 102 104 105 106 107 56 57 57 58 59 59 60
99 108 108 109 111 112 113 114 64 64 65 65 66 67 67
2 50 85 85 87 88 89 91 91 43 44 44 45 46 46 47
90 98 99 100 101 103 104 105 57 58 58 59 60 61 61
95 102 103 104 105 107 108 109 61 62 62 63 64 65 65
99 109 110 111 112 114 115 116 69 69 70 70 71 72 72
3 50 86 87 88 89 91 92 93 47 48 48 49 50 50 51
90 100 100 102 103 104 106 106 61 62 62 63 64 64 65
95 104 104 105 107 108 109 110 65 66 66 67 68 68 69
99 111 111 113 114 115 116 117 73 73 74 74 75 76 76
4 50 88 88 90 91 92 94 94 50 50 51 52 52 53 54
90 101 102 103 104 106 107 108 64 64 65 66 67 67 68
95 105 106 107 108 110 111 112 68 68 69 70 71 71 72
99 112 113 114 115 117 118 119 76 76 76 77 78 79 79
5 50 89 90 91 93 94 95 96 52 53 53 54 55 55 56
90 103 103 105 106 107 109 109 66 67 67 68 69 69 70
95 107 107 108 110 111 112 113 70 71 71 72 73 73 74
99 114 114 116 117 118 120 120 78 78 79 79 80 81 81
6 50 91 92 93 94 96 97 98 54 54 55 56 56 57 58
90 104 105 106 108 109 110 111 68 68 69 70 70 71 72
95 108 109 110 111 113 114 115 72 72 73 74 74 75 76
99 115 116 117 119 120 121 122 80 80 80 81 82 83 83
7 50 93 93 95 96 97 99 99 55 56 56 57 58 58 59
90 106 107 108 109 111 112 113 69 70 70 71 72 72 73
95 110 111 112 113 115 116 116 73 74 74 75 76 76 77
99 117 118 119 120 122 123 124 81 81 82 82 83 84 84
8 50 95 95 96 98 99 100 101 57 57 57 58 59 60 60
90 108 109 110 111 113 114 114 71 71 71 72 73 74 74
95 112 112 114 115 116 118 118 75 75 75 76 77 78 78
99 119 120 121 122 123 125 125 82 82 83 83 84 85 86
9 50 96 97 98 100 101 102 103 58 58 58 59 60 61 61
90 110 110 112 113 114 116 116 72 72 72 73 74 75 75
95 114 114 115 117 118 119 120 76 76 76 77 78 79 79
99 121 121 123 124 125 127 127 83 83 84 84 85 86 87
10 50 98 99 100 102 103 104 105 59 59 59 60 61 62 62
90 112 112 114 115 116 118 118 73 73 73 74 75 76 76
95 116 116 117 119 120 121 122 77 77 77 78 79 80 80
99 123 123 125 126 127 129 129 84 84 85 86 86 87 88
11 50 100 101 102 103 105 106 107 60 60 60 61 62 63 63
90 114 114 116 117 118 119 120 74 74 74 75 76 77 77
95 118 118 119 121 122 123 124 78 78 78 79 80 81 81
99 125 125 126 128 129 130 131 85 85 86 87 87 88 89
12 50 102 103 104 105 107 108 109 61 61 61 62 63 64 64
90 116 116 117 119 120 121 122 75 75 75 76 77 78 78
95 119 120 121 123 124 125 126 79 79 79 80 81 82 82
99 127 127 128 130 131 132 133 86 86 87 88 88 89 90
13 50 104 105 106 107 109 110 110 62 62 62 63 64 65 65
90 117 118 119 121 122 123 124 76 76 76 77 78 79 79
95 121 122 123 124 126 127 128 80 80 80 81 82 83 83
99 128 129 130 132 133 134 135 87 87 88 89 89 90 91
14 50 106 106 107 109 110 111 112 63 63 63 64 65 66 66
90 119 120 121 122 124 125 125 77 77 77 78 79 80 80
95 123 123 125 126 127 129 129 81 81 81 82 83 84 84
99 130 131 132 133 135 136 136 88 88 89 90 90 91 92
15 50 107 108 109 110 111 113 113 64 64 64 65 66 67 67
90 120 121 122 123 125 126 127 78 78 78 79 80 81 81
95 124 125 126 127 129 130 131 82 82 82 83 84 85 85
99 131 132 133 134 136 137 138 89 89 90 91 91 92 93
16 50 108 108 110 111 112 114 114 64 64 65 66 66 67 68
90 121 122 123 124 126 127 128 78 78 79 80 81 81 82
95 125 126 127 128 130 131 132 82 82 83 84 85 85 86
99 132 133 134 135 137 138 139 90 90 90 91 92 93 93
17 50 108 109 110 111 113 114 115 64 65 65 66 67 67 68
90 122 122 123 125 126 127 128 78 79 79 80 81 81 82
95 125 126 127 129 130 131 132 82 83 83 84 85 85 86
99 133 133 134 136 137 138 139 90 90 91 91 92 93 93
Nota: Adolescentes com pressão arterial ≥ 120/80mmHg devem ser considerados pré-hipertensos, mesmo se o valor do percentil
90 for superior a esta marca. Esta situação pode ocorrer para pressão sistólica em maiores de 12 anos e para pressão diastólica
em maiores de 16 anos.
hipertensão arterial (esclerose tuberosa, neurofibromatose ganho pondero-estatural, irritabilidade, má-aceitação

etc.), aumento de pressão intracraniana e uso de medi- alimentar, vômitos, cianose, dispnéia, insuficiência car-
cação crônica associada à elevação de pressão arterial. díaca e convulsões. Na criança maior a hipertensão é
A criança que apresentar medida de PA acima do geralmente silenciosa, à exceção dos casos mais graves.
percentil 90 deve ser reavaliada, se possível semanalmen- Quanto menor a criança e mais elevado o valor da medida
te, para confirmação de que se trata realmente de um pa- de PA, maior a chance de se tratar de hipertensão de causa
ciente pré-hipertenso 8. Após confirmação diagnóstica do secundária. Na grande maioria dos pacientes de até 10
estado de pré-hipertensão, recomenda-se monitorização anos de idade pode-se identificar uma causa para o
clínica de seis em seis meses8. Se ao longo do tempo a PA desenvolvimento de hipertensão arterial, em geral
de consultório atingir valor igual ou superior ao percentil associada a doença renal 16.
95, está firmado o diagnóstico de hipertensão arterial, e a O exame físico deve tentar identificar sinais su-
criança deve ser encaminhada para investigação etiológica. gestivos de hipertensão secundária, como manchas “café
com leite” (neurofibromatose/feocromocitoma), massas
A Pré-hipertensão e Hipertensão arterial abdominais (tumor de Wilms, neuroblastoma), sopros
(coarctação de aorta, outras alterações vasculares congê-
Há poucos dados epidemiológicos recentes sobre nitas ou inflamatórias), diferencial de PA entre membros
etiopatogenia de hipertensão arterial na infância e ado- superiores e inferiores, aumento de volume da glândula
lescência. Balachandra e cols.13, em estudo retrospectivo tireóide (hipertireoidismo), virilização (doenças da glân-
de uma população predominantemente não caucasiana, dula adrenal) ou estigmas de síndromes genéticas (Bardet-
demonstrou que a distribuição por faixa etária dos -Biedl, von Hippel-Landau, Williams, Turner). A hiper-
pacientes foi 7% de 0 a 1 ano de idade, 24% de 1 a 6 anos, tensão sistólica predomina na criança17. A presença de
24% de 6 a 12 anos e 45% de 12 a 18 anos. A etiologia alterações de fundo de olho, cardiomegalia, insuficiência
predominante foi doença parenquimatosa renal, seguida cardíaca ou déficit neurológico, em geral se correlaciona
de hipertensão essencial e hipo-displasia renal. A hiper- com a cronicidade e a gravidade da hipertensão arterial5.
tensão renovascular foi a causa mais prevalente na faixa A avaliação da história familiar de doença deve
etária de 0 a 1 ano de idade. A hipertensão primária foi abordar a ocorrência de eventos cardiovasculares, doença
mais freqüente em crianças maiores, estando geralmente vascular periférica e diabetes mellitus em familiares de
associada à obesidade e ao diabetes mellitus. primeiro e segundo grau. A PA de pais e irmãos da crian-
O aumento da prevalência de obesidade na criança ça afetada deve ser medida para que o diagnóstico de hi-
e no adolescente deslocou a manifestação da hipertensão pertensão familiar de causa primária ou secundária possa
primária associada à síndrome plurimetabólica, tradi- ser estabelecido.
cionalmente encontrada no adulto, para a faixa etária A avaliação diagnóstica da hipertensão na criança
pediátrica. A hipertensão primária na criança apresenta-se e no adolescente deve ser adequada ao quadro clínico,
em geral como “hipertensão estágio 1”, freqüentemente história familiar, valor medido de PA e idade de apre-
se associa a antecedentes familiares de hipertensão ou sentação5,16. A chance de detectar uma causa secundária
doença cardiovascular e é mais comumente diagnosticada na avaliação da criança hipertensa é diretamente rela-
em crianças com sobrepeso/obesidade. A criança obesa cionada à gravidade da hipertensão e inversamente
com freqüência demonstra algum grau de resistência relacionada à idade da criança. Hipertensão grave na
periférica à insulina, uma condição pré-diabética, assim criança (estágio 2) independentemente da idade deve ser
como outras alterações tipicamente associadas à síndrome exaustivamente investigada à procura de etiologia secun-
plurimetabólica como hipertrigliceridemia, baixa concen- dária. Indivíduos com hipertensão estágio 1, apresentando
tração do colesterol tipo HDL e obesidade truncal14. Em dados inocentes de anamnese e exame físico, devem ser
estudos recentes, a resistência periférica à insulina foi avaliados através dos seguintes exames, considerados
diagnosticada em 30% dos adolescentes com índice de como básicos:
massa corpórea igual ou superior ao percentil 9515. Estes Exames de sangue: Hemograma completo, uréia
dados reforçam a necessidade de ênfase à pesquisa destas e creatinina, eletrólitos, ácido úrico, perfil lipídico em
alterações como parte da anamnese, exame físico e inves- jejum, glicemia de jejum;
tigação da hipertensão na faixa etária pediátrica8.
O diagnóstico clínico de hipertensão arterial se Exames de urina: Urina 1, cultura de urina;
baseia em anamnese cuidadosa e exame físico detalhado. Outros: Ultra-som de rins e vias urinárias com
Os sintomas de apresentação no neonato são em geral de Doppler, avaliação de órgãos-alvo: fundoscopia ocular,
alta gravidade e pouca especificidade, como déficit de ecodopplercardiografia bidimensional, microalbuminúria.
A avaliação de órgãos alvo em hipertensão cada somente quando se estiver contemplando a possi-
pediátrica é de extrema importância e deve ser realizada bilidade de correção anatômica por radiologia inter-
em todos os pacientes diagnosticados (estágios 1 e 2)8, vencionista ou revascularização cirúrgica28. A dosagem
uma vez que a hipertensão arterial leve e moderada na da atividade plasmática de renina (APR), quando baixa,
faixa etária pediátrica está associada a aumento da massa aponta para a possibilidade de hipertensão por meca-
de ventrículo esquerdo18,19, hiperfiltração glomerular19 e nismo mineralocorticóide 8. Pacientes com hipertensão
alterações na fundoscopia ocular19 em grande número de renovascular tendem a apresentar valores normais ou
pacientes. elevados de APR8.
Outros recursos diagnósticos podem ser utilizados
para pacientes selecionados, seja devido a alterações Bases Terapêuticas da Hipertensão Pediátrica
verificadas na investigação básica inicial, seja em con-
tinuidade à busca etiológica da hipertensão em pacientes A terapêutica não farmacológica deve ser introdu-
com hipertensão estágio 2. Em crianças com história zida para todos os pacientes pediátricos com valores de
prévia de infecção urinária, a cintilografia renal com PA acima do percentil 907,8. Envolve redução de peso,
99mTc ácido dimercaptosuccínico (DMSA) é aconse- programação de exercício físico e intervenção dietética7,8.
lhável. A investigação de malformações urinárias deve A massa corpórea é o maior determinante da PA na faixa
incluir a uretrocistografia miccional e eventualmente a etária pediátrica 7,8. A redução de peso apresenta bons re-
cintilografia renal dinâmica com 99mTc ácido dietileno sultados no tratamento da criança hipertensa obesa29. O
triamino pentacético (DTPA) ou uma urografia excre- exercício físico é um bom instrumento para redução de
tora. A presença de hematúria e proteinúria, em asso- peso e de PA, apresentando efeito melhor sobre os valores
ciação à hipertensão arterial, pode indicar a necessidade de pressão sistólica do que sobre a diastólica30,31. Reco-
de uma biópsia renal. menda-se atividade aeróbica regular, isto é, 30-60 minu-
A monitorização ambulatorial de pressão arterial tos de exercício físico moderado, se possível diariamente,
está indicada em casos selecionados, para confirmação do com redução das atividades sedentárias de lazer, no
diagnóstico de hipertensão do avental branco e em situa- sentido de prevenir obesidade, hipertensão e outros riscos
ções clínicas nas quais a avaliação do ritmo circadiano de cardiovasculares. O treinamento de resistência pode ser
pressão arterial está indicada8, como na diabetes mellitus realizado pela criança portadora de hipertensão arterial, à
tipo 1. exceção do levantamento de peso. Esportes competitivos
O estudo do sono, através da polissonografia, está não são recomendados para pacientes com hipertensão
indicado para adolescentes com distúrbio de sono detec- arterial em estágio 2 32.
tado pela anamnese, uma vez que existe, na faixa etária
pediátrica, associação entre estes distúrbios e elevação da Terapêutica Farmacológica da Hipertensão Pediátrica
pressão arterial8.
Em caso de suspeita de feocromocitoma, uma A terapêutica farmacológica deve ser iniciada para
forma potencialmente curável de hipertensão arterial, o casos pediátricos com hipertensão sintomática, hiperten-
diagnóstico se baseia na evidência bioquímica da pro- são secundária, evidência de lesão de órgão-alvo, diabetes
dução de catecolaminas pelo tumor, através da dosagem, mellitus tipo 1 ou 2 e hipertensão persistente não-respon-
em amostra urinária, da normetanefrina e da metanefrina, siva a terapêutica não-farmacológica8 e objetiva, na hiper-
ou mais recentemente da metanefrina plasmática livre20, tensão não-complicada, redução da PA a valores infe-
cuja determinação parece apresentar os melhores valores riores ao percentil 95 e, na hipertensão complicada,
de sensibilidade e especificidade para o diagnóstico caracterizada por lesão de órgão alvo, co-morbidades ou
laboratorial do feocromocitoma 21. presença de fatores de risco como a dislipidemia, redução
A prevalência de doença renovascular na para valores abaixo do percentil 90. Recomenda-se iniciar
hipertensão pediátrica é estimada em 3-5%; dentre as com um agente anti-hipertensivo, otimizar a dose do
etiologias mais freqüentes destaca-se a neurofibroma- mesmo e, se o controle adequado da PA não for obtido,
tose22,23 e a displasia fibromuscular 23. O avanço tecno- utilizar adições de outros grupos medicamentosos em
lógico tem permitido a realização de técnicas de imagem seqüência, se necessário. Considera-se aceitável a intro-
pouco invasivas, como angio-ressonância magnética e dução para uso pediátrico das seguintes classes de
tomografia computadorizada tridimensional também na medicamentos anti-hipertensivos: inibidores da enzima
faixa etária pediátrica24-27; no entanto, arteriografia renal de conversão da angiotensina, bloqueadores de receptor
permanece como método diagnóstico de escolha para a de angiotensina, beta-bloqueadores, bloqueadores de
hipertensão renovascular pediátrica, devendo ser indi- canal de cálcio e diuréticos8.
Tabela 4. Medicamentos orais mais utilizados para o tratamento da hipertensão arterial crônica pediátrica8.
Medicamento Dose Inicial (mg/kg/dose) Dose máxima (mg/kg/dia) Intervalo
Amlodipina
(6-17 anos) 2,5 mg/dia 5 mg/dia 24h
Nifedipina XL 0,25 – 0,5 3 (máx: 120mg/dia) 12 – 24h
Captopril
Criança 0,3 – 0,5 6 8h
Neonato 0,03 – 0,15 2 8 – 24h
Enalapril 0,08 0,6 12 – 24h
Losartan 0,7 (máx: 50mg/dia) 1,4 (máx: 100mg/dia) 24h
Propranolol 1–2 4(máx: 640mg/dia) 8 – 12h
Atenolol 0,5 – 1 2 (máx: 100mg/dia) 12 – 24h
Furosemide 0,5 – 2 6 4 – 12h
Hidroclorotiazida 1 3 (máx: 50mg/dia) 12h
Triamterene 1–2 3 – 4 (máx: 300mg/dia) 12h
Espironolactona 1 3,3 (máx: 100mg/dia) 6 – 12h
Clonidina
(≥ 12 anos) 0,2mg/dia 2,4mg/dia 12h
Prazosin 0,05 – 0,1 0,5 8h
Hidralazina 0,75 7,5 (máx: 200mg/dia) 6h
Minoxidil
< 12 anos 0,2 50mg/dia 6-8h
≥ 12 anos 5mg/dia 100mg/dia
máx: máximo; h: horas
A tabela 4 demonstra as doses pediátricas atua- hipertensiva se caracteriza por elevação também impor-
lizadas para os hipotensores mais prescritos para o tante de pressão arterial em paciente sob risco de evolução
tratamento da hipertensão crônica. Crianças com hiper- para lesão progressiva de órgãos-alvo, mas sem evidência
tensão secundária devem ter a terapêutica farmacológica de acometimento recente. Em termos práticos, a emergên-
adequada ao tratamento da doença de base. Após a cia hipertensiva requer redução imediata do nível de PA,
instituição do Modernization Act pelo Food and Drug enquanto a urgência hipertensiva requer que se inicie uma
Administration (FDA), houve um ímpeto para o desen- estratégia medicamentosa para que, sob monitorização, a
volvimento de dados pediátricos de eficácia e segurança pressão arterial seja reduzida em 24-48 horas8,35.
de medicamentos em geral, e de hipotensores especifi- Na emergência hipertensiva, a redução da PA deve
camente33; estes dados, há muito esperados, terão efeito acontecer de maneira lenta e progressiva36,37 com redução
positivo para o refinamento da introdução da terapêutica de 30% do programado em 6-12 horas, 30% em 24 horas,
medicamentosa da hipertensão pediátrica e demonstrarão com ajuste final em 2-4 dias36. A redução muito rápida de
quais as melhores classes de hipotensores para uso nas pressão arterial é contra-indicada, pois leva à hipotensão,
diferentes condições associadas à hipertensão arterial na falência de mecanismos auto-reguladores e possibilidade
criança e no adolescente. A literatura pediátrica envol- de isquemia cerebral e visceral 37. A emergência hiperten-
vendo a utilização de hipotensores é ampla e a discussão siva deve ser tratada com drogas por via parenteral,
de cada classe em particular foge ao escopo deste artigo; enquanto a urgência hipertensiva pode ser controlada com
revisões recentes sobre o assunto8,34 podem ser consul- os medicamentos por via oral38 usados para hipertensão
tadas para informações adicionais. crônica. O medicamento mais utilizado em nosso meio
para o tratamento da emergência hipertensiva é o nitro-
A crise hipertensiva prussiato de sódio, um agente vasodilatador de veias e
artérias, de ação instantânea e efeito efêmero que evanes-
A crise hipertensiva pode ser classificada em ur- ce em 30-60 segundos após a parada de infusão. Reco-
gência e emergência. A emergência hipertensiva carac- menda-se iniciar com dose baixa de 0,5-1µg/kg/minuto,
teriza-se por descompensação rápida de funções vitais com aumento progressivo até 8µg/kg/minuto, quando
causada por grande elevação da PA em presença de lesão necessário8. Recomenda-se que o frasco e a linha de infu-
evidente e recente de órgãos-alvo. Esta condição clínica são do nitroprussiato permaneçam encobertos durante a
exige controle rápido dos níveis pressóricos. A urgência infusão, pois o nitroprussiato é sensível à luz. O nitro-
Tabela 5. Principais medicamentos e doses pediátricas 6. Update on the 1987 Task Force Report on High Blood
utilizadas para controle da emergência hipertensiva8. Pressure in Children and Adolescents: a working group report
Medicamento Via DOSE Início da ação from the National High Blood Pressure Education Program.
Nitroprussiato IV 0,5-10µg/kg/min Segundos National High Blood Pressure Education Program Working
de sódio Group on Hypertension Control in Children and Adolescents.
Labetolol IV 0,25-3mg/kg/h 5-10 minutos Pediatrics 1996;98:649-58.
Nicardipina IV 1-3µg/kg/min Minutos 7. Centers for Disease Control and Prevention, National Center
Hidralazina IV 0,2-0,6mg/kg em bolo 10-30 minutos for Health Statistics. National Health and Nutrition
IM IV ou via IM Examination Survey (NHANHES III), 1988-1991, data
computed for the National Heart, Lung and Blood Institute,
Esmolol IV 100-500µg/kg/min Segundos
Atlanta, GA: Centers for Disease Control and Prevention.
Enalaprilato IV 0,05-0,1mg/kg em bolo 15 minutos
(até 1,25mg/dose) 8. National High Blood Pressure Education Program Working
a cada 8-24h Group on High Blood Pressure in Children and Adolescents.
The Fourth Report on the Diagnosis, Evaluation, and
Treatment of High Blood Pressure in Children and
Adolescents. Pediatrics 2004;114:555-76.
prussiato é metabolizado a cianeto, cianeto e tiocianeto
podem causar acidose metabólica, confusão mental e 9. Centers for Disease Control and Prevention, National Center
for Health Statistics. 2000 CDC growth charts: United States.
deterioração do estado clínico, portanto administração de Disponível em: http://www.cdc.gov/growthcharts.
nitroprussiato por mais de 24 horas requer monitorização
do nível sérico de cianeto37. Esta droga deve ser evitada 10. Muntner P, He J, Cutler JA, Wildman RP, Whelton PK.
Trends in blood pressure among children and adolescents.
em adolescentes grávidas e em pacientes com hipoper- JAMA 2004;291:2107-13.
fusão do sistema nervoso central35. Cuidado especial é
11. Hulman S, Edwards R, Chen YQ, Polansky M, Falkner B.
necessário também quando da administração deste medica-
Blood pressure patterns in the first three days of life. J
mento a pacientes com insuficiência renal. Recomenda-se Perinatol 1991;11:231-4.
que imediatamente após estabilização do paciente e
12. Zubrow A, Hulman S, Kushner H, Falkner B. Determinants of
controle inicial da pressão arterial com nitroprussiato de
blood pressure in infants admitted to neonatal intensive care
sódio seja associado hipotensor por via oral, para que a units: a prospective multicenter study. J Perinatol
redução da dose do nitroprussiato se faça em vigência do 1995;15:470-9.
mesmo e ocorra de maneira segura, mas rápida, evitando-
13. Balachandra S, Singh A, Tejani A. Epidemiology of
se assim a intoxicação por seus metabólitos. É importante hypertension in children in an inner city population. Pediatr
chamar a atenção que as diretrizes de 2004 enfatizam que Res 1997;41:275.
o tratamento da emergência hipertensiva deva ser rea- 14. Sinaiko AR, Steinberger J, Moran A, Prineas RJ, Jacobs DR
lizado somente com drogas de uso parenteral, como de- Jr. Relation of insulin resistance to blood pressure in
monstrado na tabela 5. childhood. J Hypertens 2002;20:509-17.
15. Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH.
Prevalence of a metabolic syndrome phenotype in
REFERÊNCIAS adolescents: findings from the Third National Health and
Nutrition Examination Survey, 1988–1994. Arch Pediatr
1. Lauer RM, Clarke WR. Childhood risk factors for high adult Adolesc Med 2003;157:1-827.
blood pressure: the Muscatine Study. Pediatrics 1989;
84:633-41. 16. Sinaiko AR. Current Concept: Hypertension in Children. N
Engl J Med 1996;335:1968-73.
2. Hoq S, Chen W, Srinivasan SR, et al. Childhood blood
pressure predicts adult microalbuminuria in African 17. Sorof JM. Systolic hypertension in children: benign or
Americans, but not in whites: the Bogalusa heart study. Am J beware? Pediatr Nephrol 2001;16:517-25.
Hypertens 2002;15:1036-41. 18. Sorof JM. Prevalence and consequence of systolic
3. Gillman MW, Ellison RC. Childhood prevention of essential hypertension in children. Am J Hypertens 2002;15:57S-60S.
hypertension. Pediatr Clin N Am 1993;40:179-94. 19. Daniels SR, Meyer RA, Strife CF, Lipman M, Loggie JM.
4. National Heart, Lung, and Blood Institute. Report of the Task Distribution of target-organ abnormalities by race and sex in
Force on Blood Pressure Control in Children. Pediatrics children with essential hypertension. J Hum Hypertens
1977;59:797-820. 1990;4:103-4.
5. Report of the Second Task Force on Blood Pressure Control 20. Eisenhofer G, Huynh TT, Hiroi M, Pacak K. Understanding
in Children. Task Force on Blood Pressure Control in catecholamine metabolism as a guide to the biochemical
Children. National Heart, Lung and Blood Institute, Bethesda, diagnosis of pheochromocytoma. Rev Endocrinol Metab
Maryland. Pediatrics 1987;79:1-25. Disord 2001;2:297-311.
21. Lenders JW, Pacak K, Walther MM, Linehan WM, Mannelli M, 31. Hansen HS, Hyldebrandt N, Froberg K, Nielsen JR. Blood
Friberg P, et al. Biochemical diagnosis of pressure and physical fitness in a population of children – the
pheochromocytoma: which test is best? JAMA Odense Schoolchild Study. J Hum Hypertens 1990;4:615-20.
2002;287:1427-34.
32. American Academy of Pediatrics, Committee on Sports
22. McTaggart SJ, Gulati S, Walker RG, Powell HR, Jones CL. Medicine Fitness. Athletic participation by children and
Evaluation and long-term outcome of pediatric renovascular adolescents who systemic hypertension. Pediatrics
hypertension. Pediatr Nephrol 2000;14:1022-9. 1997;99:637-8.
23. Deal JE, Snell MF, Barratt TM, Dillon MJ. Renovascular 33. Wells TG. Trials of antihypertensive therapies in children.
disease in childhood. J Pediatr 1992;121:378-84. Blood Press Monit 1999;4:189-92.
24. Binkert CA, Debatin JF, Schneider E, et al. Can MR 34. Temple ME, Nahata MC. Treatment of Pediatric
measurement of renal artery flow and renal volume predict Hypertension. Pharmacotherapy 2000;20:140-50.
the outcome of percutaneous transluminal renal angioplasty?
35. Fivush B, Neu A, Furth S. Acute hypertensive crises in
Cardiovasc Intervent Radiol 2001;24:233-9.
children: emergencies and urgencies. Curr Opin Pediatr
25. Marcos HB, Choyke PL. Magnetic resonance angiography of 1997;9:233-6.
the kidney. Semin Nephrol 2000;20:450-5.
36. Adelman RD, Coppo R, Dillon MJ. The emergency
26. Debatin JF, Spritzer CE, Grist TM, et al. Imaging of the renal management of severe hypertension. Pediatr Nephrol
arteries: value of MR angiography. Am J Roentgenol 2000;14:422-7.
1991;157:981-90.
37. Deal JE, Barratt TM, Dillon MJ. Management of hypertensive
27. Vade A, Agrawal R, Lim-Dunham J, Hartoin D. Utility of emergencies. Arch Dis Child 1992;67:1089-92.
computed tomographic renal angiogram in the management
38. Abdelwahab W, Frishman W, Landau A. Management of
of childhood hypertension. Pediatr Nephrol 2002;17:741-7.
hypertensive urgencies and emergencies. J Clin Pharmacol
28. Shahdadpuri J, Frank R, Gauthier BG, Siegel DN, Trachtman 1995;35:747-62.
H. Yield of renal arteriography in the evaluation of pediatric
hypertension. Pediatr Nephrol 2000;14:816-9.
29. Rocchini AP, Katch V, Anderson J, Hinderliter J, Becque D,
Martin M, et al. Blood pressure in adolescents: effect of
weight loss. Pediatrics 1988;82:16-23.
Endereço para correspondência:
30. Hagberg JM, Goldring D, Holloszy JO. Effect of exercise
training on the blood pressure and hemodynamic features of Vera Hermina Koch
hypertensive adolescents. Am J Cardiol 1983;52:763-8. E-mail:vkoch@terra.com.br
Global Recommendations on Physical Activity for Health
WHO Library Cataloguing-in-Publication Data
Global recommendations on physical activity for health.
1.Exercise. 2.Life style. 3.Health promotion. 4.Chronic disease - prevention and control. 5.National health
programs. I.World Health Organization.
ISBN 978 92 4 159 997 9 (NLM classification: QT 255)
© World Health Organization 2010

All rights reserved. Publications of the World Health Organization can be obtained from WHO Press,
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Printed in Switzerland
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3
LIST OF ABBREVIATIONS
AFRO: WHO Regional Office for Africa
AMRO/ PAHO: WHO Regional Office for the Americas
CDC: Centres for Disease Control and Prevention
CHD: Coronary Heart Disease
CVD: Cardio Vascular Disease
DPAS: Global Strategy on Diet, Physical Activity & Health
EMRO: WHO Regional Office for the Eastern Mediterranean
EURO: WHO Regional Office for Europe
GPAQ: Global Physical Activity Questionnaire
GSHS: Global School-based Health Survey
GRC: Guidelines Review Committee
HQ: Headquarters
LMIC: Low- and Middle-Income Countries
NCDs: Non-communicable Diseases
PA: Physical Activity
RO: Regional Officer
S: Strong Recommendation (WHO Guidelines Review Committee Definition)
SEARO: WHO Regional Office for South-East Asia
STEPS: The WHO STEPwise approach to Surveillance
W: Weak Recommendation (WHO Guidelines Review Committee Definition)
WHO: World Health Organization
WPRO: WHO Regional Office for the Western Pacific
AckNOwLEdgEmENTS:
The development of this document was financially supported through the WHO/CDC Cooperative
Agreements (2006/2010). The United Kingdom Government provided financial support to the face-to-face
meeting of the guideline group members which was held in London, United Kingdom in October 2009.
Declarations of interests have been collected for all members of the guideline group (Appendix 4). These
have been discussed with the WHO legal department. None of the members of the guideline group declared
interest in terms of receiving commercial or non-commercial financial support for research and consulting
from private bodies in the field of physical activity for health. It was concluded that none of the selected
members presented conflict of interest.
PHOTO cREdITS:
Cover: V. Pierre; V. Candeias; P Merchez; V. Collazos
Chapter 2: V. Collazos; P. Desloovere; V. Pierre; A. Waak; V. Candeias; H. Anenden; E. Elsheikh
Chapter 3: P. Desloovere; A. Waak; C. Gaggero; V. Pierre; V. Collazos; B. Maloto-Adurias
Capter 4: P. Desloovere; F. Bull; C. Khasnabis; E. Elsheikh; M. Ciecierska. Age group: 5-17 years old: G. Xuereb;
V. Collazos; V. Pierre; M. Kokic; V. Candeias; Franck. Age group: 18-64 years old: C. Gaggero; V. Pierre; MC.
Engelsman; V. Collazos; N. Moindot; C. Sherer. Age group: 64 years old and above: A. Waak; P Gerace; J.
Smith; V. Candeias; C. Gaggero
Chapter 5: V. Manso Castello Branco; B. Maloto-Adurias; V. Collazos; E. Engelsman; MC. Engelsman; S. Onur;
V. Pierre
4
TABLE OF cONTENTS
1. Executive Summary 7
2. Physical activity for health 9

2.1 Public health significance of physical activity 10
2.2 Mandate on physical activity for health 10
2.3 Importance of national and regional physical activity guidelines 11
3. Development of recommendations for physical activity for health 13

3.1 Scope and target audience 14
3.2 Development process 14
4. Recommended population levels of physical activity for health 15

4.1 Introduction 16
4.2 Age group: 5–17 years old 17
4.3 Age group: 18–64 years old 23
4.4 Age group: 65 years old and above 29
4.5 Future review of recommendations and research gaps 33
5. How to use the recommended levels of physical activity for health 35

5.1 Introduction 36
5.2 National adaptation of the global recommendations 36
5.2.1 Low-and-middle income countries 37
5.3 Supportive policies in promoting physical activity 37
5.4 Strategies for communicating the global recommendations at national level 38
5.5 Monitoring and evaluation 38
6. Resources 39
7. Appendices 41
Appendix 1 - Detailed description of the methodology used for developing 42
the Global Recommendations on Physical Activity for Health
Appendix 2 - Detailed reference of literature 46
Appendix 3 - Examples of messages used to promote physical activity at national level and 49
consistent with the global recommendations
Appendix 4 - Guideline group members 51
Appendix 5 - Glossary 52
Appendix 6 - List of peer reviewers 54
Appendix 7 - WHO Regional Offices Consulted 54
Appendix 8 - WHO Secretariat 54
References 55
5
1. EXEcUTIVE SUmmARy
Physical inactivity is now identified as the fourth leading risk factor for global mortality. Physical inactivity
levels are rising in many countries with major implications for the prevalence of noncommunicable diseases
(NCDs) and the general health of the population worldwide.
The significance of physical activity on public health, the global mandates for the work carried out by WHO
in relation to promotion of physical activity and NCDs prevention, and the limited existence of national
guidelines on physical activity for health in low- and middle-income countries (LMIC) make evident the
need for the development of global recommendations that address the links between the frequency,
duration, intensity, type and total amount of physical activity needed for the prevention of NCDs.
The focus of the Global Recommendations on Physical Activity for Health is primary prevention of NCDs
through physical activity at population level, and the primary target audience for these Recommendations
are policy-makers at national level.
Issues not addressed in this document are clinical control and the management of disease through
physical activity. Guidance on how to develop interventions and approaches to promote physical activity
in population groups are similarly not addressed.
The following steps summarize the process undertaken by the WHO Secretariat in preparation of the Global
Recommendations on Physical Activity for Health:
1. Review and compilation of the scientific evidence available for three age groups, for the following
outcomes: cancer, cardiorespiratory, metabolic, musculoskeletal and functional health.
2. Setting out of a process to develop the Recommendations.
3. Establishment of a global guideline group with expertise both in subject matter and in policy
development and implementation.
4. Meeting and electronic consultation of the guideline group to prepare the final draft of the Global
Recommendations on Physical Activity for Health.
5. Peer review of the Recommendations and consultation with the WHO Regional Offices.
6. Finalization of the Recommendations, approval by the WHO Guideline Review Committee.
7. Translation, publication and dissemination.
The recommendations set out in this document address three age groups: 5–17 years old; 18–64 years old;
and 65 years old and above. A section focusing on each age group includes the following:
• a narrative summary of scientific evidence;
• the current physical activity recommendations;
• the interpretation and justification for the recommendations made.
REcOmmENdEd LEVELS OF
PHySIcAL AcTIVITy FOR HEALTH
5–17 years old
For children and young people of this age group physical activity includes play, games, sports, transportation,
recreation, physical education or planned exercise, in the context of family, school, and community activities.
In order to improve cardiorespiratory and muscular fitness, bone health, cardiovascular and metabolic
health biomarkers and reduced symptoms of anxiety and depression, the following are recommended:
1. Children and young people aged 5–17 years old should accumulate at least 60 minutes of moderate-
to vigorous-intensity physical activity daily.
2. Physical activity of amounts greater than 60 minutes daily will provide additional health benefits.
3. Most of daily physical activity should be aerobic. Vigorous-intensity activities should be incorporated,
including those that strengthen muscle and bone, at least 3 times per week.
7
18–64 years old
For adults of this age group, physical activity includes recreational or leisure-time physical activity,
transportation (e.g walking or cycling), occupational (i.e. work), household chores, play, games, sports or
planned exercise, in the context of daily, family, and community activities.
In order to improve cardiorespiratory and muscular fitness, bone health and reduce the risk of NCDs and
depression the following are recommended:
1. Adults aged 18–64 years should do at least 150 minutes of moderate-intensity aerobic physical
activity throughout the week, or do at least 75 minutes of vigorous-intensity aerobic physical activity
throughout the week, or an equivalent combination of moderate- and vigorous-intensity activity.
2. Aerobic activity should be performed in bouts of at least 10 minutes duration.
3. For additional health benefits, adults should increase their moderate-intensity aerobic physical
activity to 300 minutes per week, or engage in 150 minutes of vigorous-intensity aerobic physical
activity per week, or an equivalent combination of moderate- and vigorous-intensity activity.
4. Muscle-strengthening activities should be done involving major muscle groups on 2 or more days a
week.
65 years old and above

For adults of this age group, physical activity includes recreational or leisure-time physical activity,
transportation (e.g walking or cycling), occupational (if the person is still engaged in work), household
chores, play, games, sports or planned exercise, in the context of daily, family, and community activities.
In order to improve cardiorespiratory and muscular fitness, bone and functional health, and reduce the risk
of NCDs, depression and cognitive decline, the following are recommended:
1. Adults aged 65 years and above should do at least 150 minutes of moderate-intensity aerobic physical
activity throughout the week, or do at least 75 minutes of vigorous-intensity aerobic physical activity
throughout the week, or an equivalent combination of moderate- and vigorous-intensity activity.
3. For additional health benefits, adults aged 65 years and above should increase their moderate-
intensity aerobic physical activity to 300 minutes per week, or engage in 150 minutes of vigorous-
intensity aerobic physical activity per week, or an equivalent combination of moderate- and vigorous-
intensity activity.
4. Adults of this age group with poor mobility should perform physical activity to enhance balance and
prevent falls on 3 or more days per week.
5. Muscle-strengthening activities should be done involving major muscle groups, on 2 or more days a
week.
6. When adults of this age group cannot do the recommended amounts of physical activity due to health
conditions, they should be as physically active as their abilities and conditions allow.
Overall, across all the age groups, the benefits of implementing the above recommendations, and of being
physically active, outweigh the harms. At the recommended level of 150 minutes per week of moderate-
intensity activity, musculoskeletal injury rates appear to be uncommon. In a population-based approach, in
order to decrease the risks of musculoskeletal injuries, it would be appropriate to encourage a moderate
start with gradual progress to higher levels of physical activity.
8
2 PHySIcAL AcTIVITy FOR HEALTH

9
2.1 Physical inactivity has been identified as the fourth leading risk factor for
PUBLIc HEALTH global mortality (6% of deaths globally). This follows high blood pressure
(13%), tobacco use (9%) and high blood glucose (6%). Overweight and
SIgNIFIcANcE OF
obesity are responsible for 5% of global mortality (1).
PHySIcAL AcTIVITy
Levels of physical inactivity are rising in many countries with major
implications for the general health of people worldwide and for the
prevalence of NCDs such as cardiovascular disease, diabetes and cancer
and their risk factors such as raised blood pressure, raised blood sugar
and overweight. Physical inactivity is estimated as being the principal
cause for approximately 21–25% of breast and colon cancer burden, 27%
of diabetes and approximately 30% of ischaemic heart disease burden
(1). In addition, NCDs now account for nearly half of the overall global
burden of disease. It is estimated currently that of every 10 deaths, 6 are
attributable to noncommunicable conditions (2).
Global health is being influenced by three trends: population-ageing, rapid

unplanned urbanization, and globalization, all of which result in unhealthy
environments and behaviours. As a result, the growing prevalence of NCDs
and their risk factors has become a global issue affecting both low- and
middle-income countries. Nearly 45% of the adult disease burden in these
countries is now attributable to NCDs. Many low- and middle-income
countries are beginning to suffer the double burden of communicable and
noncommunicable diseases, and health systems in these countries are now
having to cope with the additional costs of treating both.
It has been shown that participation in regular physical activity reduces

the risk of coronary heart disease and stroke, diabetes, hypertension,
colon cancer, breast cancer and depression. Additionally, physical activity
is a key determinant of energy expenditure, and thus is fundamental to
energy balance and weight control (1–6).
2.2 In May 2004, the Fifty-seventh World Health Assembly endorsed

mANdATE ON PHySIcAL Resolution WHA57.17: Global Strategy on Diet, Physical Activity and
AcTIVITy FOR HEALTH Health and recommended that Member States develop national physical
activity action plans and policies to increase physical activity levels in
their populations (5). Furthermore, in May 2008, the Sixty-first World
Health Assembly endorsed Resolution WHA61.14: Prevention and Control
of Noncommunicable Diseases: Implementation of the Global Strategy and
the Action Plan for the Global Strategy for the Prevention and Control of
Noncommunicable Diseases (7).
This Action Plan urges Member States to implement national guidelines

on physical activity for health and encourages them to develop and put
into practice policies and interventions that:
• develop and implement national guidelines on physical activity for
health;
• introduce transport policies that promote active and safe methods
of travelling to and from schools and workplaces, such as walking or
cycling;
• ensure that physical environments support safe active commuting,
and create space for recreational activity.
The action plan urges WHO to provide countries with technical support in
either implementing or strengthening nationwide actions to reduce risk
factors for NCDs.
10
2.3 The limited existence of national guidelines on physical activity for health
ImPORTANcE OF in low- and middle-income countries, the public health significance of
physical activity and the global mandates for the work of WHO, related
NATIONAL ANd
to promotion of physical activity and NCD prevention, make evident the
REgIONAL PHySIcAL
need for the development of global recommendations that address the
AcTIVITy gUIdELINES links between the frequency, duration, intensity, type and total amount of
physical activity needed for the prevention of NCDs.
Scientifically-informed recommendations, with a global scope, on the

benefits, type, amount, frequency, intensity, duration and total amount
of the physical activity necessary for health benefits are key information
for policy-makers wanting to address physical activity at population level
and who are involved in the development of guidelines and policies at
regional and national levels on prevention and control of NCDs.
The development and publication of science-based national or regional

physical activity guidelines can:
• inform national physical activity policies and other public health
interventions;
• provide the starting point to the establishment of goals and objectives
for physical activity promotion at national level;
• foster intersectoral collaboration and contribute to setting up national
goals and objectives regarding physical activity promotion;
• provide a foundation for physical activity promotion initiatives;
• justify the allocation of resources to physical activity promotion
interventions;
• create a framework for joint action for all other relevant stakeholders
around the same goal;
• provide an evidence-based document that enables all relevant
stakeholders to transfer policy into action with the allocation of the
appropriate resources; and
• facilitate national surveillance and monitoring mechanisms to monitor
population levels of physical activity.
11
3
dEVELOPmENT OF THE gLOBAL
REcOmmENdATIONS ON PHySIcAL
AcTIVITy FOR HEALTH
13
3.1 The Global Recommendations on Physical Activity for Health aim to provide
ScOPE ANd TARgET guidance on the dose-response relationship between physical activity
and health benefits (i.e. the frequency, duration, intensity, type and total
AUdIENcE
amount of physical activity needed for health enhancement and prevention
of NCDs). The primary prevention of NCDs through physical activity, at
population level, is the focus of this document, while the management of
disease through physical activity, and clinical control are not addressed.
By reviewing the evidence and compiling it in the format of recommendations

on the frequency, duration, intensity, type and total amount of physical
activity to be achieved at the population level, this document aims to assist
policy-makers in the development of public health policies. National-level
policy-makers are the primary target audience of these recommendations,
as these are expected to constitute a resource for them in the development
of national guidelines for health-enhancing physical activity.
Guidance on how to develop interventions and approaches to promote

physical activity in population groups is an issue that is not addressed in the
document. However, information for this can be found in the publication:
A guide for population-based approaches to increasing levels of physical
activity: implementation of the Global Strategy on Diet, Physical Activity and
Health (3).
3.2 The Recommendations set out in this document were developed according
dEVELOPmENT PROcESS to the process outlined in the figure below. A detailed description of the
methodology used for developing the Global Recommendations on Physical
Activity for Health is included in Appendix 1.
FIg.1: dEVELOPmENT OF THE gLOBAL REcOmmENdATIONS

ON PHySIcAL AcTIVITy FOR HEALTH
Defining scope, content and target audience

JANUARy 2008 of recommendations.
JUNE 2010
Expert group meeting (Mexico)
Consensus decision to use the evidence
review of the USA to develop the WHO Approved by
global recommendations. GRC
FEBRUARy 2009
JUNE OcTOBER 2008
Search questions developed by WHO
Secretariat Publication of USA’s evidence review and the
recommendations by the Physical Activity Guidelines
Advisory Committee.
mARcH APRIL 2009 APRIL mAy 2010

Compilation and assessment of scientific
WHO Secretariat finalizes recommendations
evidence
mARcH 2010
JUNE 2009 Final revision by Regional Offices
Approval of process by WHO Guideline
Review Committee (GRC)
JAN. FEB. 2010
Appointment of
Guideline group Peer review of recommendations
AUgUST 2009
WHO Secretariat prepares draft of NOV. dEc. 2010
recommendations and shares evidence with
guideline group members WHO Secretariat finalizes draft
recommendations
SEPT. NOV. 2009 OcTOBER 2009

WHO Secretariat prepares draft of recommendations and Meeting of guideline group to discuss draft
shares evidence with guideline group members recommendations
14
4 REcOmmENdEd POPULATION LEVELS

OF PHySIcAL AcTIVITy FOR HEALTH
15
4.1 The following section presents the recommended levels of physical activity
INTROdUcTION for three age groups: 5–17 years old, 18–64 years old and 65 years old
and above. These age groups were selected taking into consideration the
nature and availability of the scientific evidence relevant to the selected
outcomes. The recommendations do not address the age group of children
less than 5 years old. Although children in this age range benefit from being
active, more research is needed to determine what dose of physical activity
provides the greatest health benefits.
Each section includes:

• remarks on the target population;
• a narrative summary of the scientific evidence;
• the recommendations on physical activity for health; and
• the interpretation and justification for the recommendations presented.
The Global Recommendations on Physical Activity for Health are relevant for
the following health outcomes:
• Cardiorespiratory health (coronary heart disease, cardiovascular
disease, stroke and hypertension).
• Metabolic health (diabetes and obesity).
• Musculoskeletal health (bone health, osteoporosis).
• Cancer (breast and colon cancer).
• Functional health and prevention of falls.
• Depression.
The recommendations presented in this document use the concepts of

frequency, duration, intensity, type and total amount of physical activity
needed for health enhancement and prevention of NCDs. Box 1 includes
definitions of these and other useful concepts. Further information can be
found in the Glossary in Appendix 5.
BOX 1: dEFINITIONS OF cONcEPTS USEd IN THE REcOmmENdEd LEVELS OF PHySIcAL AcTIVITy
Type of physical activity (What type). The mode of participation in physical activity. The type of
physical activity can take many forms: aerobic, strength, flexibility, balance.
Duration (For how long). The length of time in which an activity or exercise is performed. Duration
is generally expressed in minutes.
Frequency (How often). The number of times an exercise or activity is performed. Frequency is
generally expressed in sessions, episodes, or bouts per week.
Intensity (How hard a person works to do the activity). Intensity refers to the rate at which the
activity is being performed or the magnitude of the effort required to perform an activity or
exercise.
Volume (How much in total). Aerobic exercise exposures can be characterized by an interaction
between bout intensity, frequency, duration, and longevity of the programme. The product of
these characteristics can be thought of as volume.
Moderate-intensity physical activity. On an absolute scale, moderate intensity refers to activity

that is performed at 3.0–5.9 times the intensity of rest. On a scale relative to an individual’s
personal capacity, moderate-intensity physical activity is usually a 5 or 6 on a scale of 0–10.
Vigorous-intensity physical activity. On an absolute scale, vigorous intensity refers to activity

that is performed at 6.0 or more times the intensity of rest for adults and typically 7.0 or more
times for children and youth. On a scale relative to an individual’s personal capacity, vigorous-
intensity physical activity is usually a 7 or 8 on a scale of 0–10.
Aerobic activity. Aerobic activity, also called endurance activity, improves cardiorespiratory
fitness. Examples of aerobic activity include: brisk walking, running, bicycling, jumping rope, and
swimming.
16
17
TARgET POPULATION These guidelines are relevant to all children aged 5–17 years unless
specific medical conditions indicate to the contrary. Children and youth
should be encouraged to participate in a variety of physical activities that
support the natural development and are enjoyable and safe.
Whenever possible, children and youth with disabilities should meet

these recommendations. However they should work with their health
care provider to understand the types and amounts of physical activity
appropriate for them considering their disability.
These recommendations are applicable for all children and youth

irrespective of gender, race, ethnicity, or income level. However
the communication strategies, dissemination and messaging of the
recommendations may differ so as to be most effective in various
population subgroups.
The recommended levels of physical activity for children and youth included
in this section, should be achieved above and beyond the physical activity
accumulated in the course of normal daily non-recreational activities.
All children and youth should be physically active daily as part of play,
games, sports, transportation, recreation, physical education, or planned
exercise, in the context of family, school, and community activities.
For inactive children and youth, a progressive increase in activity to

eventually achieve the target shown below is recommended. It is
appropriate to start with smaller amounts of physical activity and
gradually increase duration, frequency and intensity over time. It should
also be noted that if children are currently doing no physical activity,
doing amounts below the recommended levels will bring more benefits
than doing none at all.
NARRATIVE SUmmARy The scientific evidence available for the age group 5–17 years supports
OF ScIENTIFIc EVIdENcE the overall conclusion that physical activity provides fundamental health
(9–11) benefits for children and youth. This conclusion is based on findings of
observational studies in which higher levels of physical activity were
found to be associated with more favourable health parameters as well
as experimental studies in which physical activity interventions were
associated with improvements in health indicators. The documented health
benefits include increased physical fitness (both cardiorespiratory fitness
and muscular strength), reduced body fatness, favourable cardiovascular
and metabolic disease risk profiles, enhanced bone health and reduced
symptoms of depression. (9-11)
Physical activity is positively related to cardiorespiratory and metabolic

health in children and youth. To examine the relation between physical
activity and cardiovascular and metabolic health, the guideline group
reviewed literature from the CDC Literature review (2008) and the evidence
reviews from Janssen (2007) and Janssen, Leblanc (2009). (9-11)
A dose-response relationship appears to exist, in that greater doses of

physical activity are associated with improved indicators of cardiorespiratory
and metabolic health. Taken together, the observational and experimental
18
evidence supports the hypothesis that maintaining high amounts and

intensities of physical activity starting in childhood and continuing into
adult years will enable people to maintain a favourable risk profile and
lower rates of morbidity and mortality from cardiovascular disease and
diabetes later in life. Collectively, the research suggests that moderate- to
vigorous-intensity physical activity for at least 60 minutes per day would
help children and youth maintain a healthy cardiorespiratory and metabolic
risk profile. In general it appears that higher volumes or intensities of
physical activity are likely to have greater benefit, but research in this area
is still limited. (9-11)
Physical activity is positively related to cardiorespiratory fitness in

children and youth, and both preadolescents and adolescents can achieve
improvements in cardiorespiratory fitness with exercise training. In
addition, physical activity is positively related to muscular strength. In
both children and youth, participation in muscle-strengthening activities
2 or 3 times per week significantly improves muscular strength. For this
age group, muscle-strengthening activities can be unstructured and part of
play, such as playing on playground equipment, climbing trees or pushing
and pulling activities. (9-11)
Normal-weight youth who have relatively high levels of physical activity

tend to have less adiposity than youth with low levels. Among overweight
and obese youth, interventions that increase the levels of physical activity
tend to show beneficial effects on health.
Bone-loading physical activity increases bone mineral content and bone

density. Targeted weight-loading activities that simultaneously influence
muscular strength, performed 3 or more days per week are effective. For
this age group, bone-loading activities can be performed as part of playing
games, running, turning or jumping. The literature used for the rationale
and dose-response pattern related to bone health was obtained from
the CDC literature review (2008), and the evidence reviews from Janssen
(2007) and Janssen, Leblanc (2009). (9-11)
The review of the literature relating muscular strength to the relation and
dose-response pattern included literature from the CDC literature review
(2008), and the evidence reviews from Janssen (2007) and Janssen,
Leblanc (2009).
An overall evaluation of the evidence suggests that important health

benefits can be expected to accrue in most children and youth who
accumulate 60 or more minutes of moderate to vigorous physical activity
daily. (9-11)
The concept of accumulation refers to meeting the goal of 60 minutes per

day by performing activities in multiple shorter bouts spread throughout
the day (e.g. 2 bouts of 30 minutes), then adding together the time spent
during each of these bouts. Furthermore, certain specific types of physical
activity must be included in an overall physical activity pattern in order for
children and youth to gain comprehensive health benefits (9-11).
19
These include regular participation in each of the following types of
physical activity on 3 or more days per week:
• resistance exercise to enhance muscular strength in the large muscle
groups of the trunk and limbs;
• vigorous aerobic exercise to improve cardiorespiratory fitness,
cardiovascular risk factors and other metabolic disease risk factors;
weight-loading activities to promote bone health.
These specific types of physical activity can be integrated to achieve 60

minutes or more per day of health and fitness promoting activity.
A detailed reference of the literature used by the guidelines group to

develop these recommendations can be found in Appendix 2.
REcOmmENdATIONS For children and young people, physical activity includes play, games,
sports, transportation, recreation, physical education, or planned exercise,
in the context of family, school and community activities.
The guidelines group reviewed the above cited literature and

recommended that in order to improve cardiorespiratory and muscular
fitness, bone health, cardiovascular and metabolic health biomarkers and
reduce symptoms of anxiety and depression:
1. Children and youth aged 5–17 should accumulate at least 60 minutes of moderate- to vigorous-
intensity physical activity daily.
2. Amounts of physical activity greater than 60 minutes provide additional health benefits.
3. Most of the daily physical activity should be aerobic. Vigorous-intensity activities should be
incorporated, including those that strengthen muscle and bone, at least 3 times per week.
INTERPRETATION There is conclusive evidence that the physical fitness and health status of
ANd JUSTIFIcATION children and youth are substantially enhanced by frequent physical activity.
Compared to inactive young people, physically active children and youth
have higher levels of cardiorespiratory fitness, muscular endurance and
muscular strength, and well-documented health benefits include reduced
body fat, more favourable cardiovascular and metabolic disease risk profiles,
enhanced bone health, and reduced symptoms of anxiety and depression.
Aerobic-type activities should make up the majority of the daily discretionary

physical activity.
These recommendations represent a minimum target for daily physical

activity that allows for health enhancement and prevention of NCDs.
The costs of adopting these recommendations are minimal and essentially

related to the translation into country settings, communication and
dissemination. Implementation of comprehensive policies that facilitate
the achievement of the recommended levels of physical activity will
require additional resource investment.
20
The benefits of being physically active and implementing the above

recommendations outweigh the harms. Any existing risk can be
significantly reduced by a progressive increase in the activity level,
especially in children who are inactive.
In order to reduce the risk of injuries, the use of protective equipment,

such as helmets, should be encouraged in all types of activity that can
potentially pose these risks (12).
It should be noted that in populations that are already active, the national
physical activity guidelines should not promote a physical activity target
that would encourage a reduction in current levels.
21
23
TARgET POPULATION These guidelines are relevant to all healthy adults aged 18–64 years
unless specific medical conditions indicate to the contrary. The guidelines
also apply to individuals in this age range with chronic noncommunicable
conditions not related to mobility such as hypertension or diabetes.
Pregnant, postpartum women and persons with cardiac events may need
to take extra precautions and seek medical advice before striving to
achieve the recommended levels of physical activity for this age group.
Inactive adults or adults with disease limitations will have added health
benefits if moving from the category of “no activity” to “some levels”
of activity. Adults who currently do not meet the recommendations for
physical activity should aim to increase duration, frequency and finally
intensity as a target to achieving the recommended guidelines.
These recommendations are applicable for all adults irrespective of

gender, race, ethnicity or income level. However, to be most effective, the
type of physical activity, the communication strategies, dissemination
and messaging of the recommendations, may differ in various population
groups. The retirement age, which varies from country to country, should
also be taken into consideration when implementing interventions to
promote physical activity.
These recommendations can be applied to adults with disabilities.

However they may need to be adjusted for each individual based on their
exercise capacity and specific health risks or limitations.
NARRATIVE SUmmARy The review of the literature relating cardiorespiratory fitness, muscular
OF ScIENTIFIc EVIdENcE strength, metabolic health and bone health to the rationale for relation
(11, 13–19) and dose response patterns was based on an evaluation from the CDC
literature review (2008), the evidence reviews from Warburton et al (2007
and 2009) and the review by Bauman et al (2005). (11, 13–19)
The dose-response pattern related to depression was reviewed from the

CDC literature review (2008). (11)
There is a direct relationship between physical activity and

cardiorespiratory health (risk reduction of CHD, CVD, stroke,
hypertension). Physical activity improves cardiorespiratory fitness.
Fitness has direct dose-response relations between intensity, frequency,
duration and volume. There is a dose-response relation for CVD and
CHD. Risk reductions routinely occur at levels of 150 minutes of at least
moderate-intensity activity per week. (11, 13–19)
Literature from Cook (2008) and Steyn (2005) related to The INTERHEART
Africa Study and Nocon (2008) and Sofi (2008) related to cardiovascular
disease and mortality were also considered during the peer review
process and related specifically to the context of Africa and cardiovascular
disease. (14-17)
There is a direct relationship between physical activity and metabolic

health, including reduction of risk of diabetes and metabolic syndrome
(11, 13–19). Data indicate that 150 minutes per week of moderate- to
vigorous-intensity physical activity bring significantly lower risks.
24
There is a favourable and consistent effect of aerobic physical activity

on achieving weight maintenance. Accumulation of energy expenditure
due to physical activity is what is important to achieving energy balance.
Accumulation of physical activity can be obtained in short multiple
bouts of at least 10 minutes, or one long bout to meet physical activity
expenditure goals for weight maintenance. The evidence is less consistent
for resistance training, in part, because of the compensatory increase
in lean mass, and the smaller volumes of exercise employed. There is
substantial inter-individual variability with physical activity and weight
maintenance; more than 150 minutes of moderate-intensity activity per
week may be needed to maintain weight. Data from recent well-designed
randomized control trials lasting up to 12 months indicate that aerobic
physical activity performed to achieve a volume of at least 150 minutes
per week is associated with approximately 1–3% weight loss, which is
generally considered to represent weight maintenance. (11)
Physically active adults are likely to have less risk of a hip or vertebral
fracture. Increases in exercise training can minimize the decrease in spine
and hip bone mineral density. Increases in exercise training enhance
skeletal muscle mass, strength, power, and intrinsic neuromuscular
activation. (11, 13, 18, 19)
Weight-bearing endurance and resistance types of physical activity (i.e.

exercise training) are effective in promoting increases in bone mass
density (e.g. moderate- to vigorous-intensity activity performed 3–5 days
per week, 30–60 minutes per session).
Regular practice of physical activity is linked to prevention of breast and

colon cancer. Data indicate that moderate- to vigorous-intensity physical
activity performed at least 30–60 minutes per day is needed to see
significantly lower risks of these cancers.
Overall, strong evidence demonstrates that compared to less active adult

men and women, individuals who are more active have lower rates of
all-cause mortality, coronary heart disease, high blood pressure, stroke,
diabetes, metabolic syndrome, colon cancer, breast cancer, and depression.
Strong evidence also supports the conclusion that, compared to less
active people, physically active adults and older adults exhibit a higher
level of cardiorespiratory and muscular fitness, have a healthier body
mass and composition, and a biomarker profile that is more favourable for
preventing cardiovascular disease and type 2 diabetes and for enhancing
bone health.
A detailed reference of the literature used by the guidelines group to

25
REcOmmENdATIONS In adults aged 18–64, physical activity includes leisure time physical
activity, transportation (e.g. walking or cycling), occupational (i.e. work),
household chores, play, games, sports or planned exercise, in the context
of daily, family, and community activities.

fitness, bone health, reduce the risk of NCDs and depression:
1. Adults aged 18–64 should do at least 150 minutes of moderate-intensity aerobic physical activity
throughout the week or do at least 75 minutes of vigorous-intensity aerobic physical activity
throughout the week or an equivalent combination of moderate- and vigorous-intensity activity.
3. For additional health benefits, adults should increase their moderate-intensity aerobic physical
activity to 300 minutes per week, or engage in 150 minutes of vigorous-intensity aerobic physical
activity per week, or an equivalent combination of moderate- and vigorous-intensity activity.
4. Muscle-strengthening activities should be done involving major muscle groups on 2 or more days
a week.
INTERPRETATION Conclusive scientific evidence, based on a wide range of well-conducted

ANd JUSTIFIcATION studies, shows that physically active people have higher levels of health-
related fitness, a lower risk profile for developing a number of disabling
medical conditions, and lower rates of various chronic noncommunicable
diseases than do people who are inactive.
There are multiple ways of accumulating the total of 150 minutes per week.
The concept of accumulation refers to meeting the goal of 150 minutes
per week by performing activities in multiple shorter bouts of at least 10
minutes each, spread throughout the week then adding together the time
spent during each of these bouts: e.g. 30 minutes of moderate-intensity
activity 5 times per week.
Evidence of acute effects on biomedical markers points to benefits of

undertaking regular physical activity throughout the week (such as 5
or more times per week). Moreover this has the potential to encourage
integrating physical activity as part of daily lifestyle such as active travel
through walking and cycling.
The recommendations listed above are applicable to the following

health conditions: cardiorespiratory health (coronary heart disease,
cardiovascular disease, stroke and hypertension); metabolic health
(diabetes and obesity); bone health and osteoporosis; breast and colon
cancer and depression.
The volume of physical activity associated with the prevention of different

chronic NCDs varies. However, the evidence is currently insufficiently
precise to warrant separate guidelines for each specific disease, but it is
strong enough to cover all health outcomes selected.
26
Higher volumes of activity (i.e. greater than 150 minutes per week) are
associated with additional health benefits. However the evidence is not
available to identify additional or increased benefits for volumes greater
than 300 minutes per week.
The costs of adopting these recommendations are minimal and essentially

related to the translation into country settings, communication and
dissemination. Implementation of comprehensive policies that will
facilitate the achievement of the recommended levels of physical activity
will require additional resource investment.
These recommendations are applicable in low- and middle-income

countries. However national authorities need to adapt and translate
them into culturally appropriate forms for country level, taking into
consideration, among other factors, the need to identify and adapt to the
physical activity domain which is most prevalent at the population level
(e.g. leisure time, occupational or transportation physical activity).
Activity-related adverse events such as musculoskeletal injuries are

common but are usually minor especially for moderate-intensity
activities such as walking. Overall, the benefits of being physically active
and implementing the above recommendations outweigh the harms.
The inherent risk of adverse events can be significantly reduced by a
progressive increase in the activity level, especially in inactive adults.
Selecting low-risk activities and adopting prudent behaviour while doing
any activity can minimize the frequency and severity of adverse events
and maximize the benefits of regular physical activity. In order to reduce
the risk of injuries, the use of protective equipment, such as helmets,
should be encouraged.
It should be noted that, in populations that are already active the national
physical activity guidelines should not promote a physical activity target
that would encourage a reduction in current levels.
27
29
TARgET POPULATION These guidelines are relevant to all healthy adults aged 65 years and
above. They are also relevant to individuals in this age range with chronic
NCDs. Individuals with specific health conditions, such as cardiovascular
disease and diabetes, may need to take extra precautions and seek
medical advice before striving to achieve the recommended levels of
physical activity for older adults.
These recommendations are applicable for all older adults irrespective

of gender, race, ethnicity or income level. However, the communication
strategies, dissemination and messaging of the recommendations may
differ in various population groups in order to be most effective.
The recommendations can be applied to older adults with disabilities

however they may need to be adjusted for each individual, based on their
exercise capacity and specific health risks or limitations.
NARRATIVE SUmmARy The review of the literature relating cardio respiratory fitness, muscular
OF ScIENTIFIc EVIdENcE strength, metabolic health and bone health to the rationale for relation
(11, 13, 20, 21) and dose response patterns was based on an evaluation from the CDC
literature review (2008) the evidence reviews from Warburton et al (2007
and 2009), the review by Bauman et al (2005) and the systematic reviews
by Paterson et al (2007 and 2009). (11, 13, 20, 21)
There is strong scientific evidence that regular physical activity produces

major and extensive health benefits in both adults aged 18–64 and in
older adults aged 65 and above. In some cases the evidence of health
benefits is strongest in older adults because the outcomes related to
inactivity are more common in older adults. This results in an increased
ability of observational studies to detect the protective effect of physical
activity in this age group. Overall, conclusive evidence shows that both
moderate-intensity and vigorous-intensity activity provide similar health
benefits in both adult age groups. (11, 13, 20, 21)
The overall evidence for adults aged 65 years and above demonstrates
that, compared to less active individuals, men and women who are more
active have lower rates of all-cause mortality, coronary heart disease,
high blood pressure, stroke, type 2 diabetes, colon cancer, breast cancer,
a higher level of cardiorespiratory and muscular fitness, healthier body
mass and composition, and a biomarker profile that is more favourable
for the prevention of cardiovascular disease, type 2 diabetes and the
enhancement of bone health. (11, 13, 20, 21)
These benefits are observed in adults in the older age range, with or
without existing NCDs. Hence inactive adults of the 65 years and above
age group, including those with NCDs, are likely to gain health benefits
by increasing their level of physical activity. If they cannot increase
activity to levels required to meet guidelines, they should be active to
the level their abilities and health conditions allow. Older adults who
currently do not meet the recommendations for physical activity should
aim to increase physical activity gradually, starting with increasing
duration and frequency of moderate-intensity activity before considering
increasing the intensity to vigorous-intensity activity. In addition, strong
evidence indicates that being physically active is associated with higher
levels of functional health, a lower risk of falling, and better cognitive
30
function. There is observational evidence that mid-life and older adults

who participate in regular physical activity have reduced risk of moderate
and severe functional limitations and role limitations. In older adults with
existing functional limitations, there is fairly consistent evidence that
regular physical activity is safe and has a beneficial effect on functional
ability. However, there is currently little or no experimental evidence in
older adults with functional limitations that physical activity maintains
role ability or prevents disability. The CDC literature Review (2008) and
the systematic reviews by Paterson (2007) and Patterson and Warburton
(2009) were used to develop the recommendation related to limited
mobility due to health conditions. The dose-response pattern related to
depression and cognitive decline were reviewed from the CDC Literature
review (2008). (11, 20, 21)
In older adults with poor mobility, there is consistent evidence that

regular physical activity is safe and reduces risk of falls by nearly 30%. For
prevention of falls, most evidence supports a physical activity pattern of
balance training and moderate-intensity muscle-strengthening activities
three times per week. There is no evidence that planned physical activity
reduces falls in adults and older adults who are not at risk of falls. Evidence
specific for this age group related to the maintenance or improvement
of balance for those at risk of falling was reviewed from the systematic
reviews by Paterson (2007) and Patterson and Warburton (2009). (20, 21)
A more detailed reference of the literature used by the guidelines group to

REcOmmENdATIONS In older adults of the 65 years and above age group, physical activity
includes leisure time physical activity, transportation (e.g. walking
or cycling), occupational (if the individual is still engaged in work),
household chores, play, games, sports or planned exercise, in the
context of daily, family and community activities.

fitness, bone and functional health, reduce the risk of NCDs, depression
and cognitive decline:
1. Adults aged 65 years and above should do at least 150 minutes of moderate-intensity aerobic
physical activity throughout the week or do at least 75 minutes of vigorous-intensity aerobic
physical activity throughout the week or an equivalent combination of moderate- and vigorous-
intensity activity.
3. For additional health benefits, adults aged 65 years and above should increase their moderate-
intensity aerobic physical activity to 300 minutes per week, or engage in 150 minutes of vigorous-
intensity aerobic physical activity per week, or an equivalent combination of moderate-and
vigorous-intensity activity.
4. Adults of this age group, with poor mobility, should perform physical activity to enhance balance
and prevent falls on 3 or more days per week.
5. Muscle-strengthening activities should be done involving major muscle groups, on 2 or more days
a week.
6. When adults of this age group cannot do the recommended amounts of physical activity due to
health conditions, they should be as physically active as their abilities and conditions allow.
31
JUSTIFIcATION Despite the similarities between the recommendations for adults aged
ANd INTERPRETATION 18–65 and for adults aged 65 and above, separate recommendations
should be adopted and implemented. Promoting and facilitating the
regular practice of physical activity in older adults is especially important
because this population group is very often the least physically active.
Efforts to promote physical activity in older adults will generally place less
emphasis on attaining high volumes of activity, or engaging in vigorous-
intensity activity. However, the health status and abilities of older adults
vary widely, and some older adults are capable of, and regularly perform,
high volumes of moderate- and vigorous-intensity activity.
Conclusive scientific evidence based on a wide range of well-conducted

studies shows that adults of the 65 years and above age group, who are
physically active, have higher levels of cardiorespiratory fitness, a lower
risk profile for developing a number of disabling medical conditions, and
lower rates of various chronic noncommunicable diseases than do those
who are inactive.
If an individual has a low exercise capacity (i.e. low physical fitness), the
intensity and amount of activity needed to achieve many health-related
and fitness benefits are less than for an individual who has a higher level of
activity and fitness. Because the exercise capacity of adults tends to decrease
as they age, older adults generally have lower exercise capacities than
younger persons. They therefore need a physical activity plan that is of lower
absolute intensity and amount (but similar in relative intensity and amount)
than is appropriate for people of greater fitness, especially when they have
led sedentary lifestyles and are starting out on an activity programme.
As with adults of the 18–65 age group, there are a number of ways older
adults can accumulate the total of 150 minutes per week. The concept
of accumulation refers to meeting the goal of 150 minutes per week by
performing activities in multiple shorter bouts of at least 10 minutes
each spread throughout the week then adding together the time spent
during each of these bouts: e.g. 30 minutes of moderate-intensity activity
5 times per week.
It is worth noting that the recommended moderate- to vigorous-intensity

activity is relative to the capacity of the individual to perform such activities.
Evidence of acute effects on biomedical markers points to benefits of

undertaking regular physical activity throughout the week (such as 5 or
more times per week). This also has the potential to encourage integrating
physical activity as part of daily lifestyle such as active travel through
walking and cycling.
The recommendations listed above are applicable to the following

health conditions: cardio-respiratory health (coronary heart disease,
cardiovascular disease, stroke and hypertension); metabolic health
(diabetes and obesity); bone health and osteoporosis; breast and colon
cancer and prevention of falls, depression and cognitive decline.
The volume of physical activity associated with the prevention of different

chronic NCDs varies. Although the current evidence is insufficiently
precise to warrant separate guidelines for each specific disease, it is
sufficiently sound to cover all the health outcomes selected.
32
Higher levels of activity (i.e. greater than 150 minutes per week) are
associated with additional health benefits. However the evidence
suggests there is decreasing marginal benefit from engaging in physical
activity above volumes equivalent to 300 minutes per week of moderate-
intensity activity, and an increased risk of injuries.
The costs of endorsing these recommendations are minimal

and essentially related to the translation into country settings,
communication and dissemination. Implementation of comprehensive
policies that will facilitate the achievement of the recommended levels
of physical activity will require additional resource investment.
These recommendations are applicable in low- and middle-income

countries. However, national authorities need to adapt and translate
them into culturally appropriate forms for country level taking into
consideration, among other factors, the physical activity domain which
is more prevalent at population level (i.e. leisure time, occupational or
transportation physical activity).
Overall, the benefits of being physically active and implementing the

above recommendations outweigh the harms. Activity-related adverse
events such as musculoskeletal injuries are common but are usually
mild, especially for moderate-intensity activities such as walking.
The inherent risk of adverse events can be significantly reduced by a
progressive increase in the activity level, especially in sedentary older
adults. A series of small increments in physical activity, each followed by
a period of adaptation, is associated with lower rates of musculoskeletal
injuries than is an abrupt increase to the same final level. For sudden
cardiac adverse events, intensity of activity, rather than frequency or
duration appears to have more adverse effect. The selection of low-risk
activities, and prudent behaviour while performing any activity, can
minimize the frequency and severity of adverse events and maximize
the benefits of regular physical activity.
It should be noted that in populations that are already active, the

national physical activity guidelines should not promote a physical
activity target that would encourage a reduction in their current levels.
Results expected in the following few years regarding objectively

4.5 measured physical activity levels, and the scientific knowledge being
FUTURE REVIEw OF
accumulated in areas such as sedentary behaviours, will necessitate a
REcOmmENdATIONS review of these recommendations by the year 2015.
ANd RESEARcH gAPS
The following are research areas that require further investigation:
1) Sedentary behaviour contributing to disease risk profile.

2) Health-enhancing physical activity in children under 5 years old.
3) Health-enhancing physical activity in pregnant women.
4) Physical activity and disabilities.
5) Weight loss or maintenance of weight loss.
6) Physical activity doses for the clinical treatment of people with an
NCD (e.g. cardiovascular disease, diabetes, cancer, obesity, mental
health conditions, etc.).
33
5
HOw TO USE THE REcOmmENdEd LEVELS
OF PHySIcAL AcTIVITy FOR HEALTH
35
5.1 This section includes general principles for using the recommended levels
INTROdUcTION of physical activity for health in the development of national policies,
and highlights issues to be considered by policy-makers in the process of
adaptation to the national context.
The Global Recommendations on Physical Activity for Health outlined in

this document can play an important role in guiding the overall efforts on
promotion of health-enhancing physical activity. Additionally these can:
• support the development of physical activity policy;
• be used by all relevant stakeholders to communicate valid and consistent
messages on the frequency, duration, intensity, type and total amount of
physical activity for health;
• be used by health professionals to inform patients;
• have the potential to become a tool to link communication between
scientists, health professionals, journalists, interest groups and the
general public and represent the translation of research findings into
actionable, achievable and measurable messages for practitioners,
policy-makers and communities;
• be used as benchmarks for public health monitoring and surveillance
purposes.
5.2 The Global Recommendations should be understood as an evidence-based

NATIONAL AdAPTATION starting point for policy-makers looking to promote physical activity at
OF THE gLOBAL national level.
REcOmmENdATIONS
Policy-makers at national level are encouraged to adopt the recommended
levels of physical activity for health proposed in this document.
Policy-makers are encouraged to incorporate the global recommended

levels of physical activity for health to national policies, taking into
consideration the most adequate and feasible options according to their
needs, characteristics, physical activity domain and national resources while
aiming to be participatory and socially inclusive, particularly of the most
vulnerable groups.
In addition, the adaptation and translation of the recommended levels of

physical activity at national level must take into consideration the cultural
background, gender issues, ethnic minorities and burden of disease relevant
to the country. Listed below are additional issues to be considered by policy-
makers when using the global recommended levels of physical activity for
health in national or local interventions:
• Social norms.
• Religious values.
• Security situation at national and/or local levels.
• Availability of safe spaces for the practice of physical activity.
• Geographical settings, seasons and climate.
• Gender issues.
• Involvement of all concerned sectors and actors.
• Role of municipalities and local leadership.
• Access and attendance to schools and worksite, especially with regard to
girls and women.
• Existing transport infrastructures, sports and recreational facilities
and urban design.
• Patterns of participation in all domains of physical activity (leisure,
transportation and occupational).
36
5.2.1 In many low- and middle-income countries, the levels of participation in

LOw-ANd-mIddLE leisure time physical activity may be limited, and moderate to vigorous
physical activity may be performed in the context of transport and/or
INcOmE cOUNTRIES
occupational and/or domestic activities. These characteristics and patterns
of physical activity must be taken into consideration for a more tailored and
targeted implementation of interventions aiming at promoting the global
recommended levels of physical activity for health.
In countries with high levels of occupational and transportation physical

activity, policy-makers need to acknowledge that, although these high levels
of activity may not be the result of efforts to improve health, such levels of
activity provide major health benefits for the population. Caution is therefore
needed when implementing policies and infrastructure changes which may
lead to a reduction in the levels of physical activity in any domain.
For those communities who currently do not achieve the global

recommendations of physical activity for health, science supports health
benefits for both moderate- and vigorous-intensity activity. However the
net health benefit (benefits versus risks) in community-based programmes
is likely to be higher if the main focus is on moderate-intensity activity.
Moderate-intensity activity is more relevant to the public health goals
of policy implementation than vigorous-intensity activity because of
the lower risk of orthopaedic injuries and other medical complications
potentially acquired during moderate-intensity activity. If the focus of
policy implementation is in promoting vigorous-intensity activity, issues
related to potential risks, especially for older adults and populations with
various morbidities, need to be taken into consideration. For both levels of
intensity, the use of appropriate protective equipment should always be
encouraged.
5.3 National guidelines or recommendations on physical activity for the

general population are needed to inform the population on the frequency,
SUPPORTIVE POLIcIES
duration, intensity, types and total amount of physical activity necessary
IN PROmOTINg for health. However, increasing levels of physical activity in the population
PHySIcAL AcTIVITy demands a population-based, multisectoral, multidisciplinary, and culturally
relevant approach. National policies and plans on physical activity should
comprise multiple strategies aimed at supporting the individual and creating
supportive environments for physical activity to take place. (3,5)
Current evidence shows that environmental policies that impact on the

mode of transport people use or that increase public space for recreational
activities have the potential to increase physical activity levels in the
population and consequently provide significant health benefits. This is of
particular relevance to LMIC. (3, 22)
Possible physical activity promoting interventions include:

• reviewing urban and town planning and environmental policies at
national and local level to ensure that walking, cycling and other forms of
physical activity are accessible and safe;
• providing local play facilities for children (e.g. building walking trails);
• facilitating active transport to work (e.g. cycling and walking) and other
physical activity strategies for the working population;
• ensuring that school policies support the provision of opportunities and
programmes for physical activity;
37
• providing schools with safe and appropriate spaces and facilities so that
students can spend their time actively;
• providing advice or counsel in primary care; and
• creating social networks that encourage physical activity. (3, 22, 23)
5.4 Adopting the global recommendations and integrating them to national

policies, programmes and interventions is an important initial step in
STRATEgIES FOR
communicating physical activity levels to communities and the public.
cOmmUNIcATINg
However, in order to encourage acceptance, uptake and adherence to physical
THE gLOBAL activity promotion activities by the target populations, nationally adapted
REcOmmENdATIONS messages need to be developed and widely disseminated to all relevant
AT NATIONAL LEVEL stakeholders, professional groups and to the general community.
Effective dissemination of the recommended levels of physical activity for

health requires strategic planning, strong collaborations between various
groups and resources for supporting communication and dissemination
efforts (3, 24).
Countries with differing levels of physical activity will likely need to

communicate and disseminate different strategies and messages to their
communities and to the public. Consequently, when taking into consideration
national and subnational cultural and environmental factors, it is advisable
to develop a comprehensive, communication strategy for effective
dissemination of the global recommended levels of physical activity for
health, which addresses all possible variance.
It is similarly advisable to adopt a communication strategy that includes simple,

understandable and adaptable messages which are culturally sensitive. It
should be highlighted, however, that while the messages used may vary from
country to country, or may even differ within the same country, policy-makers
and communication experts should aim to retain the core recommended levels
of physical activity for health outlined in the previous section.
Appendix 3 gives examples of messages consistent with the recommended

levels of physical activity for health which have been used to promote
physical activity in various countries, and can be used as guidance for LMIC
when developing their national communication strategies.
5.5 Evaluation and ongoing monitoring of the process and outcomes of actions
mONITORINg for the promotion of physical activity is necessary in order to:
ANd EVALUATION • examine programme success and to identify target areas for future plans
of action;
• ensure the policy, plan or programme is being implemented as intended;
• contribute to ongoing learning and continuous improvement of the
actions implemented;
• assist policy-makers in decision-making regarding existing policies, plans
and programmes, including the development of new ones; and
• facilitate transparency and accountability. (25)
(Additional resources for monitoring and evaluation processes are included

in the following section.)
38
6
RESOURcES
39
INTROdUcTION The development and dissemination of national physical activity guidelines
should be seen as one element of a broader policy and planning process
to promote physical activity. To achieve effective change in awareness and
set the agenda for behaviour and environmental change, it is necessary to
integrate the guidelines into a national physical activity policy and plan of
action.
In some countries it might also be necessary to link physical activity
guidelines to other public health and prevention issues. For example, in the
health sector, guidelines might be linked to the prevention and control of
noncommunicable diseases, or to specific health issues such as diabetes or
obesity. In the sport sector, physical activity guidelines might be linked to
community participation in organized and non-organized sport and leisure
pursuits. Greater gains can be achieved by positioning physical activity
guidelines as part of a comprehensive planning of noncommunicable
diseases prevention and control or other public health issues, such as
framing the guidelines as part of objectives setting, intervention selection
and implementation, and monitoring and surveillance.
Listed below are some of the key resources available to WHO to support
Member States in the development, implementation, monitoring and
evaluation of policies related to physical activity promotion:
POLIcy dEVELOPmENT • A guide for population-based approaches to increasing levels of

ANd ImPLEmENTATION: physical activity: implementation of the Global Strategy on Diet,
Physical Activity and Health (3):
http://www.who.int/dietphysicalactivity/PA-promotionguide-2007.pdf.
• Report of joint WHO/World Economic Forum event on prevention of
noncommunicable diseases in the workplace (26):
http://www.who.int/dietphysicalactivity/workplace.
• A school policy framework focusing on diet and physical activity (23):
http://www.who.int/dietphysicalactivity/schools.
• Interventions on Diet and Physical Activity: What Works. Implementation
of the Global Strategy on Diet, Physical Activity and Health (22):
http://www.who.int/dietphysicalactivity/whatworks.
• Pacific Physical Activity Guidelines for Adults: Framework for
Accelerating the Communication of Physical Activity Guidelines (24):
http://www.wpro.who.int/NR/rdonlyres/6BF5EE82-8509-4B2F-8388-
2CE9DBCCA0F8/0/PAG_layout2_22122008.pdf.
SURVEILLANcE, • The WHO STEPwise approach to surveillance (STEPS):

mONITORINg http://www.who.int/chp/steps/en.
ANd EVALUATION: • The Global school-based student health survey (GSHS):
http://www.who.int/school_youth_health/assessment/gshs/en.
• The WHO Global InfoBase: WHO global comparable estimates:
http://infobase.who.int.
• The Global Questionnaire on Physical Activity for Health (GPAQ):
http://www.who.int/chp/steps/GPAQ.
• A framework to monitor and evaluate implementation: Global Strategy
on Diet, Physical Activity and Health (25):
http://www.who.int/dietphysicalactivity/DPASindicators.
40
7
APPENdIcES
41
APPENdIX 1 dETAILEd dEScRIPTION OF THE mETHOdOLOgy USEd FOR dEVELOPINg
THE gLOBAL REcOmmENdATIONS ON PHySIcAL AcTIVITy FOR HEALTH
The following steps summarize the actions by the WHO Secretariat for the development of
the Global Recommendations on Physical Activity for Health:
First phase: Scope and target audience

1) A global expert meeting was arranged in January 2008 in Mexico to examine the scientific
evidence available on physical activity and health and to assess the need to develop
global recommendations on physical activity for health. The experts who participated in
this meeting concluded that there was the need and enough evidence for WHO to develop
global recommendations on physical activity for health. Moreover, it was highlighted
that the comprehensive review being prepared by the CDC, included in Physical Activity
Guidelines Advisory Committee Report, 2008 (11), should be part of the bulk of scientific
evidence considered for the development of the Global Recommendations on Physical
activity for Health. In addition, the scope, content and target audience of the global
recommendations were defined by the participating experts by discussion and consensus.
Second phase: Evidence collection and analysis

1) Evidence collection: A vast and strong body of evidence has been used for the
development of the first draft. This includes:
• the 2008 CDC literature Review presented in the report to the USA Secretary of
Health and Human Services titled “Physical Activity Guidelines Advisory Committee
Report” (11);
• Bauman et al 2005: the 2005 systematic review of the evidence on “The Health
Benefits of Physical Activity in Developing Countries” which has been carried out by
the Centre for Physical Activity and Health, University of Sydney) (13);
• Evidence reviews conducted as part of the process to update the Canadian physical
activity guidelines (9, 10, 18- 21);
• a review of the relevant literature in Chinese and Russian using the same search
framework that had been used by the 2008 CDC literature review.
Table 1. Overview of evidence documents used
Source of evidence used by WHO Rational for selecting this review Considerations by guideline group
secretariat and guideline group
The 2008 CDC Literature Review This publication was a result of the search of the Medline Study design, limitations of the
presented in the report to the USA literature - covering the period of January 1, 1995 studies, sample size, statistical power,
Secretary of Health and Human -November 2007 - 14,472 abstracts were triaged, and of precision of results, measurement
Services titled “Physical Activity these, 1,598 papers were reviewed. The review included: methods, follow-up, adherence were
Guidelines Advisory Committee cohort studies, case control studies, randomized control considered to conclude that this
Report” (11) trials, non randomized control trial, meta analysis, review provided strong evidence
observational studies, prospective studies and cross for the development of the global
sectional studies. All cause mortality, cardiorespiratory recommendations.
health, metabolic health, musculo-skeletal health,
functional health, cancer, mental health and adverse
events. The populations studied were children and youth,
adults and older adults. This is an extensive, global, high
quality and up to date review which covers the outcomes
of interest.
The 2005 systematic review of the This is a global review, focusing on grey and peer reviewed The strength of dose-response
evidence on “The Health Benefits literature from low and middle income countries. relationships is assessed based on the
of Physical Activity in Developing To identify relevant published epidemiological studies volume of data available and the level
Countries” - Centre for Physical on physical activity and health in developing countries of consistency between the various
Activity and Health, University of multiple electronic databases were searched. These study findings. This was considered
Sydney (13) included NIH Pub Med, Medline, Psycinfo and two evidence to provide strong evidence for
based directories, The Cochrane Library and DARE. the development of the global
Additional papers were identified via hand searching. The recommendations.
search strategy was restricted to English language papers
published from January 1980 – March 2007.
47 studies conducted in low and middle income countries,
with different designs were included in this review: cross
sectional surveys (descriptive and analytic), cohort studies,
randomized control trials and case control studies.
They covered all cause mortality, cardiovascular disease
diabetes, cancers, injuries and bone health, mental health
and associated risk factors.
42
2007 evidence reviews conducted These reviews of the literature provide an analysis of The strength of dose-response
as part of the process to update the the epidemiology related to physical activity for health, relationships is assessed based on the
Canadian physical activity guidelines and the strength of the relationship between physical volume of data available and the level
(9, 18, 20) activity and specific health outcomes is evaluated, with of consistency between the various
particular emphasis on minimal and optimal physical study findings. This was considered
activity requirements. Meta analysis, systematic reviews, to provide strong complementary
epidemiological studies and randomized control trials evidence for the development of the
were included in this review. global recommendations.
Cardiorespiratory health, hypertension, breast and
colon cancer, diabetes, adiposity, mental health osteo-
musculoskeletal health, osteoporosis, injuries and
asthma were health outcomes included in these reviews.
These are comprehensive and high quality reviews
which cover the outcomes of interest and the relevant
age groups.
2009 Evidence reviews conducted For all 3 papers, the literature was obtained through Study design, limitations of the
as part of the process to update the searching electronic databases. All articles included in studies, sample size, statistical power,
Canadian physical activity guidelines these reviews were reviewed to complete standardized precision of results, measurement
(10, 19, 21) data extraction tables, and assess study quality. An methods, follow-up, adherence were
established system of assessing the level and grade of considered to conclude that the three
evidence for the recommendations was employed by age specific reviews provided strong
the research groups. Various study types were included evidence for the development of the
in this review: prospective cohort studies randomized global recommendations.
control trials, and non-RCT study types 86 studies were
included in the review focusing on children and youth.
The volume, intensity, and type of physical activity were
considered.
A total of 254 articles met the eligibility criteria for the
review focusing on adults.
100 studies were included in the review focusing on
older adults.
The systematic research of the This ensured that all studies relevant to the outcomes of The evidence found was consistent
literature to search for evidence interest and published in languages other than English with the other literature reviews and
published in Chinese and Russian will be included in the evidence, strengthening its added no extra knowledge for the
(the same inclusion and exclusion global coverage. guideline group to consider.
criteria and the same time frame The additional evidence from other languages was
of research used in the CDC review assessed using the same criteria that have been used for
were used to conduct this additional the CDC systematic review.
search). 10 articles in the Russian language and 164 articles in
Chinese were retrieved. Three articles in Russian and 71
in Chinese were considered relevant to the outcomes.
2) Summarizing the evidence collected

The WHO Secretariat reviewed and analysed all the sources of evidence listed above. Based
on this body of evidence, narrative descriptions summarizing the evidence available for the
relevant health outcomes were prepared.
These narrative descriptions of the evidence included information on: the number and
type of studies included in each review, magnitude of effect, the quality of the evidence,
characteristics of the physical activity most likely to produce the outcome and the evidence
of a dose response for the age group and health outcomes selected.
Third phase: Preparation of the draft for the Global Recommendations on Physical Activity
for Health
1) After all the evidence had been collected and analysed, the WHO Secretariat led by the
Surveillance and Population-based Prevention Unit at WHO-HQ in collaboration with the WHO
Regional Offices:
• established the process for developing the Global Recommendations on Physical Activity
for Health and cleared it with the WHO Guideline Review Committee;
• established a guideline group (see Appendix 4 for members), which took into
consideration: global representation, gender balance and area of expertise both in the
subject matter as well as in policy development and implementation;
• prepared a narrative summary of the evidence relevant to the health outcomes previously
selected; and
• developed a first draft of the Global Recommendations on Physical Activity for Health.
2) The draft of the Global Recommendations on Physical Activity for Health was used in a first
round of electronic consultations with the guideline group through the online “community
43
of practice” website. To collect the comments from all the guideline group members, the
WHO Secretariat prepared a template with specific questions, The template requested
comments on:
• the overall quality of the evidence for major health outcomes and to evaluate the
issues of dose response for these outcomes;
• health conditions to which the recommendations are applicable;
• the content and formulation of the recommendations;
• generalizability and applicability of the recommendations in low and middle income
countries;
• benefits and harms; and
• costs of developing and endorsing the physical activity recommendations.
All comments made by the guideline group members were compiled by the WHO
Secretariat and presented at the meeting of the guideline group.
3) The draft of the Global Recommendations on Physical Activity for Health was used in
a first round of electronic consultations with the Guideline group. A standard reporting
form was used to collect the comments from all the group members in order to focus the
discussions of the experts on:
• the scientific evidence used;
• the health conditions to which the recommendations are applicable;
• the content and formulation of the recommendations;
• the applicability of the recommendations in low- and middle-income countries;
• the potential benefits and harms; and
• the costs of developing and endorsing the physical activity recommendations.
Fourth phase: Meeting of the guideline group

The guideline group met on the 23rd Oct 2009 with the aim of:
• reviewing face-to-face the draft Global Recommendations on Physical Activity for
Health proposed by the Secretariat;
• discussing the comments raised by the different guideline group members during the
electronic consultation; and
• finalizing the recommendations.
At the meeting, the Secretariat presented the below information:

• what is expected from the guideline group members during the meeting;
• the expected outcomes for the meeting;
• an overview of the process used for the development of the Global Recommendations
on Physical Activity for Health;
• a narrative summary of the evidence used to prepared the first draft of the Global
Recommendations;
• a summary of the comments received from all guideline group members in the
electronic consultation phase.
The meeting was conducted in the format of plenary session. Three main sessions were
organized according to the age groups being discussed: children, adults and older adults.
At the beginning of each age specific session, the summary of the age specific evidence,
comments submitted by the members of the guideline group were presented.
Finalizing the recommendations:

For finalizing each recommendation presented in “Chapter 4”, the following steps were
followed:
1) The draft recommendations were presented by the WHO Secretariat, with reference to the
relevant evidence summary.
2) The evidence was reviewed and discussed by the group. To determine the quality of
the evidence, the guideline group considered the types of studies that addressed each
specific question, the general quality of these studies (e.g., design, sample size, statistical
power, measurement methods, follow-up, adherence) for each major outcome.
3) The draft recommendations were reviewed by the guideline group considering:

• wording formulation considering concepts of: duration/volume, intensity, type, and
frequency for physical activity
• health conditions to which each recommendation are applicable
• the balance of evidence for benefits and harms
• costs
• applicability in low and middle income countries
• values, preferences.
44
4) After the discussion, the draft recommendation was modified (if necessary) and a final
recommendation was presented to the guideline group.
The same process was repeated for all recommendations presented in chapter 4.
The finalized recommendations were considered to be applicable in low-middle income

countries after the appropriate adaptation and tailoring for implementation by national
authorities. Details on the national adaptation of the Global Recommendations on Physical
Activity for Health are provided in Chapter 5.
Fifth phase: Finalization and dissemination

1) Peer review of the recommendations and consultation with the WHO Regional Offices
and relevant departments within WHO-Headquarters (Child and Adolescent Health,
Ageing, Health Promotion and Violence and Injury Prevention).
2) Finalization of the recommendations and approval by the WHO Guideline Review

Committee.
3) Translation, printing and dissemination.
Sixth phase: Implementation

The Global Recommendations on Physical Activity for Health will be integrated in
the activities planned for the implementation of the 2008-2013 Action Plan for the
Prevention and Control of NCD, and will be integrated as one of the key tools in the “DPAS
Implementation Toolbox”, which is available on the WHO website. Additionally, these
recommendations will be a key component of the regional and sub-regional training and
capacity building workshops being held by EURO, EMRO, WPRO and AFRO for 2010; and
AMRO/PAHO and SEARO for 2011.
45
APPENdIX 2 dETAILEd REFERENcE OF LITERATURE
Evidence used for the age group: 5 - 17 years old
For enhanced Supporting evidence in 2008 CDC 2005, “The Health Benefits of Evidence reviews conducted as
cardio-respiratory Literature Review (11) Physical Activity in Developing part of the process to update
health1: (relevant page n°) Countries” (13) the Canadian physical activity
guidelines (9,10)
Frequency & duration Part E: E-1 - E- 3 Not applicable as the review only Janssen 2007
E-17 - E-19 included studies with adults Janssen, Leblanc 2009
Part G9: G9-1-G9-14
G9-20 - G9-21
Intensity Part E: E-1 - E- 3 Not applicable as the review only Janssen 2007
Part G9: G9-1-G9-5
G9-9 - G9-14
G9-20 - G9-21
Intensity & frequency Part E: E-1 - E- 3 Not applicable as the review only Janssen 2007
Part G9: G9-1-G9-5
G9-9 - G9-14
G9-20 - G9-21
Type & frequency Part E: E-1 - E- 3 Not applicable as the review only Janssen 2007
Part G9: G9-1-G9-5
G9-9 - G9-14
G9-20 - G9-21
metabolic health2: Literature Review (11) Physical Activity in Developing part of the process to update
(relevant page n°) Countries” (13) the Canadian physical activity
guidelines (9,10)
Part G9: G9-1-G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
1
Cardiorespiratory health refers to risk reduction of coronary heart disease, cardiovascular disease, stroke and hypertension
2
Metabolic Health refers to risk reduction of diabetes and obesity
46
musculo-skeletal Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (9,10)
Part G9: G9-1-G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
Part G9: G9-1- G9-10
G9-20 - G9-21
Evidence used for the age group: 18 - 64 years old
For enhanced cardio- Supporting evidence in 2008 CDC 2005, “The Health Benefits of Evidence reviews conducted as
respiratory health4: Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (18,19)
Frequency, duration Part E: E-1 - E- 3 Section 4.1.2: page 23 Warburton et al 2007

and Intensity E-5 - E-6 Section 4.1.7: page 29 Warburton et al 2009
Part G2: G2-1- G9-40 Section 4.2.3: page 34-36
Section 4.2.6: page 38
Section 5: page 41-43
Type & frequency Part E: E-1 - E- 3 Section 4.1.2: page 23 Warburton et al 2007
E-5 - E-6 Section 4.1.7: page 29 Warburton et al 2009
Part G2: G2-1- G9-40 Section 4.2.3: page 34-36
Section 4.2.6: page 38
metabolic health5: Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (18,19)
Frequency, duration Part E: E-1 - E- 3 Section 4.1.3: page 24 Warburton et al 2007

and Intensity E-6 - E-10 Section 4.1.7: page 29 (20-55 years old)
Part G3: G3-9- G3-29 Section 4.2.3: page 30-33 Warburton et al 2009
Part G4: G4-1 - G4-8 Section 4.2.6: pages 39, 40
G4-10 - G4-20 Section 5: page 41-43
Type & frequency Part E: E-1 - E- 3 Section 4.1.3: page 24 Warburton et al 2007
E-6 - E-10 Section 4.1.7: page 29 (20-55 years old)
Part G4: G4-1 - G4-8 Section 4.2.6: pages 39, 40
G4-10 - G4-20 Section 5: page 41-43
3
For this age group musculo-skeletal health refers to improved bone health
4
Cardiorespiratory health refers to risk reduction of coronary heart disease, cardiovascular disease, stroke and hypertension
5
Metabolic Health refers to risk reduction of diabetes and obesity
47
musculo-skeletal Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (18,19)
Frequency, duration Part E: E-1 - E- 3 Section 4.1.5: pages 27, 28 Warburton et al 2007
and Intensity E-11 - E-13 Section 4.1.7: page 29 (20-55 years old)
Part G5: G5-31 - G5-38 Section 5: page 41-43
Type & frequency Part E: E-1 - E- 3 Section 4.1.5: pages 27, 28 Warburton et al 2007
E-11 - E-13 Section 4.1.7: page 29 (20-55 years old)
Part G5: G5-31 - G5-38 Section 5: page 41-43
For cancer Supporting evidence in 2008 CDC 2005, “The Health Benefits of Evidence reviews conducted as
prevention7: Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (18,19)
Frequency, duration Part E: E-1 - E- 3 Section 4.1.4: pages 25, 26 Warburton et al 2007
and Intensity E-15 - E-16 Section 5: page 41-43 (20-55 years old)
Part G7: G7-1 - G7-22 Warburton et al 2009
Type & frequency Part E: E-1 - E- 3 Section 4.1.4: pages 25, 26 Warburton et al 2007
E-15 - E-16 Section 5: page 41-43 (20-55 years old)
Part G7: G7-1 - G7-22 Warburton et al 2009
For prevention Supporting evidence in 2008 CDC 2005, “The Health Benefits of Evidence reviews conducted as
of depression: Literature Review (11) Physical Activity in Developing part of the process to update
(relevant page n°) Countries”8 (13) the Canadian physical activity
guidelines9 (18,19)
Frequency, type, Part E: E-16 - E- 17 See footnote 9 See footnote 10

duration and Part G8: G8-1 - G8-12
Intensity
Evidence used for the age group: 65 + years old
For the following outcomes: cardiorespiratory health, metabolic health, musculo-skeletal health, cancer prevention10 and depression,
the supporting evidence to older adults are the same as stated in the 18-64 years old group.
functional health11: Literature Review (11) Physical Activity in Developing part of the process to update
guidelines (20,21)
Frequency, duration Part E: E-1 - E- 3 Section 4.1.5: pages 27, 28 Paterson 2007
and Intensity E-13 - E-15 Section 4.1.7: page 29 Paterson, Warburton D 2009
Part G6: G6-1 - G6-22 Section 4.2.3: page 36-38
Type & frequency Part E: E-1 - E- 3 Section 4.1.5: pages 27, 28 Paterson 2007
E-13 - E-15 Section 4.1.7: page 29 Paterson, Warburton D 2009
Part G6: G6-1 - G6-22 Section 4.2.3: page 36-38
6
For this age group musculo-skeletal health refers to improved bone health and risk reduction of osteoporosis
7
Cancer prevention refers to reduction of risk of breast and colon cancer
8
Section 4.1.6: page 28 states that NO studies examining the relationship between mental health and physical activity in adults living in developing countries were identified
9
Not applicable as the review did not include any aspect of mental health
10
Cardiorespiratory health refers to risk reduction of coronary heart disease, cardiovascular disease, stroke and hypertension. Metabolic Health refers to risk reduction of diabetes and
obesity. Musculo-skeletal health refers to improved bone health and risk reduction of osteoporosis. Cancer refers to reduction of risk of breast and colon cancer.
11
Functional Health refers to prevention of falls
48
Evidence specific for this age group related to maintenance or improvement of balance for those at risk of falling was also found
in Paterson 2007 and Paterson, Warburton D 2009.
Limited Ability due Supporting evidence in 2008 CDC 2005, “The Health Benefits of Evidence reviews conducted as
to health conditions literature Review (11) Physical Activity in Developing part of the process to update
guidelines (20,21)
Part E: E-1 - E- 3 Not applicable as review didn’t Paterson 2007

E-13 - E-15 focused specifically on older Paterson, Warburton D 2009
Part G6: G6-1 - G6-22 adults
APPENdIX 3 EXAmPLES OF mESSAgES USEd TO PROmOTE PHySIcAL AcTIVITy

AT NATIONAL LEVEL ANd cONSISTENT wITH THE gLOBAL
REcOmmENdATIONS
Age group: 5–17 years
Country/Region Target population Messages used
Australia 5–12 Ideally, your child shouldn’t spend more than two hours a day doing these things, particularly
Australia’s years of age at times when they could be enjoying more active pursuits.
Physical Activity If your child is just starting to get active, begin with moderate-intensity activity - say 30
Recommendations for minutes a day – and steadily increase.
5–12 year olds (27). More vigorous activities will make kids “huff and puff” and include organized sports such
as football and netball, as well as activities such as ballet, running and swimming laps.
Children typically accumulate activity in intermittent bursts ranging from a few seconds to
several minutes, so any sort of active play will usually include some vigorous activity. Most
importantly, kids need the opportunity to participate in a variety of activities that are fun
and suit their interests, skills and abilities. Variety will also offer your child a range of health
benefits, experiences and challenges.
Australia 12–18 • Choose a range of activities you like or think you might like to try.
Australia’s years of age • Be active with your friends. You are more likely to keep active if it’s fun and you have
Physical Activity people to enjoy it with.
Recommendations for • Walk more: to school, to visit friends, to shops, or other places in your neighbourhood.
12–18 year olds (28). • Try to limit time spent watching TV, videos or DVDs, surfing the net or playing computer
games, especially during the day and on weekends.
• Take your dog or a neighbour’s dog for a walk.
• Be active with family members – in the yard and on family outings.
• Encourage and support younger brothers and sisters to be active.
• Try a new sport or go back to one you have played before.
• Take a class to learn a new skill such as yoga, kick boxing, dancing or diving.
• Check out the activities at your local recreation centre, clubs or youth centre.
• Put on some music and dance.
Canada Children 6–9 • Physical activity is fun: At home – At school – At play – Inside or Outside – On the way to
Canada’s Physical years of age and from school – With family and friends. Making physical activity a part of the day is
Activity Guide for fun and healthy.
Children, 2002 (29). • Increase time currently spent on physical activity by 30 minutes per day, and progress
to 90 minutes more per day.
• Physical activity can be accumulated in periods of 5–10 minutes.
• The 90 minute increase in physical activity should include 60 minutes of moderate
activity and 30 minutes of vigorous activity.
• Combine endurance, flexibility, and strength activities to achieve the best results.
• Reduce screen time, starting with 30 minutes less daily and progressing to 90 minutes
less daily.
49
Age group: 18–64 years old
Australia Adults • Think of movement as an opportunity, not an inconvenience. Where any form of
National Physical movement of the body is seen as an opportunity for improving health, not as a time-
Activity Guidelines for wasting inconvenience.
Adults, 2005 (30). • Be active every day in as many ways as you can. Make a habit of walking or cycling
instead of using the car, or do things yourself instead of using labour-saving machines.
• Put together at least 30 minutes of moderate-intensity physical activity on most,
preferably all, days. You can accumulate your 30 minutes (or more) throughout the day
by combining a few shorter sessions of activity of around 10–15 minutes each.
• If you can, also enjoy some regular, vigorous activity for extra health and fitness.
USA Adults • Be active your way.

Be Active Your Way. (18–64 years old) • Pick an activity you like and one that fits into your life.
A Guide for Adults, • Find the time that works best for you.
Based on the 2008 • Be active with friends and family. Having a support network can help you keep up with
Physical Activity your programme.
Guidelines for • There are many ways to build the right amount of activity into your life. Every little bit
Americans, 2008 (31). adds up and doing something is better than doing nothing.
• Start by doing what you can, and then look for ways to do more. If you have not been
active for a while, start out slowly. After several weeks or months, build up your
activities—do them longer and more often.
• Walking is one way to add physical activity to your life. When you first start, walk 10
minutes a day on a few days during the first couple of weeks.
• Add more time and days. Walk a little longer. Try 15 minutes instead of 10 minutes.
Then walk on more days a week.
• Pick up the pace. Once this is easy to do, try walking faster. Keep up your brisk walking
for a couple of months. You might want to add biking on the weekends for variety.
Pacific Region Adults • If you are not physically active (moving much), it’s not too late to START NOW! Do
Pacific physical (18–65 years old) regular physical activity and reduce sedentary activities.
activity guidelines • Be active every day in as many ways as you can, your way.
(24). • Do at least 30 minutes of moderate-intensity physical activity on five or more days each
week.
• If you can, enjoy some regular vigorous-intensity activity for extra health and fitness
benefits.
Age group: 65 years and above
Australia 65 years • Think of movement as an opportunity, not an inconvenience.

National Physical and above • Be active every day in as many ways as you can.
Activity Guidelines (Older adults) • Put together at least 30 minutes of moderate intensity physical activity on most,
for Older Adults, 2005 preferably all, days.
(30). • If you can, also enjoy some regular, vigorous activity for extra health and fitness.
• Use appropriate safety and protection equipment to maximise safety and minimize risk
of injury during physical activity, for example, use supportive footwear for walking, and
a helmet for bicycle riding.
Canada Adults 55 years • Be active your way, every day – for life. Age is no barrier. Start slowly and build up.
Canada’s Physical and above • Accumulate 30–60 minutes of moderate physical activity most days.
Activity Guide for • Minutes count – add it up 10 minutes at a time. Choose a variety of activities from each
Adults, 1999 (33). of these three groups – endurance, flexibility, strength and balance. Getting started is
easier than you think.
• Build physical activity into your daily routine. Do the activities you are doing now, more
often. Walk wherever and whenever you can.
• Start slowly with easy stretching. Move around frequently.
• Find activities that you enjoy.
50
APPENdIX 4 gUIdELINE gROUP mEmBERS
Region/Country Name Affiliation Main role of the expert
AFR Dr Rachid Hanifi Professor of Medicine of Sports Content expertise

(Alger) Faculty of Medicine of Alger
AFR Dr Vicky Lambert Professor and Researcher on Bioenergetics of exercise Content expertise
(South Africa) Sports Science Institute of South Africa, University of Cape
Town, South Africa
AMR Dr Janet Fulton Division of Nutrition, Physical Activity, and Obesity Content expertise
(USA) Centers for Disease Control and Prevention, USA
AMR Dr William Haskell Professor, Stanford Prevention Research Center, Stanford Content and
(USA) University School of Medicine methodological expertise
Chair of the US Physical Activity Guidelines Advisory in developing guidelines
Committee related to physical activity
AMR Dr David Buchner University of Illinois, USA Content and

(USA) methodological expertise
in developing guidelines
related to physical activity
AMR Dr Mark Tremblay Director, Healthy Active Living and Obesity Research (HALO) Content expertise
(Canada) Scientist and Professor, Department of Pediatrics, (specific expertise: 5–17
University of Ottawa, Canada year olds)
EMR Dr Jassem Chairman of the Physiology department and the Health Content expertise
(Kuwait) Ramadan Sciences Center
Alkandari Faculty of Medicine, Kuwait University
EMR Dr Shahzad Khan Assistant Professor, Health Systems; Health Services Content expertise
(Pakistan) Academy, Ministry of Health, Islamabad, Pakistan
EUR Professor Researcher, Physical Activity and Health Methodological expertise

(UK) Fiona Bull School of Sport & Exercise Sciences, in developing guidelines
Loughborough University, UK related to physical activity
EUR Dr Pekka Oja Urho Kaleva Kekkonen Institute for Health Promotion Content expertise
(Finland) Research, Finland (retired)
SEAR Dr Grit Leetongin Division of Physical Activity and Health End user (policy-maker)
(Thailand) Ministry of Public Health, Royal Thai Government
WPR Professor Adrian Director, NSW Centre for Physical Activity & Health Methodological expertise
(Australia) Bauman* School of Public Health, University of Sydney in developing guidelines
related to physical activity
WPR Dr T H Leung* Centre for Health Protection, Department of Health, China, End user (policy-maker)
(China) Hong Kong Special Administrative Region
* Member unable to participate in the meeting held on 23 October 2009 (London, UK).
51
APPENdIX 5 gLOSSARy
Accumulation: The concept of meeting a specific physical activity dose or goal by performing activity in short bouts, then adding
together the time spent during each of these bouts. For example, a goal of 30 minutes per day can be met by performing 3 bouts of
10 minutes each throughout the day (34).
Aerobic physical activity: Activity in which the body’s large muscles move in a rhythmic manner for a sustained period of time. Aerobic
activity – also called endurance activity – improves cardiorespiratory fitness. Examples include walking, running, and swimming, and
bicycling (34).
Balance training: Static and dynamic exercises that are designed to improve an individual’s ability to withstand challenges from
postural sway or destabilizing stimuli caused by self-motion, the environment, or other objects (34).
Bone-strengthening activity: Physical activity primarily designed to increase the strength of specific sites in bones that make up the
skeletal system. Bone-strengthening activities produce an impact or tension force on the bones that promotes bone growth and strength.
Running, jumping rope, and lifting weights are examples of bone-strengthening activities (34).
Cardiorespiratory fitness (endurance): A health-related component of physical fitness. The ability of the circulatory and respiratory
systems to supply oxygen during sustained physical activity. Usually expressed as measured or estimated maximal oxygen uptake
(VO2max).
Dose: In the field of physical activity, dose refers to the amount of physical activity performed by the subject or participants. The
total dose or amount is determined by the three components of activity: frequency, duration, and intensity. Frequency is commonly
expressed in sessions, episodes, or bouts per day or per week. Duration is the length of time for each bout of any specific activity.
Intensity is the rate of energy expenditure necessary to perform the activity to accomplish the desired function (aerobic activity) or
the magnitude of the force exerted during resistance exercise (34).
Domains of physical activity: Physical activity levels can be assessed in various domains, including one of more of the following:
leisure-time activity, occupational activity, household activity, and commuting activity (34).
Dose-response: The relationship between the dose of physical activity and the health or fitness outcome of interest is considered
the dose-response. The dose can be measured in terms of a single component of activity (e.g., frequency, duration, intensity) or as
the total amount. This concept is similar to the prescription of a medication where the expected response will vary as the dose of the
medication is changed. The dose-response relationship can be linear, exponential, or hyperbolic, and it is likely to vary depending
on the primary measure of interest. For example, improvements in cardiorespiratory fitness, bone health, or adiposity are common
dose-response measures of interest. A dose of physical activity may exist below that which no effect has been detected as well as a
dose above that which no effect has been detected. These seemingly lowest and highest doses of activity may be called “thresholds,”
but the term should be used with caution as these apparent limits may be more related to limitations of measurement than to true
biological limits (34).
Duration: The length of time in which an activity or exercise is performed. Duration is generally expressed in minutes (34).
Exercise: A subcategory of physical activity that is planned, structured, repetitive, and purposeful in the sense that the improvement
or maintenance of one or more components of physical fitness is the objective. “Exercise” and “exercise training” frequently are used
interchangeably and generally refer to physical activity performed during leisure time with the primary purpose of improving or
maintaining physical fitness, physical performance, or health.
Flexibility: A health- and performance-related component of physical fitness that is the range of motion possible at a joint. Flexibility
is specific to each joint and depends on a number of specific variables including, but not limited to, the tightness of specific ligaments
and tendons. Flexibility exercises enhance the ability of a joint to move through its full range of motion (34).
Frequency: The number of times an exercise or activity is performed. Frequency is generally expressed in sessions, episodes, or bouts
per week (34).
Guidelines and Recommendations: A WHO guideline is any document that contains recommendations about health interventions,
whether they are clinical, public health or policy interventions. Recommendations provide information about what policy-makers,
health care providers, or patients should do. They imply a choice between different interventions that have an impact on health and
that have ramifications for resource use (8).
Health-enhancing physical activity: Activity that, when added to baseline activity, produces health benefits. Brisk walking, jumping
rope, dancing, playing tennis or soccer, lifting weights, climbing on playground equipment at recess, and doing yoga are all examples
of health-enhancing physical activity (34).
52
Intensity: Intensity refers to the rate at which work is being performed or the magnitude of the effort required to perform an activity
or exercise. Intensity can be expressed either in absolute or relative terms:
• Absolute: The absolute intensity of an activity is determined by the rate of work being performed and does not take into account
the physiological capacity of the individual. For aerobic activity, absolute intensity typically is expressed as the rate of energy
expenditure (e.g. milliliters per kilogram per minute of oxygen being consumed, kilocalories per minute, or METs) or, for some
activities, simply as the speed of the activity (e.g. walking at 3 miles an hour, jogging at 6 miles an hour), or physiological response
to the intensity (e.g. heart rate). For resistance activity or exercise, intensity frequently is expressed as the amount of weight
lifted or moved.
• Relative: Relative intensity takes into account or adjusts to an individual’s exercise capacity. For aerobic exercise, relative intensity
is expressed as a percentage of an individual’s aerobic capacity (VO2max) or VO2 reserve, or as a percentage of an individual’s
measured or estimated maximum heart rate (heart rate reserve). It also can be expressed as an index of how hard an individual
feels he or she is exercising (e.g. on a 0–10 scale).
Leisure-time physical activity: Physical activity performed by an individual that is not required as an essential activity of daily living
and is performed at the discretion of the individual. Such activities include sports participation, exercise conditioning or training, and
recreational activities such as going for a walk, dancing, and gardening (34).
Maximal oxygen uptake (VO2max): The body’s capacity to transport and use oxygen during a maximal exertion involving dynamic
contraction of large muscle groups, such as during running or cycling. It is also known as maximal aerobic power and cardiorespiratory
endurance capacity. Peak oxygen consumption (VO2peak) is the highest rate of oxygen consumption observed during an exhaustive
exercise test (34).
MET: MET refers to metabolic equivalent and 1 MET is the rate of energy expenditure while sitting at rest. It is taken by convention to
be an oxygen uptake of 3.5 milliliters per kilogram of body weight per minute. Physical activities frequently are classified by their
intensity, using the MET as a reference.
Moderate-intensity physical activity: On an absolute scale, moderate intensity refers to the physical activity that is performed at
3.0–5.9 times the intensity of rest. On a scale relative to an individual’s personal capacity, moderate-intensity physical activity is
usually a 5 or 6 on a scale of 0–10 (34).
Muscle-strengthening activity: Physical activity and exercise, that increases skeletal muscle strength, power, endurance, and mass
(e.g. strength training, resistance training, or muscular strength and endurance exercises) (34).
Physical activity: Any bodily movement produced by skeletal muscles that requires energy expenditure (5).
Physical inactivity: An absence of physical activity or exercise.
Primary prevention: Actions that seek to reduce risks in the entire population regardless of each individual’s level of risk and potential
benefits. The intention of primary prevention interventions is to move the profile of the whole population in a healthier direction.
Small changes in risk factors in the majority who are at low to moderate risk can have a significant impact in terms of population-
attributable risk of death and disability (6).
Secondary prevention: Focuses actions on the people likely to benefit, or benefit most. Secondary prevention interventions are based
on screening exposed populations for the early onset of sub-clinical illnesses and administering treatment (6).
Sport: Sport covers a range of activities performed within a set of rules and undertaken as part of leisure or competition. Sporting
activities usually involve physical activity carried out by teams or individuals and are supported by an institutional framework, such
as a sporting agency (24).
Vigorous-intensity physical activity: On an absolute scale, vigorous intensity refers to physical activity that is performed at 6.0 or
more times the intensity of rest for adults and typically 7.0 or more times for children and youth. On a scale relative to an individual’s
personal capacity, vigorous-intensity physical activity is usually a 7 or 8 on a scale of 0–10 (34).
Major muscle groups: Major muscle groups include the legs, hips, back, abdomen, chest, shoulders and arms (34).
Type of physical activity: The mode of participation in physical activity. The type of physical activity can take on many forms: aerobic,
strength, flexibility, balance.
Volume: Aerobic exercise exposures can be characterized by an interaction between bout intensity, frequency, duration, and longevity
of the programme. The product of these characteristics can be thought of as volume and can be represented by the total energy
expenditure (EE) of the exercise exposure (34).
53
APPENdIX 6 LIST OF PEER REVIEwERS (IN ALPHABETIcAL ORdER)
Dr Randy Adams (Centre for Health Promotion, Public Health Agency of Canada, Canada)
Ms Frances Cuevas (Department of Health, Philippines)
Dr Luiz Gomez (Fundación FES in Bogotá, Colombia)
Mr Benaziza Hamadi (World Health Organization, Switzerland; retired)
Professor I-Min Lee (Harvard School of Public Health, USA)
Dr Sonja Kahlmeier (Institute for Social and Preventive Medicine of the University of Zurich,
Switzerland)
Dr Bill Kohl (University of Texas School of Public Health, Michael & Susan Dell Center for
Advancement of Healthy Living USA)
Professor Salome Kruger (Centre of Excellence for Nutrition, North-West University, South
Africa)
Dr Jean Claude Mbanya (Department of Internal Medicine and Specialties, University of
Yaoundé; International Diabetes Federation, Cameroon)
Dr Karim Omar (Institute for Sport Science and Sport; FA University Erlangen-Nürnberg
Germany)
Dr Vincent Onywera (Kenyatta University, Nairobi, Kenya)
Dr Michael Pratt (Centres for Disease Control and Prevention, USA)
Dr Krissada Raungarreerat (Thai Health Promotion Foundation, Thailand)
Professor Nizal Sarrafzadegan (Isfahan Cardiovascular Research Center; Isfahan University
of Medical Science Iran)
Dr Trevor Shilton (Australian Heart Foundation, Australia)
Professor Nick Watson (Department of Sociology, Anthropology and Applied Social Sciences
University of Glasgow UK)
Dr Wanda Wendel-Vos (Centre for Prevention and Health Services Research; National
Institute for Public Health and the Environment, the Netherlands)
APPENdIX 7 wHO REgIONAL OFFIcES cONSULTEd

AFRO (Dr Hamas Boureima-Sambo; Dr Sidi Allal Louazani; Dr Chandralla Sookram)
AMRO/PAHO (Dr Carl James Hospedales;Dr Enrique R Jacoby)
EMRO (Dr Jaffar Hussain)
EURO (Ms Lideke Middelbeek; Dr Sonia Kahlmeier, until December 2009; Ms Trudy Wijnhoven)
SEARO (Dr Jerzy Leowski)
WPRO (Dr Andrew Colin Bell; Dr Luca Tomaso Cavalli-Sforza; Dr Cherian Varghese)
WHO-HQ
Department of Chronic Diseases and Health Promotion (Dr Gauden Galea; Dr Shanthi Mendis)
Department of Ageing and Life Course (Dr John Beard)
Department of Nutrition for Health and Development (Dr Francesco Branca)
Department of Protection of the Human Environment (Dr Maria Purificacion Neira)
Department of Child and Adolescent Health and Development (Mr Paulus Joannes Bloem)
APPENdIX 8 wHO SEcRETARIAT
WHO-HQ Department of Chronic Diseases and Health Promotion: Dr Timothy Armstrong,

Ms Vanessa Candeias, Mr Eddy Engelsman, Ms Regina Guthold, Ms Hilda Muriuki, Mr Godfrey
Xuereb
WPRO, South Pacific Office: Dr Temo Waqanivalu
54
REFERENcES
55
1. Global health risks: mortality and burden of disease attributable to selected major risks.
Geneva, World Health Organization, 2009.
2. The global burden of disease: 2004 update. World Health Organization, Geneva, 2008.
3. A guide for population-based approaches to increasing levels of physical activity:
implementation of the WHO Global Strategy on Diet, Physical Activity and Health. Geneva,
World Health Organization, 2007.
4. Preventing chronic diseases: a vital investment. Geneva, World Health Organization,
2005.
5. Resolution WHA57.17. Global Strategy on Diet, Physical Activity and Health. In: Fifty-
seventh World Health Assembly, Geneva, 17–22 May 2004. Resolutions and decisions,
annexes. Geneva, World Health Organization, 2004.
6. World Health Report 2002: Reducing risks, promoting healthy life. Geneva, World Health
Organization, 2002.
7. 2008–2013 Action Plan for the Global Strategy for the Prevention and Control of
Noncommunicable Diseases. Geneva, World Health Organization, 2008.
8. WHO Handbook for guideline development, October 2009. Geneva, World Health
Organization, 2009.
9. Janssen I. Physical activity guidelines for children and youth. Applied Physiology
Nutrition and Metabolism, 2007, 32:S109–S121.
10. Janssen I, Leblanc A. Systematic Review of the Health Benefits of Physical Activity
in School-Aged Children and Youth. International Journal of Behavioural Nutrition and
Physical Activity, 2009 [under review for publication].
11. Physical Activity Guidelines Advisory Committee (PAGAC). Physical Activity Guidelines
Advisory Committee Report, 2008. Washington, DC, US Department of Health and Human
Services, 2008.
12. World report on child injury prevention. World Health Organization, UNICEF, 2008.
13. Bauman A, Lewicka M, Schöppe S. The Health Benefits of Physical Activity in Developing
Countries. Geneva, World Health Organization, 2005.
14. Cook I, Alberts M, Lambert EV. Relationship between adiposity and pedometer-assessed
ambulatory activity in adult, rural African women. International Journal of Obesity, 2008,
32: 1327–1330.
15. Nocon M et al. Association of physical activity with all-cause and cardiovascular
mortality: a systematic review and meta-analysis. European Journal of Cardiovascular
Prevention & Rehabilitation, 2008, 15:239–46.
16. Steyn K et al. Risk factors associated with myocardial infarction in Africa: the
INTERHEART Africa study. Circulation, 2005, 112(23):3554–3561.
17. Sofi F et al. Physical activity during leisure time and primary prevention of coronary heart
disease: an updated meta-analysis of cohort studies. European Journal of Cardiovascular
Prevention & Rehabilitation, 2008, 15:247–57.
18. Warburton D et al. Evidence-informed physical activity guidelines for Canadian adults.
Applied Physiology Nutrition and Metabolism, 2007, 32:S16–S68.
19. Warburton D et al. A systematic review of the evidence for Canada’s Physical Activity
Guidelines for Adults. International Journal of Behavioural Nutrition and Physical Activity,
2009 [under review for publication].
20. Paterson DH, Jones GR, Rice CL. Ageing and physical activity: evidence to develop
exercise recommendations for older adults. Applied Physiology, Nutrition and Metabolism,
2007, 32:S69–S108.
21. Paterson D, Warburton D. Physical activity and functional limitations in older adults: a
systematic review related to Canada’s Physical Activity Guidelines. International Journal
of Behavioural Nutrition and Physical Activity, 2009 [under review for publication].
22. Interventions on diet and physical activity: what works: summary report. Geneva, World
Health Organization, 2009.
56
23. School policy framework: implementation of the WHO global strategy on diet, physical
activity and health. Geneva, World Health Organization, 2008.
24. Pacific physical activity guidelines for adults: framework for accelerating the
communication of physical activity guidelines. World Health Organization, Western Pacific
Region, 2008.
25. Global Strategy on Diet, Physical Activity and Health: A framework to monitor and
evaluate implementation. Geneva, World Health Organization, 2008.
26. Preventing noncommunicable disease in the workplace through diet and physical activity.
WHO/World Economic Forum report of a joint event. Geneva, World Health Organization,
2008.
27. Australia’s Physical Activity Recommendations for 5–12 Year olds [brochure]. Australian
Government Department of Health and Ageing, 2005. (http://www.health.gov.au/
internet/main/publishing.nsf/Content/9D7D393564FA0C42CA256F970014A5D4/$File/
kids_phys.pdf, accessed 23 February 2010).
28. Australia’s Physical Activity Recommendations for 12–18 Year olds [brochure].
Australian Government Department of Health and Ageing, 2005. (http://www.health.gov.
au/internet/main/publishing.nsf/Content/0D0EB17A5B838081CA256F9700136F60/$Fi
le/youth_phys.pdf, accessed 23 February 2010).
29. Canada’s physical activity guide for children, 2002 (http://www.phac-aspc.gc.ca/hp-

ps/hl-mvs/pag-gap/cy-ej/index-eng.php, accessed 24 April 2010).
30. National Physical Activity Guidelines for Adults. Australian Government Department
of Health and Ageing, 2005. (http://www.health.gov.au/internet/main/publishing.nsf/
Content/health-pubhlth-strateg-phys-act-guidelines, accessed 11 January 2010).
31. Be Active Your Way: A Guide for Adults. Based on the 2008 Physical Activity Guidelines
for Americans. ODPHP Publication No. U0037. Office of Disease Prevention & Health
Promotion, US Department of Health and Human Services, October 2008. (http://www.
health.gov/paguidelines/pdf/adultguide.pdf, accessed 11 January 2010).
32. UKK Institute’s Physical Activity Pie. UKK Institute, Finland, 2009. (http://www.
ukkinstituutti.fi/en/liikuntavinkit/1004, accessed 11 January 2010).
33. Be Active, Your Way, Every Day for Life! Canada’s physical activity guide for older adults.
(http://www.phac-aspc.gc.ca/hp-ps/hl-mvs/pag-gap/pdf/guide-older-eng.pdf, accessed
April 2010).
34. 2008 Physical Activity Guidelines for Americans. Office of Disease Prevention & Health
Promotion, US Department of Health and Human Services, October 2008. (www.health.
gov/paguidelines, accessed 11 January 2010).
57
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ADC Online First, published on January 29, 2015 as 10.1136/archdischild-2014-307985
Review
Paediatric non-alcoholic fatty liver disease:

a practical overview for non-specialists
Jake P Mann,1 Rajiv Goonetilleke,2 Pat McKiernan3
1
Department of paediatrics, ABSTRACT develop fibrosis and potentially cirrhosis, with the
University of Cambridge, Non-alcoholic fatty liver disease (NAFLD) is the most reversibility diminishing with more advanced
Cambridge, UK
2
Children’s unit,
common paediatric liver disease with a prevalence of disease (see figure 1).
Hinchingbrooke Hospital, almost 10%; therefore, the majority of affected patients
Huntingdon, UK are under the care of general practitioners and non- WHICH CHILDREN ARE AT RISK OF NAFLD?
3
Liver unit, Birmingham specialists. The condition is caused by central obesity
Children’s Hospital, Obesity is the main risk factor for NAFLD. Several
with insulin resistance with additional factors influencing studies have assessed the histological prevalence of
Birmingham, UK
inflammatory activity (steatohepatitis). Ongoing NAFLD: 9.6% in healthy-weight children and 38%
Correspondence to inflammation leads to fibrosis and end-stage liver in obese children.27 Therefore, with 28% of UK
Dr Jake P Mann, Department disease, though this will usually occur after children have children overweight or obesei 8 there are potentially
of Paediatrics, University of transitioned into adult care. However, their main
Cambridge, Box 116, Level 8, a huge number of patients with undiagnosed
Addenbrooke’s Hospital, Hills morbidity and mortality is from type 2 diabetes and NAFLD. Other common risk factors are listed in
Rd, Cambridge CB2 0QQ, UK; complications of atherosclerosis. The minority of children table 2; however, it is not yet clearly established
jakemann@doctors.org.uk undergo biopsy but currently there is no other method to which factors put patients at a higher risk of NASH
accurately assess the stage of disease. Management is or fibrosis, rather than more benign steatosis.
Received 29 November 2014
Accepted 7 January 2015
focused at weight loss through a combination of diet
and exercise. Here, we present a current review of
paediatric NAFLD aimed at non-specialists, with practice WHAT IS THE CAUSE OF NAFLD?
NAFLD is a multifactorial condition due to envir-
points for implementation.
onmental and genetic influences. It has been
described with a ‘multiple-hit hypothesis’ where
the first ‘hit’ is an increase in liver fat, followed by
INTRODUCTION multiple additional factors that trigger the inflam-
Non-alcoholic fatty liver disease (NAFLD), some- matory activity.13 19
times referred to as just ‘fatty liver’, is the most The development of hepatic steatosis is intim-
common liver disease in UK children.1 2 Since ately related to insulin resistance: raised plasma
1983, when it was first recognised in children,3 its insulinii in the fasting state with reduced glucose-
prevalence has rapidly increased, paralleling the lowering ability.30 31 It seems that hepatic steatosis
rise in obesity.4–8 In recent years, there have been is both caused by and exacerbates insulin resistance,
numerous reviews of the condition,1 9–21 but there though this is an area of much study.32 In almost
is a need for more practical advice aimed at non- all cases, the initiating factor is the development of
specialists.22 With such high numbers of patients excess visceral adipose, combined with reduced
affected, general paediatricians and general practi- muscle mass. Therefore, the key environmental
tioners, rather than hepatologists, will care for the influences are, unsurprisingly, an energy-dense diet
majority of affected children. of high fat and high fructose combined with
NAFLD encompasses a spectrum of disease (see reduced physical activity.33–35 Sugar-sweetened bev-
table 1) that is defined histologically. erages have been identified as a particular culprit,
Simple steatosis is defined as greater than 5% of especially when coupled with low fibre.34 36
hepatocytes with fat infiltration.23 24 The term Only a small percentage of patients progress
NAFLD may also be used to describe a state of from steatosis to steatohepatitis.21 This is due to a
steatosis in association with the metabolic syn- number of influences: changes in the type and
drome or mild hepatic inflammation, which may be redox state of hepatic lipids, gut microbiota,
reflected by abnormal liver function tests (LFTs). genetic factors (eg, a polymorphism in PNPLA3),
Normal LFTs do not exclude NAFLD in children. mitochondrial dysfunction and hormone (adipo-
However, if a patient has biopsy-proven inflamma- kine) abnormalities.11 These lead to excess inflam-
tory activity, he/she would then be diagnosed with matory activity (with stellate cell activation and
non-alcoholic steatohepatitis (NASH). At the histo- raised tumour necrosis factor-α) that characterises
logical level there are significant differences NASH and fibrosis.15
between paediatric and adult NASH in the pattern
of inflammation that is seen, the cause and implica-
tions of which are not yet understood.25–29 Biopsy i
Where overweight is defined as over 85th body mass
To cite: Mann JP, may demonstrate a variable amount of fibrosis such index (BMI) centile and obese as over 95th, as is used in
Goonetilleke R,
McKiernan P. Arch Dis Child
that, in the most advanced cases, there is disruption the National Child Measurement Programme. However,
of the normal hepatic architecture and extensive the National Institute for Clinical Excellence defines
Published Online First: obese as over 98th BMI centile.
[please include Day Month fibrosis defined as cirrhosis. ii
Significantly raised fasting insulin levels are: Tanner
Year] doi:10.1136/ It is generally believed that patients progress 1-2≥15 IU/L, Tanner 3-4≥30 IU/L, Tanner 5≥20 IU/L; or
archdischild-2014-307985 from simple steatosis to steatohepatitis, then HOMA-IR of >4.4
Mann JP, et al. Arch Dis Child 2015;0 :1–5. doi:10.1136/archdischild-2014-307985 1

Copyright Article author (or their employer) 2015. Produced by BMJ Publishing Group Ltd (& RCPCH) under licence.
Review
Table 1 Definitions/spectrum of non-alcoholic fatty liver disease Table 2 Risk factors for non-alcoholic fatty liver disease (NAFLD)
(NAFLD), adapted from Vajro et al23 Modifiable risk factors Non-modifiable risk factors
Simple steatosis Microvesicular or macrovesicular fat deposition in >5%
hepatocytes Obesity Male
Non-alcoholic fatty Steatosis with the metabolic syndrome and/or Waist circumference >95th centile Hispanic origin
liver disease abnormal liver function tests Sedentary lifestyle Family history of NAFLD or T2DM
Non-alcoholic Biopsy-proven inflammatory activity in association High intake of sugar-sweetened beverages Parental (maternal) obesity
steatohepatitis with steatosis, with or without fibrosis Obstructive sleep apnoea Low birth weight
Cirrhosis Advanced fibrosis with disruption of hepatic Not breastfed Genetic polymorphisms
architecture and regenerative nodules (eg, in PNPLA3)
Note that ‘NAFLD’ can refer to both the whole spectrum of disease and one T2DM=type 2 diabetes mellitus.
sub-group of the spectrum.
NAFLD, non-alcoholic fatty liver disease.
Hepatomegaly and acanthosis nigricans are the most common

WHAT IS THE PROGNOSIS FOR CHILDREN WITH NAFLD? clinical findings, but examination usually only reveals central
There are only a few studies describing the natural history of adiposity. It is important to thoroughly examine for splenomeg-
NAFLD in children,37 but it is generally accepted that some aly and other signs of portal hypertension that may suggest
patients with uncontrolled steatohepatitis will develop fibrosis more advanced disease.23
and eventually cirrhosis.38 39 There are reports of children with
cirrhosis, end-stage liver disease and hepatocellular carcinoma as
a result of NAFLD.40 41 It is certainly established that there is WHAT INVESTIGATIONS ARE REQUIRED FOR DIAGNOSIS?
significant liver-related morbidity and mortality from NAFLD in Ultrasonography and LFTs are the basic first-line investigations. In
adults; it is reasonable to assume that our adult physician collea- general paediatric practice, for children with raised alanine trans-
gues may end up managing the end-stage complications of chil- aminase (ALT) or aspartate transaminase (AST), it is reasonable to
dren with NASH.2 17 screen for common conditions that can masquerade as NAFLD
Despite this, the complications of the metabolic syndrome and include blood tests that give an indication of the systemic
will be the main cause of morbidity in children with NAFLD.19 metabolic dysfunction (see box 2).45 These conditions can coexist
As much as 43%–45% of children with NAFLD have impaired with NAFLD; for example, both Wilson’s disease and NASH may
glucose tolerance or type 2 diabetes42 and they have an be found on biopsy. In specialist clinics, a more extensive set of
extremely atherogenic phenotype.12 However, many patients tests may be performed to look for rare cases of steatosis.19 23
will transition into adult care before their cardiac disease or Every patient should be tested for diabetes, initially by meas-
other diabetic complications become clinically manifest. uring HbA1c and progressing to an oral glucose tolerance test
(OGTT) if there is high suspicion of diabetes. Formal diagnosis
HOW DOES NAFLD PRESENT? of T2DM in children requires an OGTT in all cases; it also
Almost all NAFLD presents incidentally, examples are given in gives opportunity to measure preprandial and postprandial
box 1. They most commonly present at 11–13 years of age, insulin levels.
which may be related to peripubertal hormonal changes.43 44 An essential part of the diagnosis of NAFLD, particularly in
Patients occasionally present with non-specific abdominal pain, adolescents, is an alcohol history. The thresholds for a diagnosis
malaise and fatigue. These symptoms have been linked to more of NAFLD in adults in UK are consumption of <210 g (21
advanced NAFLD in a few circumstances;2 however, they are units) alcohol per week for men and <140 g (14 units) per
usually of a separate aetiology (eg, non-specific abdominal pain). week for women.17
Box 1 Presentation of non-alcoholic fatty liver disease

(NAFLD)
Case 1: Jonny, a 13-year-old boy, is admitted to the general

paediatrics ward with an acute, severe asthma attack. His body
mass index is above the 95% age-matched and sex-matched
centile. He is found to have an alanine transaminase (ALT)=67
IU/L, with the remainder of his liver function tests (LFTs) normal.
His discharge letter to the general practitioner (GP) asks his
LFTs to be repeated in 1–2 months time to see if his ALT has
normalised.
Case 2: Zainab, an 11-year-old girl, is admitted under the general
surgeons with symptoms suggestive of appendicitis. She has an
abdominal ultrasound scan, which demonstrates ‘diffusely
increased hepatic echogenicity consistent with fatty infiltration’.
Figure 1 Natural progression of non-alcoholic fatty liver disease After her appendicectomy, the general paediatricians are contacted
(NAFLD) from steatosis, to steatohepatitis with fibrosis, and finally for advice regarding Zainab’s liver.
cirrhosis. The reversibility diminishes as the condition progresses.
2 Mann JP, et al. Arch Dis Child 2015;0 :1–5. doi:10.1136/archdischild-2014-307985

Review
Table 3 Classification of secondary causes of fatty liver disease

Box 2 Tests included in liver screen and initial tests in
arranged in approximate order of frequency
non-alcoholic fatty liver disease (NAFLD)
Genetic/congenital
conditions Drugs Nutritional Other
Basic screen for alternative causes of abnormal liver function
tests (LFTs): Cystic fibrosis Corticosteroids Parenteral Alcohol
nutrition
▸ Full blood count, alanine transaminase, aspartate
Haemochromatosis Chemotherapy Rapid weight Polycystic ovarian
transaminase, bilirubin, albumin, coagulation screen, urea loss syndrome
and electrolytes Glycogen storage Oestrogens Kwashiorkor Hepatitis C virus
▸ Serum immunoglobulins and liver autoantibodies. diseases
▸ Hepatitis B and C virus serology, cytomegalovirus serology, Wilson disease Antiretrovirals Jejuno-ileal Obstructive sleep
Epstein–Barr virus serology bypass apnoea
▸ α1-antitrypsin level, serum caeruloplasmin, ferritin Prader–Willi syndrome Nifedipine Hypothyroidism
▸ Ultrasound scan of liver, spleen and portal vein Bardet–Biedl syndrome Amiodarone Bacterial
Metabolic tests in work-up of NAFLD: overgrowth
▸ Lipid profile (total cholesterol, high-density lipoprotein, Lipodystrophy
low-density lipoprotein, triglycerides) Alstrom’s syndrome
▸ HbA1c and, if indicated, fasting glucose, fasting insulin, or
oral glucose tolerance test.
▸ Thyroid function tests
are a number of causes that result in secondary fatty liver
disease (see table 3).48
DOES EVERY CHILD NEED A LIVER BIOPSY? It may be tempting to assume a diagnosis of NAFLD in obese
Liver biopsy remains the gold standard for diagnosis and staging children with a mildly raised ALT but, in an important study
of NAFLD, but it is only a minority of children who undergo looking at primary care referrals, Schwimmer et al49 found that
this relatively invasive procedure. Guidelines from the European 18% of patients referred for suspected fatty liver were diag-
Society of Gastroenterology, Hepatology and Nutrition suggest nosed with hepatic conditions other than NAFLD. In addition,
that biopsy should be performed when there is diagnostic uncer- secondary metabolic causes are much more likely in children
tainty ( particularly in children aged under 10 years or those aged under 3 years and NAFLD is still comparatively rare at
who are not obese), a higher risk of advanced disease (eg, <10 years of age.
splenomegaly on ultrasonography) or with persistently raised The main clinical indicator of ( primary) NAFLD is obesity
transaminases (AST and/or ALT) after 3–6 months of lifestyle but whether or not to screen is a difficult question. Several sets
intervention.23 of expert opinion have been produced that recommend screen-
Unfortunately, there is no reliable correlation between trans- ing using AST and ALT in children with a body mass index
aminase levels or ultrasound appearances and liver histology in (BMI) above 85th–95th centile (see box 4);23 50 51 however,
NAFLD.26 46 Some studies have suggested that raised AST and, this would apply to vast numbers of children. Focusing screen-
in particular, a raised AST: ALT ratio47 predict more advanced ing on children with a waist circumference of >98th centile
disease, but this and a recently developed scoring system to may be more helpful.42 Though, in spite of this, obese children
predict fibrosis42 are not yet fully validated. Unlike in adults, are generally underscreened,52 and in UK practice, there is even
Fibroscan (measuring hepatic transient elastography) is not vali- a lack of routine anthropomorphic measurements.53
dated in children.18 However, there is promise for a range of
serum biomarkers that may ultimately allow non-invasive predic-
tion of hepatic fibrosis.10 WHEN SHOULD A SPECIALIST REFERRAL BE MADE?
There are some situations where the decision to refer is straight-
forward, for example, an obese teenager with a persistently
WHEN SHOULD AN ALTERNATIVE DIAGNOSIS BE raised ALT of 200 IU/L. But paediatricians may be less certain of
CONSIDERED? when to refer if AST or ALT is only just above the upper limit of
Fatty liver disease can be classified as primary or secondary.
Primary NAFLD occurs as part of the metabolic syndrome
where there is no other underlying diagnosis. However, there
Box 4 Key points for practice
Screen obese children (body mass index >85th centile) and refer
Box 3 When to refer children with suspected fatty liver those with suspected non-alcoholic fatty liver disease
disease Advice for children and their families:
▸ Maximum 1 h screen-time per day
▸ High transaminases (alanine transaminase or aspartate ▸ Minimum 1 h physical activity per day
transaminase) >3× upper limit of normal ▸ Eat breakfast
▸ Non-obese ▸ Remove all sugar-sweetened beverages from the house,
▸ Under 10 years of age including fruit juices
▸ Persistently raised transaminases for 6 months, despite ▸ At least five portions of fruit or vegetables per day
6 months of lifestyle modification Sensitively ask about children’s mental health.
▸ Clinical or ultrasonographic evidence of splenomegaly Check vitamin D, lipids and HbA1c.

Review
normal. Evidence suggests that we generally underestimate the stage, we cannot state that treatment of deficiency will necessar-
severity of NAFLD in obese children with only mildly abnormal ily improve NAFLD by itself; however, the benefits of vitamin
LFTs. It is possible to be anywhere on the NAFLD spectrum D replacement probably outweigh the risks in children.
with normal transaminases. One study found advanced fibrosis Similarly, despite being overweight, children may suffer from
in 11% of obese children referred from primary care with raised iron deficiency anaemia due to malnourishment.75
ALT,49 but exactly what cut-off above the age-specific/sex- Bariatric surgery is rarely performed for children in the UK;
specific upper limit of normal is not yet known, though it is however, it is more established in the USA.76 So far, data seem
likely to be too high.54 55 So, while ALT is far from a perfect to be positive, though long-term follow-up is still needed.77
screening test for NAFLD, it is simple, non-invasive and corre- While it is not yet a treatment primarily for NAFLD, a signifi-
lated with insulin resistance and central adiposity.56 57 cant improvement in liver disease is found with the dramatic
While specialist clinics will not be able to provide long-term weight loss many patients achieve.14
follow-up for all children with NAFLD, referral is recom- The majority of children with NAFLD will be under the care
mended where the diagnosis is uncertain, persistently raised of general practitioners or paediatricians for their long-term
transaminases or features suggestive of severe disease (see box 3) follow-up. At least annual LFTs and ultrasonography are per-
considered. In the foreseeable future, non-invasive scoring formed for monitoring. Specialist hepatologists may trial use of
systems (analogous to the NASH fibrosis score for adults58) may a variety of therapies including vitamin E and metformin, but
allow general paediatricians to risk stratify adolescents with these would not usually be commenced in primary care.
NAFLD.
HOW SHOULD NAFLD BE MANAGED? CONCLUSIONS

Weight loss is the single most beneficial treatment for patients Children with NAFLD are a group of patients with severe meta-
with NAFLD.14 59 60 It will improve their liver disease, metabolic derangement, at high risk of type 2 diabetes and complica-
bolic dysfunction and long-term prognosis. However, it is diffi- tions of atherosclerosis later in life. Management is focused on
cult to achieve in practice, and even in dedicated paediatric weight loss through a combination of diet and exercise, though
obesity clinics, sustained weight loss is hard to maintain. Ideally, achieving this is challenging, even with a dedicated multidiscip-
weight loss should be gradual, at 500 g/week or less; more rapid linary team.
loss can have deleterious effects and is more likely to be
Twitter Follow Jake Mann at @MannGsy
regained.61 62 Loss of 3%–5% weight improves steatosis, with
Contributors JPM drafted the manuscript. RG and PMcK reviewed and edited the
10% loss improving inflammatory activity, but no threshold
manuscript. All authors approved the manuscript prior to submission.
effect has been demonstrated.63 A reduction of at least 0.25
Competing interests None.
BMI SDs is needed to demonstrate systemic metabolic benefit.64
In prepubescent children or adolescents, aiming for weight Provenance and peer review Not commissioned; externally peer reviewed.
maintenance, rather than weight loss, will allow an improve-
ment in BMI during growth.
REFERENCES
Achieving and maintaining weight loss requires a multidiscip- 1 Berardis S, Sokal E. Pediatric non-alcoholic fatty liver disease: an increasing public
linary, family-centred approach tackling physical activity and health issue. Eur J Pediatr 2014;173:131–9.
diet.65 66 It seems that almost any form of physical activity is 2 Schwimmer JB, Deutsch R, Kahen T, et al. Prevalence of fatty liver in children and
beneficial: resistance training and vigorous and sustained exer- adolescents. Pediatrics 2006;118:1388–93.
3 Moran JR, Ghishan FK, Halter SA, et al. Steatohepatitis in obese children: a cause
cise all have evidence supporting their use.67 68 The UK govern-
of chronic liver dysfunction. Am J Gastroenterol 1983;78:374–7.
ment recommends at least 60 min physical activity every day, 4 Cohen JC, Horton JD, Hobbs HH. Human fatty liver disease: old questions and new
but more is required if weight loss is to be achieved and then insights. Science 2011;332:1519–23.
maintained.69 A practical method of increasing general activity 5 The NHS Information Centre for health and social care. Dunn W, Xu R, Wingard
levels is to reduce sedentary screen time.70 Experts recommend DDL, et al. Suspected nonalcoholic fatty liver disease and mortality risk in a
population-based cohort study. Am J Gastroenterol 2008;103:2263–71.
a maximum of 1 or 2 h screen time per day.66 71 6 Ogden CL, Carroll MD, Kit BK, et al. Prevalence of obesity and trends in body mass
Dietary advice can seem confusing and overwhelming to fam- index among US children and adolescents, 1999-2010. JAMA 2012;307:483–90.
ilies, particularly if it challenges their current eating habits and 7 Peters H, Whincup PH, Cook DG, et al. Trends in resting pulse rates in
cultural practices. For this reason, involvement of a dietician is 9–11-year-old children in the UK 1980-2008. Arch Dis Child 2014;99:10–14.
8 Craig R, Mindell J. Health Survey for England 2012. London, 2013.
vital, as part of a multidisciplinary clinic. Macronutrients and
9 Awai HI, Newton KP, Sirlin CB, et al. Evidence and recommendations for imaging
micronutrients have been studied for their individual and col- liver fat in children, based on systematic review. Clin Gastroenterol Hepatol
lective benefits in NAFLD.66 72 From this, the evidence suggests 2014;12:765–73.
that a low energy-dense diet, low in sugar ( particularly fructose) 10 Fitzpatrick E, Dhawan A. Noninvasive biomarkers in non-alcoholic fatty liver disease:
and fat but high in fibre should be strived towards. This equates current status and a glimpse of the future. World J Gastroenterol
2014;20:10851–63.
to a low glycaemic index diet that includes a significant quantity 11 Hassan K, Bhalla V, Ezz El Regal M, et al. Nonalcoholic fatty liver disease: a
of fruit and vegetables with addition of ω-3 polyunsaturated comprehensive review of a growing epidemic. World J Gastroenterol
fatty acids (found in ‘oily’ fish). Simply eating breakfast is 2014;20:12082–101.
known to help achieve a healthy metabolic state.71 12 Pacifico L, Chiesa C, Anania C, et al. Nonalcoholic fatty liver disease and the heart
in children and adolescents. World J Gastroenterol 2014;20:9055–71.
There are several other important points to consider; as for
13 Ozturk Y, Soylu OB. Fatty liver in childhood. World J Hepatol 2014;6:33–40.
managing all children with obesity, psychological factors should 14 Mitchel E, Lavine J. Review article: the management of paediatric nonalcoholic fatty
be addressed. Depression, low self-esteem and bullying are liver disease. Aliment Pharmacol 2014;40:1155–70.
much more frequent in obese children.73 The exact influence of 15 Berlanga A, Guiu-jurado E, Porras JA, et al. Molecular pathways in non-alcoholic
psychological factors on weight gain is complex, but clinicians fatty liver disease. Clin Exp Gastroenterol 2014;7:221–39.
16 Firneisz G. Non-alcoholic fatty liver disease and type 2 diabetes mellitus: the liver
should acknowledge their importance and refer appropriately. disease of our age? World J Gastroenterol 2014;20:9072–89.
Vitamin D deficiency is frequently found in association with 17 Sattar N, Forrest E, Preiss D. Non-alcoholic fatty liver disease. BMJ 2014;347:
NAFLD and has been implicated in its pathogenesis.74 At this g4596–g4596.
4 Mann JP, et al. Arch Dis Child 2015;0 :1–5. doi:10.1136/archdischild-2014-307985

Review
18 Yang HR. Noninvasive diagnosis of pediatric nonalcoholic fatty liver disease. Korean 51 August GP, Caprio S, Fennoy I, et al. Prevention and treatment of pediatric obesity:
J Pediatr 2013;56:45–51. an Endocrine Society Clinical Practice guideline based on expert opinion. J Clin
19 Giorgio V, Prono F, Graziano F, et al. Pediatric non alcoholic fatty liver disease: old Endocrinol Metab 2008;93:4576–99.
and new concepts on development, progression, metabolic insight and potential 52 Riley MR, Bass NM, Rosenthal P, et al. Underdiagnosis of pediatric obesity and
treatment targets. BMC Pediatr 2013;13:40. underscreening for fatty liver disease and metabolic syndrome by pediatricians and
20 Nobili V, Svegliati-Baroni G, Alisi A, et al. A 360-degree overview of paediatric pediatric subspecialists. J Pediatr 2005;147:839–42.
NAFLD: Recent insights. J Hepatol 2013;58:1218–29. 53 Abbey I, Rudolf M. Do paediatricians miss the diagnosis of obesity? Arch Dis Child
21 Wree A, Broderick L, Canbay A, et al. From NAFLD to NASH to cirrhosis-new 2010;95:A51–2.
insights into disease mechanisms. Nat Rev Gastroenterol Hepatol 2013;10:627–36. 54 Engelmann G, Hoffmann GF, Grulich-Henn J, et al. Alanine aminotransferase
22 Anonymous. Finding fatty livers. Arch Dis Child 2014;99:515. elevation in obese infants and children: A marker of early onset non alcoholic fatty
23 Vajro P, Lenta S, Socha P, et al. Diagnosis of nonalcoholic fatty liver disease in liver disease. Hepat Mon 2014;14:e14112.
children and adolescents: position paper of the ESPGHAN Hepatology Committee. J 55 Schwimmer JB, Dunn W, Norman GJ, et al. SAFETY Study: alanine aminotransferase
Pediatr Gastroenterol Nutr 2012;54:700–13. cutoff values are set too high for reliable detection of pediatric chronic liver disease.
24 Ludwig J, Viggiano TR, McGill DB, et al. Nonalcoholic steatohepatitis: Mayo Clinic Gastroenterology 2010;138.
experiences with a hitherto unnamed disease. Mayo Clin Proc 1980;55:434–8. 56 Fraser A, Longnecker MP, Lawlor DA. Prevalence of elevated
25 Ko JS, Yoon JM, Yang HR, et al. Clinical and histological features of nonalcoholic alanine-aminotransferase (ALT) among US adolescents and associated factors :
fatty liver disease in children. Dig Dis Sci 2009;54:2225–30. NHANES 1999–2004. 2008;133:1814–20.
26 Molleston JP, Schwimmer JB, Yates KP, et al. Histological abnormalities in children 57 Burgert TS, Taksali SE, Dziura J, et al. Alanine aminotransferase levels and fatty liver
with nonalcoholic fatty liver disease and normal or mildly elevated alanine in childhood obesity: associations with insulin resistance, adiponectin, and visceral
aminotransferase levels. J Pediatr 2014;164:707–713.e3. fat. J Clin Endocrinol Metab 2006;91:4287–94.
27 Schwimmer JB, Behling C, Newbury R, et al. Histopathology of pediatric 58 Angulo P, Hui JM, Marchesini G, et al. The NAFLD fibrosis score: a noninvasive
nonalcoholic fatty liver disease. Hepatology 2005;42:641–9. system that identifies liver fibrosis in patients with NAFLD. Hepatology
28 Carter-Kent C, Yerian LM, Brunt EM, et al. Nonalcoholic steatohepatitis in children: 2007;45:846–54.
a multicenter clinicopathological study. Hepatology 2009;50:1113–20. 59 Koot BGP, van der Baan-Slootweg OH, Tamminga-Smeulders CLJ, et al. Lifestyle
29 Swiderska-Syn M, Suzuki A, Guy CD, et al. Hedgehog pathway and pediatric intervention for non-alcoholic fatty liver disease: prospective cohort study of its
nonalcoholic fatty liver disease. Hepatology 2013;57:1814–25. efficacy and factors related to improvement. Arch Dis Child 2011;96:669–74.
30 Parker VER, Semple RK. Genetics in endocrinology: genetic forms of severe insulin 60 Nobili V, Manco M, Devito R, et al. Effect of vitamin E on aminotransferase levels
resistance: what endocrinologists should know. Eur J Endocrinol 2013;169:R71–80. and insulin resistance in children with non-alcoholic fatty liver disease. Aliment
31 Viner RM, White B, Barrett T, et al. Assessment of childhood obesity in secondary Pharmacol Ther 2006;24:1553–61.
care: OSCA consensus statement. Arch Dis Child Educ Pr Ed 2012;97:98–105. 61 Agostoni C, Braegger C, Decsi T, et al. Role of dietary factors and food habits in
32 Shulman GI. Ectopic fat in Insulin resistance, dyslipidemia, and cardiometabolic the development of childhood obesity: a commentary by the ESPGHAN Committee
disease. N Engl J Med 2014;371:1131–41. on Nutrition. J Pediatr Gastroenterol Nutr 2011;52:662–9.
33 Nseir W, Hellou E, Assy N. Role of diet and lifestyle changes in nonalcoholic fatty 62 Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of
liver disease. World J Gastroenterol 2014;20:9338–44. non-alcoholic fatty liver disease: practice guideline by the American
34 Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. Hepatology Gastroenterological Association, American Association for the Study of Liver
2013;57:2525–31. Diseases, and American College of Gastroenterology. Gastroenterology
35 Jin R, Welsh J a, Le N-A, et al. Dietary fructose reduction improves markers of 2012;142:1592–609.
cardiovascular disease risk in Hispanic-American adolescents with NAFLD. Nutrients 63 Reinehr T, Schmidt C, Toschke AM, et al. Lifestyle intervention in obese children
2014;6:3187–201. with non-alcoholic fatty liver disease: 2-year follow-up study. Arch Dis Child
36 Mollard RC, Sénéchal M, MacIntosh AC, et al. Dietary determinants of hepatic 2009;94:437–42.
steatosis and visceral adiposity in overweight and obese youth at risk of type 2 64 Ford AL, Hunt LP, Cooper A, et al. What reduction in BMI SDS is required in obese
diabetes. Am J Clin Nutr 2014;99:804–12. adolescents to improve body composition and cardiometabolic health? Arch Dis
37 Feldstein AE, Charatcharoenwitthaya P, Treeprasertsuk S, et al. The natural history Child 2010;95:256–61.
of nonalcholic fatty liver disease in children: a follow-up study for up to 20-years. 65 Turner KM, Salisbury C, Shield JPH. Parents’ views and experiences of childhood
Gut 2009;58:1538–44. obesity management in primary care: a qualitative study. Fam Pract
38 Patton HM, Sirlin C, Behling C, et al. Pediatric nonalcoholic fatty liver disease: a 2012;29:476–81.
critical appraisal of current data and implications for future research. J Pediatr 66 Spear BA, Barlow SE, Ervin C, et al. Recommendations for treatment of child and
Gastroenterol Nutr 2006;43:413–27. adolescent overweight and obesity. Pediatrics 2007;120(Suppl):S254–88.
39 Matteoni CA, Younossi ZM, Gramlich T, et al. Nonalcoholic fatty liver disease: 67 Fedewa MV, Gist NH, Evans EM, et al. Exercise and insulin resistance in youth: a
a spectrum of clinical and pathological severity. Gastroenterology meta-analysis. Pediatrics 2014;133:e163–74.
1999;116:1413–19. 68 Kistler KD, Brunt EM, Clark JM, et al. Physical activity recommendations, exercise
40 Alisi A, Feldstein AE, Villani A, et al. Pediatric nonalcoholic fatty liver disease: a intensity, and histological severity of nonalcoholic fatty liver disease. Am J
multidisciplinary approach. Nat Rev Gastroenterol Hepatol 2012;9:152–61. Gastroenterol 2011;106:460–8; quiz 469.
41 Molleston JP, White F, Teckman J, et al. Obese children with steatohepatitis can 69 Bull F. Physical Activity Guidelines in the U.K.: Review and Recommendations.
develop cirrhosis in childhood. Am J Gastroenterol 2002;97:2460–2. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/
42 Eng K, Lopez R, Liccardo D, et al. A non-invasive prediction model for non-alcoholic 213743/dh_128255.pdf
steatohepatitis in paediatric patients with non-alcoholic fatty liver disease. Dig Liver 70 Liao Y, Liao J, Durand CP, et al. Which type of sedentary behaviour intervention is
Dis 2014;46:1008–13. more effective at reducing body mass index in children? A meta-analytic review.
43 Schwimmer JB, Celedon MA, Lavine JE, et al. Heritability of nonalcoholic fatty liver Obes Rev 2014;15:159–68.
disease. Gastroenterology 2009;136:1585–92. 71 Vos M, McClain C. Nutrition and nonalcoholic fatty liver disease in children. Curr
44 DeBoer MD. Ethnicity, obesity and the metabolic syndrome: implications on assessing Gastroenterol Rep 2008;10:308–15. http://link.springer.com/article/10.1007/
risk and targeting intervention. Expert Rev Endocrinol Metab 2011;6:279–89. s11894-008-0061-4 (accessed 8 Oct 2014).
45 Kang K-S. Abnormality on liver function test. Pediatr Gastroenterol Hepatol Nutr 72 Zivkovic AM, German JB, Sanyal AJ. Comparative review of diets for the metabolic
2013;16:225–32. syndrome: implications for nonalcoholic fatty liver disease. Am J Clin Nutr
46 Saadeh S, Younossi ZM, Remer EM, et al. The utility of radiological imaging in 2007;86:285–300.
nonalcoholic fatty liver disease. Gastroenterology 2002;123:745–50. 73 De Niet JE, Naiman DI. Psychosocial aspects of childhood obesity. Minerva Pediatr
47 Patton HM, Lavine JE, Van Natta ML, et al. Clinical correlates of histopathology 2011;63:491–505.
in pediatric nonalcoholic steatohepatitis. Gastroenterology 74 Kwok RM, Torres DM, Harrison SA. Vitamin D and nonalcoholic fatty liver
2008;135:1961–1971.e2. disease (NAFLD): Is it more than just an association? Hepatology
48 Bellentani S, Scaglioni F, Marino M, et al. Epidemiology of non-alcoholic fatty liver 2013;58:1166–74.
disease. Dig Dis 2010;28:155–61. 75 Nead KG, Halterman JS, Kaczorowski JM, et al. Overweight
49 Schwimmer JB, Newton KP, Awai HI, et al. Paediatric gastroenterology evaluation of children and adolescents: a risk group for iron deficiency. Pediatrics
overweight and obese children referred from primary care for suspected 2004;114:104–8.
non-alcoholic fatty liver disease. Aliment Pharmacol Ther 2013;38:1267–77. 76 Sachdev P, Makaya T, Marven SS, et al. Bariatric surgery in severely obese
50 Barlow SE. Expert committee recommendations regarding the prevention, adolescents: a single-centre experience. Arch Dis Child 2014;99:894–8.
assessment, and treatment of child and adolescent overweight and obesity: 77 Black JA, White B, Viner RM, et al. Bariatric surgery for obese children and
summary report. Pediatrics 2007;120(Suppl):S164–92. adolescents: a systematic review and meta-analysis. Obes Rev 2013;14:634–44.

Paediatric non-alcoholic fatty liver disease: a

practical overview for non-specialists
Jake P Mann, Rajiv Goonetilleke and Pat McKiernan
Arch Dis Child published online January 29, 2015
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REPORT OF THE COMMISSION ON
ENDING
CHILDHOOD
OBESITY
REPORT OF THE COMMISSION ON
ENDING
CHILDHOOD
OBESITY
WHO Library Cataloguing-in-Publication Data
Report of the commission on ending childhood obesity.
1.Pediatric Obesity – prevention and control. 2.Child. 3.Feeding Behavior. 4.Food Habits. 5.Exercise. 6.Diet. 7.Health Promotion.
8.National Health Programs. I.World Health Organization.
ISBN 978 92 4 151006 6 (NLM classification: WS 130)
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CONTENTS
v Glossary and definitions
vi Executive summary
2 Introduction
8 Guiding principles
12 Strategic objectives
16 Recommendations
33 Actions and responsibilities

for implementing the recommendations
38 Monitoring and accountability
40 Conclusions
42 References
46 ANNEX 1: The Commission on Ending Childhood Obesity
48 ANNEX 2: Commissioners
IV
GLOSSARY AND
DEFINITIONS
BMI Body mass index = weight (kg)/height (m2).
BMI-FOR-AGE BMI adjusted for age, standardized for children.
CHILDREN Those less than 18 years of age.1
INFANTS Those less than 12 months of age.
HEALTHY FOODS Foods that contribute to healthy diets if consumed in appropriate

amounts.2
OBESITY From birth to less than 5 years of age: weight-for-height more

than 3 Standard Deviation (SD) above the WHO Child Growth
Standards median.3
From age 5 to less than 19 years: BMI-for-age more than 2 SD

above the WHO growth reference median.4
OBESOGENIC An environment that promotes high energy intake and sedentary

ENVIRONMENT behaviour.
This includes the foods that are available, affordable, accessible

and promoted; physical activity opportunities; and the social
norms in relation to food and physical activity.
OVERWEIGHT From birth to less than 5 years of age: weight-for-height more

than 2 SD above WHO Child Growth Standards median.3
From age 5 to less than 19 years: BMI-for-age more than 1 SD

above WHO growth reference median.4
UNHEALTHY FOODS Foods high in saturated fats, trans-fatty acids, free sugars or salt
(i.e. energy-dense, nutrient-poor foods).
YOUNG CHILDREN Those less than 5 years of age.
1
Convention on the rights of the child, Treaty Series, 1577:3(1989): PART I, Article 1 defines a child as every human being below the age of eighteen years unless, under the law
applicable to the child, majority is attained earlier. The World Health Organization (WHO) defines adolescents as those between 10 and 19 years of age. The majority of adolescents
are, therefore, included in the age-based definition of “child”, adopted by the Convention on the Rights of the Child, as a person under the age of 18 years.
2
http://www.who.int/mediacentre/factsheets/fs394/en/.
3
http://www.who.int/childgrowth/standards/technical_report/en/.
4
http://www.who.int/nutrition/publications/growthref_who_bulletin/en/. The new curves are closely aligned with the WHO Child Growth Standards at 5 years, and the
recommended adult cut-offs for overweight and obesity at 19 years. They fill the gap in growth curves and provide an appropriate reference for the 5–19-year age group.
V
EXECUTIVE
SUMMARY
Childhood obesity is reaching on Ending Childhood Obesity No single intervention can halt
alarming proportions in many was established in 2014 to the rise of the growing obesity
countries and poses an urgent review, build upon and address epidemic. Addressing childhood
and serious challenge. The gaps in existing mandates and and adolescent obesity requires
Sustainable Development Goals, strategies. Having consulted consideration of the environmental
set by the United Nations in with over 100 WHO Member context and of three critical
2015, identify prevention and States and reviewed nearly 180 time periods in the life-course:
control of noncommunicable online comments (see Annex 1), preconception and pregnancy;
diseases as core priorities. Among the Commission has developed infancy and early childhood; and
the noncommunicable disease a set of recommendations to older childhood and adolescence.
risk factors, obesity is particularly successfully tackle childhood and In addition, it is important to treat
concerning and has the potential adolescent obesity in different children who are already obese,
to negate many of the health contexts around the world. for their own well-being and that of
benefits that have contributed to their children.
increased life expectancy. Many children today are
growing up in an obesogenic Obesity prevention and treatment
The prevalence of infant, environment that encourages requires a whole-of-government
childhood and adolescent obesity weight gain and obesity. approach in which policies across
is rising around the world. Energy imbalance has resulted all sectors systematically take
Although rates may be plateauing from the changes in food type, health into account, avoid harmful
in some settings, in absolute availability, affordability and health impacts, and thus improve
numbers there are more children marketing, as well as a decline population health and health
who are overweight and obese in in physical activity, with more equity.
low- and middle-income countries time being spent on screen-
than in high-income countries. based and sedentary leisure The Commission has developed
Obesity can affect a child’s activities. The behavioural and a comprehensive, integrated
immediate health, educational biological responses of a child package of recommendations to
attainment and quality of life. to the obesogenic environment address childhood obesity. It calls
Children with obesity are very can be shaped by processes for governments to take leadership
likely to remain obese as adults even before birth, placing an and for all stakeholders to
and are at risk of chronic illness. even greater number of children recognize their moral responsibility
on the pathway to becoming in acting on behalf of the child
Progress in tackling childhood obese when faced with an to reduce the risk of obesity. The
obesity has been slow and unhealthy diet and low physical recommendations are presented
inconsistent. The Commission activity. under the following areas.
VI
PROMOTE INTAKE OF
HEALTHY FOODS
WEIGHT PROMOTE
MANAGEMENT PHYSICAL ACTIVITY
1
6 2
ENDING
CHILDHOOD
OBESITY
5 3
HEALTH, NUTRITION PRECONCEPTION AND

AND PHYSICAL PREGNANCY CARE
ACTIVITY FOR SCHOOL-
AGE CHILDREN
EARLY CHILDHOOD
DIET AND PHYSICAL
ACTIVITY
VII
RECOMMENDATIONS
1 IMPLEMENT COMPREHENSIVE PROGRAMMES

THAT PROMOTE THE INTAKE OF HEALTHY FOODS
AND REDUCE THE INTAKE OF UNHEALTHY
FOODS AND SUGAR-SWEETENED BEVERAGES BY
CHILDREN AND ADOLESCENTS.
1.1 Ensure that appropriate and context-specific

nutrition information and guidelines for
both adults and children are developed and
disseminated in a simple, understandable and
accessible manner to all groups in society.
Implement an effective tax on sugar-sweetened

1.2
beverages.
Implement the Set of Recommendations on the

1.3
Marketing of Foods and Non-alcoholic Beverages
to Children to reduce the exposure of children and
adolescents to, and the power of, the marketing
of unhealthy foods.
Develop nutrient-profiles to identify unhealthy

1.4
foods and beverages.
1.5 Establish cooperation between Member States to

reduce the impact of cross-border marketing of
unhealthy foods and beverages.
1.6 Implement a standardized global nutrient labelling

system.
1.7 Implement interpretive front-of-pack labelling,

supported by public education of both adults and
children for nutrition literacy.
1.8 Require settings such as schools, child-care

settings, children’s sports facilities and events to
create healthy food environments.
1.9 Increase access to healthy foods in disadvantaged

communities.
VIII
THAT PROMOTE PHYSICAL ACTIVITY AND
REDUCE SEDENTARY BEHAVIOURS IN CHILDREN
AND ADOLESCENTS.
2.1 Provide guidance to children and adolescents,

their parents, caregivers, teachers and health
professionals on healthy body size, physical activity,
sleep behaviours and appropriate use of screen-
based entertainment.
Ensure that adequate facilities are available on

2.2
school premises and in public spaces for physical
activity during recreational time for all children
(including those with disabilities), with the provision
of gender-friendly spaces where appropriate.
3 INTEGRATE AND STRENGTHEN GUIDANCE FOR

NONCOMMUNICABLE DISEASE PREVENTION
WITH CURRENT GUIDANCE FOR PRECONCEPTION
AND ANTENATAL CARE, TO REDUCE THE RISK OF
CHILDHOOD OBESITY.
3.1 Diagnose and manage hyperglycaemia and

gestational hypertension.
Monitor and manage appropriate gestational

3.2
weight gain.
Include an additional focus on appropriate nutrition

3.3
in guidance and advice for both prospective
mothers and fathers before conception and during
pregnancy.
Develop clear guidance and support for the

3.4
promotion of good nutrition, healthy diets and
physical activity, and for avoiding the use of and
exposure to tobacco, alcohol, drugs and other
toxins.
IX
4 PROVIDE GUIDANCE ON, AND SUPPORT FOR,
HEALTHY DIET, SLEEP AND PHYSICAL ACTIVITY IN
EARLY CHILDHOOD TO ENSURE CHILDREN GROW
APPROPRIATELY AND DEVELOP HEALTHY HABITS.
4.1 Enforce regulatory measures such as The International

Code of Marketing of Breast-milk Substitutes and
subsequent World Health Assembly resolutions.
4.2 Ensure all maternity facilities fully practice the Ten

Steps to Successful Breastfeeding.
4.3 Promote the benefits of breastfeeding for both mother

and child through broad-based education to parents
and the community at large.
4.4 Support mothers to breastfeed, through regulatory

measures such as maternity leave, facilities and time
for breastfeeding in the work place.
Develop regulations on the marketing of

4.5
complementary foods and beverages, in line with
WHO recommendations, to limit the consumption of
foods and beverages high in fat, sugar and salt by
infants and young children.
Provide clear guidance and support to caregivers

4.6
to avoid specific categories of foods (e.g. sugar-
sweetened milks and fruit juices or energy-dense,
nutrient-poor foods) for the prevention of excess
weight gain.
Provide clear guidance and support to caregivers

4.7
to encourage the consumption of a wide variety of
healthy foods.
Provide guidance to caregivers on appropriate

4.8
nutrition, diet and portion size for this age group.
Ensure only healthy foods, beverages and snacks are

4.9
served in formal child care settings or institutions.
Ensure food education and understanding are

4.10
incorporated into the curriculum in formal child-care
settings or institutions.
Ensure physical activity is incorporated into the daily

4.11
routine and curriculum in formal child care settings or
institutions.
4.12 Provide guidance on appropriate sleep time, sedentary

or screen-time, and physical activity or active play for
the 2–5 years of age group.
4.13 Engage whole-of-community support for caregivers

and child care settings to promote healthy lifestyles for
young children.
X
THAT PROMOTE HEALTHY SCHOOL
ENVIRONMENTS, HEALTH AND NUTRITION
LITERACY AND PHYSICAL ACTIVITY AMONG
SCHOOL-AGE CHILDREN AND ADOLESCENTS.
5.1 Establish standards for meals provided in schools,

or foods and beverages sold in schools, that meet
healthy nutrition guidelines.
5.2 Eliminate the provision or sale of unhealthy

foods, such as sugar-sweetened beverages and
energy-dense, nutrient-poor foods, in the school
environment.
Ensure access to potable water in schools and sports

5.3
facilities.
5.4 Require inclusion of nutrition and health education

within the core curriculum of schools.
5.5 Improve the nutrition literacy and skills of parents

and caregivers.
5.6 Make food preparation classes available to children,

their parents and caregivers.
5.7 Include Quality Physical Education in the school

curriculum and provide adequate and appropriate
staffing and facilities to support this.
6 PROVIDE FAMILY-BASED, MULTICOMPONENT,

LIFESTYLE WEIGHT MANAGEMENT SERVICES FOR
CHILDREN AND YOUNG PEOPLE WHO ARE OBESE.
6.1 Develop and support appropriate weight

management services for children and adolescents
who are overweight or obese that are family-
based, multicomponent (including nutrition, physical
activity and psychosocial support) and delivered
by multi-professional teams with appropriate
training and resources, as part of Universal Health
Coverage.
XI
ACTIONS AND RESPONSIBILITIES
FOR IMPLEMENTING THE RECOMMENDATIONS
ACTIONS AND RESPONSIBILITIES FOR:
WHO A Institutionalize a cross-cutting and life-course

approach to ending childhood obesity across all
relevant technical areas in WHO headquarters,
regional and country offices.
B Develop, in consultation with Member States, a

framework to implement the recommendations of
the Commission.
C Strengthen capacity to provide technical support for

action to end childhood obesity at global, regional
and national levels.
D Support international agencies, national

governments and relevant stakeholders in building
upon existing commitments to ensure that relevant
actions to end childhood obesity are implemented at
global, regional and national levels.
E Promote collaborative research on ending childhood

obesity with a focus on the life-course approach.
F Report on progress made on ending childhood obesity.
International A Cooperate to build capacity and support Member

organizations States in addressing childhood obesity.
Members A Take ownership, provide leadership and engage

States political commitment to tackle childhood obesity
over the long term.
B Coordinate contributions of all government sectors

and institutions responsible for policies, including,
but not limited to: education; food, agriculture;
commerce and industry; development; finance and
revenue; sport and recreation; communication;
environmental and urban planning; transport and
social affairs; and trade.
C Ensure data collection on BMI-for-age of children

– including for ages not currently monitored – and
set national targets for childhood obesity.
D Develop guidelines, recommendations or policy

measures that appropriately engage relevant
sectors – including the private sector, where
applicable – to implement actions, aimed at
reducing childhood obesity, as set out in this report.
XII
Nongovernmental A Raise the profile of childhood obesity prevention
organizations through advocacy efforts and the dissemination of
information.
B
Motivate consumers to demand that governments
support healthy lifestyles and that the food and
non-alcoholic beverage industry provide healthy
products, and do not market unhealthy foods
and sugar-sweetened beverages to children.
C Contribute to the development and

implementation of a monitoring and
accountability mechanism.
The private sector A Support the production of, and facilitate access to,
foods and non-alcoholic beverages that contribute to a
healthy diet.
B Facilitate access to, and participation in, physical activity.
Philanthropic A Recognize childhood obesity as endangering child

foundations health and educational attainment and address
this important issue.
B Mobilize funds to support research, capacity-

building and service delivery.
Academic institutions A Raise the profile of childhood obesity prevention

through the dissemination of information and
incorporation into appropriate curricula.
B Address knowledge gaps with evidence to

support policy implementation.
C Support monitoring and accountability activities.
The greatest obstacle to effective systems to track the prevalence complex issue of childhood
progress on reducing childhood of childhood obesity. These obesity. WHO, international
obesity is a lack of political systems are vital in providing organizations and their Member
commitment and a failure of data for policy development and States, as well as non-State
governments and other actors to in offering evidence of the impact actors, all have a critical role to
take ownership, leadership and and effectiveness of interventions. play in harnessing momentum
necessary actions. and ensuring that all sectors
The Commission would like remain committed to working
Governments must invest in robust to stress the importance and together to reach a positive
monitoring and accountability necessity of tackling the conclusion.
XIII
XIV
GOALS OF THE
COMMISSION
The overarching goals of the Commission on

Ending Childhood Obesity are to provide policy
recommendations to governments to prevent infants,
children and adolescents from developing obesity,
and to identify and treat pre existing obesity in
children and adolescents.
The aims are to reduce the risk of morbidity and

mortality due to noncommunicable diseases, lessen
the negative psychosocial effects of obesity both in
childhood and adulthood and reduce the risk of the
next generation developing obesity.
1
INTRODUCTION
The obesity epidemic has the middle-income countries than Many countries now face the
potential to negate many of in high-income countries (3). burden of malnutrition in all its
the health benefits that have Figure 2 shows the prevalence forms, with rising rates of childhood
contributed to the increased of overweight by WHO region obesity as well as high rates of
longevity observed in the world. and World Bank income group. child undernutrition and stunting.
In 2014, an estimated 41 million Prevalence data available for Childhood obesity is often under-
children under 5 years of age older children and adolescents recognized as a public health issue
were affected by overweight are currently being verified and in these settings, where, culturally,
or obesity (1) (defined as the are due to be released by WHO an overweight child is often
proportion of children with in 2016. To date, progress in considered to be healthy.
weight-for-height z-score values tackling childhood obesity has
more than 2 SDs and more been slow and inconsistent (4). In high-income countries, the risks
than 3 SDs, respectively, from of childhood obesity are greatest
the WHO growth standard An even greater number of in lower socioeconomic groups.
median (2)). Figure 1 shows children are, even from before Although currently the converse
the prevalence of overweight birth, on the pathway to is true in most low- and middle-
children under 5 years of age developing obesity. Children income countries, a changing
worldwide. In Africa, the number who are not yet at the body- pattern is emerging. Within
of children who are overweight mass-index (BMI)-for-age countries, certain population
or obese has nearly doubled threshold for the current subgroups, such as migrant
since 1990, increasing from definition of childhood obesity and indigenous children, are
5.4 million to 10.3 million. In or overweight may be at an at a particularly high risk of
2014, of children under 5 years increased risk of developing becoming obese (5), due to rapid
of age who were overweight, obesity. The recommendations acculturation and poor access
48% lived in Asia and 25% in in this report also address to public health information.
Africa (1). The prevalence of the needs of these children. As countries undergo rapid
infant, childhood and adolescent Undernutrition in early childhood socioeconomic and/or nutrition
obesity may be plateauing in places children at an especially transitions, they face a double
some settings, but in absolute high risk of developing obesity burden in which inadequate
numbers more overweight and when food and physical activity nutrition and excess weight gain
obese children live in low- and patterns change. co-exist (6).
2
FIGURE1:
AGE-STANDARDIZED PREVALENCE OF OVERWEIGHT IN CHILDREN UNDER 5 YEARS OF AGE,
COMPARABLE ESTIMATES, 2014
Latest Prevalence
(0) No data
(1) < 5.0%
(2) 5.0 - 9.9%
(3) 10.0 - 14.9%
(4) 15.0 - 19.9%
(5) ≥ 20%
The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the World Health Organization
concerning the legal status of any country, territory, city or area, or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent
approximate border lines for which there may not yet be full agreement. All rights reserved. Copyright – WHO 2015.
Source: Tracking tool (http://www.who.int/nutrition/trackingtool)
FIGURE2:
PREVALENCE OF OVERWEIGHT IN CHILDREN UNDER 5 YEARS OF AGE, BY WHO REGION AND
WORLD BANK INCOME GROUP, COMPARABLE ESTIMATES, 2014
14
12
10
Overweight (%)
0
AFR AMR EMR EUR SEAR WPR High Upper Lower Low
income middle middle income
income income
AFR=African Region, AMR=Region of Americas, SEAR=South-East Asia Region, EUR=European Region, EMR=Eastern Mediterranean Region, WPR=Western Pacific Region.
Source: UNICEF, WHO, The World Bank. Joint Child Malnutrition Estimates. (UNICEF, New York; WHO, Geneva; The World Bank, Washington, DC; 2015).
3
Obesity arises from a a decline in physical activity for
combination of exposure of the transport or play, have resulted
child to an unhealthy environment in energy imbalance. Children
(often called the obesogenic are exposed to ultra-processed,
environment (7)) and inadequate energy-dense, nutrient-poor
behavioural and biological foods, which are cheap and
responses to that environment. readily available. Opportunities
These responses vary among for physical activity, both in and
individuals and are strongly out of school, have been reduced
influenced by developmental or and more time is spent on screen-
life-course factors. based and sedentary leisure
activities.
Many children today are
growing up in environments Cultural values and norms
that encourage weight gain influence the perception of
and obesity. With globalization healthy or desirable body weight,
and urbanization, exposure to especially for infants, young
the obesogenic environment is children and women. In some
increasing in both high-income settings, overweight and obesity
countries and low- and middle- are becoming social norms
income countries and across all and thus contributing to the
socioeconomic groups. Changes perpetuation of the obesogenic
in food availability and type, and environment.
10.3 MILLION
In Africa, the number of children
who are overweight or obese
has nearly doubled since 1990,
increasing from 5.4 million to
10.3 million.
4
5
The risk of obesity can be passed placental insufficiency. The mother entering pregnancy with
from one generation to the next, underlying processes involve obesity or pre-existing diabetes,
as a result of behavioural and/ environmental effects on gene or developing gestational
or biological factors. Behavioural function (epigenetic effects) that diabetes. This predisposes the
influences continue through do not necessarily have obvious child to increased fat deposits
generations as children inherit effects on measures such as birth associated with metabolic disease
socioeconomic status, cultural weight (8). Children who have and obesity. This pathway
norms and behaviours, and suffered from undernutrition and may also involve epigenetic
family eating and physical activity were born with low birth weight processes. Recent research
behaviours. or are short-for-age (stunted), are indicates that paternal obesity
at far greater risk of developing can also contribute to a greater
Biological factors can lead to overweight and obesity when risk of obesity in the child (9),
an increase in the risk of obesity faced with energy-dense diets probably through epigenetic
in children through two general and a sedentary lifestyle later mechanisms. Inappropriate early
developmental pathways: in life. Attempts to deal with infant feeding also impacts on
undernutrition and stunting during the child’s developing biology.
(i) The “mismatch” pathway. childhood may have led to the Appropriate interventions before
This results from malnutrition unintended consequences of conception, during pregnancy
– sometimes subtle – during obesity risk for these children. and in infancy may prevent some
fetal and early childhood of these effects, but these may
development, due, for example, (ii) The developmental pathway. not easily be reversed once a
to poor maternal nutrition or This is characterized by the critical period of development
In absolute
numbers more
overweight and
obese children
live in low- and
middle-income
countries than
in high-income
countries.
6
has passed. Since many women education and establishing of noncommunicable diseases
do not consult a healthcare regulatory frameworks to address impair the individual’s lifetime
professional until the end of developmental and environmental educational attainment and labour
the first trimester, it is essential risks, in order to support families’ market outcomes and place a
to promote knowledge of the efforts to change behaviours. significant burden on health-care
importance of healthy behaviours Parents, families, caregivers and systems, family, employers and
in adolescents, young women and educators also play a critical society as a whole (20).
men before conception and in role in encouraging healthy
early pregnancy. behaviours. Prevention of childhood obesity
will result in significant economic
Overweight and obesity are Obesity has physical and intergenerational benefits that
not absolute cut-offs and many and psychological health currently cannot be accurately
children are on the pathway to consequences during childhood, estimated or quantified. Spill-over
obesity when they are within adolescence and into adulthood. benefits also include improved
the normal range for BMI-for- Obesity itself is a direct cause maternal and reproductive health
age. The health consequences of morbidities in childhood and a reduction in obesogenic
of overweight and obesity are including gastrointestinal, exposure for all members of
also continuous and can affect musculoskeletal and orthopaedic the population, thus further
a child’s quality of life before complications, sleep apnoea, strengthening the case for urgent
BMI-for-age cut-offs are reached. and the accelerated onset of action.
Across the distribution of BMI cardiovascular disease and
there is a trend for individuals type-2 diabetes, as well as the
to have more body fat and comorbidities of the latter two
less lean muscle mass than in noncommunicable diseases
previous generations (10). The (12). Obesity in childhood
pattern of fat deposit in the can contribute to behavioural
body is also important in terms and emotional difficulties, such
of health outcomes (11). Some as depression, and can also
population groups have more lead to stigmatization and
fat deposits and less lean muscle poor socialization and reduce
mass than others at the same educational attainment (13, 14).
BMI. Although BMI is the simplest
means to identify children who Critically, childhood obesity is a
are overweight and obese, it strong predictor of adult obesity,
does not necessarily identify which has well known health and
children with abdominal fat economic consequences, both
deposits that put them at greater for the individual and society
risk of health complications. as a whole (15, 16). Although
While new methodologies are longitudinal studies suggest that
available, such as dual-energy improving BMI in adulthood can
X-ray absorptiometry, magnetic reduce the risk of morbidity and
resonance imaging or body mortality (17), childhood obesity
impedance to measure body fat will leave a permanent imprint on
and lean mass, these are currently adult health (18).
beyond the scope of population- Childhood obesity
based surveys. Evidence on the lifetime cost of is a strong
childhood obesity is developing,
None of these upstream causal but is scarce compared with predictor of adult
factors are in the control of that on the economic burden of obesity, which has
the child. Therefore, childhood adult obesity. To date, studies
obesity should not be seen as a have concentrated primarily on well known health
result of voluntary lifestyle choices, healthcare expenditure, ignoring and economic
particularly by the younger child. other costs, including the cost of
Given that childhood obesity the accelerated onset of adult consequences,
is influenced by biological and diseases and the tendency for both for the
contextual factors, governments childhood obesity to continue
must address these issues by into adulthood with attendant
individual and
providing public health guidance, economic costs (19). Early onset society as a whole.
7
GUIDING
PRINCIPLES
THE COMMISSION The child’s right to health: A whole-of-government

AFFIRMS THE Government and society have approach: Obesity prevention
a moral responsibility to act on and treatment requires a whole-
FOLLOWING behalf of the child to reduce the of-government approach in
PRINCIPLES AND risk of obesity. Tackling childhood which policies across all sectors
STRATEGIES: obesity resonates with the systematically take health
universal acceptance of the rights into account, avoid harmful
of the child to a healthy life as health impacts and so improve
well as the obligations assumed population health and health
by State Parties to the Convention equity. The education sector
of the Rights of the Child.1 plays a critical role in providing
nutrition and health education,
Government commitment increasing the opportunities for
and leadership: Rates of physical activity and promoting
childhood obesity are reaching healthy school environments.
alarming proportions in many Agriculture and trade policies
countries, posing an urgent and the globalization of the
and serious challenge. These food system impact on food
increasing rates cannot be affordability, availability and
ignored and governments need quality at national and local
to accept primary responsibility levels. In 2013, WHO Member
in addressing this issue on behalf States adopted a resolution to
of the children they are ethically consider the interplay between
bound to protect. A failure to act international trade and health
will have major medical, social through multistakeholder
and economic consequences. dialogue.2 Urban planning
1
Committee on the Rights of the Child: General comment No. 15 (2013) on the right of the child to the enjoyment of the highest attainable standard of health (art. 24), para 47;
CRC/C/GC/15.
2
Resolution WHA59.26 on international trade and health.
8
9
and design, and transport engagement of all sectors of improvements in social and health
planning, all impact directly society at the national, regional capital, and increase inequity.
on opportunities for physical and global levels. Without
activity and access to healthy joint ownership and shared Aligning with the global
foods. Intersectoral government responsibility, well-meaning and development agenda:
structures can facilitate cost-effective interventions have The Sustainable Development
coordination, identify mutual limited reach and impact. Goals (SDG) call for an end to
interest, collaboration and malnutrition in all its forms (SDG
exchange of information through Equity: Governments should target 2.2) and a reduction
coordinating mechanisms. ensure equitable coverage of in premature mortality from
interventions, particularly for noncommunicable diseases (SDG
A whole-of-society excluded, marginalized or target 3.4). Childhood obesity
approach: The complexity of otherwise vulnerable population undermines the physical, social
obesity calls for a comprehensive groups, who are at high risk both and psychological well-being
approach involving all actors, of malnutrition in all its forms of children and is a known risk
including governments, parents, and of developing obesity. These factor for adult obesity and
caregivers, civil society, population groups often have noncommunicable diseases.
academic institutions and the poor access to healthy foods, safe Progress will be made in achieving
private sector. Moving from places for physical activity and these goals by tackling this issue.
policy to action to address preventative health services and
childhood obesity demands support. Obesity and its associated Accountability: Political and
a concerted effort and an morbidities erode the potential financial commitment is imperative
10
in combatting childhood Declaration of the High-level fundamental right to health, while
obesity. A robust mechanism Meeting of the General Assembly reducing the burden on the health
and framework is needed to on the Prevention and Control of system.
monitor policy development and Non-communicable diseases,3
implementation, thus facilitating and the Rome Declaration of the Universal Health Coverage6
the accountability of governments, Second International Conference and treatment of obesity:
civil society and the private sector on Nutrition.4 There are a number Sustainable Development Goal
on commitments made. of current WHO and other United target 3.8 calls for the achievement
Nations agencies strategies and of Universal Health Coverage
Integration into a life- implementation plans related to through integrated health services
course approach: Integrating optimizing maternal, infant and that enable people to receive a
interventions to address childhood child nutrition and adolescent continuum of health promotion,
obesity with existing WHO and health that are highly relevant to disease prevention, diagnosis,
other initiatives, using a life-course key elements of a comprehensive treatment and management,
approach, will offer additional approach to obesity prevention. over the course of a lifetime.7 As
benefits for longer-term health. Relevant principles and such, prevention of overweight
These initiatives include the United recommendations can be found and obesity and the treatment of
Nations Secretary General’s in documents providing guidance children already obese, and those
Global Strategy for Women’s, throughout the life-course.5 with overweight who are on the
Children’s and Adolescent’s Initiatives to address childhood pathway to obesity, should be
Health,1 the Every Woman, Every obesity should build upon these considered an element of Universal
Child initiative,2 the Political to help children realize their Health Coverage.
Without joint ownership and shared

responsibility, well-meaning and cost-
effective interventions have limited
reach and impact.
1
http://www.who.int/life-course/partners/global-strategy/global-strategy-2016-2030/en/.
2
http://www.everywomaneverychild.org.
3
http://www.who.int/nmh/events/un_ncd_summit2011/political_declaration_en.pdf.
4
http://www.fao.org/3/a-ml542e.pdf.
5
WHA Resolutions: WHA53.17 on Prevention and Control of Noncommunicable Diseases; WHA57.17 on the Global
Strategy on Diet, Physical Activity and Health; WHA61.14 on Prevention and Control of Noncommunicable Diseases:
Implementation of the Global Strategy; WHA63.14 on Marketing of Food and Non-alcoholic Beverages to Children;
WHA65.6 on the Comprehensive Implementation Plan on Maternal, Infant and Young Child Nutrition; and WHA66.10
on the follow-up to the Political Declaration of the High-level Meeting of the General Assembly on the Prevention and
Control of Non-communicable diseases; WHA68.19 Outcome of the Second International Conference on Nutrition.
Meeting to Develop a Global Consensus on Preconception Care to Reduce Maternal and Childhood Mortality and
Morbidity, WHO, 2013; The optimal duration of exclusive breastfeeding. Report of an expert consultation, WHO,
2001; Complementary feeding. Report of global consultation: summary of guiding principles, WHO, 2002; Global
recommendations on physical activity for health, WHO, 2012; Population-based approaches to childhood obesity
prevention, WHO, 2010; PAHO/AMRO Plan of Action for the Prevention of Obesity in Children and Adolescents, 53rd
Directing Council, 66th Session of the Regional Committee of WHO for the Americas, October 2014; Resolution EUR/
RC63/R4 Vienna Declaration on Nutrition and Noncommunicable Diseases in the Context of Health 2020; WPR/RC63.
R2 Scaling up Nutrition in the Western Pacific Region.
6
http://www.who.int/universal_health_coverage/en/.
7
United Nations General Assembly Resolution A/67/L36 Global Health and Foreign Policy.
11
STRATEGIC
OBJECTIVES
No single intervention can halt the rise of the
growing obesity epidemic. To successfully
challenge childhood obesity requires
addressing the obesogenic environment as
well as critical elements in the life-course.
TACKLE THE
OBESOGENIC
ENVIRONMENT
AND NORMS
1 2
The major goals of addressing agreements, fiscal and agricultural the feeding of children and the
the environmental components policies and food systems); the status associated with higher body
include improving healthy eating built environment (availability of mass in some population groups,
and physical activity behaviours healthy foods, infrastructure and social restrictions on physical
of children. A number of factors opportunities for physical activity activity) and family environment
influence the obesogenic in the neighbourhood); social (parental nutrition knowledge and
environment, including political norms (body weight and image behaviours, family economics,
and commercial factors (trade norms, cultural norms regarding family eating behaviours).
12
REDUCE THE RISK OF
OBESITY BY ADDRESSING
CRITICAL ELEMENTS
IN THE LIFE-COURSE
3 4 5
Developmental factors change both the biology and behaviour of individuals from
before birth and through infancy, such that they develop with a greater or lesser
risk of developing obesity. The Commission considers it essential to address both the
environmental context and three critical time periods in the life-course: preconception and
pregnancy, infancy and early childhood and older childhood and adolescence.
It is the primary responsibility at each stage of the life-course. approach can be integrated into
of governments to ensure that By focusing attention on these other components of the maternal-
policies and actions address sensitive periods of the life-course, neonatal-child health agenda,
the obesogenic environment interventions can address specific and to the broader effort to tackle
and to provide guidance and risk factors, both individually noncommunicable diseases across
support for optimal development and in combination. Such an the whole population.
13
TREAT CHILDREN
WHO ARE OBESE
TO IMPROVE THEIR
CURRENT AND
FUTURE HEALTH
6
When children are already will face different challenges

overweight or obese, additional in responding to the need for
goals include reduction in treatment services for those
the level of overweight, with obesity. However, the
improvement in obesity-related management of children with
comorbidities and improvement overweight and obesity should
in risk factors for excess weight be included in effective services
gain. The health sector in each extended under Universal Health
country varies considerably and Coverage.
ROLES AND
RESPONSIBILITIES
The Commission recognizes that local levels. They should also
the scope of potential policy gather data on nutrition, eating
recommendations to address behaviours and physical activity
childhood obesity is broad and of children and adolescents
contains a number of novel across different socioeconomic
elements, including a focus on the groups and settings. Although
life-course dimension and on the some data are collected (21),
education sector. A multisectoral there remains a significant gap
approach will be essential for for children over 5 years of age
sustained progress. that needs addressing. This data
will guide the development of
Countries should measure BMI-for- appropriate policy priorities and
age to establish the prevalence provide a baseline against which
and trends in childhood obesity to measure the success of policies
at national, regional and and programmes.
14
15
RECOMMENDATIONS
The recommendations and accompanying rationales,
presented below, were developed by the Commission
following the review of the scientific evidence, the
reports of the ad hoc working groups to the WHO
Director-General, and feedback from the regional
and online consultations. The effectiveness, cost-
effectiveness, affordability and applicability of
policies and interventions were also considered.
16
IMPLEMENT COMPREHENSIVE PROGRAMMES
1 THAT PROMOTE THE INTAKE OF HEALTHY FOODS
AND REDUCE THE INTAKE OF UNHEALTHY
FOODS AND SUGAR-SWEETENED BEVERAGES BY
CHILDREN AND ADOLESCENTS.
Nutrition information can be of trade reform can affect diet

confusing and thus poorly and nutrition transition. The
understood by many people. health and equity impacts of
Given that individuals and national and international
families choose their diets, economic agreements and
the population needs to be policies need to be considered
empowered to make healthier (22). Processed, energy-
choices about what to eat dense, nutrient-poor foods and
and provide their infants and sugar-sweetened beverages,
children. This is not possible in increasing portion size,
unless nutrition literacy is at affordable prices have
universal and provided in replaced minimally-processed
a manner that is useful, fresh foods and water in many
understandable and accessible settings at school and family
to all members of society. meals. The easy access to
energy-dense foods and sugar-
Recent trends in food sweetened beverages and
production, processing, trade, the tacit encouragement to
marketing and retailing have “size-up” through commercial
contributed to the rise in diet- promotions have contributed to
related noncommunicable the rising caloric intake in many
diseases. The potential impact populations.
RECOMMENDATIONS RATIONALE
It is not sufficient to rely on nutrient labelling or simple codes such as

1.1
traffic light labels or health star ratings. All governments must lead in
Ensure that appropriate developing and disseminating appropriate and context-specific food-
and context specific based dietary guidelines for both adults and children. The necessary
nutrition information and information should be provided through media and educational outlets
guidelines for both adults and public health messaging in ways that reach all segments of the
and children are developed population, such that all of society is empowered to make healthier
and disseminated in a choices.
simple, understandable and
accessible manner to all As children enter school, health and nutrition literacy should be
groups in society. included in the core curriculum and supported by a health-promoting
school environment (see recommendations for early childhood, school-
age children and adolescents).
17
1.2 The adoption of fiscal measures for obesity prevention has received
a great deal of attention (23) and is being implemented in a
Implement an effective number of countries.1 Overall, the rationale for taxation measures
tax on sugar-sweetened to influence purchasing behaviours is strong and supported by the
beverages. available evidence (24, 25). Further evidence will become available
as countries that implement taxes on unhealthy foods and/or sugar-
sweetened beverages monitor their progress.2 The Commission
believes there is sufficient rationale to warrant the introduction of an
effective tax on sugar-sweetened beverages.
It is well established that the consumption of sugar-sweetened

beverages is associated with an increased risk of obesity (26, 27).
Consumption patterns may vary in different settings (28) and more
detail is needed about the patterns of intake in children in different
settings. Low-income consumers and their children have the greatest
risk of obesity in many societies and are most influenced by price.
Fiscal policies may encourage this group of consumers to make
healthier choices (provided healthier alternatives are made available)
as well as providing an indirect educational and public health signal
to the whole population.
Available evidence indicates that taxes on products such as sugar-

sweetened beverages are the most feasible to implement with data
indicating an impact on consumption.
Some countries may consider taxes on other unhealthy foods, such as

those high in fats and sugar. Taxing energy-dense, nutrient-poor foods
would require the development of nutrient profiles (29) and modelling
suggests this may reduce consumption.
1.3 There is unequivocal evidence that the marketing of unhealthy foods

and sugar-sweetened beverages is related to childhood obesity (30,
Implement the Set of 31). Despite the increasing number of voluntary efforts by industry,
Recommendations on the exposure to the marketing of unhealthy foods remains a major issue
Marketing of Foods and demanding change that will protect all children equally. Any attempt
Non-alcoholic Beverages to tackle childhood obesity should, therefore, include a reduction in
to Children to reduce the exposure of children to, and the power of, marketing.
exposure of children and
adolescents to, and the Settings where children and adolescents gather (such as schools and
power of, the marketing of sports facilities or events) and the screen-based offerings they watch
unhealthy foods. or participate in, should be free of marketing of unhealthy foods and
sugar-sweetened beverages. The Commission notes with concern the
failure of Member States to give significant attention to Resolution
WHA 63.14 endorsed by the World Health Assembly in 20103
and requests that they address this issue. Parents and caregivers are
increasingly the target of marketing for foods and beverages high in
fats and sugar, aimed at their children (32).
1
http://www.wcrf.org/int/policy/nourishing-framework/use-economic-tools.
2
See preliminary data on Mexico tax on sugar-sweetened beverages which has been submitted for publication (http://www.insp.mx/epppo/blog/3666-reduccion-consumo-bebidas.html).
3
WHA63.14 on the Marketing of Food and Non-alcoholic Beverages to Children.
18
1.4 There is wide variation in the types of business, attitudes and

behaviour within the food and non-alcoholic beverage, retail
Develop nutrient-profiles to and marketing industries. Even voluntary initiatives must conform
identify unhealthy foods and to guidelines determined by government and must be subject to
beverages. independent audit. Governments must define clear parameters,
enforcement and monitoring mechanisms and, if necessary, consider
regulatory and statutory approaches. Regulation would provide equal
1.5 protection to all children regardless of socioeconomic group and
ensure equal responsibility by large, regional, multinational and small
Establish cooperation
local producers and retailers.
between Member States
to reduce the impact of
Clarity on the range of healthy products that can be marketed without
cross-border marketing
restriction is needed, as is consideration of both direct and indirect
of unhealthy foods and
marketing strategies, including pricing, promotion (including portion-
beverages.
size promotion) and placement. Such approaches require identifying
healthy and unhealthy foods using independent nutrient profiling.
These considerations must also take into account issues of food
security, where this is relevant, either at a national, sub-national or
sub-population level.
The WHO Framework for implementing the set of recommendations

on the marketing of foods and non-alcoholic beverages to children
(33) provides practical guidance to Member States on the
development and implementation of policy and monitoring and
evaluation frameworks.
The Commission recognizes that in certain settings adolescents

consume alcohol, and that alcohol is particularly obesogenic.
Although this is beyond their scope of work, the Commission notes
that it is very difficult to market alcoholic products targeted at young
adult consumers, in particular, without exposing cohorts of adolescents
under the legal age to the same marketing. The exposure of children
and young people to appealing marketing is of particular concern.
A precautionary approach to protecting young people against the
marketing of such products is needed.
1.6 A standardized system of food labelling, as recommended by the

Codex Alimentarius Commission1 can support nutrition and health
Implement a standardized literacy education efforts, if mandatory for all packaged foods and
global nutrient labelling beverages.
system.
1
WHA56.23 Joint FAO/WHO evaluation of the work of the Codex Alimentarius Commission.
19
Healthy eating habits can be nurtured from infancy and have both
1.7
biological and behavioural dimensions. This requires caregiver
Implement interpretive front- understanding of the relationship between diet and health, and
of-pack labelling supported behaviours to encourage and support the development of such healthy
by public education of both habits. Simple, easy to understand food labelling systems can support
adults and children for nutrition education and help caregivers and children to make healthier
nutrition literacy. choices.
1.8 Nutrition and food literacy and knowledge will be undermined if

there are conflicting messages in the settings where children gather.
Require settings such as Schools, child-care and sports facilities should support efforts to
schools, child-care settings, improve children’s nutrition by making the healthy choice the easy
children’s sports facilities and choice and not providing or selling unhealthy foods and beverages.
events to create healthy food
environments.
1.9 Nutrition literacy and knowledge of healthy food choices also cannot
be acted upon if such foods are not readily available or affordable.
Increase access to healthy Influencing the food environment requires a collaborative approach
foods in disadvantaged to food production, processing, accessibility, availability and
communities. affordability. Where access to healthy foods is limited, ultra-processed
foods are often the only available and affordable alternatives. A
number of public and private sector initiatives to promote healthier
food behaviours have been developed and the limited evidence
available indicates the potential to promote healthier choices among
consumers (34). Such initiatives, where they are supported by
evidence, are to be encouraged.
20
2 THAT PROMOTE PHYSICAL ACTIVITY AND REDUCE
SEDENTARY BEHAVIOURS IN CHILDREN AND
ADOLESCENTS.
Recent evidence shows that Urban planning and design has

physical activity declines from the potential to both contribute
the age of school entry (35). to the problem and offer the
Globally, in 2010, 81% of opportunity to form part of the
adolescents aged 11–17 years solution. Increased recreational
were insufficiently physically space and safe walking-
active. Adolescent girls were and cycling-paths for active
less active than adolescent transport, help make physical
boys, with 84% of girls and activity functions of daily life.
78%1 of boys not attaining
the 60 minutes of moderate to Physical activity behaviours
vigorous physical activity daily across the life-course can be
as recommended by WHO heavily influenced by childhood
(36). Low physical activity is experience. Creating safe,
rapidly becoming the social physical activity-friendly
norm in most countries, and communities, which enable,
is an important factor in the and encourage the use of active
obesity epidemic. Physical transport (walking, cycling etc.)
activity can reduce the risk and participation in an active
of diabetes, cardiovascular lifestyle and physical activities,
disease and cancers (37), and will benefit all communities.
improve children’s ability to Particular attention needs to
learn, their mental health and be given to improving access
well-being. Recent evidence to, and participation in,
suggests that obesity, in turn, physical activity for children
reduces physical activity, already affected by overweight
creating a vicious cycle of and obesity, disadvantaged
increasing body fat levels and children, girls and children with
declining physical activity. disabilities.
81%
of adolescents do not achieve
the recommended 60 minutes
of physical activity each day.
1
http://apps.who.int/gho/data/view.main.2482ADO?lang=en.
21
2.1 All members of society, including parents, need to appreciate the

importance of both adequate growth and the consequences of
Provide guidance to excess body fat deposition to the short-term and long-term health
children and adolescents, and well-being of the child. The Commission recognizes that in
their parents, caregivers, some cultures this may be in conflict with traditional perceptions and
teachers and health practice.
professionals on healthy
body size, physical activity, Physical activity provides fundamental health benefits for children
sleep behaviours and and adolescents, including increased cardiorespiratory and muscular
appropriate use of screen- fitness, reduced body fatness and enhanced bone health.
based entertainment.
Context-specific guidance on how to achieve physical activity

2.2
recommendations and the appropriate number of hours that
Ensure that adequate children should sleep or watch television (38–40), for example,
facilities are available should be a component of any healthy-living education provided to
on school premises and children or caregivers.
in public spaces for
physical activity during Increasing the opportunities for safe, appropriate and gender-
recreational time for all friendly structured and unstructured physical activity, both in and
children (including those out of school, including active transport (walking and cycling), will
with disabilities), with the have positive health, behavioural and educational spill-over effects
provision of gender-friendly for all children and adolescents.
spaces where appropriate.
Physical activity can reduce

the risk of diabetes,
cardiovascular disease and
cancers, and improve children’s
ability to learn, their mental
health and well-being.
22
23
INTEGRATE AND STRENGTHEN GUIDANCE FOR
3 NONCOMMUNICABLE DISEASE PREVENTION
WITH CURRENT GUIDANCE FOR PRECONCEPTION
AND ANTENATAL CARE, TO REDUCE THE RISK OF
CHILDHOOD OBESITY.
The care that women receive to include advice to would-be

before, during and after fathers.
pregnancy has profound
implications for the later health Current guidance for
and development of their preconception and antenatal
children. Timely and good-quality care focuses on the prevention
care throughout these periods of fetal undernutrition. Given
provides important opportunities changing obesogenic exposures,
to prevent the intergenerational guidelines are needed that
transmission of risk and has a address malnutrition in all
high impact on the health of its forms (including caloric
the child throughout the life- excess) and later obesity risk in
course.1 Evidence shows that the offspring. Interventions to
maternal undernutrition (whether address childhood obesity risk
global or nutrient-specific), factors also prevent other adverse
maternal overweight or obesity, pregnancy outcomes (47) and so
excess pregnancy weight gain, contribute to improving maternal
maternal hyperglycaemia and newborn health. Maternal
(including gestational diabetes), overweight and obesity increase
smoking or exposure to toxins the risk of complications during
can increase the likelihood pregnancy, labour and delivery
of obesity during infancy and (including stillbirth), and maternal
childhood (41–46). Evidence undernutrition increases the risk
is emerging that the health of of low birth weight. These factors
fathers at the time of conception can put the child at greater risk of
can influence the risk of obesity infant mortality, childhood obesity
in their children (9). Healthy and adult noncommunicable
lifestyle guidance thus needs diseases.
The care that a woman

receives before, during and
after pregnancy has profound
implications for the later health
and development of her child.
1
Committee on the Rights of the Child: General comment No. 15 (2013) on the right of the child to the enjoyment of the highest attainable standard of health (art. 24), para 53;
CRC/C/GC/15.
24
There is a need for screening and appropriate management of pre-

3.1
existing diabetes mellitus and hypertension in pregnant women; early
Diagnose and manage diagnosis and effective management of gestational diabetes and
hyperglycaemia and pregnancy-induced hypertension, depression and mental health issues;
gestational hypertension. gestational weight gain pattern (48); and ensuring dietary quality and
appropriate physical activity.
3.2
Monitor and manage

appropriate gestational
weight gain.
3.3 Interventions that integrate guidance related to all forms of malnutrition

should address undernutrition and unbalanced diets, including excess
Include an additional focus nutrition and specific nutrition deficiencies (49). Young people are
on appropriate nutrition often unaware of what constitutes a healthy diet. This highlights the
in guidance and advice need for governments to take leadership in ensuring nutrition and food
for both prospective literacy.
mothers and fathers before
conception and during There is evidence for the beneficial effects of appropriate exercise
pregnancy. programmes in pregnancy on maternal BMI, gestational weight gain
and birth outcomes, which are linked to a later risk of childhood
obesity (50).
3.4
There is limited, but growing, evidence that paternal health prior to
Develop clear guidance and
conception has some impact on offspring health (9). There are, thus,
support for the promotion of
direct reasons to also target paternal behaviour and health.
good nutrition, healthy diets
and physical activity, and
for avoiding the use of and
exposure to tobacco, alcohol,
drugs and other toxins.
25
PROVIDE GUIDANCE ON AND SUPPORT FOR
4 HEALTHY DIET, SLEEP AND PHYSICAL ACTIVITY IN
EARLY CHILDHOOD TO ENSURE CHILDREN GROW
APPROPRIATELY AND DEVELOP HEALTHY HABITS.
The first years of life are critical risk factors for childhood obesity.
in establishing good nutrition Encouraging the intake of a variety
and physical activity behaviours of healthy foods, rather than
that reduce the risk of developing unhealthy, energy-dense, nutrient-
obesity. Exclusive breastfeeding poor foods and sugar-sweetened
for the first six months of life, beverages, during this critical
followed by the introduction of period supports optimal growth and
appropriate complementary foods, development. Health-care providers
is a significant factor in reducing can use routine growth monitoring
the risk of obesity (51). Appropriate opportunities to track children’s
complementary feeding with BMI-for-age and give appropriate
continued breastfeeding can reduce advice to caregivers to help prevent
the risk of undernutrition and excess children developing overweight
body fat deposition in infants, both and obesity.
26
Breastfeeding is core to optimizing infant development, growth and

4.1
nutrition and may also be beneficial for postnatal weight management
Enforce regulatory in women.
measures such as The
International Code of Given the changes in women’s lifestyles and roles, the ability to
Marketing of Breast- breastfeed outside of the home, and to sustain breastfeeding when a
milk Substitutes1 and mother returns to work, are critical to achieving the recommendations.
subsequent World Health
Assembly resolutions.2 Policies that establish the rights of women and the responsibilities of
employers are needed and some are in place. However, to protect
all mothers and infants, regardless of social or economic status, these
4.2 should be universal.
Ensure all maternity
facilities fully practice the
Ten Steps to Successful
Breastfeeding.3
4.3
Promote the benefits of

breastfeeding for mother
and child through broad-
based education to parents
and the community at
large.
4.4
Support mothers to
breastfeed, through
regulatory measures
such as maternity leave,
facilities and time for
breastfeeding in the work
place.4
1
WHA34.22 International Code of Marketing of Breast-milk Substitutes.
2
WHA35.26, WHA37.30, WHA39.28, WHA41.11, WHA43.3, WHA45.34, WHA47.5, WHA49.15, WHA54.2, WHA55.25, WHA58.32, WHA59.21, WHA61.20 and WHA63.23 on
Infant and Young Child Nutrition; WHA65.6 Comprehensive Implementation Plan on Maternal, Infant and Young Child Nutrition.
3
WHO UNICEF Baby-Friendly Hospital Initiative, 1991, updated 2009 (http://www.who.int/nutrition/publications/infantfeeding/bfhi_trainingcourse/en/).
4
International Labour Organization, Maternity Protection Convention 183, 2000.
27
4.5 Established global guidance for infant and young child feeding
primarily targets undernutrition. It is also important to consider the
Develop regulations on the risks created by unhealthy diets in infancy and childhood.
marketing of complementary
foods and beverages, in line Guidelines that address both undernutrition and obesity risk are
with WHO recommendations, clearly needed for countries where there is malnutrition in all its
to limit the consumption of forms (32).
foods and beverages high in
fat, sugar and salt by infants Current complementary feeding guidelines (52) provide guidance
and young children. on the timing of introduction, responsive feeding, quantity and
types of foods needed.
4.6 Family attitudes to eating and perceptions of ideal body weight are
important determinants of complementary feeding behaviours and
Provide clear guidance and
need to be considered.
support to caregivers to
avoid specific categories Recent evidence shows that sensory experiences related to food
of foods (e.g. sugar- begin in utero and continue during breastfeeding, and that the
sweetened milks and fruit flavours of foods mothers eat are transmitted to their infants. This
juices or energy-dense, and appropriate complementary feeding can play an important
nutrient-poor foods) for role in establishing food preferences and appetite control.
the prevention of excess Encouraging healthy food variety in children through repeated,
weight gain. positive exposure to new foods (53), seeing caregivers and family
members enjoy healthy foods, and limiting their exposure to
4.7 unhealthy foods (that may lead to preferences for very sweet foods
and drinks), all help develop good food habits in children and their
Provide clear guidance and families (54).
support to caregivers to
encourage the consumption
of a wide variety of healthy
foods.
Breastfeeding is core to
optimizing infant development,
growth and nutrition.
28
4.8 There is evidence that poor sleeping patterns, low physical activity
and an excess number of hours spent on screen-based entertainment
Provide guidance to are associated with increased risk of obesity in childhood (38–40).
caregivers on appropriate The evidence to support early interventions to prevent obesity in high-
nutrition, diet and portion income countries is still emerging, but looks very promising. Evidence
size for this age group. supports interventions in pre-school and child-care settings for children
aged 2–5 years for early child feeding, activity patterns, media
exposures and sleep that help to promote healthy behaviours and
4.9 weight trajectories in this period of life (55).
Ensure only healthy foods,
Several strategies in this age group have also supported parents
beverages and snacks are
and caregivers to ensure appropriate television/screen viewing,
served in formal child-care
encourage active play, establish healthy eating behaviours and diets,
settings or institutions.
promote healthy sleep routines and role-model healthy caregiver and
family lifestyle (55).
4.10
The evidence shows that interventions to improve child nutrition, sleep
Ensure food education and physical activity are most effective if these are comprehensive and
and understanding are involve caregivers and the community at large (55). Societal changes
incorporated into the and transitions require a more deliberate and concerted interventions,
curriculum in formal including support for parents and other caregivers to enable them to
child-care settings or contribute to the recommended behaviour changes.
institutions.
4.11
Ensure physical activity is

incorporated into the daily
routine and curriculum in
formal child-care settings
or institutions.
4.12
Provide guidance on
appropriate sleep time,
sedentary or screen-time and
physical activity or active
play for the 2–5 years of age
group.
4.13
Engage the whole-of-the-
community to support
caregivers and child-care
settings to promote healthy
lifestyles for young children.
29
5 THAT PROMOTE HEALTHY SCHOOL
ENVIRONMENTS, HEALTH AND NUTRITION
LITERACY AND PHYSICAL ACTIVITY AMONG
SCHOOL-AGE CHILDREN AND ADOLESCENTS.
School-age children and (e.g. reading, science); and c)

adolescents, whether in formal positioning of school-based efforts
education or out of school, face within the context of broader
particular challenges. They educational and community
are highly susceptible to the efforts.
marketing of unhealthy foods
and sugar-sweetened beverages, To be successful, programmes
peer pressure and perceptions of to improve the nutrition and
ideal body image. Adolescents, physical activity of children and
in particular, may have more adolescents need to engage with
freedom in food and beverage a number of stakeholders. Obesity
choices made outside the home. prevention and health promotion
Physical activity often also has traditionally been the remit
declines at this age. of ministries of health. Key to
success will be the integration of
Although a significant number activities into a health-promoting
of school-age children are school initiative, with active
unfortunately not in formal engagement of the education
education, the compulsory school sector. Interventions that will be
years provide an easy entry incorporated into the school day
point to engage this age group or curriculum will then be seen as
and embed healthy eating and part of their own remit. The most
physical activity habits for lifetime frequently mentioned challenge
obesity prevention. Given that to implementation is competition
governments in most countries with the schools’ primary
control the education sector, mission (55). By appropriate
effective collaboration between engagement with teachers, such
health and education can ensure education can be integrated
that school environments are effectively into mainstream topics,
healthy environments, where both rather than requiring separate
nutrition literacy and physical time allocation. Collaboration
activity are promoted. To ensure and exchange of information, the
equity, further attention is needed use evidence-based approaches
to develop programmes to reach appropriately adapted to context,
children and adolescents outside and resource-sharing between
formal education. education and health ministries
will help to move this agenda
There is a growing evidence forward.
base to support interventions for
children and adolescents in school Older children and adolescents
settings and the wider community also need to be engaged in the
as an obesity prevention strategy development and implementation
(23). Qualitative assessments of interventions to reduce
suggest that their effectiveness childhood obesity (56). Only
on obesity prevention behaviours through their active contribution
and outcomes is related to: a) in the process will interventions
quality of implementation; b) be shaped to meet their specific
the educational rigour of the needs, such that they, and their
programme and its integration peers, can fully participate and
within mainstream curricula benefit.
30
5.1 Energy-dense, nutrient-poor foods and sugar-sweetened beverages

are important drivers of the obesity epidemic in school-age children
Establish standards for and adolescents globally, acting both to induce and maintain
meals provided in schools, overweight and obesity. It is a paradox to encourage and educate
or foods and beverages children on healthy behaviours, while allowing inappropriate foods
sold in schools, that meet and beverages to be sold or marketed within the school environment.
healthy nutrition guidelines. To establish healthier behavioural norms and make the environment
less obesogenic it is necessary to reduce access to, or provision of,
unhealthy foods and sugar-sweetened beverages in places where
5.2 children gather.
Eliminate the provision or
This strategy must go hand-in-hand with increasing access to,
sale of unhealthy foods,
and promotion of, lower energy density foods and to water as an
such as sugar-sweetened
alternative to sugar-sweetened beverages.
beverages and energy-
dense, nutrient-poor foods,
It may be possible to establish zones around schools where the sale
in the school environment.
of unhealthy foods and beverages is restricted, but the Commission
recognizes that this may not be feasible in a number of settings.
5.3
Ensure access to potable water

in schools and sports facilities.
Understanding the role of nutrition in good health is central to the

5.4
success of interventions to improve diet. As adolescents are the next
Require inclusion of nutrition generation of parents, the importance of health and nutrition literacy
and health education within during adolescence cannot be overestimated – indeed the school
the core curriculum in years and the mainstream curricula offer important opportunities for
schools. progress. Life-course education in schools should be co-constructed
with teachers, according to educational criteria and embedded in
core curricula subjects.
5.5
Effective nutrition literacy goes beyond knowledge to actual behaviour
Improve the nutrition literacy
change. Although there is evidence of the effectiveness of interventions
and skills of parents and
to improve nutrition knowledge and understanding, the impact of these
caregivers.
interventions on dietary behaviour is less clear. Combining nutrition
literacy interventions and clear context-specific nutrition advice to
5.6 children and their caregivers and providing additional knowledge
on food preparation in the context of an improved obesogenic
Make food preparation environment, would enable children, adolescents and their parents/
classes available to children, caregivers to make healthier choices.
their parents and caregivers.
Regular participation in quality physical education and other forms of

5.7 physical activity can improve a child’s attention span, enhance their
Include Quality Physical cognitive control and processing (57). It can challenge stigma and
Education1 in the school stereotypes, reduce symptoms of depression and improve psychosocial
curriculum and provide outcomes. It is important that school-based physical education is
adequate and appropriate inclusive of all children, of all abilities, rather than focused on the
staffing and facilities to potential elite sportsperson.
support this.
1
UNESCO Quality physical education (QPE). Guidelines for policy-makers, Paris 2015.
31
PROVIDE FAMILY-BASED, MULTICOMPONENT
6 LIFESTYLE WEIGHT MANAGEMENT SERVICES FOR
CHILDREN AND YOUNG PEOPLE WHO ARE OBESE.
When children are already to identify children at risk of

overweight or obese additional developing obesity. Low-energy
goals include reduction in the diets can be effective in the short
level of overweight, improvement term for the management of
in obesity-related comorbidities obesity, but reducing inactivity
and improvement in risk factors and increasing physical activity
for excess weight gain. The will increase the effectiveness
health sector in each country of interventions. There is little
varies considerably and will written on models of health
face different challenges in service delivery for the provision
responding to the need for of obesity treatment in children
treatment services for those and adolescents, but it is clear
with obesity. However, the that these efforts can only be
management of children with effective with the involvement
overweight and obesity should of the whole family or care
be included in effective services environment.
extended under Universal Health
Coverage. Health workers and others may
discriminate against children
Primary health-care services who are overweight or obese.
are important for the early All such forms of discrimination
detection and management are unacceptable and must be
of obesity and its associated eliminated (58). The mental
complications, such as diabetes. health needs of children,
Regular growth monitoring at the including issues of stigmatization
primary health-care facility or at and bullying, need to be given
school provides an opportunity special attention.
Evidence reviews of childhood obesity show that family-focused

6.1
behavioural lifestyle interventions can lead to positive outcomes in
Develop and support weight, BMI and other measures of body fatness. This is the case
appropriate weight for both children and adolescents (59). Such an approach is the
management services for foundation for all treatment interventions. However, very few studies
children and adolescents have been undertaken in low- and middle-income countries.
who are overweight or
obese that are family- For the morbidly obese child, in the face of failure of life-style
based, multicomponent modification, pharmacological and/or surgical options may be
(including nutrition, necessary (60).
physical activity and
psychosocial support) Health professionals and all those providing services to children and
and delivered by multi- adolescents need appropriate training on nutrition and diet, physical
professional teams with activity and the risk factors for developing obesity.
appropriate training and
resources, as part of
Universal Health Coverage.
32
ACTIONS AND RESPONSIBILITIES
FOR IMPLEMENTING
THE RECOMMENDATIONS
The Commission recognizes that successful implementation of the recommendations requires
the committed input, focus and support of a number of agencies. Necessary actions and
responsibilities would involve the following:
WHO
ACTION RATIONALE
It is essential that momentum is maintained to address this complex

A
and critical issue. WHO can lead and convene high-level dialogue
Institutionalize a cross- within the United Nations system and with and between Member
cutting and life-course States, to build upon the commitments made in the Sustainable
approach to ending Development Goals, the Political Declaration of the High-level meeting
childhood obesity across all of United Nations General Assembly on the Prevention and Control
relevant technical areas in of Non-communicable diseases, the Rome Declaration of the Second
headquarters, regional and International Conference on Nutrition and others, to address the
country offices. actions detailed in this report to end childhood obesity.
Using its normative function, both globally and through its network of
B regional and country offices, WHO can provide technical assistance
by developing or building on guidelines, tools and standards to
Develop, in consultation
support the recommendations of the Commission and other relevant
with Member States, a
WHO mandates at country level.
framework to implement
the recommendations of the
WHO can disseminate guidance for implementation, monitoring and
Commission.
accountability, and monitor and report on progress to end childhood
obesity.
C
Strengthen capacity to
provide technical support
for action to end childhood
obesity at global, regional
and national levels.
D
Support international
agencies, national
governments and relevant
stakeholders in building
upon existing commitments
to ensure that relevant
actions to end childhood
obesity are implemented
at global, regional and
national level.
33
ACTION RATIONALE
Promote collaborative
research on ending childhood
obesity with a focus on the
life-course approach.
Report on progress made on

ending childhood obesity.
International organizations
ACTION RATIONALE
A Cooperation between international organizations including other United

Nations agencies can promote the establishment of global and regional
Cooperate to build capacity partners and networks for advocacy, resource mobilization, capacity-
and support Member States in building and collaborative research. The United Nations Inter-Agency
addressing childhood obesity. Task Force on noncommunicable diseases can support Member States in
addressing childhood obesity.
Members States
ACTION RATIONALE
A Governments hold the ultimate responsibility in ensuring their

citizens have a healthy start in life. Thus, taking an active role to
Take ownership, provide address childhood obesity should not be interpreted as interference
leadership and make political with individual choice, rather as the state taking ownership of
commitment to tackle childhood the development of their human capital. It is clear that to address
obesity over the long term. childhood obesity effectively, the active engagement of multiple
agencies of government is needed. There is an understandable
tendency to see obesity as a problem for the health sector. However,
B
preventing childhood obesity requires the coordinated contributions
of all government sectors and institutions responsible for policies.
Coordinate contributions of
Governments must establish appropriate whole-of-government
all government sectors and
approaches to address childhood obesity. Further, regional and local
institutions responsible for
governments must understand their obligations and harness resources
policies, including, but not
and efforts to ensure a coordinated and comprehensive response to
limited to: education; food;
the issue.
agriculture; commerce and
industry; development;
finance/revenue; sport and
recreation; communication;
environmental and urban
planning; transport and social
affairs; and trade.
34
ACTION RATIONALE
Using these data, governments can establish obesity

C
targets and intermediate milestones, consistent with the
Ensure data collection on global nutrition and noncommunicable disease targets
BMI-for-age of children established by the World Health Assembly. They should
– including for ages not include in their national monitoring frameworks agreed
currently monitored – and international indicators for obesity outcomes (to track
set national targets for progress in achieving national targets), diet and physical
childhood obesity. activity programme implementation (including coverage
of interventions) and the obesity policy environment
D
(including institutional arrangements, capacities
and investments in obesity prevention and control).
Monitoring should be conducted, to the fullest possible
Develop guidelines,
extent, through existing monitoring mechanisms.
recommendations or policy
measures that appropriately
engage relevant sectors –
including the private sector,
where applicable – to
implement actions, aimed at
reducing childhood obesity,
as set out in this report.
NON-STATE ACTORS
There are many ways in which non- As this report shows, the risk school and social environment, by
State actors can play an important of childhood obesity is greatly cultural attitudes to body image, by
and supportive role in addressing influenced by food, physical activity the behaviour of adults and by the
the challenge of childhood obesity. and eating behaviours, by the conduct of the private sector.
Nongovernmental organizations
ACTION RATIONALE
A Although building the policy framework is undertaken by government,

in some countries developing nutrition information and education
Raise the profile of childhood campaigns, implementing programmes, and monitoring and holding
obesity prevention through actors to account for commitments made, may be tasks shared between
advocacy efforts and the government and civil society.
dissemination of information.
Social movements can engage members of the community and provide
a platform for advocacy and action.
B
Motivate consumers to demand

that governments support
healthy lifestyles and that
the food and non-alcoholic
beverage industry provide
healthy products, and do not
market unhealthy foods and
sugar-sweetened beverages to
children.
35
ACTION RATIONALE
Contribute to the
development and
implementation of
a monitoring and
accountability mechanism.
The private sector
ACTION RATIONALE
The private sector is not a homogeneous entity and includes the

A
agricultural food production sector, the food and non-alcoholic beverage
Support the production of, industry, retailers, catering companies, sporting-goods manufacturers,
and facilitate access to, advertising and recreation businesses, and the media. It is, therefore,
foods and non-alcoholic important to consider those entities whose activities are directly or
beverages that contribute to indirectly related to childhood obesity either positively or negatively.
a healthy diet. Countries need to engage constructively with the private sector to
encourage implementation of policies and interventions.
B The Commission is aware of a number of private sector initiatives that

have the potential to impact positively on childhood obesity. These need
Facilitate access to, and
to be encouraged where they are supported by an evidence base. As
participation in, physical
many companies operate globally, international collaboration is vital.
activity.
However, attention must also be given to local and regional entities and
artisans. Cooperative relationships with industry have already led to some
encouraging outcomes related to diet and physical activity. Initiatives by
the food manufacturing industry to reduce fat, sugar and salt content,
and portion sizes of processed foods, and to increase the production of
innovative, healthy and nutritious choices, could accelerate health gains
worldwide.
The Commission believes that real progress can be made by constructive,

transparent and accountable engagement with the private sector.
36
Philanthropic foundations
ACTION RATIONALE
Philanthropic foundations are uniquely placed to make significant

A
contributions to global public health and can also engage in
Recognize childhood obesity monitoring and accountability activities.
as endangering child health
and educational attainment
and thus address this
important issue.
Mobilize funds to support

research, capacity-building
and service delivery.
Academic institutions
ACTION RATIONALE
Academic institutions can contribute to addressing childhood obesity

A
through studies on biological, behavioural and environmental risk factors
Raise the profile of and determinants, and the effectiveness of interventions in each of these.
childhood obesity
prevention through the
dissemination of information
and incorporation into
appropriate curricula.
Address knowledge gaps

with evidence to support
policy implementation.
C
Support monitoring and
accountability activities.
37
MONITORING AND
ACCOUNTABILITY
The greatest risk to effective therefore begin with the adoption currently exist which countries
progress on childhood obesity of meaningful policies that give could draw upon and integrate
is a lack of political commitment clear guidance on the actions into a comprehensive national
and that governments and required and the timeframe for monitoring framework for
other actors will fail to take doing so. childhood obesity. These include
ownership, leadership and the the Global Monitoring Framework
necessary actions. A whole Governments should prioritize for Noncommunicable Diseases1
of society approach offers the investment in building robust and the Global Monitoring
best opportunity for addressing systems with specific indicators Framework for Maternal, Infant
childhood obesity. Both that measure childhood obesity and Young Child Nutrition.2
governments and other actors, and related determinants (such
notably, civil society can hold as fitness and nutrition) in a National strategic leadership
each other and private sector standardized manner. This is includes establishing the
entities to account, to ensure they critical to demonstrating the scale governance structures across
adopt policies and comply with of the problem, providing data a variety of sectors that are
standards. Strong commitments for setting national targets and necessary to manage the
must be accompanied by strong guiding policy development. development and implementation
implementation systems and Well established monitoring of laws, policies and
well-defined accountability systems can provide evidence programmes. National leadership
mechanisms. of the impact and effectiveness is also necessary to manage
of interventions in reducing the engagement with non-State
Governments bear primary prevalence of childhood obesity. actors, such as nongovernmental
responsibility for setting the policy organizations, the private
and regulatory framework for The Commission is aware that sector and academic institutions
the prevention and management governments do not want to to successfully implement
of childhood obesity at the increase the reporting burden. A programmes, activities and
country level. Accountability must number of monitoring mechanisms investments.
1
WHA66.8 Global Monitoring Framework for Noncommunicable Diseases.
2
WHA68.9 Indicators for the Global Monitoring Framework for Maternal, Infant and Young Child Nutrition.
38
A whole-of-government approach sector (including retailers, food in ensuring accountability.
requires that a clear chain of manufacturers, food services, While these examples do not
responsibility and accountability insurers) to address obesity that cover all potential accountability
is established and that relevant are supported by an independent mechanisms, optimal results will
institutions, tasked with developing evidence base, should be be achieved by using a mix of
or implementing interventions, considered. Conflict of interest risks accountability tools and strategies.
are held accountable for the need to be identified, assessed
performance of those tasks. and managed in a transparent The Commission has noted
and appropriate manner. Codes the important influence that
Civil society can play a critical of conduct and independently trade policies can have on the
role in bringing social, moral and audited assessments of compliance obesogenic environment. This
political pressure on governments with government oversight are is particularly the case for small
to fulfil their commitments (61). therefore important. island states that are highly
Ending childhood obesity should dependent on imported foods
now form part of civil society’s Governments can use their and where the nature of the
agenda for advocacy and regulatory power to improve the food supply and pricing are
accountability. food environment, to enforce largely determined by the trade
regulatory standards, to implement dynamics. The Commission
The Commission recognizes the internationally-recognized acknowledges the complexity of
important role the private sector standards such as the WHO international trade, particularly
can play in addressing childhood International Code of Marketing in food and agricultural products,
obesity but that additional of Breast-milk Substitutes,1 and the but urges Member States and
accountability strategies, including WHO Set of Recommendations on those involved in international
legal, market-based and media- the Marketing of Foods and Non- trade arrangements to seek ways
based mechanisms (62) are often alcoholic Beverages to Children.2 to address the trade issues that
necessary. Initiatives of the private Scorecards can be useful tools impact on child obesity.
The greatest risk to

effective progress
on childhood
obesity is a
lack of political
commitment and
that governments
and other actors
will fail to take
ownership,
leadership and the
necessary actions.
1
WHA34.22 International Code of Marketing of Breast-
milk Substitutes.
2
WHA63.14 Marketing of Food and Non-alcoholic
Beverages to Children.
39
CONCLUSIONS
Childhood obesity undermines the physical,

social and psychological well-being of children
and is a known risk factor for adult obesity and
noncommunicable diseases. There is an urgent need
to act now to improve the health of this generation
and the next.
The Commission recognizes that the scope of

potential policy recommendations to address
childhood obesity is broad and contains a number
of novel elements. However, it is only by taking a
multisectoral approach through a comprehensive,
integrated package of interventions that address the
obesogenic environment, the life-course dimension
and the education sector, that sustained progress can
be made. This requires government commitment and
leadership, long-term investment and engagement of
the whole of society to protect the rights of children to
good health and well-being. The Commission believes
that progress can be made if all actors remain
committed to working together towards a collective
goal of ending childhood obesity.
40
41
REFERENCES
1. UNICEF, WHO, World Bank. Levels 6. Food and Agriculture Organization. 12. Lobstein T, Jackson-Leach R.
and trends in child malnutrition: The double burden of malnutrition. Estimated burden of paediatric
UNICEF-WHO-World Bank joint Case studies from six developing obesity and co-morbidities in
child malnutrition estimates. countries. Food and Nutrition Paper. Europe. Part 2. Numbers of children
UNICEF, New York; WHO, Geneva; 2006;84:1–334. with indicators of obesity-related
World Bank, Washington DC: disease. International Journal of
2015. 7. Lake A, Townshend T. Obesogenic Pediatric Obesity. 2006;1:33–41.
environments: exploring the built
2. WHO Multicentre Growth Reference and food environments. J R Soc 13. Pizzi MA, Vroman K. Childhood
Study Group. WHO child growth Promot Health. 2006;126:262–7. obesity: effects on children’s
standards based on length/height, participation, mental health, and
weight and age. Acta Paediatr. 8. Hanson MA, Gluckman PD. Early psychosocial development. Occup
2006;Suppl 450:76–85. developmental conditioning of later Ther Health Care. 2013;27:99–112.
health and disease: physiology or
3. Ng M, Fleming T, Robinson M, pathophysiology? Physiological 14. Pediatr ResMiller AL, Lee HJ, Lumeng
Thomson B, Graetz N, Margono reviews. 2014;94:1027–76. JC. Obesity-associated biomarkers
C, et al. Global, regional, and and executive function in children.
national prevalence of overweight 9. McPherson NO, Fullston T, Aitken Pediatr Res. 2015;77:143–7.
and obesity in children and adults RJ, Lane M. Paternal obesity,
during 1980–2013: a systematic interventions, and mechanistic 15. Litwin SE. Childhood Obesity and
analysis for the Global Burden pathways to impaired health Adulthood Cardiovascular Disease:
of Disease Study 2013. Lancet. in offspring. Ann Nutr Metab. Quantifying the Lifetime Cumulative
2014;384:766–81. 2014;64:231–8. Burden of Cardiovascular Risk
Factors. J Am Coll Cardiol.
4. Roberto CA, Swinburn B, Hawkes 10. Tanamas SK, Lean ME, Combet 2014;64:1588-90.
C, Huang TTK, Costa SA, Ashe E, Vlassopoulos A, Zimmet PZ,
M, et al. Patchy progress on Peeters A. Changing guards: time 16. Nader PR, O’Brien M, Houts R,
obesity prevention: emerging to move beyond body mass index Bradley R, Belsky J, Crosnoe R,
examples, entrenched barriers, for population monitoring of excess et al. Identifying risk for obesity
and new thinking. Lancet. adiposity. QJM. 2015;Nov 1. in early childhood. Pediatrics.
2015;385:2400–9. 2006;118:e594–e601.
11. Eastwood SV, Tillin T, Dehbi HM,
5. Taveras EM, Gillman MW, Kleinman Wright A, Forouhi NG, Godsland 17. Juonala M, Magnussen CG,
K, Rich-Edwards JW, Rifas-Shiman I, et al. Ethnic differences in Berenson GS, Venn A, Burns
SL. Racial/ethnic differences in associations between fat deposition TL, Sabin MA, et al. Childhood
early-life risk factors for childhood and incident diabetes and adiposity, adult adiposity, and
obesity. Pediatrics. 2010;125:686– underlying mechanisms: the SABRE cardiovascular risk factors. N Engl J
95. study. Obesity. 2015;23:699–706. Med. 2011;365:1876–85.
42
18. Kelsey MM, Zaepfel A, Bjornstad for improving public health: a childhood. Curr Opin Endocrinol
P, Nadeau KJ. Age-related systematic review of prices, demand Diabetes Obes. 2015;22:41–7.
consequences of childhood obesity. and body weight outcomes. Obesity
Gerontology. 2014;60:222–8. Reviews. 2013;14:110–28. 40. Taveras EM, Gillman MW, Pena
MM, Redline S, Rifas-Shiman
19. Finkelstein EA, Graham WC, 30. Hastings G, Stead M, McDermott L, SL. Chronic sleep curtailment
Malhotra R. Lifetime direct medical Forsyth A, MacKintosh AM, Rayner and adiposity. Pediatrics.
costs of childhood obesity. M, et al. Review of research on 2014;133:1013–22.
Pediatrics. 2014;133:854–62. the effects of food promotion to
children – final report. Report to the 41. Yu Z, Han S, Zhu J, Sun X, Ji C,
20. Muller-Riemenschneider F, Food Standards Agency. Glasgow: Guo X. Pre-pregnancy body mass
Reinhold T, Berghofer A, Willich University of Strathclyde, Centre for index in relation to infant birth
SN. Health-economic burden of Social Marketing, 2003. weight and offspring overweight/
obesity in Europe. Eur J Epidemiol. obesity: a systematic review
2008;23:499–509. 31. McGinnis JM, Gootman JA, Kraak and meta-analysis. PLoS One.
VI. Food marketing to children 2013;8:e61627.
21. Global reference list of 100 core and youth. Threat or opportunity?
health indicators. Geneva: World Washington, DC: Institute of 42. Eriksson JG, Sandboge S, Salonen
Health Organization, 2015. Medicine, National Academies MK, Kajantie E, Osmond C. Long-
Press; 2006. term consequences of maternal
22. Commission on Social Determinants overweight in pregnancy on
of Health. Closing the gap in a 32. Lobstein T, Jackson-Leach R, offspring later health: findings from
generation: health equity through Moodie ML, Hall KD, Gortmaker the Helsinki Birth Cohort Study. Ann
action on the social determinants SL, Swinburn BA, et al. Child and Med. 2014;46:434–8.
of health. Final Report of the adolescent obesity: part of a bigger
Commission on Social Determinants picture. Lancet. 2015;385:2510– 43. Okubo H, Crozier SR, Harvey NC,
of Health. Geneva: World Health 20. Godfrey KM, Inskip HM, Cooper
Organization, 2008. C, et al. Maternal dietary glycemic
33. A framework for implementing index and glycemic load in early
23. Hawkes C, Smith TG, Jewell J, the set of recommendations pregnancy are associated with
Wardle J, Hammond RA, Friel on the marketing of foods and offspring adiposity in childhood: the
S, et al. Smart food policies non-alcoholic beverages to Southampton Women’s Survey. Am J
for obesity prevention. Lancet. children. Geneva: World Health Clin Nutr. 2014;100:676–83.
2015;385:2410–21. Organization, 2012.
44. Poston L. Maternal obesity,
24. Using price policies to promote 34. An R, Patel D, Segal D, Sturm R. gestational weight gain and
healthier diets. Copenhagen, Eating better for less: a national diet as determinants of offspring
Denmark: World Health discount program for healthy food long term health. Best practice &
Organization Regional Office for purchases in South Africa. American Research Clinical Endocrinology &
Europe, 2014. journal of health behavior. Metabolism. 2012;26:627–39.
2013;37:56–61.
25. Arantxa Colchero M, Popkin BM, 45. Oken E, Levitan EB, Gillman MW.
Rivera JA, Nh SW. Beverage 35. Tremblay MS, Gray CE, Akinroye Maternal smoking during pregnancy
purchases from stores since the start K, Harrington DM, Katzmarzyk PT, and child overweight: systematic
of the Mexican sugar-sweetened Lambert EV, et al. Physical activity review and meta-analysis. Int J Obes
beverage excise tax: a year out. of children: a global matrix of (Lond). 2008;32:201–10.
BMJ. 2016;352:h6704. grades comparing 15 countries.
Journal of physical activity & health. 46. Janesick A, Blumberg B. Endocrine
26. Ebbeling CB, Feldman HA, Chomitz 2014;11:S113–25. disrupting chemicals and the
VR, Antonelli TA, Gortmaker SL, developmental programming of
Osganian SK, et al. A randomized 36. Global recommendations on adipogenesis and obesity. Birth
trial of sugar-sweetened beverages physical activity for health. Geneva: defects research Part C, Embryo
and adolescent body weight. N World Health Organization, 2010. today: reviews. 2011;93:34–50.
Engl J Med. 2012;367:1407–16.
37. Food, nutrition, physical activity, 47. Temel S, van Voorst SF, Jack BW,
27. de Ruyter JC, Olthof MR, Seidell and the prevention of cancer: a Denktas S, Steegers EA. Evidence-
JC, Katan MB. A trial of sugar-free global perspective. Washington, based preconceptional lifestyle
or sugar-sweetened beverages and DC: World Cancer Research interventions. Epidemiologic
body weight in children. N Engl J Fund, America Institute of Cancer Reviews. 2014;36:19–30.
Med. 2012;367:1397–406. Research, 2007.
48. Institute of Medicine and National
28. Popkin BM, Hawkes C. Sweetening 38. LeBlanc AG, Spence JC, Carson Research Council. Weight gain
of the global diet, particularly V, Connor Gorber S, Dillman C, during pregnancy: Reexamining
beverages: patterns, trends, and Janssen I, et al. Systematic review the guidelines. Washington DC:
policy responses. Lancet Diabetes of sedentary behaviour and health National Academies Press; 2009.
Endocrinol. 2015. indicators in the early years (aged
0–4 years). Appl Physiol Nutr 49. Hanson MA, Bardsley A, De-Regil
29. Powell LM, Chriqui JF, Khan T, Metab. 2012;37:753–72. LM, Moore SE, Oken E, Poston L, et
Wada R, Chaloupka FJ. Assessing al. The International Federation of
the potential effectiveness of food 39. Miller AL, Lumeng JC, LeBourgeois Gynecology and Obstetrics (FIGO)
and beverage taxes and subsidies MK. Sleep patterns and obesity in recommendations on adolescent,
43
preconception, and maternal 56. School policy framework.
nutrition: “Think Nutrition First”. Int J Implementation of the WHO global
Gynecol Obstet. 2015;131:S213– strategy on diet, physcial activity
S53. and health. Geneva: World Health
Organization, 2008.
50. Choi J, Fukuoka Y, Lee JH.
The effects of physical activity 57. Rasberry CN, Lee SM, Robin L, Laris
and physical activity plus diet BA, Russell LA, Coyle KK, et al.
interventions on body weight in The association between school-
overweight or obese women who based physical activity, including
are pregnant or in postpartum: a physical education, and academic
systematic review and meta-analysis performance: a systematic review of
of randomized controlled trials. Prev the literature. Prev Med. 2011;52
Med. 2013;56:351–64. Suppl 1:S10–20.
51. Horta BL, Loret de Mola C, Victora 58. Dietz WH, Baur LA, Hall K,
CG. Long-term consequences Puhl RM, Taveras EM, Uauy R,
of breastfeeding on cholesterol, et al. Management of obesity:
obesity, systolic blood pressure and improvement of health-care training
type 2 diabetes: a systematic review and systems for prevention and
and meta-analysis. Acta Paediatr care. Lancet. 2015;385:2521–33.
Suppl. 2015;104:30–7.
59. Oude Luttikhuis H, Baur L, Jansen H,
52. Guiding principles for Shrewsbury VA, O’Malley C, Stolk
complementary feeding of the RP, et al. Interventions for treating
breastfed child. Washington, DC: obesity in children. The Cochrane
Pan American Health Organization database of systematic reviews.
and World Health Organization, 2009:CD001872.
2002.
60. Spear BA, Barlow SE, Ervin C,
53. Mennella JA, Nicklaus S, Jagolino Ludwig DS, Saelens BE, Schetzina
AL, Yourshaw LM. Variety is KE, et al. Recommendations for
the spice of life: strategies for treatment of child and adolescent
promoting fruit and vegetable overweight and obesity. Pediatrics.
acceptance during infancy. Physiol 2007;120:S254–S88.
Behav. 2008;94:29–38.
61. Huang TTK, Cawley JH, Ashe M,
54. Liem DG, Mennella JA. Sweet and Costa SA, Frerichs LM, Zwicker L,
sour preferences during childhood: et al. Mobilisation of public support
role of early experiences. for policy actions to prevent obesity.
Developmental psychobiology. Lancet. 2015;385:2422–31.
2002;41:388–95.
62. Swinburn B, Kraak V, Rutter
55. Waters E, de Silva-Sanigorski A, H, Vandevijvere S, Lobstein T,
Hall BJ, Brown T, Campbell KJ, Gao Sacks G, et al. Strengthening of
Y, et al. Interventions for preventing accountability systems to create
obesity in children. The Cochrane healthy food environments and
database of systematic reviews. reduce global obesity. Lancet.
2011:CD001871. 2015;385:2534–45.
44
CHILDHOOD OBESITY
UNDERMINES THE
PHYSICAL, SOCIAL AND
PSYCHOLOGICAL WELL-
BEING OF CHILDREN
AND IS A KNOWN
RISK FACTOR FOR
ADULT OBESITY AND
NONCOMMUNICABLE
DISEASES. THERE IS
AN URGENT NEED TO
ACT NOW TO IMPROVE
THE HEALTH OF THIS
GENERATION AND
THE NEXT.
45
ANNEX 1:
THE COMMISSION
ON ENDING
CHILDHOOD OBESITY
The prevalence of infant, childhood and eminent individuals from a During the second meeting, held
and adolescent obesity is variety of relevant backgrounds. in Geneva on 13 and 14 January
increasing in many countries, with The Commission was tasked with 2015, the Commission reviewed
the most rapid rises occurring in preparing a consensus report the second report of the Ad hoc
low- and middle-income countries. specifying the approaches and Working Group on Science and
Without intervention, obese infants combinations of interventions Evidence and the first report of
and young children are likely that are likely to be most effective the Ad hoc Working Group on
to continue to be obese during in tackling childhood and Implementation, Monitoring and
childhood, adolescence and adolescent obesity in different Accountability, and developed the
adulthood. contexts around the world. The Interim Report of the Commission
Commission reviewed, built upon on Ending Childhood Obesity.
Childhood obesity is associated and addressed gaps in existing This provided the rationale for
with a wide range of health mandates and strategies on the tackling childhood obesity and the
complications and an increased prevention of childhood obesity. imperative for governments to take
risk of premature onset of The work of the Commission was the lead in addressing the issue.
illnesses, including diabetes and supported by two ad hoc working The Interim Report highlighted
heart disease. Many causes and groups for ending childhood potential policy options for tackling
potential solutions to this problem obesity – one on the science the obesogenic environment,
exist. However, as is the case and evidence, and the other on reducing the risk of obesity by
with all public health strategies, implementation, monitoring and addressing critical elements in
there are many challenges to accountability. the life-course approach and the
implementation. Only through management of children with
a combination of community The Commission held four meetings obesity to improve their current and
partnerships, government support and, as part of its working future health.
and scientific research will the best methods, undertook regional
recommendations be developed consultations with Member States The Interim Report also served as
and implemented worldwide. as well as hearings with non- the basis for an online consultation
State actors. The first meeting from 16 March to 5 June 2015.
In order to better inform and took place in Geneva on 17 and Eighty-one entities, including
fashion a comprehensive response 18 July 2014, during which the Member States, nongovernmental
to childhood obesity, the WHO Commission reviewed the report organizations, philanthropic
Director-General established of the first meeting of the Ad hoc foundations, academia,
a high-level Commission on Working Group on Science and researchers, the private sector and
Ending Childhood Obesity, Evidence and developed its method individuals submitted comments on
comprising fifteen accomplished of work. the Interim Report.
46
THE MANILA CAIRO
COMMISSION The Philippines Egypt
ALSO HELD
SEVEN 24/25 March 2/3 July
for the Western Pacific for the Eastern
REGIONAL Region mainland Mediterranean Region
CONSULTATIONS countries countries
WITH MEMBER
STATES:
AUCKLAND MEXICO CITY

New Zealand Mexico
27/28 July 26/28 August

for the Western Pacific for countries of the
Region Island Countries Region of the Americas
and Territories
NEW DELHI ACCRA

India Ghana
28/29 September 22/23 October
for the South-East Asia for the African Region
Region countries countries
VALLETTA
Malta
28/29 October
for the European
Region countries
The Commission convened its the Ad hoc Working Group on from September to November
third meeting on 22 and 23 June Implementation, Monitoring and 2015 for comments by relevant
2015 in Hong Kong Special Accountability and an evidence stakeholders; 98 submissions
Administrative Region, Republic update from the Ad hoc Working were received and reviewed.
of China. During this meeting Group on Science and Evidence.
the Commission reviewed the Following the period of
comments received from Member At the third meeting, the consultations, the Commission held
States on agenda item 13.3 at Commission developed its its fourth meeting in Geneva on
the 68th World Health Assembly, final draft report detailing 30 November and 1 December
the feedback received from potential policy directions for the 2015, to review the feedback
the online consultations as well consideration of Member States. received, consider the reports of
as the regional consultation The draft final report served as the the two ad hoc working groups
and hearings with the Western basis for regional consultations and develop their final report. This
Pacific mainland countries. The for the Region of the Americas, final report of the Commission on
Commission also received from South-East Asia Region, African Ending Childhood Obesity will be
the WHO Director-General a Region and European region. The submitted to the WHO Director-
report of the second meeting of report was also placed online General in January 2016.
47
ANNEX 2:
COMMISSIONERS
Sir George Alleyne Ms Betty King Professor Hoda Rashad

Director Emeritus Former Ambassador Research Professor and Director
Pan American Health Permanent Mission of the Social Research Center
Organization (PAHO) United States of America to the American University in Cairo
United Nations Office and other Egypt
Dr Constance Chan Hon Yee International Organizations at
Director of Health Department Geneva Professor K. Srinath Reddy
of Health Hong Kong Special President Public Health
Administrative Region Ms Nana Oye Lithur Foundation of India Institute of
China Minister of Gender, Children and Studies in Industrial Development
Social Protection (ISID) Campus
Ms Helen Clark Ghana India
Administrator
United Nations Development Dr David Nabarro Dr Jacques Rogge
Programme Coordinator, Scaling up Honorary President International
(UNDP) Nutrition (SUN) Movement Olympic Committee (IOC)
Special Representative of the Switzerland
Sir Peter Gluckman UN Secretary General for
(co-chair) Food Security and Nutrition Ms Sachita Shrestha
Chief Science Advisor to the Coordinator for the High Level Youth Advocate
Prime Minister of New Zealand Task Force Nepal
& Liggins Institute University of
Auckland Dr Sania Nishtar (co-chair) Dr Colin Tukuitonga
New Zealand Founder, Heartfile Director-General
Pakistan Secretariat of the Pacific
Mr Adrian Gore Community (SPC)
Founder and Chief Executive Officer Ms Paula Radcliffe New Caledonia
Discovery Group Athlete and parent
South Africa United Kingdom
48
49
Photo credits
Cover:
© 2007 Iryna Shabaykovych, Courtesy of Photoshare
© 2013 Valerie Caldas/ Johns Hopkins University Center
for Communication Programs, Courtesy of Photoshare
© 2013 Alissa Zhu, Courtesy of Photoshare
P. xiv © WHO / SEARO /Payden

P. 5 © 2014 Jose Ramos II, Courtesy of Photoshare
P. 6 © 2008 Pablo P Yori, Courtesy of Photoshare
P. 9 © 2007 Jose M. Marin, Courtesy of Photoshare
P. 10 © 2008 Kunle Ajayi, Courtesy of Photoshare
P. 13 © 2014 Lorine Ghabranious/MSH, Courtesy of Photoshare
P. 15 © 2013 Anil Gulati, Courtesy of Photoshare
P. 16 © 2012 Sharvari Raval, Courtesy of Photoshare
P. 23 © 2013 Kyle Sherman, Courtesy of Photoshare
P. 25 © WHO / SEARO /SB Rai
P. 26 © WHO / SEARO /Anuradha Sarup
P. 27 © WHO / SEARO /SB Rainow
P. 29 © 2013 Valerie Caldas, Courtesy of Photoshare
P. 35 © WHO /Isadore Brown
P. 37 © 2013 David Huamaní, Courtesy of Photoshare
P. 39 © 2012 David Snyder for CRWRC, Courtesy of Photoshare
P. 41 © 2005 Anil Gulati, Courtesy of Photoshare
P. 49 © 2011 Lawrence Ko, Courtesy of Photoshare
50
RELATO DE CASO
Consenso da Associação Brasileira de

Nutrologia sobre manejo da dislipidemia
secundária à obesidade infanto-juvenil
1
2
3
Patrícia Piccoli de Mello
4
Paula Daniel de Mello
5
Renato Augusto Zorzo
6
Durval Ribas Filho
1
MD, MSc, PhD, Universidade de Ribeirão Preto, ABRAN
2
MD, MSc, PhD, Universidade Federal do Rio Grande do Sul, ABRAN
3
MD, MSc, Universidade Federal do Rio Grande do Sul
4
AC, University of Cologne
5
MD, MSC, Universidade Federal de São Carlos
6
MD, MSC, PhD, Faculdade de Medicina da Fundação Padre Albino, ABRAN
RESUMO
Objetivo
Estabelecer consenso sobre o manejo da dislipidemia secundária à obesidade infanto-juvenil.
Métodos
Foi realizada pesquisa bibliográfica nas bases de dados Medline, Scielo e LILACS. Com base nas
evidências científicas, o grupo de trabalho estabeleceu as condutas recomendadas pelo Departamento
de Nutrologia Pediátrica da ABRAN.
Resultados
Os autores redigiram o consenso que foi aprovado pela Diretoria da Associação Brasileira de Nutrologia
- ABRAN.
Conclusões
São apresentadas, com base nas evidências científicas, as recomendações para a condução dos casos
de dislipidemia associados à obesidade na infância e adolescência.
Palavras-Chave: Dislipidemia, lipídeos, aterosclerose, crianças e adolescentes.
INTRODUÇÃO ção infanto-juvenil, que apresenta prevalência de

sobrepeso de 31,6% nos Estados Unidos1. No
A obesidade é um fenômeno global, cuja pre- Brasil, segundo os últimos dados do IBGE, 51,4%
valência vem aumentando nas últimas décadas, dos meninos e 43,8% das meninas entre 5 e 9 anos
chegando a assumir caráter de epidemia. Dados de idade apresentam excesso de peso, números que
recentes confirmam o crescimento acelerado de indi- mostram a importância desta entidade mórbida na
víduos com excesso de peso também na popula- esfera da saúde pública1, 2. O acúmulo de gordura
corporal, em especial na localização visceral, senvolvimento, havendo duas fases de aumento

associa-se ao aumento do desenvolvimento de expressivo de seus níveis: até o segundo ano de
comorbidades e agrega risco para a gênese de Do- vida e durante a maturação sexual18. São maiores
enças Crônicas Não Transmissíveis (DCNT) ainda nas crianças e adolescentes do sexo feminino
na infância, como hipertensão arterial sistêmica e essa diferença é mais expressiva durante a
(HAS), dislipidemia, resistência periférica à insulina adolescência. Em média, as meninas apresentam
e síndrome metabólica3. níveis mais elevados de CT, lipoproteínas de alta
A dislipidemia é uma das complicações mais densidade (HDL-colesterol) e LDL-colesterol, quan-
frequentes da obesidade4-7. Trata-se de distúrbio do comparadas aos meninos8.
metabólico caracterizado por concentrações Os níveis elevados de lipídeos circulantes
anormais de lipídeos e/ou lipoproteínas no san- estão relacionados a alterações na função do
gue, sendo determinada por fatores genéticos e endotélio, resultando em formação de placas de
ambientais3. A prevalência das dislipidemias na ateroma. Sugere-se que o processo de formação
infância e adolescência varia entre 24 e 40%8-10, da aterosclerose começa na infância19 e progride
com aumento progressivo dessas taxas ao longo lentamente até a vida adulta, através da formação
dos anos. Pesquisa realizada no Hospital de Clínicas de placas lipídicas, ou ateromas, que se depositam
da Universidade Estadual de Campinas (SP) en- na parede arterial, podendo obstruir a luz dos
controu valores alterados de colesterol total (CT), vasos sanguíneos20. Estudos experimentais mos-
lipoproteínas de baixa densidade (LDL-colesterol) e tram, inicialmente, espessamento da camada ín-
triglicerídeos (TG) em 44%, 36% e 56% das crianças tima das artérias21,22 com infiltração de lipídeos e
de 2 a 9 anos de idade e em 44%, 36% e 50% nos proteoglicanos e, posteriormente, infiltração de
adolescentes de 10 a 19 anos respectivamente, macrófagos e formação de células espumosas,
demonstrando o impacto negativo deste importante resultando em disfunção endotelial23. Além disso,
desvio de hábitos alimentares nessa população11. também ocorre elevação nas concentrações de
A alimentação é um item que deve permear mediadores inflamatórios, como interleucina-18 e
a orientação em saúde em todas as idades, em proteína C reativa, evidenciando perfil sugestivo de
especial nos primeiros anos de vida. Os primeiros um estado inflamatório subclínico24. Essas alterações
1.000 dias, como é conhecida a época que vai são potencializadas pela obesidade, em decorrência
da concepção ao final do segundo ano de vida, do sinergismo do efeito inflamatório e do aumento da
exercem importância vital na programação da saúde relação entre leptina e adiponectina, presentes nos
e da doença do indivíduo12. Tanto o crescimento sujeitos com excesso de peso. Todos esses achados
retardado como o excessivo nos períodos embri- indicam que ocorre progressão da aterosclerose já
onário, fetal e na primeira infância, podem ser fatores na adolescência25.
de risco para o desenvolvimento de DCNT13,15. A dislipidemia na faixa etária infanto-juvenil
Estudos observacionais indicam que lactentes que pode ser um evento primário. Entretanto, ela é mais
ingerem exclusivamente leite materno, rico em frequentemente secundária à obesidade e, nesse
gorduras saturadas, apresentam níveis elevados caso, as alterações mais comuns são os níveis
de colesterol no início da vida, entretanto, na idade reduzidos de HDL-colesterol e elevados de CT, TG
adulta, desenvolvem melhor regulação hepática e LDL-colesterol, com predomínio das subclasses
do metabolismo de lipoproteínas. Dessa forma, as de colesterol com menor tamanho molecular, que
crianças que foram alimentadas com leite materno tem maior poder aterogênico5, 26. Por esse motivo,
desenvolveriam posteriormente perfil lipídico mais torna-se essencial procurar avançar nos métodos de
favorável quando comparadas àquelas que rece- prevenção e diagnóstico adequados de dislipidemia
beram fórmulas artificiais na infância16, 17. na infância e adolescência, visando instituir tera-
Os níveis de lipídeos e lipoproteínas séricos pêuticas que visem reduzir a morbimortalidade na
sofrem mudanças durante o crescimento e o devida adulta.
CONSENSO DA ASSOCIAÇÃO BRASILEIRA DE NUTROLOGIA SOBRE
MANEJO DA DISLIPIDEMIA SECUNDÁRIA À OBESIDADE INFANTO-JUVENIL
A correlação entre os níveis alterados de lipídeos DISLIPIDEMIA

na população pediátrica e a presença de lesões
ateroscleróticas em necropsias já foi demonstrada O colesterol é o esteroide mais comum no
previamente27, 28. Está bem estabelecido que células corpo humano, estando presente em todos os
gordurosas estão presentes na aorta de indivíduos tecidos e também no plasma. Apresenta-se nas
aos 10 anos de idade e nas artérias coronárias aos formas livre ou combinado com ácidos graxos de
20 anos, e que o período de maior progressão das cadeia longa na forma de éster de colesteril, que
estrias gordurosas para placas fibrosas ocorre a partir é a sua estrutura de armazenamento. É um lipídeo
dos 15 anos de idade29. O fator de maior influência anfipático, componente estrutural essencial da
na aceleração da progressão da aterosclerose é a membrana plasmática de todas as células do corpo
dislipidemia, especialmente quando os níveis de CT, humano, além de ser precursor de várias moléculas
LDL-colesterol e TG estão elevados e os de HDL- biologicamente ativas, como o ácido cólico (um
colesterol estão reduzidos30. constituinte dos ácidos biliares), a vitamina D (atra-
A principal implicação patológica das vés de seu derivado 7-deidro), além de estrógenos,
dislipidemias é a doença arterial coronariana andrógenos, progesterona e a maioria dos hormônios
(DAC), que atualmente é uma das principais adrenocorticais35.
causas de morbidade e mortalidade em adultos O colesterol pode ser consumido em fontes
de todo o mundo7, 31. A DAC é a manifestação dietéticas (colesterol exógeno), sendo absorvido
clínica do desenvolvimento lento e gradual de lentamente pelo trato gastrointestinal. No entanto,
placas ateroscleróticas nas artérias coronárias. A a maior parte é produzido pelo fígado (colesterol
aterosclerose é considerada doença progressiva de endógeno) e circula pelos vasos na forma de lipopro-
etiologia multifatorial, sendo resultado de processo teínas, que permitem solubilização e transporte dos
não apenas decorrente do acúmulo de lipídeos nas lipídeos, uma vez que são substâncias hidrofóbicas.
paredes das artérias, mas também consequente As lipoproteínas são divididas, de acordo com sua
da disfunção endotelial e da ativação dos sistemas composição, em quilomícrons, lipoproteínas de densi-
inflamatório e imunológico32. dade muito baixa (VLDL-colesterol), LDL-colesterol,
Estudos observacionais mostram que os lipoproteínas de alta densidade (HDL-colesterol)
níveis de CT em crianças se associam diretamente e lipoproteínas de densidade intermediária (IDL-
à prevalência de DAC nos adultos, evidenciando colesterol). O transporte dos lipídeos absorvidos no
forte tendência das crianças em manterem os intestino é realizado pelos quilomícrons, sofrendo
mesmos percentis de colesterol até a vida adulta33. ação das lipases lipoproteica e hepática durante o
Resultados do Bogalusa Heart Study demonstraram metabolismo digestivo. O colesterol endógeno é
que aproximadamente 50% das crianças com transportado através de VLDL-colesterol, IDL-coles-
CT acima do percentil 75 da curva de referência terol e LDL-colesterol. Por último, o HDL-colesterol
apresentaram valores elevados de LDL-colesterol 10 é responsável pelo transporte reverso do colesterol,
a 15 anos mais tarde34. processo pelo qual o colesterol excedente é removido
O manejo consciente das dislipidemias desde dos tecidos para o fígado36.
tenra idade é fundamental, posto que as doenças A dislipidemia relacionada com a obesidade é
relacionadas ao excesso de lipídeos circulantes são caracterizada por aumento dos níveis de TG, queda
preveníveis com medidas simples de orientação dos níveis de HDL-colesterol e composição anormal
em relação ao estilo de vida. Nesse sentido, a de LDL-colesterol, com maior proporção de partículas
elaboração deste consenso visa possibilitar a ampla pequenas e mais densas. Essas alterações lipídicas
orientação a pediatras gerais e nutrólogos que parecem estar intimamente associadas à resistência
atendem pacientes obesos na faixa etária pediátrica, insulínica, situação em que há comprometimento na
a fim de que as medidas de prevenção, diagnóstico atividade da lipase lipoproteica, promovendo menor
e tratamento sejam aplicadas no momento propício. captação de glicose e maior liberação de ácidos
graxos livres e glicerol na circulação, o que propicia a dosagem do CT objetivando mensurar risco
maior produção hepática de TG e VLDL-colesterol. cardiovascular seja recomendada por programas
Os TG do VLDL-colesterol são transferidos de rastreamento, tal valor pode ser enganoso
para o LDL-colesterol, o que resulta na formação quando obtido isoladamente, sendo necessária a
de partículas menores e mais densas, as quais têm dosagem das frações do CT (LDL-colesterol e HDL-
maior acesso à camada íntima arterial que se tornam colesterol). De uma forma geral, utilizam-se valores
mais suscetíveis à oxidação. A formação do HDL- de referência procedentes de outros países, por
colesterol também é comprometida, predominando exemplo, a V DBDPA utiliza valores transcritos do
moléculas pequenas e densas, com menor potencial National Cholesterol Education Program (NCEP),
antiaterogênico. O aumento de VLDL-colesterol adotado nos EUA a partir de 199238.
e TG, a redução do HDL-colesterol e a elevação Em 2005, a Sociedade Brasileira de Cardiologia
do LDL-colesterol rico em partículas pequenas e publicou a I Diretriz de Prevenção da Aterosclerose
densas resultam em perfil lipídico bastante atero- na Infância e Adolescência (I DPAIA)40, propondo
gênico. Há de se destacar ainda o papel das valores de referência para faixa etária de 2 a 19
citocinas secretadas pelo próprio tecido adiposo, anos, com nível de evidência D, conforme Tabela 1.
a saber: interleucina-6, fator de necrose tumoral e A I DPAIA orienta triagem seletiva para
inibidor do ativador de plasminogênio 1, na atividade crianças de 2 a 10 anos de idade, com solicitação
inflamatória vascular, predispondo à formação de de perfil lipídico na presença dos seguintes fatores
de risco: pais ou avós com história de DAC precoce
estrias e placas ateromatosas37.
(homens <55 anos e mulheres <65 anos), parentes
de primeiro grau com hipercolesterolemia ou
RASTREAMENTO E DIAGNÓSTICO
hipertrigliceridemia, diabetes mélito, infecção pelo
DA DISLIPIDEMIA
HIV, síndrome nefrótica, lúpus eritematoso sistêmico,
história de pancreatite aguda, presença de xantomas
A V Diretriz Brasileira de Dislipidemias e
ou xantelasmas ao exame físico, história familiar
Prevenção da Aterosclerose (V DBDPA)36 recomen-
desconhecida, HAS, obesidade, tabagismo e dieta
da rastreamento seletivo do perfil lipídico em crianças
rica em gorduras saturadas e/ou trans. Além disso,
e jovens de 2 a 19 anos de idade. A triagem seletiva,
orienta triagem universal a partir dos 10 anos de
recomendada pela National Cholesterol Education
idade, com solicitação de perfil lipídico para todas
Program (NCEP), orienta triagem, com solicitação
as crianças. Também recomenda aconselhamento
de CT, LDL-colesterol, HDL-colesterol e TG, para dietético para valores de CT a partir de 150mg/dL
crianças com história familiar positiva para início e supervisão rotineira a partir de 170mg/dL para
precoce de DAC (homens <55 anos e mulheres <65 prevenção de DAC40.
anos) ou com diagnóstico de dislipidemia38. Além Sugere-se, neste consenso, que o perfil
disso, é recomendada triagem para crianças com lipídico seja sempre solicitado no momento em que
excesso de peso, independentemente da presença a criança ou o adolescente for diagnosticado como
ou não de outros fatores de risco39. em sobrepeso ou obesidade.
Entretanto, a triagem seletiva não detecta Inicialmente, sempre que os valores da coleta
muitas crianças que apresentam dislipidemia sem do perfil lipídico (TG, CT e frações) forem consi-
nenhum fator de risco associado. A triagem universal derados limítrofes ou elevados, deve-se repetir a
pode ser realizada em todas as crianças a partir dosagem sérica no mesmo laboratório, com intervalo
dos dois anos de idade, embora ainda não existam de 4 semanas para confirmação dos resultados. Para
evidências suficientemente fortes recomendando a coleta, devem-se seguir as seguintes orientações:
ou contraindicando a solicitação rotineira de perfil coleta após 8 horas de jejum (apesar de atualmente
lipídico na infância3. não ser mais recomendado jejum para coleta de
A V DBDPA relata a correlação entre CT sérico sangue para lipidograma41, como, em geral, na
elevado e incidência de DAC, revelando que, embora mesma amostra é colhida glicemia e insulinemia,
nesse consenso mantém-se a orientação para o Com relação ao tratamento farmacológico,

jejum de 8 horas), evitar atividade física vigorosa nas todos também indicam as estatinas e citam as resinas
24 horas anteriores, abstenção de consumo de álcool de absorção iônica, apesar da dificuldade prática
nas 72 horas anteriores e manter dieta habitual por que o uso dessas últimas oferecem. Citam o uso de
pelo menos nas 2 semanas anteriores40. fibratos e ômega-3 para as hipertrigliceridemias, mas
Como regra, uma vez diagnosticada a dis- com a ressalva de serem medicações de uso em
lipidemia, deve-se avaliar se a sua origem é adultos. Os consensos chileno, coreano e francês
primária ou secundária. Quando há suspeita de recomendam o uso de inibidores de absorção do
hiperlipidemia hereditária, recomenda-se a estra- colesterol (ezetimibe, na dose de 5-10mg/dia) como
tégia de rastreamento em cascata, isto é, triagem adjuvantes às estatinas nos casos refratários à
laboratorial para os familiares de 1° grau da criança monoterapia, sendo esse fármaco aprovado pelo
ou adolescente42. Food and Drugs Administration (FDA) para uso a
A principal causa associada à dislipidemia é a partir dos 10 anos de idade45-47. O consenso coreano
obesidade, sendo outras: diabetes mélito, síndrome também aborda o uso alternativo de ácido nicotínico
nefrótica, hipotireoidismo, lúpus eritematoso sistê- nos casos de elevação do LDL-colesterol, com alerta
mico e portadores de infecção por HIV em tera- para os potenciais efeitos colaterais graves, como
pia com antirretrovirais, devendo-se afastar esses hepatotoxicidade, hiperglicemia, miopatia, exantema,
diagnósticos previamente ao início do tratamento43. hiperuricemia e sintomas gastrointestinais46, que
O presente consenso é focado na dislipidemia da se mostraram reversíveis com a interrupção do
criança com sobrepeso e obesidade. tratamento53.
Metanálise de 2014 estudou o efeito do uso de
TERAPÊUTICA DAS DISLIPIDEMIAS fitoesterol na redução dos níveis de LDL-Colesterol
em crianças e adultos com Hipercolesterolemia
Os consensos sobre o tratamento da dis- Familiar e concluiu que o uso do fitoesterol como
lipidemia existentes na literatura são, em sua mai- adjuvante à dieta de redução do colesterol teve
oria, destinados à população adulta. Entretanto, impacto benéfico e estatisticamente significativo,
alguns documentos trazem orientações cientificas apesar de não ter sido possível demonstrar se o
frente à dislipidemia na população pediátrica. Os uso desta medicação também reduziria eventos
consensos existentes são o argentino44, o chileno45, secundários, como incidência de DAC54.
o coreano46 e o francês47. O espanhol aborda especi- Apesar da extensa literatura embasando o
ficamente crianças e adolescentes acometidos por uso de ômega 3 em adultos dislipidêmicos, ainda
Hipercolesterolemia Familiar48. há poucas evidências que avalizem sua indicação
Todos os documentos revisados recomendam na população pediátrica. Para a prescrição de ácido
como primeira abordagem a orientação nutrológica, desocosahexaenoico (DHA), há apenas um estudo
com adequação do valor energético total (VET) desenhado para avaliar seu efeito em 20 crianças
diário visando o peso ideal, restrição no consumo dislipidêmicas e o resultado foi positivo, demostrando
de lipídeos com adequação nas proporções de boa tolerância da medicação e redução do LDL-
ingestão de gordura saturada, monoinsaturada e colesterol de classes 1 e 3 após seis meses de uso55.
poli-insaturada (em geral, com 7-10% de saturadas) Importante citar que as apresentações comercias
com incentivo ao consumo de pescados fonte de de ômega 3 e DHA são amplamente prescritas em
ômega-3, adequação no consumo de fibras, redução adultos, sem serem observados efeitos colaterais
do tempo de exposição a telas e incentivo à prática graves56.
de atividades físicas7, 37, 40, 44-46, 49-52. No presente Uma nova classe de drogas hipolipemiantes
consenso, esses aspectos serão tratados de forma pode se tornar no futuro uma opção para os casos
diferenciada, uma vez que o foco são as crianças particularmente resistentes aos tratamentos descritos
portadoras de sobrepeso e obesidade. anteriormente. Trata-se dos inibidores de PCSK-
9, que se mostraram bastante eficazes naqueles Etapa 2

pacientes já em uso de associação de estatina com Tratamento medicamentoso.
ezetimibe, mas que não atingiam a meta de redução
de LDL-colesterol. Nesses casos, incluindo-se aqui os A figura 1 apresenta esquematicamente quais
portadores de Hipercolesterolemia Familiar, diabetes etapas se deve adotar de acordo com valores de
mélito, doença renal crônica, HIV, entre outros. Os LDL-colesterol e presença de fatores de risco.
inibidores de PCSK-9 determinariam reduções
significativas, a ponto de diminuir o risco futuro de Etapa 1 – Terapia não farmacológica
DAC no paciente. O evolocumab é liberado pelo FDA A terapêutica não farmacológica é composta de
para uso a partir dos 12 anos e a dificuldade que se duas partes que devem ser implementadas simul-
encontra atualmente é o alto custo da medicação57. taneamente: nutroterapia e orientações para prática
Com relação à abordagem da hipertrigliceridemia de atividade física (AF).
refratária ao tratamento não farmacológico, há muito
pouca literatura disponível em crianças. Entretanto, 1) Nutroterapia
artigo de revisão mostrou que o uso de fibratos Visa alteração dos hábitos alimentares, com a
em crianças acima de 4 anos por um período de 6 finalidade de se adotar dieta saudável e adequada
meses foi eficaz na redução de CT, LDL-colesterol e para o paciente com dislipidemia.
TG, embora tenham sido observadas alterações de
enzimas hepáticas durante o uso, que normalizaram
Oferta energética
com a sua suspensão56.
Inicialmente, deve-se proceder a uma avaliação
do aporte energético atual do paciente, seja por
TRATAMENTO DA DISLIPIDEMIA ASSOCIADA À
recordatório, registro ou inquérito alimentar. Para que
OBESIDADE
ocorra melhor adesão e não comprometimento do
crescimento da criança ou adolescente, recomenda-
A importância em diagnosticar corretamente a
se que o cálculo do VET do novo plano alimentar
dislipidemia na criança com sobrepeso e obesidade
prescrito seja feito, inicialmente, com redução de
reside em iniciar precocemente as modificações no
20% do VET da dieta atual e, futuramente, novos
estilo de vida pois, quanto mais cedo a intervenção,
ajustes deverão ser realizados de acordo com a
melhores serão os resultados em diminuir o risco de
velocidade da perda de peso.
DAC na idade adulta6, 7, 50.
O tratamento se divide nas modalidades far-
macológico e não farmacológico. Enquanto a abor- Macronutrientes
dagem não farmacológica deve ser realizada em A dieta deve apresentar baixos teores de gordura
todas as crianças acometidas, a farmacológica é saturada, gordura trans e colesterol. Do VET total,
restrita àquelas consideradas de alto risco, que são no máximo 30% deve ser proveniente de fonte
as que apresentam níveis séricos de LDL-colesterol lipídica, sendo 7 a 10% de gorduras saturadas, 10
muito elevados ou refratários ao tratamento não a 13% de gorduras poliinsaturadas, até 10% de
farmacológico, ou as que apresentam valores mode- gorduras monoinsaturadas, até 1% de gordura trans
radamente elevados associados a outros fatores de e um máximo de 300mg de colesterol58. O restante
risco cardiovascular. do VET deve ser distribuído entre proteínas (10 a
O presente consenso propõe o tratamento da 12%) e carboidratos (58 a 60%). Ensaios clínicos
dislipidemia associada à obesidade em duas etapas: indicam que a ingestão de dieta com baixo teor de
gordura pode ser seguramente recomendada para
Etapa 1 a população pediátrica dos 2 aos 11 anos, sem
Terapia não farmacológica, que envolve tratamento alterações no crescimento ou desenvolvimento
nutrológico e estímulo à prática de atividade física. puberal52, 59, 60.
Para que a adequação do perfil de carboidratos Fibras

seja alcançada é possível utilizar programas de Denominam-se fibras os diversos compostos
computador que auxiliam a prescrição. Paralela- resistentes à ação digestiva das enzimas. As fibras
mente, propõem-se as seguintes orientações prá- da dieta são classificadas de acordo com sua
ticas gerais: solubilidade em água em solúveis e insolúveis e
ambos os tipos são encontrados naturalmente nos
a. Estímulo do consumo em forma de rodízio de: alimentos da forma como são consumidos65.
carnes bovinas (retirando toda a gordura aparente A fibra solúvel é aquela que, na presença de
antes do preparo), frango (retirando a pele e a água, se solubiliza formando um gel. Este estado
gordura aparente antes do preparo e priorizando aumenta a viscosidade dos alimentos no estômago,
o peito), porco (lombo e sem gordura aparente) e gerando maior sensação de saciedade. Há também
ovo. Em relação aos peixes de água fria e profunda benefícios em pacientes dislipidêmicos, pois as fibras
(salmão, bacalhau, truta, cavala, arenque, atum solúveis têm o poder de adsorção dos sais biliares.
e sardinha), ricos em ômega-3, sugere-se que São exemplos de fibras solúveis: pectinas, gomas,
sejam consumidos 1 vez por semana. A limitação mucilagem e polissacarídeos de armazenagem. Suas
ao uso 1 vez por semana refere-se ao risco de fontes são: aveia (em especial o seu farelo), frutas e
contaminação por metais pesados61 e à grande vegetais. As fibras insolúveis são responsáveis pela
quantidade de gordura na composição corporal formação do bolo fecal, podendo regular o trânsito
intestinal. São exemplos de insolúveis: celulose,
desses peixes, especialmente quando criados em
hemicelulose e lignina. As leguminosas e os cereais
cativeiro;
são fontes de ambos os tipos de fibras, sendo que os
b. A quantidade das carnes deverá ser de 100
cereais têm maior composição de fibras insolúveis,
gramas por porção;
em especial os integrais.
c. Dar preferência aos carboidratos complexos e de
Em relação ao metabolismo, apresentam
baixo índice glicêmico, buscando-se que 50% dos
como características: diminuição do tempo de trân-
cereais da dieta estejam na forma integral;
sito intestinal, aumento do bolo fecal e redução dos
d. Leite e derivados com baixo teor de gordura
níveis plasmáticos de glicose, insulina e do LDL-
(preferencialmente semi-desnatados62 não sendo
colesterol65. A redução do colesterol ocorre por efeito
recomendado o uso daqueles totalmente des-
mecânico (carreamento para as fezes) e também
natados devido à baixa aterogenicidade dos
devido à excreção de moléculas de colesterol
lipídeos lácteos63 e à importância dos precursores
através dos ácidos biliares, havendo a necessidade
do colesterol presentes no leite para a produção
de aumento da síntese desses ácidos a partir do
hormonal da criança37, 64); colesterol presente na circulação, ocorrendo assim
e. Frutas e verduras dentro do recomendado para a sua redução. A quantidade ideal de fibras a serem
idade (tabela 2); consumidas diariamente na faixa etária pediátrica
f. Alimentos excessivamente gordurosos, óleos ve- é obtida através da fórmula: Quantidade de fibras
getais de origem tropical (óleo de coco e de dendê) (em gramas) = idade (em anos) + 5. A proporção
e frituras devem ser praticamente ausentes na de fibras solúveis e insolúveis deve ser 1:1, e não
rotina alimentar; se deve ultrapassar o total de 25 g/dia. Este objetivo
g. Evitar o consumo domiciliar de produtos embu- é atingido se forem ingeridas 5 porções de frutas,
tidos, pré-prontos e de alimentos que contenham verduras e legumes por dia ou, caso isso não possa
gordura trans, além de doces e bebidas açuca- ser alcançado, através da reposição de fibras como
radas; suplemento alimentar65, 66.
h. Em adolescentes, desencorajar fortemente o con- A tabela 3 mostra o teor de fibras de alguns
sumo de álcool. alimentos.
Fitoesteroides O efeito da AF sobre a dislipidemia em crianças

Os fitoesterois são um grupo de moléculas está longe de ser completamente entendido, pois
derivados do colesterol e que têm sua fonte princi- existem dados conflitantes sobre o efeito ser ou não
palmente no reino vegetal. São subdivididos em mediado pelo controle de peso induzido pelo gasto
esteroides ou estanoides, em função respectivamente energético38, 68, 69. Apesar de não se comprovar a
da ausência ou presença de insaturações em sua relação direta entre sedentarismo e dislipidemia, o
molécula. Foram demonstradas evidências de que estímulo à AF talvez seja uma das medidas mais
o consumo de fitoesterois está associado à redução importantes para a prevenção da DAC desde a
dos níveis plasmáticos de LDL-colesterol e também infância. Até o momento, não existem evidências
aumento dos níveis de HDL-colesterol, sendo esse científicas que demonstrem a prática de exercício
último efeito potencializado quando há consumo físico por crianças e adolescentes como variável
concomitante de niacina. O principal mecanismo que independente na melhora do seu metabolismo
leva à redução do LDL-colesterol é provavelmente lipídico51, mas ainda que o efeito seja mediado
a inibição da absorção intestinal de LDL-colesterol. pelo emagrecimento, sua inclusão no tratamento é
O consumo médio de 1,8 g/dia de fitoesterois leva inquestionável.
à redução dos níveis circulantes LDL-colesterol em Como medida genérica de combate ao se-
8%67. dentarismo, praticamente todas as sociedades
Esses compostos são naturalmente encon- pediátricas do mundo têm recomendado que as
trados em frutas, vegetais, óleos vegetais, castanhas crianças e adolescentes não permaneçam mais do
e sementes. Podem também constar em alimentos que 2 horas por dia em frente a telas (televisores,
enriquecidos, como margarinas, sucos, iogurtes e tablets, celulares, computadores e vídeo-games)4,6,37.
cereais.
São fontes dietéticas de fitoesterois: Intensidades da prática de atividade física
• Cereais: farelo de arroz, germe de trigo, farelo de A Organização Mundial da Saúde recomenda
aveia, trigo, e arroz escuro; que em crianças e adultos jovens a prática de AF inclua
• Leguminosas: feijão, ervilha e lentilha; brincadeiras, jogos, esportes, atividades recreativas,
• Sementes e castanhas: amendoim, amêndoa, opção por caminhadas a fim de deslocamento entre
sementes de girassol, abóbora, e gergelim, e locais, ou mesmo AF planejada junto à família, na
nozes; escola, ou em ambientes comunitários. As reco-
• Frutas e vegetais: brócolis, couve-flor, couve de mendações que têm por objetivo melhoria das fun-
Bruxelas, maçã, abacate, tomate, mirtilo, óleos ções cardiovascular, osteomuscular e metabólicas
vegetais e germe de trigo; são4, 6, 37:
• Alimentos fortificados. 1. Crianças e adolescentes ente 5 e 17 anos devem
A tabela 4 apresenta a quantidade de fitoes- acumular diariamente pelo menos 60 minutos de
terois de alguns alimentos. AF moderada ou vigorosa;
O presente consenso recomenda que, no 2. Maiores tempos acumulados de AF, além de 60
contexto da dieta, as crianças e adolescentes obe- minutos ao dia, promovem benefícios adicionais
sos com dislipidemia recebam 1,6 g de fitoesterol na saúde;
diariamente. Caso essa quantidade não seja atin- 3. A maior parte do exercício físico diário deve ser
gida pela alimentação, incluindo-se os alimentos aeróbico, atividades de intensidade vigorosa
fortificados, recomenda-se a suplementação. devem ser incorporadas pelo menos 3 vezes
na semana, inclusive aquelas que promovem
2) Atividade física aumento de força muscular e óssea.
Outro aspecto para a modificação do estilo de Define-se AF moderada ou vigorosa como
vida é a prática de AF, considerada um dos fatores uma atividade que causa aumento nas frequências
determinantes na diminuição do risco de DAC36. cardíaca e respiratória. Em uma pessoa saudável,
usualmente está associada a caminhada mais veloz, neurológico ou na maturação sexual74, 75. O que não
dança, natação ou ciclismo em terreno plano. O se sabe ainda, devido à inexistência de estudos de
dispêndio energético é associado a mais de 3 METs seguimento de longo prazo, é se o tratamento na
(Equivalentes Metabólicos), e o gasto energético infância diminui o risco de DAC futura39. O uso de
maior que 3,5 kcal/min. estatinas em crianças com dislipidemia grave já está
Não existe consenso que descreva objeti- bem estabelecido na literatura39, 70. A sinvastatina,
vamente os limites de intensidade em AF correla- a lovastatina, a atorvastatina e o ezetimibe são
cionados com sinais clínicos facilmente observáveis, aprovados pela FDA e pela European Medicines
como por exemplo frequência cardíaca. Não há, Agency (EMEA) para uso em crianças acima de 10
tampouco, estudos desenhados para a determinação anos de idade. A pravastatina também está aprovada
de faixas de VO2max em crianças ou adolescentes. pela FDA e EMEA para uso em crianças acima de 8
Mesmo os que citam alguma descrição de intervalos anos de idade76. As características, doses e efeitos
de intensidade, geralmente se referem a percentuais dos medicamentos hipolipemiantes estão descritos
estimados da FC máxima utilizando a fórmula “FCmax na Tabela 5.
= 220-idade”, a qual, apesar do seu frequente uso, O presente consenso propõe que as estatinas
não apresenta sustentação científica. são as drogas de primeira escolha, devendo o
tratamento ser iniciado com a dose mais baixa, ao
Acompanhamento se deitar (Tabela 6). Adolescentes do sexo feminino
Deve-se reavaliar os pacientes em tratamento já em idade fértil devem, necessariamente, fazer
não farmacológico após 3 meses do início das uso de contraceptivo oral. Para o acompanhamento
modificações de estilo de vida, reforçando as da farmacoterapia, exames laboratoriais (creatina
orientações prévias e realizando novo controle fosfoquinase, alanina aminotransferase, aspartato
laboratorial. aminotransferase e perfil lipídico) devem ser
repetidos 12 semanas após o inicio da terapêutica,
Etapa 2 – Tratamento medicamentoso ou mais cedo se houver surgimento de sinais e
A NCEP recomenda o início do tratamento sintomas, para determinar a eficácia da medicação
medicamentoso a partir dos 10 anos de idade, e avaliar possíveis efeitos adversos musculares e
idealmente a partir do estágio II de Tanner, e após hepáticos.
falha das modificações de estilo de vida por 6 a 12 Para os casos mais complexos de dislipide-
meses38. A American Heart Association e a American mias, que não respondem adequadamente ao uso
Academy of Pediatrics sugeriram modificação da de estatinas, pode-se considerar a prescrição de
idade de início do tratamento farmacológico da ezetimibe, apesar de poucos estudos pediátricos,
dislipidemia para 8 anos de idade39, 70. No presente e da colestiramina, muito pouco tolerada, além de
consenso, propõe-se que, após nova dosagem de encaminhamento para serviços especializados em
perfil lipídico, a criança que permanecer com LDL- dislipidemia pediátrica.
colesterol acima de 190 mg/dL ou com LDL-colesterol O controle com exames laboratoriais deve ser
acima de 160 mg/dL com fator de risco (parentes de realizado a cada 3 meses, para se reavaliar se o
primeiro grau com DAC prematura, HDL-colesterol < paciente deve permanecer nas etapas 1 e 2 ou se
35 mg/dL, tabagismo, HAS ou diabetes mélito), deva pode seguir apenas a etapa 1.
ser submetida a tratamento farmacológico71-73.
Já é aceito, com base em clinical trials, que a RECOMENDAÇÕES
terapia com estatinas em crianças com dislipidemia
familiar, comparado com placebo, diminui LDL- A formação precoce da aterosclerose durante
colesterol, sem causar efeitos adversos significativos a infância, através da presença de placas ateros-
ao longo de anos de seguimento e sem provocar cleróticas na camada média-intimal das artérias,
efeitos adversos no crescimento, no desenvolvimento reforça a necessidade de focar na prevenção de
DAC nesse período da vida. A reversibilidade das nutrológicas e de estímulo à prática de AF (Etapa
primeiras lesões ateroscleróticas deixa clara a 1) e farmacoterapia (Etapa 2);
indispensabilidade de se controlar a dislipidemia, 5. A medicação de escolha é a sinvastatina na dose
seja por modificações de estilo de vida ou com o uso inicial de 10 mg/dia. Em caso de intolerância ou
de medicamentos36. de insucesso, outras medicações podem ser
A dislipidemia infanto-juvenil deve ser avaliada usadas como substitutas ou associadas;
entre as crianças com sobrepeso e obesidade atra- 6. Pacientes em uso de farmacoterapia (Etapa 2)
vés da solicitação de perfil lipídico a partir dos 2 anos devem ser reavaliados clínica e laboratorialmente
de idade. a cada 3 meses, a fim de se verificar a presença
Uma vez que não se têm estudos de longo de indicadores de prejuízos à saúde derivados do
prazo de observação em crianças, deve-se assumir fármaco. Essa reavaliação visa também embasar
o tratamento pediátrico baseado em estudos em a decisão sobre a necessidade de continuidade da
adultos e coortes que começaram na infância. A farmacoterapia ou sua suspensão. A medicação
recomendação das terapias não farmacológica e deve ser suspensa quando o paciente apresentar
farmacológica para manejo e controle da dislipi- LDL-colesterol abaixo de 160 mg/dL. Nesse caso,
demia se deve às evidências crescentes de o paciente deve ser mantido na Etapa 1 enquanto
que a dislipidemia na infância e adolescência, o lipidograma não estiver normalizado.
especialmente quando associada à obesidade,
contribui para o desenvolvimento de aterosclerose,
DAC e DCNT, aumentando a morbimortalidade na REFERÊNCIAS BIBLIOGRÁFICAS
idade adulta. 1. Singh GK, Kogan MD, van Dyck PC. Changes in state-
specific childhood obesity and overweight prevalence in
Este Consenso propõe que: the United States from 2003 to 2007. Arch Pediatr Adolesc
1. Toda criança e adolescente com sobrepeso ou Med. 2010;164(7):598-607.
obesidade deve ter seu perfil lipídico avaliado a 2. IBGE. Pesquisa de orçamentos familiares 2008-
partir dos 2 anos de idade. Se houver resultado 2009 - Antropometria e estado nutricional de crianças,
alterado, a dosagem deve ser repetida em 4 adolescentes e adultos no Brasil. IBGE. Instituto Brasileiro
de Pesquisa Geográfica e Estatística. Ministério do
semanas a fim de se eliminar a possibilidade de
Planejamento, Orçamento e Gestão; 2010.
erro laboratorial;
2. Pacientes obesos ou com sobrepeso com LDL- 3. Lughetti L, Bruzzi P, Predieri B. Evaluation and
management of hyperlipidemia in children and
colesterol abaixo de 160mg/mL devem ser
adolescents. Curr Opin Pediatr. 2010;22(4):485-93.
tratados através de medidas nutrológicas e de
estímulo à prática de AF (Etapa 1); 4. de Mello ED, Nogueira-de-Almeida CA. Manejo da
obesidade infanto-juvenil. International Journal of
3. Pacientes obesos ou com sobrepeso e LDL-
Nutrology. 2017;10(1):322-4.
colesterol com valores entre 160 e 190 mg/
mL devem ser tratados através de medidas 5. Nogueira-de-Almeida CA, Pires LA, dos Santos RG.
nutrológicas e de estímulo à prática de AF Comparação de indicadores de perfis glicêmico e lipídico
entre crianças e adolescentes obesos egressos de serviço
(Etapa 1). Esse tratamento deve ser associado público ou privado da cidade de Ribeirão Preto (SP).
à farmacoterapia para as crianças com mais de 8 Medicina (Ribeirao Preto Online). 2016;49(6):504-10.
anos de idade (Etapa 2) quando estiver presente
6. Nogueira-de-Almeida CA, Mello ED. Obesidade. In:
pelo menos 1 fator de risco adicional à obesidade Nogueira-de-Almeida CA, Mello ED, editors. Nutrologia
(parentes de primeiro grau com DAC prematura, Pediátrica - Prática Baseada em Evidências. 1. 1 ed. São
HDL-colesterol < 35 mg/dL, tabagismo, HAS ou Paulo: Manole; 2016.
diabetes mélito); 7. Mello ED, Nogueira-de-Almeida CA, Mello PP, Mello PD.
4. Pacientes obesos ou com sobrepeso com LDL- Dislipidemia. In: Nogueira-de-Almeida C, Mello E, editors.
colesterol acima de 190 mg/mL e idade maior que Nutrologia Pediátrica - Prática Baseada em Evidências. 1.
8 anos devem ser tratados através de medidas 1 ed. São Paulo: Manole; 2016.
8. Giuliano IdCB, Coutinho MSSdA, Freitas SFTd, Pires obese children: present and future. Revista Paulista de
MMdS, Zunino JN, Ribeiro RQdC. Lípides séricos Pediatria. 2012;30(3):431-7.
em crianças e adolescentes de Florianópolis, SC:
Estudo Floripa saudável 2040. Arquivos Brasileiros de 22. Nogueira-de-Almeida CA, Garcia J, Caixe SH, Benedeti
Cardiologia. 2005;85:85-91. AC. Ultrasonographic Assessment of the Common
Carotid Intima-Media Complex in Normal Weight Children
9. Moura EC, Castro CMd, Mellin AS, Figueiredo DBd. Perfil and in Overweight/Obese Children. The FASEB Journal.
lipídico em escolares de Campinas, SP, Brasil. Revista de 2016;30(1 Supplement):1165.3-.3.
Saúde Pública. 2000;34:499-505.
23. Nakashima Y, Fujii H, Sumiyoshi S, Wight TN, Sueishi
10. Ribeiro RQC. Epidemiologia das dislipidemias em K. Early human atherosclerosis: accumulation of lipid
escolares. Belo Horizonte: UFMG; 2000. and proteoglycans in intimal thickenings followed by
macrophage infiltration. Arterioscler Thromb Vasc Biol.
11. Faria ECd, Dalpino FB, Takata R. Lípides e lipoproteínas 2007;27(5):1159-65.
séricos em crianças e adolescentes ambulatoriais de
um hospital universitário público. Revista Paulista de 24. Pinho AP, Brunetti IL, Pepato MT, Almeida CANd. Metabolic
Pediatria. 2008;26:54-8. syndrome in overweight/obese female adolescents.
Revista Paulista de Pediatria. 2012;30(1):51-6.
12. Nogueira-de-Almeida CA, Mello ED. Por que um livro de
Nutrologia Pediátrica? In: Nogueira-de-Almeida CA, Mello 25. Pilz S, Horejsi R, Moller R, Almer G, Scharnagl H,
ED, editors. Nutrologia Pediátrica - Prática Baseada em Stojakovic T, et al. Early atherosclerosis in obese juveniles
Evidências. 1. 1 ed. São Paulo: Manole; 2016. is associated with low serum levels of adiponectin.
The Journal of clinical endocrinology and metabolism.
13. Barker DJ, Eriksson JG, Forsen T, Osmond C. Fetal 2005;90(8):4792-6.
origins of adult disease: strength of effects and biological
basis. Int J Epidemiol. 2002;31(6):1235-9. 26. Ballesteros MN, Cabrera RM, Saucedo Mdel S, Aggarwal
D, Shachter NS, Fernandez ML. High intake of saturated
14. Lawlor DA, Davey Smith G, Ebrahim S. Birth weight is
fat and early occurrence of specific biomarkers may
inversely associated with coronary heart disease in post-
explain the prevalence of chronic disease in northern
menopausal women: findings from the British women’s
Mexico. The Journal of nutrition. 2005;135(1):70-3.
heart and health study. Journal of epidemiology and
community health. 2004;58(2):120-5. 27. Frontini MG, Srinivasan SR, Xu J, Tang R, Bond MG,
Berenson GS. Usefulness of childhood non-high density
15. Palinski W, Napoli C. The fetal origins of atherosclerosis:
lipoprotein cholesterol levels versus other lipoprotein
maternal hypercholesterolemia, and cholesterol-lowering
measures in predicting adult subclinical atherosclerosis:
or antioxidant treatment during pregnancy influence
the Bogalusa Heart Study. Pediatrics. 2008;121(5):924-9.
in utero programming and postnatal susceptibility to
atherogenesis. FASEB J. 2002;16(11):1348-60. 28. McGill HC, Jr., McMahan CA, Gidding SS. Preventing
heart disease in the 21st century: implications of the
16. Dietz WH. Breastfeeding may help prevent childhood
Pathobiological Determinants of Atherosclerosis in Youth
overweight. Jama. 2001;285(19):2506-7.
(PDAY) study. Circulation. 2008;117(9):1216-27.
17. Roberts SB. Prevention of hypertension in adulthood by
29. Tracy RE, Newman WP, 3rd, Wattigney WA, Berenson
breastfeeding? Lancet. 2001;357(9254):406-7.
GS. Risk factors and atherosclerosis in youth autopsy
18. Brotons C, Ribera A, Perich RM, Abrodos D, Magana P, findings of the Bogalusa Heart Study. Am J Med Sci.
Pablo S, et al. Worldwide distribution of blood lipids and 1995;310 Suppl 1:S37-41.
lipoproteins in childhood and adolescence: a review study.
30. Berenson GS, Srinivasan SR, Bao W, Newman WP, 3rd,
Atherosclerosis. 1998;139(1):1-9.
Tracy RE, Wattigney WA. Association between multiple
19. Nogueira-de-Almeida CA, Garcia J, Caixe SH, Benedeti cardiovascular risk factors and atherosclerosis in children
ACGS. Ultrasonographic Assessment of the Common and young adults. The Bogalusa Heart Study. The New
Carotid Intima-Media Complex in Normal Weight Children England journal of medicine. 1998;338(23):1650-6.
and in Overweight/Obese Children. The FASEB Journal.
2016;30(1 Supplement):1165.3. 31. Levi F, Lucchini F, Negri E, La Vecchia C. Trends in
mortality from cardiovascular and cerebrovascular
20. Francoso LA, Coates V. Anatomicopathological evidence diseases in Europe and other areas of the world. Heart.
of the beginning of atherosclerosis in infancy and 2002;88(2):119-24.
adolescence. Arq Bras Cardiol. 2002;78(1):131-42.
32. Hansson GK. Inflammation, atherosclerosis, and coronary
21. Costa KCM, Lima JC, Almeida CANd, Ciampo LAD, artery disease. The New England journal of medicine.
Souza CSBd. Variation of the brachial artery diameter in 2005;352(16):1685-95.
33. Schulpis K, Karikas GA. Serum Cholesterol and 47. Girardet JP, Luc G, Rieu D, Bruckert E, Darmaun D,
Triglyceride Distribution in 7767\’a0School-aged Greek Farnier M. Prise en charge des hypercholestérolé mies
Children. 1998;101(5). de l’enfant: recommandations du Comité de nutrition
de la Société française de pédiatrie et de la Nouvelle
34. Bao W, Srinivasan SR, Wattigney WA, Bao W, Berenson société française d’athérosclérose. Archives de Pédiatrie.
GS. Usefulness of childhood low-density lipoprotein 2011;18:12.
cholesterol level in predicting adult dyslipidemia and other
cardiovascular risks. The Bogalusa Heart Study. Arch 48. Mata P, Alonso R, Ruiz A, Gonzalez-Juanatey JR,
Intern Med. 1996;156(12):1315-20. Badimón L, Díaz-Díaz JL, et al. Diagnóstico y tratamiento
de la hipercolesterolemia familiar en España: documento
35. Botham KM, Mayers PA. Sintese, transporte e excreção de consenso. Atención Primaria. 2015;47(1):56-65.
do colesterol. In: Rodwell VW, Bender DA, Botham KM,
Kennelly PJ, Weil PA, editors. Bioquímica Ilustrada de 49. Caramelli B, Giuliana ICB. Dislipidemia em crianças e
Harper. Porto Alegre: AMGH; 2017. p. 267-79. adolescentes. Rev Soc Cardiol Estado de São Paulo.
2005;6:6.
36. Xavier HT, Izar MC, Faria Neto JR, Assad MH, Rocha VZ,
Sposito AC, et al. V Diretriz Brasileira de Dislipidemias 50. Holmes KW, Kwiterovich PO, Jr. Treatment of
e Prevenção da Aterosclerose. Arq Bras Cardiol. dyslipidemia in children and adolescents. Curr Cardiol
2013;101(4):22. Rep. 2005;7(6):445-56.
37. SBP. Obesidade na infância e adolescência - Manual de 51. Kavey R-EW, Daniels SR, Lauer RM, Atkins DL, Hayman
Orientação. São Paulo; 2012. LL, Taubert K. American Heart Association Guidelines
for Primary Prevention of Atherosclerotic Cardiovascular
38. National Cholesterol Education Program (NCEP):
Disease Beginning in Childhood. Circulation.
Highlights of the Report of the Expert Panel on Blood
2003;107(11):1562-6.
Cholesterol Levels in Children and Adolescents.
Pediatrics. 1992;89(3):495-501. 52. Zappalla FR, Gidding SS. Lipid management in children.
39. Daniels SR, Greer FR, Committee on N. Lipid screening Endocrinol Metab Clin North Am. 2009;38(1):171-83.
and cardiovascular health in childhood. Pediatrics. 53. Colletti RB, Neufeld EJ, Roff NK, McAuliffe TL, Baker AL,
2008;122(1):198-208.
Newburger JW. Niacin treatment of hypercholesterolemia
40. I Diretriz de Prevenção da Aterosclerose na Infância e in children. Pediatrics. 1993;92(1):78-82.
na Adolescência. Arquivos Brasileiros de Cardiologia.
54. Malhotra A, Shafiq N, Arora A, Singh M, Kumar R,
2005;85:3-36.
Malhotra S. Dietary interventions (plant sterols, stanols,
41. Consenso Brasileiro para a Normatização da omega-3 fatty acids, soy protein and dietary fibers) for
Determinação Laboratorial do Perfil Lipídico, (2017). familial hypercholesterolaemia. Cochrane Database Syst
Rev. 2014(6):CD001918.
42. Pereira A, Gagliardi A, Lottenberg A, Chacra A, Faludi A,
Sposito A, et al. I Diretriz Brasileira de Hipercolesterolemia 55. Engler MM, Engler MB, Malloy MJ, Paul SM, Kulkarni
Familiar (HF). Arquivos Brasileiros de Cardiologia. KR, Mietus-Snyder ML. Effect of docosahexaenoic acid
2012;99:1-28. on lipoprotein subclasses in hyperlipidemic children (the
EARLY study). Am J Cardiol. 2005;95(7):869-71.
43. Non LR, Escota GV, Powderly WG. HIV and its relationship
to insulin resistance and lipid abnormalities. Transl Res. 56. Kennedy MJ, Jellerson KD, Snow MZ, Zacchetti ML.
2017;183:41-56. Challenges in the pharmacologic management of obesity
and secondary dyslipidemia in children and adolescents.
44. [Consensus on management of dyslipidemia in pediatrics]. Paediatr Drugs. 2013;15(5):335-42.
Archivos argentinos de pediatria. 2015;113(2):177-86.
57. Achimastos A, Alexandrides T, Alexopoulos D, Athyros
45. S BY, L. CBM, C. BL, I. HBM. Diagnóstico y tratamiento V, Bargiota A, Bilianou E, et al. Expert consensus on the
de las dislipidemias en niños y adolescentes: rational clinical use of proprotein convertase subtilisin/
Recomendaciones de la Rama de Nutrición de la kexin type 9 (PCSK9) inhibitors. Hormones (Athens,
Sociedad Chilena de Pediatría. Revista chilena de Greece). 2016;15(1):8-14.
pediatría. 2014;85:367-77.
58. Kersting M, Alexy U, Clausen K. Using the concept of
46. Yoon JM. Dyslipidemia in Children and Adolescents: Food Based Dietary Guidelines to Develop an Optimized
When and How to Diagnose and Treat? Pediatric Mixed Diet (OMD) for German children and adolescents.
Gastroenterology, Hepatology & Nutrition. 2014;17(2):85- Journal of pediatric gastroenterology and nutrition.
92. 2005;40(3):301-8.
59. Lughetti L, Predieri B, Balli F, Calandra S. Rational scientific statement from the American Heart Association
approach to the treatment for heterozygous familial Atherosclerosis, Hypertension, and Obesity in Youth
hypercholesterolemia in childhood and adolescence: Committee, Council of Cardiovascular Disease in the
a review. Journal of endocrinological investigation. Young, with the Council on Cardiovascular Nursing.
2007;30(8):700-19. Circulation. 2007;115(14):1948-67.
60. Olson RE. Is it wise to restrict fat in the diets of 71. Tonstad S. Role of lipid-lowering pharmacotherapy in
children? Journal of the American Dietetic Association. children. Paediatr Drugs. 2000;2(1):11-22.
2000;100(1):28-32.
72. Williams CL, Hayman LL, Daniels SR, Robinson TN,
61. Mohammed A, Mohammed T. Mercury, arsenic, cadmium Steinberger J, Paridon S, et al. Cardiovascular health in
and lead in two commercial shark species (Sphyrna lewini childhood: A statement for health professionals from the
and Caraharinus porosus) in Trinidad and Tobago. Marine Committee on Atherosclerosis, Hypertension, and Obesity
pollution bulletin. 2017;119(2):214-8. in the Young (AHOY) of the Council on Cardiovascular
Disease in the Young, American Heart Association.
62. Lichtenstein AH, Appel LJ, Brands M, Carnethon
Circulation. 2002;106(1):143-60.
M, Daniels S, Franch HA, et al. Diet and lifestyle
recommendations revision 2006: a scientific statement 73. Xydakis AM, Guyton JR, Chiou P, Stein JL, Jones PH,
from the American Heart Association Nutrition Committee. Ballantyne CM. Effectiveness and tolerability of ezetimibe
Circulation. 2006;114(1):82-96. add-on therapy to a bile acid resin-based regimen for
hypercholesterolemia. Am J Cardiol. 2004;94(6):795-7.
63. Kris-Etherton PM, Griel AE, Psota TL, Gebauer SK,
Zhang J, Etherton TD. Dietary stearic acid and risk of 74. Arambepola C, Farmer AJ, Perera R, Neil HA. Statin
cardiovascular disease: intake, sources, digestion, and treatment for children and adolescents with heterozygous
absorption. Lipids. 2005;40(12):1193-200. familial hypercholesterolaemia: a systematic review and
64. Santos RD, Gagliardi ACM, Xavier HT, Magnoni CD, meta-analysis. Atherosclerosis. 2007;195(2):339-47.
Cassani R, Lottenberg AMP, et al. I Diretriz sobre o 75. O’Gorman CS, Higgins MF, O’Neill MB. Systematic
consumo de gorduras e saúde cardiovascular. Arquivos
review and metaanalysis of statins for heterozygous
Brasileiros de Cardiologia. 2013;100:1-40.
familial hypercholesterolemia in children: evaluation of
65. Mello PP, Mello ED, Nogueira-de-Almeida CA. cholesterol changes and side effects. Pediatric cardiology.
Constipação Intestinal. In: Nogueira-de-Almeida C, Mello 2009;30(4):482-9.
E, editors. Nutrologia Pediátrica - Prática Baseada em
76. Van der Graaf A, Kastelein JJ, Wiegman A. Heterozygous
Evidências. 1. 1 ed. São Paulo: Manole; 2016.
familial hypercholesterolaemia in childhood:
66. Santos ZEA. Necessidades Nutricionais de Crianças e cardiovascular risk prevention. J Inherit Metab Dis.
Adolescentes Saudáveis. In: Nogueira-de-Almeida C, 2009;32(6):699-705.
Mello E, editors. Nutrologia Pediátrica - Prática Baseada
77. Nogueira-de-Almeida CA, Mello ED. Como Fazer um
em Evidências. 1. 1 ed. São Paulo: Manole; 2016.
Plano Alimentar. In: Nogueira-de-Almeida CA, Mello
67. Jakulj L, Vissers MN, Rodenburg J, Wiegman A, ED, editors. Nutrologia Pediátrica - Prática Baseada em
Trip MD, Kastelein JJP. Plant stanols do not restore Evidências. 1. 1 ed. São Paulo: Manole; 2016.
endothelial function in pre-pubertal children with
familial hypercholesterolemia despite reduction of low- 78. Anderson JW. Plant Fiber in Foods. 2 ed: HCF Nutrition
density lipoprotein cholesterol levels. The Journal of Research Foundation; 1990.
Pediatrics.148(4):495-500.
79. Silva GLd. Fontes dietéticas de fitoesteróis e seu efeito na
68. Executive Summary of The Third Report of The National saúde humana. 2016.
Cholesterol Education Program (NCEP) Expert Panel
on Detection, Evaluation, And Treatment of High Blood
Cholesterol In Adults (Adult Treatment Panel III). Jama.
2001;285(19):2486-97.
69. Boreham C, Twisk J, Murray L, Savage M, Strain JJ, Cran Revisado em 25/09/2017
Aceito em 01/10/2017
G. Fitness, fatness, and coronary heart disease risk in
adolescents: the Northern Ireland Young Hearts Project.
Med Sci Sports Exerc. 2001;33(2):270-4. Autor Correspondente:
70. McCrindle BW, Urbina EM, Dennison BA, Jacobson MS, R. São José, 2591 - Subsetor Sul 1, Ribeirão Preto - SP, 14025-180
Steinberger J, Rocchini AP, et al. Drug therapy of high- email: dr.nogueira@me.com
risk lipid abnormalities in children and adolescents: a Fone: 3877 5034
Tabela 1 - Valores de referência lipídica propostos para faixa etária de 2 a 19 anos pela Sociedade
Brasileira de Cardiologia40.
Desejáveis Limítrofes Aumentados

Lipídeos (mg/dL) (mg/dL) (mg/dL)
Colesterol total <150 150-169 ≥170

LDL-colesterol <100 100-129 ≥130
HDL-colesterol ≥45
Triglicerídeos <100 100-129 ≥130
Tabela 2 - Porções de frutas e verduras conforme faixa etária77.
Faixa etária Frutas Verduras e Legumes
1 a 3 anos 4 porções 3 porções
4 a 6 anos 3 porções 3 porções
Idade escolar 3 porções 3 porções
Adolescentes do sexo feminino 4 porções 4 e ½ porções
Adolescentes do sexo masculino 4-5 porções 4,5-5 porções
Tabela 3 - Conteúdo de fibra alimentar em porções comuns78.
Total de fibra Fibra solúvel Fibra insolúvel

Alimento por porção or porção por porção Porção
Vegetais, cozidos
Aspargos 2,8 1,7 1,1 ½ xícara
Beterraba, crua somente 1,8 0,8 1,0 ½ xícara
Brócolis 2,4 1,2 1,2 ½ xícara
Milho, enlatado 1,6 0,2 1,4 ½ xícara
Cenoura, fatiada 2,0 1,1 0,9 ½ xícara
Vagem 2,0 0,7 1,8 ½ xícara
Couve 2,5 0,7 1,8 ½ xícara
Quiabo, congelado 4,1 1,0 3,1 ½ xícara
Ervilhas, congelada 4,3 1,3 3,0 ½ xícara
Batata doce, crua somente 4,0 1,8 2,2 ½ xícara
Espinafre 1,6 0,5 1,1 ½ xícara
Molho de tomate 1,7 0,8 0,9 ½ xícara
Nabo 4,8 1,7 3,1 ½ xícara
Frutas e vegetais crus
Repolho vermelho 1,5 0,6 0,9 1 xícara
Cenoura 2,3 1,1 1,2 1,7 ½ ao longo
Aipo 1,7 0,1 1,0 1 xícara picado
Pepino 0,5 0,2 0,3 1 xícara
Alface 0,5 0,1 0,4 1 xícara

Cogumelos 0,8 0,1 0,7 1 xícara picado
Cebola 1,7 0,9 0,8 1 xícara picado
Pimentão verde 1,7 0,7 1,0 1 xícara picado
Tomate, fresco 1,0 0,1 0,9 1 médio
Maça, com casca 2,8 1,0 1,8 1 pequena
Molho de maçã 2,0 0,7 1,3 ½ xícara
Damasco, seco 2,0 1,1 0,9 7 metades
Damasco, fresco com casca 3,5 1,8 1,7 4 unidades
Banana, fresca 1,1 0,3 0,8 ½ pequena
Mirtilo, fresco 1,4 0,3 1,1 ¾ xícara
Cereja preta, fresca 1,3 0,6 0,7 12 grandes
Figo, seco 3,0 1,4 1,6 1½
Toranja, fresca 1,6 1,1 0,5 ½ média
Uva, fresca com casca 0,5 0,2 0,3 15 pequenas
Kiwi, fresco 1,7 0,7 1,0 1 grande
Manga 2,9 1,7 1,2 ½ pequena
Melão 1,1 0,3 0,8 1 copo, picado
Laranja 2,9 1,8 1,1 1 pequena
Pêssego, fresca com casca 2,0 1,0 1,0 1 médio
Pera, fresca com casca 2,9 1,1 1,8 ½ grande
Ameixa vermelha, fresca 2,4 1,1 1,3 2 médias
Ameixa seca 1,7 1,0 0,7 3 médias
Uva passa seca 0,4 0,2 0,2 3 colheres sopa
Morangos, frescos 2,8 1,1 1,7 1 ¼ xícara
Melancia 0,6 0,4 0,2 1 ¼ xícara, cubos
Leguminosas (cozidas)
Feijão preto 6,1 2,4 3,7 ½ xícara
Lentilha 5,2 0,6 4,6 ½ xícara
Feijão 4,3 1,1 3,2 ½ xícara
Feijão branco 6,5 2,2 4,3 ½ xícara
Massa, Arroz, Grãos
Cevada, cozida 3,0 0,8 2,2 ½ xícara
Milho de pipoca 2,0 0,1 1,9 3 xícaras
Arroz branco, cozido 0,8 Traço 0,8 ½ xícara
Espaguete branco, cozido 0,9 0,4 0,5 ½ xícara
Espaguete de trigo, cozido 2,7 0,6 2,1 ½ xícara
Farelo de trigo 12,3 1,0 11,3 ½ xícara
Gérmen de trigo 3,9 0,7 3,2 3 colheres sopa
Pão e bolachas
Pão de centeio 2,7 1,2 1,5 1 fatia
Pão branco 0,6 0,3 0,3 1 fatia
Pão integral 1,5 0,3 1,2 1 fatias
Nozes e sementes
Amêndoas 0,6 0,1 0,5 6 unidades
Linhaça 3,3 1,1 2,2 1 colher sopa
Pasta de amendoim 1,0 0,3 0,7 1 colher sopa
Amendoim torrado 0,6 0,2 0,4 10 unidades
Sementes de gergelim 0,5 0,2 0,3 1 colher sopa
Nozes 0,3 0,1 0,2 2 unidades
Tabela 4 - Fontes alimentares de fitoesteróis79.
Fonte Porção Quantidade de fitoesterol
Amêndoa 30g 30mg

Maçã 1 unidade média 25mg
Grão de bico 30g 10mg
Gergelim 1 colher de sopa 100mg
Óleo de milho 1 colher de sopa 135mg
Margarina fortificada 2 colheres de sopa (20g) 1.600 mg
Iogurte líquido fortificado 1 pote (75g) 1.100 mg
Tabela 5 - Características gerais das drogas hipolipemiantes usadas no tratamento da dislipidemia6, 7, 36, 37, 40, 42, 44-46, 52, 70.
Classe Mecanismo de ação Dose Efeito esperado Efeitos adversos
↓ síntese endógena de colesterol por Sinvastatina: ↓ 20-55% LDL-colesterol; Elevação de transaminases,

inibição HGM-CoA redutase; 10-40mg/dia ↓ 5-10% TG; elevação de creatinoquinase e
↑ atividade receptores de LDL- ↑ 5-10% HDL-colesterol miopatia
colesterol no fígado Lovastatina:
10-40mg/dia Contraindicado durante a gestação
Estatinas por potencial efeito aterogênico
Atorvastatina:
10-20mg/dia
Pravastatina:
20-40mg/dia
Inibidores absorção Inibidor específico da absorção do Ezetimiba: ↓ 17-20% LDL-colesterol ↑ síntese de colesterol
do colesterol colesterol, agindo sobre a borda 10mg/dia
estriada do enterócito
Sequestradores Agem no intestino se ligando aos Colestiramina: ↓ 13-20% LDL-colesterol Náusea, dor abdominal,
de ácidos biliares ácidos biliares e evitando sua 4-16g/dia hipertrigliceridemia e alteração na
(resinas) reabsorção, promovendo excreção Colestipol: absorção de vitaminas lipossolúveis
e remoção do ciclo do colesterol 5-20g/dia e ácido fólico
Não há absorção sistêmica
Fibratos ↓ síntese de VLDL-colesterol 10-20mg/dia ↓ TG; ↑ níveis HDL-colesterol; Distúrbios gastrointestinais,

efeito variável sobre os níveis colelitíase, elevação de
de LDL- transaminases e da
colesterol creatinoquinase
Niacinaª ↓ síntese hepática de LDL 100mg até 1g/dia ↓5-25% LDL-colesterol; Rubor, diarreia, insuficiência
-colesterol, ↓20-50% TG; ↑15-35% HDL- hepática, elevação de
↓ secreção de de VLDL colesterol transaminases, miopatia,
-colesterol intolerância a glicose e hiperuricemia
Nutracêuticos Melhoram função endotelial Ácidos graxos ↓ TG --

ômega-3: 2-4g/dia
Tabela 6 - Orientações para prescrição de estatinas6, 7, 36, 37, 40, 42, 44-46, 52, 70
Estatina Dose Uso Reação Adversa Contraindicação Monitorização
Sinvastatina <10 anos: iniciar com 5mgà noite, Agente hipolipemiante; Fibrilação atrial, edema, Alergia a componentes da No início do tratamento, solicitar
aumentar para 10mg após 4 via oral; vertigem, cefaleia, sinvastatina, TGO/TGP/CPK/perfil lipídico.
semanas e aumentar novamente Uso preferencial à noite; eczema, dor abdominal, hepatopatia, elevação
para 20mg após 4 semanas efeito máximo após 2 constipação, dispepsia, persistente de Repetir TGO e TGP 4 semanas
semanas de adesão nausea, elevação de transaminases, gestação após o início do tratamento. Se
≥10 anos: iniciar com 10mg transaminases, mialgia, e lactação, medicamentos normais, realizar controles
à noite, aumentar para 20mg elevação de CPK, inibidores de CYP3A4*, uso a cada 3 meses no
após 6 semanas e aumentar broncoespasmo. concomitante de ciclosporina primeiro ano.
novamente para 40mg
após 6 semanas Após o primeiro ano, realizar
controle a cada 6 meses.
Máximo: 80mg/dia
Dose ajustada para função renal
Lovastatina >10 anos: 10-40mg 1x/dia Agente hipolipemiante; Cefaléia, tontura, rash Alergia a componentes da No início do tratamento, solicitar
via oral; cutâneo, dor abdominal, lovastatina, TGO/TGP/CPK/perfil lipídico.
preferencialmente à noite constipação, diarréia, hepatopatia, elevação
dispepsia, flatulência, persistente de Repetir TGO e TGP 4 semanas
náusea, câimbras, transaminases, gestação, após o início do tratamento. Se
mialgia, fraqueza, lactação, medicamentos normais, realizar controles a
elevação de CPK inibidores de CYP3A4* cada 3 meses no primeiro ano.
Após o primeiro ano, realizar

Atorvastatina ≥10 anos: iniciar com 10mg/dia Agente hipolipemiante; Insônia, diarréia, Alergia a componentes da No início do tratamento, solicitar
e aumentar para 20mg/dia em via oral; dispepsia, náusea, atorvastatina, hepatopatia, TGO/TGP/CPK/perfil lipídico.
4-12sem infecção do trato elevação persistente de
urinário, elevação de transaminases, gestação, Repetir TGO e TGP 4 semanas
Máximo: 20mg/dia transaminases, artralgia, lactação após o início do tratamento.
espasmo muscular, dor Se normais, realizar controles a
musculoesquelética, cada 3 meses no primeiro ano.
mialgia, nasofaringite
Pravastatina 8-13 anos: 20mg 1x/dia Agente hipolipemiante; Dor no peito, tontura, Alergia a componentes da No início do tratamento, solicitar
via oral; fatiga, cefaléia, rash pravastatina, hepatopatia, TGO/TGP/CPK/perfil lipídico.
14-18anos: 40mg 1x/dia cutâneo, diarréia, pirose, elevação persistente de
náusea, vômito, transaminases, gestação, Repetir TGO e TGP 4 semanas
elevação de lactação após o início do tratamento.
transaminases, Se normais, realizar controles a
mialgia, tosse, gripe cada 3 meses no primeiro ano.

Rosuvastatina 10-17 anos: 5-20mg 1x/dia, Agente hipolipemiante; Tontuta, cefaléia, diabetes Alergia a componentes da No início do tratamento, solicitar
aumento a cada 4 semanas via oral; mellitus, dor abdominal, rosuvastatina, hepatopatia, TGO/TGP/CPK/perfil lipídico.
constipação, náusea, elevação persistente de
Máximo: 20mg/dia elevação de TGP, transaminases, gestação, Repetir TGO e TGP 4 semanas
artralgia, elevação lactação, presença de fator após o início do tratamento.
de CPK, mialgia de risco para rabdomiólise, Se normais, realizar controles a
e fraqueza hipotireoidismo, alcoolismo cada 3 meses no primeiro ano.

Figura 1 - Etapas da opção terapêutica de acordo com valores de LDL-colesterol e presença de fatores de risco
(valores de LDL expressos em mg/dL).
1
1. Tabela de peso e estatura (percentil 50) utilizando como referencial o NCHS 77/8 - gênero masculino
Anos Mês Estatura Peso Anos Mês Estatura Peso Anos Mês Estatura Peso Anos Mês Estatura Peso
0,0 0,0 50,5 3,3 3,0 11,0 102,3 16,5 8,0 11,0 131,7 27,9 13,0 11,0 162,6 50,3
0,0 1,0 54,6 4,3 4,0 0,0 102,9 16,7 9,0 0,0 132,2 28,1 14,0 0,0 163,1 50,8
0,0 2,0 58,1 5,2 4,0 1,0 103,6 16,9 9,0 1,0 132,6 28,4 14,0 1,0 163,6 51,3
0,0 3,0 61,1 6,0 4,0 2,0 104,2 17,0 9,0 2,0 133,0 28,6 14,0 2,0 164,2 51,8
0,0 4,0 63,7 6,7 4,0 3,0 104,8 17,2 9,0 3,0 133,5 28,9 14,0 3,0 164,7 52,3
0,0 5,0 65,9 7,3 4,0 4,0 105,4 17,4 9,0 4,0 133,9 29,2 14,0 4,0 165,2 52,8
0,0 6,0 67,8 7,8 4,0 5,0 106,0 17,5 9,0 5,0 134,4 29,5 14,0 5,0 165,7 53,3
0,0 7,0 69,5 8,3 4,0 6,0 106,6 17,7 9,0 6,0 134,8 29,7 14,0 6,0 166,2 53,8
0,0 8,0 71,0 8,8 4,0 7,0 107,1 17,9 9,0 7,0 135,3 30,0 14,0 7,0 166,7 54,3
0,0 9,0 72,3 9,2 4,0 8,0 107,7 18,0 9,0 8,0 135,7 30,3 14,0 8,0 167,2 54,8
0,0 10,0 73,6 9,5 4,0 9,0 108,3 18,2 9,0 9,0 136,1 30,6 14,0 9,0 167,6 55,2
0,0 11,0 74,9 9,9 4,0 10,0 108,8 18,3 9,0 10,0 136,6 30,9 14,0 10,0 168,1 55,7
0,0 12,0 76,1 10,2 4,0 11,0 109,4 18,5 9,0 11,0 137,1 31,1 14,0 11,0 168,6 56,2
0,0 13,0 77,2 10,4 5,0 0,0 109,9 18,7 10,0 0,0 137,5 31,4 15,0 0,0 169,0 56,7
0,0 14,0 78,3 10,7 5,0 1,0 110,5 18,8 10,0 1,0 138,0 31,7 15,0 1,0 169,4 57,2
0,0 15,0 79,4 10,9 5,0 2,0 111,0 19,0 10,0 2,0 138,4 32,0 15,0 2,0 169,9 57,7
0,0 16,0 80,4 11,1 5,0 3,0 111,5 19,2 10,0 3,0 138,9 32,4 15,0 3,0 170,3 58,1
0,0 17,0 81,4 11,3 5,0 4,0 112,1 19,3 10,0 4,0 139,4 32,7 15,0 4,0 170,7 58,6
0,0 18,0 82,4 11,5 5,0 5,0 112,6 19,5 10,0 5,0 139,9 33,0 15,0 5,0 171,1 59,1
0,0 19,0 83,3 11,7 5,0 6,0 113,1 19,7 10,0 6,0 140,3 33,3 15,0 6,0 171,5 59,5
0,0 20,0 84,2 11,8 5,0 7,0 113,6 19,8 10,0 7,0 140,8 33,6 15,0 7,0 171,8 60,0
0,0 21,0 85,1 12,0 5,0 8,0 114,1 20,0 10,0 8,0 141,3 33,9 15,0 8,0 172,2 60,4
0,0 22,0 86,0 12,2 5,0 9,0 114,6 20,2 10,0 9,0 141,8 34,3 15,0 9,0 172,6 60,8
0,0 23,0 86,8 12,4 5,0 10,0 115,1 20,3 10,0 10,0 142,3 34,6 15,0 10,0 172,9 61,3
0,0 24,0 87,6 12,6 5,0 11,0 115,6 20,5 10,0 11,0 142,8 35,0 15,0 11,0 173,2 61,8
0,0 25,0 88,5 12,8 6,0 0,0 116,1 20,7 11,0 0,0 143,3 35,3 16,0 0,0 173,5 62,1
0,0 26,0 89,2 13,0 6,0 1,0 116,6 20,9 11,0 1,0 143,8 35,6 16,0 1,0 173,8 62,5
0,0 27,0 90,0 13,1 6,0 2,0 117,1 21,0 11,0 2,0 144,3 36,0 16,0 2,0 174,1 62,9
0,0 28,0 90,8 13,3 6,0 3,0 117,5 21,2 11,0 3,0 144,8 36,4 16,0 3,0 174,4 63,3
0,0 29,0 91,6 13,5 6,0 4,0 118,0 21,4 11,0 4,0 145,3 36,7 16,0 4,0 174,7 63,7
0,0 30,0 92,3 13,7 6,0 5,0 118,5 21,6 11,0 5,0 145,8 37,1 16,0 5,0 174,9 64,0
0,0 31,0 93,0 13,8 6,0 6,0 119,0 21,7 11,0 6,0 146,4 37,5 16,0 6,0 175,2 64,4
0,0 32,0 93,7 14,0 6,0 7,0 119,4 21,6 11,0 7,0 146,9 37,8 16,0 7,0 175,4 64,7
0,0 33,0 94,5 14,2 6,0 8,0 119,9 22,1 11,0 8,0 147,4 38,2 16,0 8,0 175,6 65,1
0,0 34,0 95,2 14,4 6,0 9,0 120,3 22,3 11,0 9,0 148,0 38,6 16,0 9,0 175,8 65,4
0,0 35,0 95,8 14,5 6,0 10,0 120,8 22,5 11,0 10,0 148,5 39,0 16,0 10,0 175,9 65,7
0,0 36,0 96,5 14,7 6,0 11,0 121,2 22,7 11,0 11,0 149,1 39,4 16,0 11,0 176,1 66,0
2,0 0,0 85,6 12,3 7,0 0,0 121,7 22,9 12,0 0,0 149,7 39,8 17,0 0,0 176,2 66,3
2,0 1,0 86,4 12,5 7,0 1,0 122,1 23,0 12,0 1,0 150,2 40,2 17,0 1,0 176,3 66,6
2,0 2,0 87,2 12,7 7,0 2,0 122,6 23,2 12,0 2,0 150,8 40,6 17,0 2,0 176,4 66,8
2,0 3,0 88,1 12,9 7,0 3,0 123,0 23,4 12,0 3,0 151,3 41,0 17,0 3,0 176,5 67,1
2,0 4,0 88,9 13,1 7,0 4,0 123,5 23,6 12,0 4,0 151,9 41,4 17,0 4,0 176,6 67,3
2,0 5,0 89,7 13,3 7,0 5,0 123,9 23,8 12,0 5,0 152,5 41,8 17,0 5,0 176,7 67,6
2,0 6,0 90,4 13,5 7,0 6,0 124,4 24,0 12,0 6,0 153,0 42,3 17,0 6,0 176,7 67,8
2,0 7,0 91,2 13,7 7,0 7,0 124,8 24,2 12,0 7,0 153,6 42,7 17,0 7,0 176,8 68,0
2,0 8,0 92,0 13,9 7,0 8,0 125,2 24,4 12,0 8,0 154,2 43,1 17,0 8,0 176,8 68,2
2,0 9,0 92,7 14,1 7,0 9,0 125,7 24,7 12,0 9,0 154,8 43,6 17,0 9,0 176,8 68,4
2,0 10,0 93,5 14,3 7,0 10,0 126,1 24,9 12,0 10,0 155,3 44,0 17,0 10,0 176,8 68,6
2,0 11,0 94,2 14,4 7,0 11,0 126,5 25,1 12,0 11,0 155,9 44,5 17,0 11,0 176,8 68,7
3,0 0,0 94,9 14,6 8,0 0,0 127,0 25,3 13,0 0,0 156,5 45,0 18,0 0,0 176,8 68,9
3,0 1,0 95,6 14,8 8,0 1,0 127,4 25,5 13,0 1,0 157,0 45,4
3,0 2,0 96,3 15,0 8,0 2,0 127,8 25,7 13,0 2,0 157,6 45,9
3,0 3,0 97,0 15,2 8,0 3,0 128,3 26,0 13,0 3,0 158,2 46,4 P/I = peso da criança
3,0 4,0 97,7 15,3 8,0 4,0 128,7 26,2 13,0 4,0 158,7 46,8 peso para idade
3,0 5,0 98,4 15,5 8,0 5,0 129,1 26,4 13,0 5,0 159,3 47,3
3,0 6,0 99,1 15,7 8,0 6,0 129,6 26,7 13,0 6,0 159,9 47,8 E/I = Altura da criança
3,0 7,0 99,7 15,8 8,0 7,0 130,0 26,9 13,0 7,0 160,4 48,3 Altura para idade
3,0 8,0 100,4 16,0 8,0 8,0 130,4 27,1 13,0 8,0 161,0 48,8
P/E = peso da criança
3,0 9,0 101,0 16,2 8,0 9,0 130,9 27,4 13,0 9,0 161,5 49,3
peso para altura
3,0 10,0 101,7 16,4 8,0 10,0 131,3 27,6 13,0 10,0 162,1 49,8
Fonte: World Health Organization: Physical Status: The use and interpretation of anthropometry. WHO Technical Report Series 854,
Geneva, 1995, p. 452
2
2. Tabelas de peso e estatura (percentil 50) utilizando como referencial o NCHS 77/8 - gênero feminino
Anos Mês Estatura Peso Anos Mês Estatura Peso Anos Mês Estatura Peso Anos Mês Estatura Peso
0,0 0,0 49,9 3,2 3,0 11,0 101,0 15,8 8,0 11,0 131,7 28,1 13,0 11,0 160,2 50,0
0,0 1,0 53,5 4,0 4,0 0,0 101,6 16,0 9,0 0,0 132,2 28,5 14,0 0,0 160,4 50,3
0,0 2,0 56,8 4,7 4,0 1,0 102,2 16,1 9,0 1,0 132,7 28,8 14,0 1,0 160,5 50,6
0,0 3,0 59,5 5,4 4,0 2,0 102,8 16,2 9,0 2,0 133,2 29,1 14,0 2,0 160,7 50,9
0,0 4,0 62,0 6,0 4,0 3,0 103,4 16,4 9,0 3,0 133,7 29,4 14,0 3,0 160,8 51,2
0,0 5,0 64,1 6,7 4,0 4,0 104,0 16,5 9,0 4,0 134,2 29,8 14,0 4,0 161,0 51,5
0,0 6,0 65,9 7,2 4,0 5,0 104,5 16,7 9,0 5,0 134,7 30,1 14,0 5,0 161,1 51,8
0,0 7,0 67,6 7,7 4,0 6,0 105,1 16,8 9,0 6,0 135,2 30,5 14,0 6,0 161,2 52,1
0,0 8,0 69,1 8,2 4,0 7,0 105,6 17,0 9,0 7,0 135,7 30,8 14,0 7,0 161,3 52,4
0,0 9,0 70,4 8,6 4,0 8,0 106,2 17,1 9,0 8,0 136,2 31,1 14,0 8,0 161,4 52,7
0,0 10,0 71,8 8,9 4,0 9,0 106,7 17,2 9,0 9,0 136,8 31,5 14,0 9,0 161,5 52,9
0,0 11,0 73,1 9,2 4,0 10,0 107,3 17,4 9,0 10,0 137,3 31,8 14,0 10,0 161,6 53,2
0,0 12,0 74,3 9,5 4,0 11,0 107,8 17,5 9,0 11,0 137,8 32,2 14,0 11,0 161,7 53,4
0,0 13,0 75,5 9,8 5,0 0,0 108,4 17,7 10,0 0,0 138,3 32,5 15,0 0,0 161,8 53,7
0,0 14,0 76,7 10,0 5,0 1,0 108,9 17,8 10,0 1,0 138,8 32,9 15,0 1,0 161,9 53,9
0,0 15,0 77,8 10,2 5,0 2,0 109,5 18,0 10,0 2,0 139,4 33,3 15,0 2,0 161,9 54,1
0,0 16,0 78,9 10,4 5,0 3,0 110,0 18,1 10,0 3,0 139,9 33,6 15,0 3,0 162,0 54,4
0,0 17,0 79,9 10,6 5,0 4,0 110,5 18,3 10,0 4,0 140,4 34,0 15,0 4,0 162,0 54,6
0,0 18,0 80,9 10,8 5,0 5,0 111,0 18,4 10,0 5,0 140,9 34,4 15,0 5,0 162,1 54,8
0,0 19,0 81,9 11,0 5,0 6,0 111,6 18,6 10,0 6,0 141,5 34,7 15,0 6,0 162,1 55,0
0,0 20,0 82,9 11,2 5,0 7,0 112,1 18,7 10,0 7,0 142,0 35,1 15,0 7,0 162,2 55,1
0,0 21,0 83,8 11,4 5,0 8,0 112,6 18,9 10,0 8,0 142,6 35,5 15,0 8,0 162,2 55,3
0,0 22,0 84,7 11,5 5,0 9,0 113,1 19,0 10,0 9,0 143,1 35,8 15,0 9,0 162,3 55,5
0,0 23,0 85,6 11,7 5,0 10,0 113,6 19,2 10,0 10,0 143,7 36,2 15,0 10,0 162,3 55,6
0,0 24,0 86,5 11,9 5,0 11,0 114,1 19,4 10,0 11,0 144,2 36,6 15,0 11,0 162,4 55,8
0,0 25,0 87,3 12,1 6,0 0,0 114,6 19,5 11,0 0,0 144,8 37,0 16,0 0,0 162,4 55,9
0,0 26,0 88,2 12,3 6,0 1,0 115,1 19,7 11,0 1,0 145,3 37,3 16,0 1,0 162,5 56,0
0,0 27,0 89,0 12,4 6,0 2,0 115,6 19,9 11,0 2,0 145,9 37,7 16,0 2,0 162,5 56,1
0,0 28,0 89,8 12,6 6,0 3,0 116,1 20,0 11,0 3,0 146,5 38,1 16,0 3,0 162,6 56,2
0,0 29,0 90,6 12,8 6,0 4,0 116,6 20,2 11,0 4,0 147,0 38,5 16,0 4,0 162,6 56,3
0,0 30,0 91,3 12,9 6,0 5,0 117,1 20,4 11,0 5,0 147,6 38,8 16,0 5,0 162,7 56,4
0,0 31,0 92,1 13,1 6,0 6,0 117,6 20,6 11,0 6,0 148,2 39,2 16,0 6,0 162,7 56,4
0,0 32,0 92,8 13,3 6,0 7,0 118,1 20,8 11,0 7,0 148,8 39,6 16,0 7,0 162,8 56,5
0,0 33,0 93,5 13,4 6,0 8,0 118,6 21,0 11,0 8,0 149,3 40,0 16,0 8,0 162,8 56,6
0,0 34,0 94,2 13,6 6,0 9,0 119,1 21,2 11,0 9,0 149,9 40,4 16,0 9,0 162,9 56,6
0,0 35,0 94,9 13,8 6,0 10,0 119,6 21,4 11,0 10,0 150,4 40,8 16,0 10,0 162,9 56,6
0,0 36,0 95,6 13,9 6,0 11,0 120,1 21,6 11,0 11,0 151,0 41,1 16,0 11,0 163,0 56,7
2,0 0,0 84,5 11,8 7,0 0,0 120,6 21,8 12,0 0,0 151,5 41,5 17,0 0,0 163,1 56,7
2,0 1,0 85,4 12,0 7,0 1,0 121,1 22,1 12,0 1,0 152,1 41,9 17,0 1,0 163,1 56,7
2,0 2,0 86,2 12,2 7,0 2,0 121,5 22,3 12,0 2,0 152,6 42,3 17,0 2,0 163,2 56,7
2,0 3,0 87,0 12,4 7,0 3,0 122,0 22,5 12,0 3,0 153,1 42,7 17,0 3,0 163,2 56,7
2,0 4,0 87,9 12,6 7,0 4,0 122,5 22,8 12,0 4,0 153,6 43,1 17,0 4,0 163,3 56,7
2,0 5,0 88,7 12,8 7,0 5,0 123,0 23,0 12,0 5,0 154,1 43,5 17,0 5,0 163,3 56,7
2,0 6,0 89,5 13,0 7,0 6,0 123,5 23,3 12,0 6,0 154,6 43,8 17,0 6,0 163,4 56,7
2,0 7,0 90,2 13,2 7,0 7,0 124,0 23,5 12,0 7,0 155,0 44,2 17,0 7,0 163,5 56,7
2,0 8,0 91,0 13,4 7,0 8,0 124,5 23,8 12,0 8,0 155,5 44,6 17,0 8,0 163,5 56,7
2,0 9,0 91,7 13,6 7,0 9,0 124,9 24,0 12,0 9,0 155,9 45,0 17,0 9,0 163,6 56,7
2,0 10,0 92,5 13,8 7,0 10,0 125,4 24,3 12,0 10,0 156,3 45,4 17,0 10,0 163,6 56,7
2,0 11,0 93,2 13,9 7,0 11,0 125,9 24,6 12,0 11,0 156,7 45,7 17,0 11,0 163,7 56,6
3,0 0,0 93,9 14,1 8,0 0,0 126,4 24,8 13,0 0,0 157,1 46,1 18,0 0,0 163,7 56,6
3,0 1,0 94,6 14,3 8,0 1,0 126,9 25,1 13,0 1,0 157,5 46,5
3,0 2,0 95,3 14,4 8,0 2,0 127,4 25,4 13,0 2,0 157,8 46,8
3,0 3,0 96,0 14,6 8,0 3,0 127,8 25,7 13,0 3,0 158,2 47,2
P/I = peso da criança
3,0 4,0 96,6 14,8 8,0 4,0 128,3 26,0 13,0 4,0 158,5 47,6 peso para idade
3,0 5,0 97,3 14,9 8,0 5,0 128,8 26,3 13,0 5,0 158,8 47,9
3,0 6,0 97,9 15,1 8,0 6,0 129,3 26,6 13,0 6,0 159,0 48,3 E/I = Altura da criança
3,0 7,0 98,6 15,2 8,0 7,0 129,8 26,9 13,0 7,0 159,3 48,6 Altura para idade
3,0 8,0 99,2 15,4 8,0 8,0 130,3 27,2 13,0 8,0 159,5 49,0
3,0 9,0 99,8 15,5 8,0 9,0 130,8 27,5 13,0 9,0 159,8 49,3 P/E = peso da criança
peso para altura
3,0 10,0 100,4 15,7 8,0 10,0 131,2 27,8 13,0 10,0 160,0 49,6
Fonte: World Health Organization: Physical Status: The use and interpretation of anthropometry. WHO Technical Report Series 854,
Geneva, 1995, p. 452
3
3. Tabelas de peso e estatura (percentil 50) utilizando como padrão OMS, 2006 para ambos os gêneros
Meninos (p50) Meninas (p50)

Ano Mês Estatura Peso Ano Mês Estatura Peso
0:0 0 49,5 3,3 0:0 0 49,1 3,2
0:1 1 54,7 4,5 0:1 1 53,7 4,2
0:2 2 58,4 5,5 0:2 2 57,1 5,1
0:3 3 61,4 6,4 0:3 3 59,8 5,8
0:4 4 63,9 7,0 0:4 4 62,1 6,4
0:5 5 65,9 7,5 0:5 5 64,0 6,9
0:6 6 67,6 7,9 0:6 6 65,7 7,3
0:7 7 69,2 8,3 0:7 7 67,3 7,6
0:8 8 70,6 8,6 0:8 8 68,7 7,9
0:9 9 72,0 8,9 0:9 9 70,1 8,2
0:10 10 73,3 9,2 0:10 10 71,5 7,5
0:11 11 74,5 9,4 0:11 11 72,8 8,7
1:0 12 75,7 9,6 1:0 12 74,0 8,9
1:1 13 76,9 9,9 1:1 13 75,2 9,2
1:2 14 78,0 10,1 1:2 14 76,4 9,4
1:3 15 79,1 10,3 1:3 15 77,5 9,6
1:4 16 80,2 10,5 1:4 16 78,6 9,8
1:5 17 81,2 10,7 1:5 17 79,7 10,0
1:6 18 82,3 10,9 1:6 18 80,7 10,2
1:7 19 83,2 11,1 1:7 19 81,7 10,4
1:8 20 84,2 11,3 1:8 20 82,7 10,6
1:9 21 85,1 11,5 1:9 21 83,7 10,9
1:10 22 86,0 11,8 1:10 22 84,6 11,1
1:11 23 86,9 12,0 1:11 23 85,5 11,3
2:0 24 87,8 12,2 2:0 24 86,4 11,5
2:1 25 88,0 12,4 2:1 25 86,6 11,7
2:2 26 88,8 12,5 2:2 26 87,4 11,9
2:3 27 89,6 12,7 2:3 27 88,3 12,1
2:4 28 90,4 12,9 2:4 28 89,1 12,3
2:5 29 91,2 13,1 2:5 29 89,9 12,5
2:6 30 91,9 13,3 2:6 30 90,7 12,7
2:7 31 92,7 13,5 2:7 31 91,4 12,9
2:8 32 93,4 13,7 2:8 32 92,2 13,1
2:9 33 94,1 13,8 2:9 33 92,9 13,3
2:10 34 94,8 14,0 2:10 34 93,6 13,5
2:11 35 95,4 14,2 2:11 35 94,4 13,7
3:0 36 96,1 14,3 3:0 36 95,1 13,9
3:1 37 96,7 14,5 3:1 37 95,7 14,0
3:2 38 97,4 14,7 3:2 38 96,4 14,2
3:3 39 98,0 14,8 3:3 39 97,1 14,4
3:4 40 98,6 15,0 3:4 40 97,7 14,6
3:5 41 99,2 15,2 3:5 41 98,4 14,8
3:6 42 99,9 15,3 3:6 42 99,0 15,0
3:7 43 100,4 15,5 3:7 43 99,7 15,2
3:8 44 101,0 15,7 3:8 44 100,3 15,3
3:9 45 101,6 15,8 3:9 45 100,9 15,5
3:10 46 102,2 16,0 3:10 46 101,5 15,7
3:11 47 102,8 16,2 3:11 47 102,1 15,9
4:0 48 103,3 16,3 4:0 48 102,7 16,1
4:1 49 103,9 16,5 4:1 49 103,3 16,3
4:2 50 104,4 16,7 4:2 50 103,9 16,4
4:3 51 105,0 16,8 4:3 51 104,5 16,6
4:4 52 105,6 17,0 4:4 52 105,0 16,8
4:5 53 106,1 17,2 4:5 53 105,6 17,0
4:6 54 106,7 17,3 4:6 54 106,2 17,2
4:7 55 107,2 17,5 4:7 55 106,7 17,3
4:8 56 107,8 17,7 4:8 56 107,3 17,5
4:9 57 108,3 17,8 4:9 57 107,8 17,7
4:10 58 108,9 18,0 4:10 58 108,4 17,9
4:11 59 109,4 18,2 4:11 59 108,9 18,0
5:0 60 110,0 18,3 5:0 60 109,4 18,2
Fonte: WHO child growth standards: length/height-for-age, weight-for-age, weight-for-length, weight-forheight and body mass index-for-
age: methods and development. WHO, 2006
4
4. Distribuição em percentis do índice de massa corporal segundo gênero e idade de acordo com Must, 1992
MASCULINO FEMININO
Idade Percentil Idade Percentil
(anos) n 5 15 50 85 95 (anos) n 5 15 50 85 95
6 165 12.86 13.43 14.54 16.64 18.02 6 161 12.83 13.37 14.31 16.17 17.49
7 164 13.24 13.85 15.07 17.37 19.18 7 174 13.17 13.79 14.98 17.17 18.93
8 149 13.63 14.28 15.62 18.11 20.33 8 153 13.51 14.22 15.66 18.18 20.36
9 177 14.03 14.71 16.17 18.85 21.47 9 173 13.87 14.66 16.33 19.19 21.78
10 177 14.42 15.15 16.72 19.60 22.60 10 194 14.23 15.09 17.00 20.19 23.20
11 169 14.83 15.59 17.28 20.35 23.73 11 163 14.60 15.53 17.67 21.18 24.59
12 204 15.24 16.06 17.87 21.12 24.89 12 177 14.98 15.98 18.35 22.17 25.95
13 177 15.73 16.62 18.53 21.93 25.93 13 199 15.36 16.43 18.95 23.08 27.07
14 173 16.18 17.20 19.22 22.77 26.93 14 192 15.67 16.79 19.32 23.88 27.97
15 175 16.59 17.76 19.92 23.63 27.76 15 164 16.01 17.16 19.69 24.29 28.51
16 172 17.01 18.32 20.63 24.45 28.53 16 173 16.37 17.54 20.09 24.74 29.10
17 167 17.31 18.68 21.12 25.18 29.32 17 159 16.59 17.81 20.36 25.23 29.72
18 120 17.54 18.89 21.45 25.92 30.02 18 140 16.71 17.99 20.57 25.56 30.22
19 137 17.80 19.20 21.86 26.36 30.66 19 142 16.87 18.20 20.80 25.85 30.72
20-24 514 18.66 20.21 23.07 26.87 31.26 20-24 1244 17.38 18.64 21.46 26.14 31.20
25-29 671 19.11 20.98 24.19 28.08 31.72 25-29 1307 17.84 19.09 22.10 27.68 33.16
30-34 466 19.52 21.51 24.90 28.75 31.99 30-34 1092 18.23 19.54 22.69 28.87 34.58
35-39 451 19.55 21.71 25.25 29.18 32.23 35-39 1017 18.51 19.91 23.25 29.54 35.35
40-44 474 19.52 21.75 25.49 29.37 32.41 40-44 999 18.65 20.20 23.74 30.11 35.85
45-49 532 19.45 21.72 25.55 29.39 32.40 45-49 603 18.71 20.45 24.17 30.56 36.02
50-54 531 19.35 21.66 25.54 29.31 32.27 50-54 615 18.79 20.66 24.54 30.79 35.95
55-59 468 19.25 21.58 25.51 29.24 32.18 55-59 492 18.88 20.86 24.92 31.00 35.88
60-64 378 19.15 21.49 25.47 29.17 32.08 60-64 463 18.96 21.06 25.29 31.21 35.80
65-69 1084 19.05 21.39 25.41 29.08 31.98 65-69 1157 19.03 21.25 25.66 31.40 35.70
70-74 752 18.94 21.29 25.33 28.99 31.87 70-74 848 19.09 21.44 26.01 31.58 35.58
Fonte: Must A, Dallal GE, Dietz WH. Reference data for obesity: 85th and 95th percentiles of body mass index (wt/ht2) and triceps
skinfold thickness. Am J Clin Nutr 1991; 53:839-46.
5
5. Distribuição em percentis da prega cutânea tricipital segundo gênero e idade de acordo com Frisancho, 1990
Idade Percentil
(anos) 5 10 15 25 50 75 85 90 95
Masculino
1,0-1,9 6,5 7 7,5 8 10 12 13 14 15,5
2,0-2,9 6 6,5 7 8 10 12 13 14 15
3,0-3,9 6 7 7 8 9,5 11,5 12,5 13,5 15
4,0-4,9 5,5 6,5 7 7,5 9 11 12 12,5 14
5,0-5,9 5 6 6 7 8 10 11,5 13 14,5
6,0-6,9 5 5,5 6 6,5 8 10 12 13 16
7,0-7,9 4,5 5 6 6 8 10,5 12,5 14 16
8,0-8,9 5 5,5 6 7 8,5 11 13 16 19
9,0-9,9 5 5,5 6 6,5 9 12,5 15,5 17 20
10,0-10,9 5 5,5 6 7,5 10 14 17 20 24
11,0-11,9 5 6 6,5 7,5 10 16 19,5 23 27
12,0-12,9 4,5 6 6 7,5 10,5 14,5 18 22,5 27,5
13,0-13,9 4,5 5 5,5 7 9 13 17 20,5 25
14,0-14,9 4 5 5 6 8,5 12,5 15 18 23,5
15,0-15,9 5 5 5 6 7,5 11 15 18 23,5
16,0-16,9 4 5 5,1 6 8 12 14 17 23
17,0-17,9 4 5 5 6 7 11 13,5 16 19,5
18,0-24,9 4 5 5,5 6,5 10 14,5 17,5 20 23,5
25,0-29,9 4 5 6 7 11 15,5 19 21,5 25
30,0-34,9 4,5 6 6,5 8 12 16,5 20 22 25
35,0-39,9 4,5 6 7 8,5 12 16 18,5 20,5 24,5
40,0-44,9 5 6 6,9 8 12 16 19 21,5 26
45,0-49,9 5 6 7 8 12 16 19 21 25
50,0-54,9 5 6 7 8 11,5 15 18,5 20,8 25
55,0-59,9 5 6 6,5 8 11,5 15 18 20,5 25
60,0-64,9 5 6 7 8 11,5 15,5 18,5 20,5 24
65,0-69,9 4,5 5 6,5 8 11 15 18 20 23,5
70,0-74,9 4,5 6 6,5 8 11 15 17 19 23
Feminino
1,0-1,9 6 7 7 8 10 12 13 14 16
2,0-2,9 6 7 7,5 8,5 10 12 13,5 14,5 16
3,0-3,9 6 7 7,5 8,5 10 12 13 14 16
4,0-4,9 6 7 7,5 8 10 12 13 14 15,5
5,0-5,9 5,5 7 7 8 10 12 13,5 15 17
6,0-6,9 6 6,5 7 8 10 12 13 15 17
7,0-7,9 6 7 7 8 10,5 12,5 15 16 19
8,0-8,9 6 7 7,5 8,5 11 14,5 17 18 22,5
9,0-9,9 6,5 7 8 9 12 16 19 21 25
10,0-10,9 7 8 8 9 12,5 17,5 20 22,5 27
11,0-11,9 7 8 8,5 10 13 18 21,5 24 29
12,0-12,9 7 8 9 11 14 18,5 21,5 24 27,5
13,0-13,9 7 8 9 11 15 20 24 25 30
14,0-14,9 8 9 10 11,5 16 21 23,5 26,5 32
15,0-15,9 8 9,5 10,5 12 16,5 20,5 23 26 32,5
16,0-16,9 10,5 11,5 12 14 18 23 26 29 32,5
17,0-17,9 9 10 12 13 18 24 26,5 29 34,5
18,0-24,9 9 11 12 14 18,5 24,5 28,5 31 36
25,0-29,9 10 12 13 15 20 26,5 31 34 38
30,0-34,9 10,5 13 15 17 22,5 29,5 33 35,5 41,5
35,0-39,9 11 13 15,5 18 23,5 30 35 37 41
40,0-44,9 12 14 16 19 24,5 30,5 35 37 41
45,0-49,9 12 14,5 16,5 19,5 25,5 32 35,5 38 42,5
50,0-54,9 12 15 17,5 20,5 25,5 32 36 38,5 42
55,0-59,9 12 15 17 20,5 26 32 36 39 42,5
60,0-64,9 12,5 16 17,5 20,5 26 32 35,5 38 42,5
65,0-69,9 12 14,5 16 19 25 30 33,5 36 40
70,0-74,9 11 13,5 15,5 18 24 29,5 32 35 38,5
Fonte: Frisancho AR. Anthropometric standards for the assessments of growth and nutritional status. University of Michigan,1990. 189p.
6
6. Distribuição em percentis da circunferência do braço segundo gênero e idade de acordo com Frisancho, 1990
Idade Percentil
(anos) 5 10 15 25 50 75 85 90 95
Masculino
1,0-1,9 14,2 14,7 14,9 15,2 16 16,9 17,4 17,7 18,2
2,0-2,9 14,3 14,8 15,1 15,5 16,3 17,1 17,6 17,9 18,6
3,0-3,9 15 15,3 15,5 16 16,8 17,6 18,1 18,4 19
4,0-4,9 15,1 15,5 15,8 16,2 17,1 18 18,5 18,7 19,3
5,0-5,9 15,5 16 16,1 16,6 17,5 18,5 19,1 19,5 20,5
6,0-6,9 15,8 16,1 16,5 17 18 19,1 19,8 20,7 22,8
7,0-7,9 16,1 16,8 17 17,6 18,7 20 21 21,8 22,9
8,0-8,9 16,5 17,2 17,5 18,1 19,2 20,5 21,6 22,6 24
9,0-9,9 17,5 18 18,4 19 20,1 21,8 23,2 24,5 26
10,0-10,9 18,1 18,6 19,1 19,7 21,1 23,1 24,8 26 27,9
11,0-11,9 18,5 19,3 19,8 20,6 22,1 24,5 26,1 27,6 29,4
12,0-12,9 19,3 20,1 20,7 21,5 23,1 25,4 27,1 28,5 30,3
13,0-13,9 20 20,8 21,6 22,5 24,5 26,6 28,2 29 30,8
14,0-14,9 21,6 22,5 23,2 23,8 25,7 28,1 29,1 30 32,3
15,0-15,9 22,5 23,4 24 25,1 27,2 29 30,3 31,2 32,7
16,0-16,9 24,1 25 25,7 26,7 28,3 30,6 32,1 32,7 34,7
17,0-17,9 24,3 25,1 25,9 26,8 28,6 30,8 32,2 33,3 34,7
18,0-24,9 26 27,1 27,7 28,7 30,7 33 34,4 35,4 37,2
25,0-29,9 27 28 28,7 29,8 31,8 34,2 35,5 36,6 38,3
30,0-34,9 27,7 28,7 29,3 30,5 32,5 34,9 35,9 36,7 38,2
35,0-39,9 27,4 28,6 29,5 30,7 32,9 35,1 36,2 36,9 38,2
40,0-44,9 27,8 28,9 29,7 31 32,8 34,9 36,1 36,9 38,1
45,0-49,9 27,2 28,6 29,4 30,6 32,6 34,9 36,1 36,9 38,2
50,0-54,9 27,1 28,3 29,1 30,2 32,3 34,5 35,8 36,8 38,3
55,0-59,9 26,8 28,1 29,2 30,4 32,3 34,3 35,5 36,6 37,8
60,0-64,9 26,6 27,8 28,6 29,7 32 34 35,1 36 37,5
65,0-69,9 25,4 26,7 27,7 29 31,1 33,2 34,5 35,3 36,6
70,0-74,9 25,1 26,2 27,1 28,5 30,7 32,6 33,7 34,8 36
Feminino
1,0-1,9 13,6 14,1 14,4 14,8 15,7 16,4 17 17,2 17,8
2,0-2,9 14,2 14,6 15 15,4 16,1 17 17,4 18 18,5
3,0-3,9 14,4 15 15,2 15,7 16,6 17,4 18 18,4 19
4,0-4,9 14,8 15,3 15,7 16,1 17 18 18,5 19 19,5
5,0-5,9 15,2 15,7 16,1 16,5 17,5 18,5 19,4 20 21
6,0-6,9 15,7 16,2 16,5 17 17,8 19 19,9 20,5 22
7,0-7,9 16,4 16,7 17 17,5 18,6 20,1 20,9 21,6 23,3
8,0-8,9 16,7 17,2 17,6 18,2 19,5 21,2 22,2 23,2 25,1
9,0-9,9 17,6 18,1 18,6 19,1 20,6 22,2 23,8 25 26,7
10,0-10,9 17,8 18,4 18,9 19,5 21,2 23,4 25 26,1 27,3
11,0-11,9 18,8 19,6 20 20,6 22,2 25,1 26,5 27,9 30
12,0-12,9 19,2 20 20,5 21,5 23,7 25,8 27,6 28,3 30,2
13,0-13,9 20,1 21 21,5 22,5 24,3 26,7 28,3 30,1 32,7
14,0-14,9 21,2 21,8 22,5 23,5 25,1 27,4 29,5 30,9 32,9
15,0-15,9 21,6 22,2 22,9 23,5 25,2 27,7 28,8 30 32,2
16,0-16,9 22,3 23,2 23,5 24,4 26,1 28,5 29,9 31,6 33,5
17,0-17,9 22 23,1 23,6 24,5 26,6 29 30,7 32,8 35,4
18,0-24,9 22,4 23,3 24 24,8 26,8 29,2 31,2 32,4 35,2
25,0-29,9 23,1 24 24,5 25,5 27,6 30,6 32,5 34,3 37,1
30,0-34,9 23,8 24,7 25,4 26,4 28,6 32 34,1 36 38,5
35,0-39,9 24,1 25,2 25,8 26,8 29,4 32,6 35 36,8 39
40,0-44,9 24,3 25,4 26,2 27,2 29,7 33,2 35,5 37,2 38,8
45,0-49,9 24,2 25,5 26,3 27,4 30,1 33,5 35,6 37,2 40
50,0-54,9 24,8 26 26,8 28 30,6 33,8 35,9 37,5 39,3
55,0-59,9 24,8 26,1 27 28,2 30,9 34,3 36,7 38 40
60,0-64,9 25 26,1 27,1 28,4 30,8 34 35,7 37,3 39,6
65,0-69,9 24,3 25,7 26,7 28 30,5 33,4 35,2 36,5 38,5
70,0-74,9 23,8 25,3 26,3 27,6 30,3 33,1 34,7 35,8 37,5
Fonte: Frisancho AR. Anthropometric standards for the assessments of growth and nutritional status. University of Michigan,1990. 189p.
7
7. Distribuição em percentis da circunferência abdominal segundo gênero e idade de acordo com Freedman, 1999
BRANCOS NEGROS
Meninos Meninas Meninos Meninas
Idade Percentil Percentil Percentil Percentil
(anos) n 50 90 n 50 90 n 50 90 n 50 90
5 28 52 59 34 51 57 36 52 56 34 52 56
6 44 54 61 60 53 60 42 54 60 52 53 59
7 54 55 61 55 54 64 53 56 61 52 56 67
8 95 59 75 75 58 73 54 58 67 54 58 65
9 53 62 77 84 60 73 53 60 74 56 61 78
10 72 64 88 67 63 75 53 64 79 49 62 79
11 97 68 90 95 66 83 58 64 79 67 67 87
12 102 70 89 89 67 83 60 68 87 73 67 84
13 82 77 95 78 69 94 49 68 87 64 67 81
14 88 73 99 54 69 96 62 72 85 51 68 92
15 58 73 99 58 69 88 44 72 81 54 72 85
16 41 77 97 58 68 93 41 75 91 34 75 90
17 22 79 90 42 66 86 31 78 101 35 71 105
Fonte: Freedman DS, Serdula MK, Srinivasan SR, Berenson GS. Relation of circemference and skinfold thicknesses to lipid and insulin
concentrations in children and adolescents: the Bogalusa Heart Study. Am J Clin Nutr 1999; 69:308-17.
8
8. Distribuição em percentis da pressão arterial segundo percentis de estatura e idade de acordo com Task Force (EUA), 2004
MASCULINO PA sistólica (mmHg) PA diastólica (mmHg)
(anos) percentil
5 10 25 50 75 90 95 5 10 25 50 75 90 95
1 50 80 81 83 85 87 88 89 34 35 36 37 38 39 39
90 94 95 97 99 100 102 103 49 50 51 52 53 53 54
95 98 99 101 103 104 106 106 54 54 55 56 57 58 58
99 105 106 108 110 112 113 114 61 62 63 64 65 66 66
2 50 84 85 87 88 90 92 92 39 40 41 42 43 44 44
90 97 99 100 102 104 105 106 54 55 56 57 58 58 59
95 101 102 104 106 108 109 110 59 59 60 61 62 63 63
99 109 110 111 113 115 117 117 66 67 68 69 70 71 71
3 50 86 87 89 91 93 94 95 44 44 45 46 47 48 48
90 100 101 103 105 107 108 109 59 59 60 61 62 63 63
95 104 105 107 109 110 112 113 63 63 64 65 66 67 67
99 111 112 114 116 118 119 120 71 71 72 73 74 75 75
4 50 88 89 91 93 95 96 97 47 48 49 50 51 51 52
90 102 103 105 107 109 110 111 62 63 64 65 66 66 67
95 106 107 109 111 112 114 115 66 67 68 69 70 71 71
99 113 114 116 118 120 121 122 74 75 76 77 78 78 79
5 50 90 91 93 95 96 98 98 50 51 52 53 54 55 55
90 104 105 106 108 110 111 112 65 66 67 68 69 69 70
95 108 109 110 112 114 115 116 69 70 71 72 73 74 74
99 115 116 118 120 121 123 123 77 78 79 80 81 81 82
6 50 91 92 94 96 98 99 100 53 53 54 55 56 57 57
90 105 106 108 110 111 113 113 68 68 69 70 71 72 72
95 109 110 112 114 115 117 117 72 72 73 74 75 76 76
99 116 117 119 121 123 124 125 80 80 81 82 83 84 84
7 50 92 94 95 97 99 100 101 55 55 56 57 58 59 59
90 106 107 109 111 113 114 115 70 70 71 72 73 74 74
95 110 111 113 115 117 118 119 74 74 75 76 77 78 78
99 117 118 120 122 124 125 126 82 82 83 84 85 86 86
8 50 94 95 97 99 100 102 102 56 57 58 59 60 60 61
90 107 109 110 112 114 115 116 71 72 72 73 74 75 76
95 111 112 114 116 118 119 120 75 76 77 78 79 79 80
99 119 120 122 123 125 127 127 83 84 85 86 87 87 88
9 50 95 96 98 100 102 103 104 57 58 59 60 61 61 62
90 109 110 112 114 115 117 118 72 73 74 75 76 76 77
95 113 114 116 118 119 121 121 76 77 78 79 80 81 81
99 120 121 123 125 127 128 129 84 85 86 87 88 88 89
10 50 97 98 100 102 103 105 106 58 59 60 61 61 62 63
90 111 112 114 115 117 119 119 73 73 74 75 76 77 78
95 115 116 117 119 121 122 123 77 78 79 80 81 81 82
99 122 123 125 127 128 130 130 85 86 86 88 88 89 90
11 50 99 100 102 104 105 107 107 59 60 61 62 63 63 63
90 113 114 115 117 119 120 121 74 75 75 76 77 78 78
95 117 118 119 121 123 124 125 78 79 80 81 82 82 82
99 124 125 127 129 130 132 132 86 87 88 89 90 90 90
12 50 101 102 104 106 108 109 110 59 60 61 62 63 63 64
90 115 116 118 120 121 123 123 74 75 75 76 77 78 79
95 119 120 122 123 125 127 127 78 79 80 81 82 82 83
99 126 127 129 131 133 134 135 86 87 88 89 90 90 91
13 50 104 105 106 108 110 111 112 60 60 61 62 63 67 67
90 117 118 120 122 124 125 126 75 75 76 77 78 79 79
95 121 122 124 126 128 129 130 79 79 80 81 82 83 83
99 128 130 131 133 135 136 137 87 87 88 89 90 91 91
14 50 106 107 109 111 113 114 115 60 61 62 63 64 65 65
90 120 121 123 125 126 128 128 75 76 77 78 79 79 80
95 124 125 127 128 130 132 132 80 80 81 82 83 84 84
99 131 132 134 136 138 139 140 87 88 89 90 91 92 92
15 50 109 110 112 113 115 117 117 61 62 63 64 65 66 66
90 122 124 125 127 129 130 131 76 77 78 79 80 80 81
95 126 127 129 131 133 134 135 81 81 82 83 84 85 85
99 134 135 136 138 140 142 142 88 89 90 91 92 93 93
16 50 111 112 114 116 118 119 120 63 63 64 65 66 67 67
90 125 126 128 130 131 133 134 78 78 79 80 81 82 82
95 129 130 132 134 135 137 137 82 83 83 84 85 86 87
99 136 137 139 141 143 144 145 90 90 91 92 93 94 94
17 50 114 115 116 118 120 121 122 65 66 66 67 68 69 70
90 127 128 130 132 134 135 136 80 80 81 82 83 84 84
95 131 132 134 136 138 139 140 84 85 86 87 87 88 89
99 139 140 141 143 145 146 147 92 93 93 94 95 96 97
Fonte: National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The
fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics 2004;114:555-
76.
9
9. Distribuição em percentis da pressão arterial segundo percentis de estatura e idade de acordo com Task Force (EUA), 2004
FEMININO PA sistólica (mmHg) PA diastólica (mmHg)
(anos) percentil
5 10 25 50 75 90 95 5 10 25 50 75 90 95
1 50 83 84 85 86 88 89 90 38 39 39 40 41 41 42
90 97 97 98 100 101 102 103 52 53 53 54 55 55 56
95 100 101 102 104 105 106 107 56 57 57 58 59 59 60
99 108 108 109 111 112 113 114 64 64 65 65 66 66 67
2 50 85 85 87 88 89 91 91 43 44 44 45 46 46 47
90 98 99 100 101 103 104 105 57 58 58 59 60 61 61
95 102 103 104 105 107 108 109 61 62 62 63 64 65 65
99 109 110 111 112 114 115 116 69 69 70 70 71 72 72
3 50 86 87 88 89 91 92 93 47 48 48 49 49 50 51
90 100 100 102 103 104 106 106 61 62 62 62 63 64 65
95 104 104 105 107 108 109 110 65 66 66 66 67 68 69
99 111 111 113 114 115 116 117 73 73 74 74 74 75 76
4 50 88 88 90 91 92 94 94 50 50 51 52 52 53 54
90 101 102 103 104 106 107 108 64 64 65 66 67 67 68
95 105 106 107 108 110 111 112 68 68 69 70 71 71 72
99 112 113 114 115 117 118 119 76 76 76 77 78 79 79
5 50 89 90 91 93 94 95 96 52 53 53 54 55 55 56
90 103 103 105 106 107 109 109 66 67 67 68 69 69 70
95 107 107 108 110 111 112 113 70 71 71 72 73 73 74
99 114 114 116 117 118 120 120 78 78 79 79 80 81 81
6 50 91 92 93 94 96 97 98 54 54 55 56 56 57 58
90 104 105 106 108 109 110 111 68 68 69 70 70 71 72
95 108 109 110 111 113 114 115 72 72 73 74 74 75 76
99 115 116 117 119 120 121 122 80 80 80 81 82 83 83
7 50 93 93 95 96 97 99 99 55 56 56 57 58 58 59
90 106 107 108 109 111 112 113 69 70 70 71 72 72 73
95 110 111 112 113 115 116 116 73 74 74 75 76 76 77
99 117 118 119 120 122 123 124 81 81 82 82 83 84 84
8 50 95 95 96 98 99 100 101 57 57 57 58 59 60 60
90 108 109 110 111 113 114 114 71 71 71 72 73 74 74
95 112 112 114 115 116 118 118 75 75 75 76 77 78 78
99 119 120 121 122 123 125 125 82 82 83 83 84 85 86
9 50 96 97 98 100 101 102 103 58 58 58 59 60 61 61
90 110 110 112 113 114 116 116 72 72 72 73 74 75 75
95 114 114 115 117 118 119 120 76 76 76 77 78 79 79
99 121 121 123 124 125 127 127 83 83 84 84 85 86 87
10 50 98 99 100 102 103 104 105 59 59 59 60 61 62 62
90 112 112 114 115 116 118 118 73 73 73 74 75 76 76
95 116 116 117 119 120 121 122 77 77 77 78 79 80 80
99 123 123 125 126 127 129 129 84 84 85 86 86 87 88
11 50 100 101 102 103 105 106 107 60 60 60 61 62 63 63
90 114 114 116 117 118 119 120 74 74 74 75 76 77 77
95 118 118 119 121 122 123 124 78 78 78 79 80 81 81
99 125 125 126 128 129 130 131 85 85 86 87 87 88 89
12 50 102 103 104 105 107 108 109 61 61 61 62 63 64 64
90 116 116 117 119 120 121 122 75 75 75 76 77 78 78
95 119 120 121 123 124 125 126 79 79 79 80 81 82 82
99 127 127 128 130 131 132 133 86 86 87 88 88 89 90
13 50 104 105 106 107 109 110 110 62 62 62 63 64 65 65
90 117 118 119 121 122 123 124 76 76 76 77 78 79 79
95 121 122 123 124 126 127 128 80 80 80 81 82 83 83
99 128 129 130 132 133 134 135 87 87 88 89 89 90 91
14 50 106 106 107 109 110 111 112 63 63 63 64 65 66 66
90 119 120 121 122 124 125 125 77 77 77 78 79 80 80
95 123 123 125 126 127 129 129 81 81 81 82 83 84 84
99 130 131 132 133 135 136 136 88 88 89 90 90 91 92
15 50 107 108 109 110 111 113 113 64 64 64 65 66 67 67
90 120 121 122 123 125 126 127 78 78 78 79 80 81 81
95 124 125 126 127 129 130 131 82 82 82 83 84 85 85
99 131 132 133 134 136 137 138 89 89 90 91 91 92 93
16 50 108 108 110 111 112 114 114 64 64 65 66 66 67 68
90 121 122 123 124 126 127 128 78 78 79 80 81 81 82
95 125 126 127 128 130 131 132 82 82 83 84 85 85 86
99 132 133 134 135 137 138 139 90 90 90 91 92 93 93
17 50 108 109 110 111 113 114 115 64 65 65 66 67 67 68
90 122 122 123 125 126 127 128 78 79 79 80 81 81 82
95 125 126 127 129 130 131 132 82 83 83 84 85 85 86
99 133 133 134 136 137 138 139 90 90 91 91 92 93 93
Fonte: National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The
fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics 2004;114:555-
76.
10
10. Tabela de velocidade de crescimento segundo gênero e idade de acordo com Tanner
MASCULINO FEMININO
(cm/ano) (cm/ano)
Idade Percentil 50 Desvio-padrão Percentil 50 Desvio-padrão
(ano) (mês)
0 2 40 36
0 4 30 26
0 6 18 2,4 19 2,4
0 10 14,5 2,3 15,9 2,3
1 1 12,3 2,0 13,5 2,0
1 4 11,1 1,0 11,8 1,9
1 6 9,9 1,1 10,6 1,1
1 10 9,1 1,7 9,6 1,7
2 3 8,6 1,5 8,7 1,5
2 9 8,0 1,4 8,1 1,4
3 3 7,6 1,3 7,7 1,3
3 9 7,2 1,2 7,2 1,2
4 3 6,8 1,1 6,8 1,1
4 9 6,6 1,1 6,6 1,1
5 3 6,4 1,0 6,4 1,0
5 9 6,2 1,0 6,2 1,0
6 3 6,0 0,9 6,0 0,9
6 9 5,8 0,9 5,8 0,9
7 3 5,7 0,8 5,7 0,8
7 9 5,6 0,8 5,6 0,1
8 3 5,5 0,8 5,5 0,8
8 9 5,4 0,8 5,5 0,8
9 3 5,3 0,7 5,5 0,8
9 9 5,2 0,7 5,4 0,8
10 3 5,1 0,7 5,5 0,9
10 9 5,0 0,7 5,9 1,0
11 3 5,0 0,7 7,2 1,0
11 9 5,0 0,7 8,3 1,1
12 3 5,0 0,8 8,2 1,1
12 9 5,6 1,0 6,6 1,1
13 3 4,5 1,1 4,5 1,0
13 6 8,7 1,1 3,7 1,0
13 9 9,3 1,2 2,9 0,9
14 0 9,5 1,2
14 3 9,2 1,2 1,9 0,8
14 6 8,2 1,2
14 9 7,0 1,2 1,1 0,6
15 3 4,7 1,1
15 9 3,2 1,0
16 3 2,1 0,8
16 9 1,2 0,6
Fonte: Tanner JM. Growth as a monitor of nutritional status. Proc Nutr Soc 1976; 35:315-22.
11
10. Classificação do perfil lipídico em crianças e adolescentes de acordo com Kwiterowich, 1989
Valor (mg/dL)
Idade (anos) Desejável Limítrofe Aumentado
Colesterol total 2 - 19 < 170 170 ¬ 199 ≥ 200
LDL-c 2 - 19 < 110 110 ¬ 119 ≥ 130
HDL-c ≤ 10 ≥ 40 110 ¬ 119

10 ¬ 19 ≥ 35
Triglicerídios ≤ 10 ≤ 100 > 100

10 ¬ 19 ≤ 130 > 130
Fonte: Kwiterovich PO. The John Hopkins complete guide avoiding heart disease. Baltimore. The John Hopkins Press, 1989.
12
1 - Gráfico de peso para estatura de acordo com o NCHS 77/8 – gênero masculino
13
2 - Gráfico de peso para estatura de acordo com o NCHS 77/8 – gênero feminino:
14
3 - Gráfico de peso para estatura (0 – 36 meses) de acordo com o CDC, 2000 – gênero masculino:
15
4 - Gráfico de peso para estatura (0 – 36 meses) de acordo com o CDC, 2000 – gênero feminino:
16
5 - Gráfico de peso para estatura de acordo com o CDC, 2000 – gênero masculino:
17
6 - Gráfico de peso para estatura de acordo com o CDC, 2000 – gênero feminino:
18
7 - Gráfico de estatura segundo idade de acordo com o CDC, 2000 – gênero masculino:
19
8 - Gráfico de estatura segundo idade de acordo com o CDC, 2000 – gênero feminino:
20
9 - Gráfico de índice de massa corporal segundo a idade de acordo com o CDC, 2000 – gênero masculino:
21
10 - Gráfico de índice de massa corporal segundo a idade de acordo com o CDC, 2000 – gênero feminino:
22
11 - Estadiamento puberal de acordo com o proposto por Tanner - Masculino:

23
12 - Estadiamento puberal de acordo com o proposto por Tanner - Feminino:

Relation of circumferences and skinfold thicknesses to lipid and
insulin concentrations in children and adolescents: the Bogalusa
Heart Study1–3
David S Freedman, Mary K Serdula, Sathanur R Srinivasan, and Gerald S Berenson
ABSTRACT is related to lipid concentrations, insulin concentrations, and

Background: Although body fat patterning has been related to hypertension (6–8). These associations, which have frequently
adverse health outcomes in adults, its importance in children and been shown to be independent of the general degree of obesity,
adolescents is less certain. have been found with the use of various skinfold-thickness and
Objective: We examined the relation of circumference (waist circumference measurements to characterize fat distribution.
and hip) and skinfold-thickness (subscapular and triceps) meas- In contrast with these findings in adults, the importance of fat
Downloaded from www.ajcn.org by on December 5, 2005

urements to lipid and insulin concentrations among 2996 chil- distribution in early life is less certain. Various fat patterns have
dren and adolescents aged 5–17 y. been associated with concentrations of lipids and insulin and
Design: This was a community-based, cross-sectional study con- with blood pressure in some studies (9–14), but equivocal or
ducted in 1992–1994. negative results have also been reported (15–19); it is also possi-
Results: A central or abdominal distribution of body fat was ble that fat patterning is associated with risk factors only after
related to adverse concentrations of triacylglycerol, LDL choles- sexual maturation (17). The study of fat distribution among chil-
terol, HDL cholesterol, and insulin; these associations were dren and adolescents can be difficult because there are marked
independent of race, sex, age, weight, and height. These associ- changes in circumferences (20), skinfold thicknesses (21), and
ations were observed whether fat patterning was characterized lipoprotein concentrations (22) during growth and development.
by using 1) waist circumference alone (after adjustment for Furthermore, the amount of intraabdominal fat, which may have
weight and height), 2) waist-to-hip ratio, or 3) principal compo- a primary role in adverse health outcomes (6, 23–25), is small
nents analysis. Compared with a child at the 10th percentile of before adulthood (26, 27).
waist circumference, a child at the 90th percentile was estimated We showed previously, in 388 children with extreme (high or
to have, on average, higher concentrations of LDL cholesterol low) concentrations of LDL and VLDL cholesterol, that truncal
(0.17 mmol/L), triacylglycerol (0.11 mmol/L), and insulin skinfold thicknesses and waist circumference are related to con-
(6 pmol/L) and lower concentrations of HDL cholesterol centrations of lipids and insulin (9, 10). The current analyses,
(!0.07 mmol/L). These differences, which were independent of which also included hip circumference, further examined these
weight and height, were significant at the 0.001 level and were associations in a larger (n = 2996), representative sample of
consistent across race-sex groups. school-aged children. The goal of the present study was to deter-
Conclusions: These findings emphasize the importance of mine whether information on skinfold thicknesses (subscapular
obtaining information on body fat distribution, waist circumfer- and triceps) and circumferences (waist and hip) can improve the
ence in particular, in children. Waist circumference, which is rel- prediction of lipid and insulin concentrations among children
atively easy to measure, may help to identify children likely to and adolescents if weights and heights are already known.
have adverse concentrations of lipids and insulin. Am J Clin
Nutr 1999;69:308–17.
KEY WORDS Fat distribution, children, lipids, insulin,

1
waist circumference, hip circumference, skinfold thickness, From the Division of Nutrition and Physical Activity, Centers for Disease
body weight, Bogalusa Heart Study Control and Prevention, Atlanta, and the Tulane Center for Cardiovascular
Health, Tulane University School of Public Health and Tropical Medicine,
New Orleans.
2
INTRODUCTION Supported by grants HL 15103 and HL 32194 from the National Heart,
Lung, and Blood Institute, National Institutes of Health, and by funds from
After Vague’s (1) observation that android obesity among the CDC and Robert W. Woodruff Foundations.
women is associated with diabetes and atherosclerosis, a prepon- 3
Address reprint requests to DS Freedman, CDC Mailstop K-26, 4770
derance of body fat in the abdomen, upper body, and trunk was Buford Highway, Atlanta, GA 30341-3717. E-mail: Dxf1@Cdc.gov.
found to be predictive of diabetes (2, 3) and cardiovascular dis- Received January 15, 1998.
ease (4, 5). Several investigators also reported that fat distribution Accepted for publication June 17, 1998.
308 Am J Clin Nutr 1999;69:308–17. Printed in USA. © 1999 American Society for Clinical Nutrition
CIRCUMFERENCES, SKINFOLDS, AND RISK FACTORS IN CHILDREN 309
SUBJECTS AND METHODS weight, Quetelet index (in kg/m2), Rohrer index (in kg/m3), and
hip circumference; 0.98 for each skinfold thickness; and 0.97 for
Study population waist circumference. The slightly lower reproducibility for the
The Bogalusa Heart Study is a community-based study of car- waist circumference was in part due to duplicate measurements
diovascular disease risk factors in early life. The eligible popula- (of 52 and 83 cm) for a 12-y-old with a Quetelet index of 28.9;
tion consists of all children and young adults living in Ward 4 of excluding this girl increased the intraclass correlation coefficient
Washington Parish, LA. Although this biracial (one-third black) to 0.98. No information is available for interobserver repro-
community is relatively poor, with an economy sustained primar- ducibility because the original and repeat measurements were
ily by a lumber mill, it is fairly typical of semirural towns in the made by the same examiner.
South; the population in 1990 was !43 000. Since 1973, cross- Because the stage of sexual maturation is associated with fat
sectional studies of the school-age population have been con- distribution (21) and lipid concentrations (22), an index of sex-
ducted every 3–5 y; the current analysis consists of 5–17-y-olds ual development was included in some analyses. Maturation was
who participated in the examination conducted between October determined by a physician according to the 5 categories of Tan-
1992 and June 1994. Participation rates in previous cross-sec- ner (29); this classification was based on a combination of the
tional studies ranged from 80% to 93% (28). Informed consent appearance of female breast or male genitalia and pubic hair
was obtained from all participants, and study protocols were development.
approved by human subjects review committees of the Louisiana
State University School of Medicine and the Tulane University Laboratory analyses
School of Public Health and Tropical Medicine. Concentrations of serum cholesterol and triacylglycerol were
Of the 3135 participants, we excluded 9 girls who reported measured, in the Bogalusa Heart Study Core Laboratory, by
that they were pregnant and 17 children who were missing one enzymatic procedures (Abbott VP, North Chicago) (30, 31). The
or more anthropometric measurements. We also excluded 7 chil- laboratory met the performance requirements of the Centers for

dren whose race-ethnicity was reported as other than white or Disease Control and Prevention (CDC) Lipid Standardization
black; the race-ethnicity of the mother was used for these classi- Program and is monitored by this program for the accuracy of
fications. Of the remaining 3102 children, cholesterol (total, total cholesterol, triacylglycerol, and HDL-cholesterol measure-
LDL, and HDL) determinations were available for 2996. Analy- ments. Measurements of LDL and HDL cholesterol were made
ses of triacylglycerol and insulin concentrations excluded an with a combination of heparin-calcium precipitation and agar-
additional 347 children who reported not having fasted; another agarose gel electrophoresis (32). Plasma insulin concentrations
133 children did not have a sample available for insulin determi- were measured in the centralized laboratory by a radioim-
nations. The resulting sample sizes in the present analyses were munoassay procedure (Phaadebas Insulin Kit; Pharmacia Diag-
2516 (insulin), 2649 (triacylglycerol), and 2996 (LDL and HDL nostics AB, Piscataway, NJ).
cholesterol). Although we observed a weak, positive association CDC-assigned quality control samples were used to monitor
(that was significant at the 0.01 level) between waist circumfer- the cholesterol and triacylglycerol analyses, and the accuracy
ence and concentrations of total cholesterol, these data are not was well within the limits set by this agency. In addition, a 10%
presented because of the opposite associations of LDL and HDL sample was randomly chosen each day to assess measurement
cholesterol with the obesity indexes. error, and with the exception of insulin concentrations (0.91),
intraclass correlation coefficients ranged from 0.95 (HDL cho-
General examinations lesterol) to 0.995 (triacylglycerol). Median concentrations of the
Height was measured twice to the nearest 0.1 cm with a man- laboratory determinations, along with the overall 10th and 90th
ual height board, and weight was measured twice to the nearest percentiles, are shown in Table 1. Lipid and insulin concentra-
0.1 kg with a balance-beam metric scale. No adjustments were tions differed substantially by race, sex, and age.
made for the weight of the gown, underpants, or socks worn dur-
ing the examination. Statistical analyses
Each skinfold thickness and circumference was measured 3 Robust lowess (locally weighted scatter plot smoother)
times. The triceps and subscapular skinfold thicknesses were curves, which rely on the data to determine functional form (33),
measured to the nearest millimeter with Lange skinfold calipers were used to summarize the relation of the anthropometric
(Cambridge Scientific Industries, Inc, Cambridge, MD) and cir- dimensions to age (calculated as the number of days between the
cumferences were measured with a nonstretchable tape. The sub- examination and birth dates divided by 365.25) within each race-
scapular skinfold thickness was measured immediately below sex group; statistical significance was assessed in regression
the inferior angle of the scapula, waist circumference was meas- models that incorporated natural splines (34). Because the distri-
ured midway between the rib cage and the superior border of the butions of several variables (triacylglycerol, insulin, and skinfold
iliac crest, and hip circumference was measured at the greater thicknesses) were skewed, nonparametric techniques, such as
trochanters. The mean value for each anthropometric character- Spearman correlation coefficients or log transformations, were
istic was used in all analyses. The subscapular-to-triceps skin- often used in the analyses. In analyses of the entire sample, a P
fold-thickness ratio (STR) and the waist-to-hip ratio (WHR), 2 value of 0.001 was used to assess significance.
widely used indexes of fat distribution, were also examined. Race, sex, age, and height were treated as covariates in all
On each of the 262 screening days during the 21 mo of data analyses, and weight was included in analyses that examined
collection, a 10% random sample of the examined children was whether the circumferences and skinfold thicknesses provided
selected to assess reproducibility. Intraclass (within-observer) additional (independent) information on risk factors. Although
correlation coefficients, based on pairs of measurements made we also included the Quetelet or Rohrer index in some regres-
by the same examiner on the same day, were > 0.99 for height, sion models, it may be more appropriate to adjust for weight
310 FREEDMAN ET AL
TABLE 1
Median lipid and insulin concentrations by race, sex, and age group
Race-sex1
White White Black Black Age group1
Overall percentiles males females males females 5–9 y 10–14 y 15–17 y
n 10 50 90 (n = 836) (n = 849) (n = 636) (n = 675) (n = 1068) (n = 1410) (n = 518)
LDL cholesterol (mmol/L) 2996 1.86 2.59 3.50 2.55 2.61 2.58 2.68 2.71 2.57 2.44
HDL cholesterol (mmol/L) 2996 1.01 1.34 1.78 1.29 1.27 1.47 1.40 1.40 1.34 1.24
Triacylglycerols (mmol/L) 2649 0.50 0.80 1.49 0.84 0.91 0.68 0.73 0.74 0.85 0.81
Insulin (pmol/L) 2516 38 67 136 61 69 63 79 52 79 71
1
Median concentrations are shown.
and height separately (7); furthermore, although the Quetelet (age 17 y) among girls and from 0.87 to 0.82 among boys (data
index is widely used as a measure of relative weight (35), it is not shown).
moderately correlated with height in schoolchildren (r = 0.55 in Most anthropometric dimensions were highly intercorrelated
the current study). (Table 2). The Quetelet index was related strongly to the indi-
Because of the differences in scale of the anthropometric vidual circumference (r: !0.9) and skinfold-thickness (r: !0.8)
dimensions, predicted differences in risk factors are presented measures; waist and hip circumferences were also strongly asso-
for children at the 10th and 90th percentiles of each skinfold ciated with each other and with the skinfold thicknesses
thickness or circumference. Furthermore, because of the diffi- (r: !0.8–0.9). In contrast, a weaker correlation (r = 0.35) was
culty in interpreting regression coefficients in the presence of seen between WHR and STR, suggesting that each might capture

highly correlated variables, several statistical tests were based on a different aspect of fat distribution. Adjustment for weight sub-
whether a set of regression coefficients was equal to 0 (chunk stantially reduced the magnitudes of most associations (values in
tests), and therefore provided no additional information on the parentheses); the largest decrease was seen in the correlation
outcome. Several results were verified by using least-trimmed between waist and hip circumferences.
squares regression; whereas ordinary least-squares regression Each anthropometric characteristic showed fairly similar (and
minimizes the sum of all squared deviations, this robust method significant) associations with concentrations of lipids and insulin
minimizes !50% of the squared deviations and provided a good (Table 3). For example, compared with a child at the 10th per-
fit for the bulk of the data (36). centile of weight, a child (of the same sex, race, age, and height)
Although ratios are widely used in studies of body fat distribution, at the 90th percentile of weight was estimated to have a 0.30-
to adequately correct for the characteristic in the denominator, it is mmol/L higher LDL-cholesterol concentration, a 0.32-mmol/L
necessary for a regression of the numerator on the denominator to higher triacylglycerol concentration, a 0.19-mmol/L lower HDL-
have a y intercept of 0 (37, 38); furthermore, the use of WHR is cholesterol concentration, and a 54-pmol/L higher insulin
analogous to modeling an interaction (without main effects) concentration. Predicted differences in LDL-cholesterol concentra-
between waist and hip!1 in regression models. We therefore tions varied little across the individual anthropometric dimensions,
focused on the individual characteristics and used principal com- with increases ranging from 0.30 mmol/L (weight and hip cir-
ponents analysis to reduce the 4 measurements (2 circumferences cumference) to 0.34 mmol/L (subscapular skinfold thickness);
and 2 skinfold thicknesses) to a smaller number of uncorrelated differences across deciles of WHR and STR tended to be smaller.
variables (4, 39). Residuals from a regression of the circumfer- Predicted changes in other risk factors also varied only slightly
ences and skinfold thicknesses on race, sex, age, weight, and across the individual anthropometric dimensions: for triacylglyc-
height were used in these analyses and we found the first principal erol, from 0.29 to 0.34 mmol/L; for HDL cholesterol, from
component to be positively correlated (r: !0.5–0.9) with all !0.16 to !0.20 mmol/L; and for insulin, from 43 to 54 pmol/L.
anthropometric dimensions, reflecting the overall level of obesity. In general, the weakest associations were seen with triceps skin-
The second component contrasted the waist circumference with fold thickness.
the hip circumference and triceps skinfold thickness and was inter- We then used lowess curves to summarize the relation of
preted as an index of central fat distribution. waist circumference to concentrations of HDL cholesterol
among 5–17-y-old black girls (n = 675) within Rohrer index
categories (Figure 2). This specific relation is shown because
RESULTS age was weakly related to concentrations of HDL cholesterol
Among these 5–17-y-olds, subscapular skinfold thickness (r = !0.09) and Rohrer index (r = 0.01) among girls; results
(Figure 1) was strongly associated with age, and thicknesses were similar among black and white girls. Although there were
were consistently higher in girls than in boys and in white boys some inconsistencies within the 9 strata shown in Figure 2, an
than in black boys. The relation of the triceps skinfold thickness increase in waist circumference from 60 to 80 cm was typically
to age differed substantially by sex: during adolescence, thick- associated with a decrease in HDL-cholesterol concentration of
nesses either remained stable or increased slightly among girls, from 0.15 to 0.25 mmol/L. Furthermore, these associations did
whereas they decreased by !20–40% among boys. Smaller race- not differ significantly by relative weight or age; among 5–9-y-
sex differences were seen for the circumferences, but white boys old black girls, for example, a 20-cm increase in waist circum-
had the largest waist girths. Because the increase with age was ference was independently associated with a 0.36-mmol/L
proportionately greater for hip circumference than for waist cir- decrease in HDL cholesterol (data not shown). Additional
cumference, mean WHRs decreased from 0.86 (age 5 y) to 0.75 regression models indicated that independently of the Rohrer

FIGURE 1. Skinfold thicknesses (subscapular and triceps) and circumferences (waist and hip) by race (black or white), sex, and age: solid lines,
males; dashed lines, females; thick lines, whites; thin lines, blacks. Each race-sex curve was constructed by using lowess (see Methods). As assessed
in linear regression models, there were significant race, sex, and age differences for all anthropometric dimensions.
index, a 20-cm increase in waist circumference among black girls scapular skinfold thickness remained associated with adverse risk
was also associated with increases of 0.16 mmol/L in triacylglyc- factor concentrations (Table 4). For example, a child with a waist
erol and 57 pmol/L in insulin, but little difference in concentra- circumference at the 90th percentile was estimated to have a 0.17-
tions of LDL cholesterol. mmol/L higher LDL-cholesterol concentration than a child at the
After adjustment for weight (in addition to race, sex, age, and 10th percentile. (Similar results were obtained by using least-
height) in regression models, waist circumference, WHR, and sub- trimmed squares rather than ordinary least-squares.) Compared with
TABLE 2
Intercorrelations among the anthropometric characteristics1
Relative weight indexes Circumferences Skinfold thicknesses
Rohrer (kg/m)3 Quetelet (kg/m2) Waist Hip WHR Subscapular Triceps
Circumferences
Waist (cm) 0.84 0.90
Hip (cm) 0.88 0.93 0.88 (0.20)2
WHR 0.37 0.33 0.58 (0.61) 0.26 (!0.32)
Skinfold thicknesses
Subscapular (mm) 0.81 0.84 0.83 (0.37) 0.83 (0.35) 0.36 (0.10)
Triceps (mm) 0.77 0.80 0.76 (0.20) 0.80 (0.31) 0.27 (!0.02) 0.84 (0.57)
STR 0.39 0.38 0.46 (0.22) 0.40 (0.04) 0.35 (0.24) 0.56 (0.42) 0.09 (!0.40)
1
Values are partial Spearman correlation coefficients that have been adjusted for race, sex, age, and height. With a sample size of 2996, a correlation
coefficient " 0.06 is significant at the 0.001 level. WHR, waist-to-hip ratio; STR, subscapular-to-triceps skinfold-thickness ratio.
2
Values in parentheses were adjusted for weight in addition to race, sex, age, and height.
312 FREEDMAN ET AL
TABLE 3
Relation of the anthropometric characteristics to lipid and insulin concentrations, adjusted for race, sex, age, and height1
Circumferences Skinfold thicknesses
Outcome Weight Waist Hip WHR Subscapular Triceps STR
LDL cholesterol
Predicted change2 (mmol/L) 0.30 0.31 0.30 0.24 0.34 0.33 0.18
t Statistic3 10 12 10 8 12 11 6
Spearman r 0.19 0.21 0.19 0.15 0.21 0.22 0.11
Triacylglycerols
Predicted change (mmol/L) 0.32 0.32 0.33 0.23 0.34 0.29 0.24
t Statistic 18 20 18 14 19 16 13
Spearman r 0.32 0.33 0.32 0.21 0.33 0.29 0.24
HDL cholesterol
Predicted change (mmol/L) !0.19 !0.19 !0.19 !0.16 !0.20 !0.16 !0.16
t Statistic 15 17 14 13 15 12 12
Spearman r !0.28 !0.29 !0.25 !0.23 !0.27 !0.20 !0.23
Insulin
Predicted change (pmol/L) 54 47 54 29 47 43 28
t Statistic 31 32 29 17 28 24 16
Spearman r 0.52 0.51 0.50 0.26 0.48 0.45 0.31
1
WHR, waist-to-hip ratio; STR, subscapular-to-triceps skinfold-thickness ratio.
2
Predicted difference in metabolic characteristics between persons at the 10th and 90th percentiles of each anthropometric dimension. Differences were
as follows: weight, 26 kg; waist circumference, 21 cm; hip circumference, 22 cm; WHR, 0.115; subscapular skinfold thickness, 1.5 (log scale); triceps skin-

fold thickness, 1.23 (log scale); and STR, 0.33 (log scale). The SDs of the risk factors were 0.67 mmol/L (LDL cholesterol), 0.46 mmol/L (triacylglycerols),
0.31 mmol/L (HDL cholesterol), and 57 pmol/L (insulin).
3
A t statistic " 3 indicates that the predicted change in the risk factor is significant at the 0.001 level.
the previous results, the smaller predicted differences shown in Table 4 were fairly similar to those seen with waist circumference, but associa-
were largely due to the reduced variability of the anthropometric tions with hip circumference and triceps skinfold thickness were small
dimensions after adjustment for weight. (The decreased variability in and inconsistent. Spearman correlation coefficients also indicated that
waist circumference after stratification by Rohrer index is evident in associations were generally strongest for waist circumference and sub-
Figure 2.) Predicted changes across subscapular skinfold thicknesses scapular skinfold thickness and weakest for hip circumference.
FIGURE 2. Relation of waist circumference to concentrations of HDL cholesterol among black females. Each of the 9 panels shows this relation,
summarized by using lowess curves, for a given range of the Rohrer index (in kg/m3); each person is represented by an open circle. Increasing values
of Rohrer index go from left to right and from bottom to top; the shaded part of the label indicates the position of the specified stratum relative to the
overall range. Additional analyses indicated that the relation of waist circumference to HDL-cholesterol concentrations did not differ across Rohrer
index strata (P = 0.16 for product term). Similar results were obtained if 4, 5, or 10 strata (rather then 9) were used.
TABLE 4
Relation of the circumferences and skinfold thicknesses to concentrations of lipids and insulin, adjusted for race, sex, age, height, and weight1
Circumferences Skinfold thicknesses
Outcome Waist Hip WHR Subscapular Triceps STR
LDL cholesterol
Predicted change2 (mmol/L) 0.17 0.03 0.12 0.18 0.15 0.06
t Statistic3 6 1 4 6 5 2
Spearman r 0.08 0.02 0.08 0.10 0.11 0.01
Triacylglycerols
Predicted change (mmol/L) 0.11 !0.01 0.09 0.10 0.03 0.08
t Statistic 7 1 6 6 2 5
Spearman r 0.09 0.02 0.10 0.12 0.06 0.09
HDL cholesterol
Predicted change (mmol/L) !0.07 0.03 !0.08 !0.04 0.02 !0.07
Spearman r !0.11 0.04 !0.14 !0.08 0.02 !0.12
Insulin
Predicted change (pmol/L) 6 !4 7 4 0 4
Spearman r 0.09 !0.01 0.09 0.09 0.07 0.07
1
WHR, waist-to-hip ratio; STR, subscapular-to-triceps skinfold-thickness ratio.
2
Predicted difference in metabolic characteristics between persons at the 10th and 90th percentiles of each anthropometric dimension. Differences were
as follows: waist circumference, 8 cm; hip circumference, 6 cm; WHR, 0.10; subscapular skinfold thickness, 0.8 (log scale); triceps skinfold thickness, 0.75

(log scale); and STR, 0.28 (log scale). The SDs of the risk factors were 0.67 mmol/L (LDL cholesterol), 0.46 mmol/L (triacylglycerols), 0.31 mmol/L (HDL
cholesterol), and 57 pmol/L (insulin).
3
A t statistic " 3 indicates that the predicted change in the risk factor is significant at the 0.001 level.
In contrast with the independent information provided by waist /r/ ≤ 0.04). Weight, however, did improve the prediction of insulin
circumference and subscapular skinfold thickness for the risk fac- concentrations beyond that achieved with waist circumference.
tors shown in Table 4, additional analyses indicated that weight Forward stepwise regression was then used to determine
provided no additional information on concentrations of LDL cho- which circumferences and skinfold thicknesses were most pre-
lesterol, triacylglycerol, or HDL cholesterol if waist circumfer- dictive of risk factor concentrations if weight and other covariates
ence (in addition to race, sex, age, and height) was known (partial were known (Table 5). Of the 4 measures, waist circumference
TABLE 5
Relation of the girth and skinfold-thickness measures to concentrations of lipids and insulin based on stepwise regression1
LDL cholesterol (mmol/L) Triacylglycerols (mmol/L) HDL cholesterol (mmol/L) Insulin (pmol/L)
Individual measures
Waist circumference 0.12 0.09 !0.07 7
Hip circumference — !0.04 0.04 !5
Subscapular skinfold thickness 0.132 0.08 — —
Triceps skinfold thickness — — — —
F statistic3 28 27 22 21
# R2 4 0.017 0.023 0.012 0.008
Ratios
WHR 0.12 0.08 !0.08 7
STR — 0.07 !0.05 —
F statistic 19 24 31 31
# R2 0.006 0.016 0.016 0.006
Principal components
1 (generalized obesity) 0.19 0.08 — —
2 (central fat patterning)5 0.08 0.08 !0.09 6
F statistic 28 36 46 31
# R2 0.017 0.021 0.012 0.007
1
All models contained race, sex, age, height, and weight. Values represent the predicted change in lipid or insulin concentration associated with a change
for each anthropometric index between the 10th and 90th percentiles; differences were as follows: waist circumference, 8 cm; hip circumference, 6 cm; sub-
scapular skinfold thickness, 0.8 (log scale); WHR, 0.10; and STR, 0.28 (log scale). All predicted changes were significant at the 0.01 level; dashed lines indi-
cate that the variable was not a significant predictor. WHR, waist-to-hip ratio; STR, subscapular-to-triceps skinfold-thickness ratio.
2
A model with waist circumference and triceps skinfold thickness (rather than subscapular skinfold thickness) yielded similar results.
3
The F statistic tests that all added anthropometric characteristics have a coefficient of 0; with 2 variables added to a model already containing 12 pre-
dictors (race, sex, age, height, weight, and quadratic terms and interactions), an F statistic of !7 would be significant at the 0.001 level given a sample size
of 2996.
4
Represents the increase in the multiple R 2 attributable to the information added by the anthropometric characteristics.
5
The second principal component was a linear contrast of the waist circumference with the hip circumference and triceps skinfold thickness.
314 FREEDMAN ET AL
TABLE 6
Relation of body fat distribution to concentrations of lipids and insulin by race, sex, and age group1
Race-sex Age group
White males White females Black males Black females 5–9 y 10–14 y 15–17 y
Index of fat patterning (n = 836) (n = 849) (n = 636) (n = 675) (n = 1068) (n = 1410) (n = 518)
LDL cholesterol (mmol/L)
Waist circumference 0.16 0.13 0.16 0.23 0.082 0.22 0.10
WHR 0.16 0.12 0.012 0.20 !0.032 0.22 0.132
HDL cholesterol (mmol/L)
Waist circumference !0.07 !0.08 !0.052 !0.08 !0.14 !0.06 !0.07
WHR !0.09 !0.09 !0.052 !0.12 !0.11 !0.07 !0.11
Triacylglycerols (mmol/L)
Waist circumference 0.09 0.14 02 0.12 0.052 0.12 0.11
WHR 0.08 0.14 02 0.07 0.022 0.12 0.13
Insulin (pmol/L)
Waist circumference 22 6 32 12 52 6 7
WHR 32 8 62 10 4 7 11
1
Values represent the predicted changes in lipid or insulin concentration associated with a change in each anthropometric index between the 10th and
90th percentiles. All models contained height and weight as covariates. WHR, waist-to-hip ratio.
2
P > 0.05; all other values were significant at the 0.05 level.
was consistently associated with concentrations of each risk fac- trasting waist circumference with the sum of the hip circumfer-

tor; other predictors (at the 0.01 level) included subscapular ence and triceps skinfold thickness. Although the differences
skinfold thickness and hip circumference. Hip circumference, observed in risk factors between the 10th and 90th percentiles of
however, was significantly related to concentrations of triacyl- the fat patterning indexes were relatively modest, they were con-
glycerol and HDL cholesterol only if circumference was also sistent across race and sex groups; furthermore, an association
included in the regression models. Triceps skinfold thickness did with concentrations of HDL cholesterol was observed even
not provide independent information on any outcome. among 5–9-y-olds. These results confirm many of the associa-
Also shown in Table 5 are the corresponding results for the tions observed in previous studies of children and adolescents
ratios and principal components. These analyses indicated that from Bogalusa (9, 10), but are based on a much larger, represen-
the second principal component, which was associated positively tative sample; the current results also emphasize that the hip cir-
(r: !0.8) with waist circumference and inversely (r: !!0.35) cumference provides little information on risk factors.
with both hip circumference and triceps skinfold thickness, was Waist circumference showed the most consistent, and gener-
associated with adverse concentrations of all risk factors. Fur- ally strongest, associations with adverse risk factor concentra-
thermore, this index of central fat patterning was uncorrelated tions. These findings likely reflect the ability of waist circumfer-
with the first component (general degree of obesity) and showed ence to function as an index of both fat distribution and
moderate to strong correlations with the adjusted waist circum- generalized obesity, as well as the relation of waist circumfer-
ference (r: !0.74), WHR (r: !0.68), and STR (r: !0.42). ence with correlates of lipid concentrations. For example, waist
In general, associations with risk factors differed only slightly circumference was strongly associated with age and Quetelet
across race and sex groups (Table 6). As assessed by product index and circumferences differed between boys and girls and
terms in regression models, the only significant differences (at between white boys and black boys. Because waist circumfer-
the 0.001 level) in the associations with fat patterning were that ence is also relatively easy to measure, it may be particularly
the strength of the relation of WHR to concentrations of both appropriate for epidemiologic studies of children. Race-, sex-,
LDL cholesterol and triacylglycerol increased with age. Among and age-specific 50th and 90th percentiles for waist circumfer-
5–9-y-olds, for example, a child with an adverse (90th per- ence based on the current sample are shown in Table 7. This
centile) WHR had, on average, a (nonsignificant) 0.03-mmol/L information may help in the identification of persons who are
lower LDL-cholesterol concentration and a 0.02-mmol/L higher likely to have adverse lipid and insulin concentrations.
triacylglycerol concentration than did a child at the 10th per- Previous studies of fat distribution among children and ado-
centile. An inverse association between waist circumference and lescents produced somewhat conflicting results: associations
concentrations of HDL cholesterol, however, was evident even with concentrations of lipids, glucose, and insulin and with
among the 5–9-y-olds. blood pressure were reported in some (9–14) but not all (15–19)
studies. These contrasting findings may in part be due to differ-
ences across studies in the examined anthropometric dimensions
DISCUSSION or outcomes, the ages of the studied children, or the statistical
Our results indicate that a relative excess of adipose tissue in analyses performed. For example, although some studies (17,
the abdominal or central region of children and adolescents is 18) measured several skinfold thicknesses and circumferences,
associated with adverse concentrations of lipids and insulin. the only lipid determination was the total cholesterol concentra-
These associations, which exist independently of weight, height, tion; furthermore, associations with blood pressure may have
and age, were similar in magnitude regardless of whether fat dis- been confounded by a lack of statistical adjustment for height, a
tribution was quantified by waist circumference (adjusted for correlate of blood pressure that is independent of age (40).
weight, height, and age), WHR, or a principal component con- Results of studies that examined intraabdominal fat (as deter-
TABLE 7
Selected percentiles of waist circumference by race, sex, and age1
White boys White girls Black boys Black girls
Percentiles Percentiles Percentiles Percentiles
Age (y) n 50 90 n 50 90 n 50 90 n 50 90
cm cm cm cm
5 28 52 59 34 51 57 36 52 56 34 52 56
6 44 54 61 60 53 60 42 54 60 52 53 59
7 54 55 61 55 54 64 53 56 61 52 56 67
8 95 59 75 75 58 73 54 58 67 54 58 65
9 53 62 77 84 60 73 53 60 74 56 61 78
10 72 64 88 67 63 75 53 64 79 49 62 79
11 97 68 90 95 66 83 58 64 79 67 67 87
12 102 70 89 89 67 83 60 68 87 73 67 84
13 82 77 95 78 69 94 49 68 87 64 67 81
14 88 73 99 54 69 96 62 72 85 51 68 92
15 58 73 99 58 69 88 44 72 81 54 72 85
16 41 77 97 58 68 93 41 75 91 34 75 90
17 22 79 90 42 66 86 31 78 101 35 71 105
1
Percentiles are based on the 1992–1994 examination of school-aged children in the Bogalusa Heart Study and were estimated separately within each
race, sex, and age group. Estimates were not smoothed.

mined by magnetic resonance imaging) in youths (12, 14, 26) circumference = 3.4 + 0.78 $ hip circumference. Other investi-
also suggest that the use of WHR to characterize fat distribution gations of children and adults have also suggested that waist cir-
(16, 19) may not be optimal. Furthermore, it is difficult to inter- cumference (7, 8, 13, 26) or various skinfold thicknesses (12, 27,
pret the results that appear to have not controlled for both weight 43) may be better measures of fat distribution than is WHR.
and height (11, 13); the strong intercorrelations with various Several limitations of the current study should be considered.
anthropometric dimensions and fat depots (41) could confound Only 2 skinfold thicknesses and 2 circumferences were obtained
associations with fat patterning. and it is possible that measurements at other sites [such as at the
It has been suggested that the amount of intraabdominal fat is chest or thigh (4, 42, 46, 47)] may have provided additional
the primary determinant of adverse outcomes (6, 23–25) and that information. Although the optimal sites are uncertain, small
the lipolysis of intraabdominal adipocytes may lead to high con- changes in the location of the waist measurement can influence
centrations of fatty acids (24). However, various metabolic out- associations with risk factors (42); the associations with STR in
comes are also associated with chest circumference (42) and the current study were influenced by the low precision of skin-
truncal subcutaneous adipose tissue (43). In agreement with our fold-thickness ratios (48). Furthermore, the current analyses
observation that triacylglycerol concentrations are independently used fasting insulin concentrations as a surrogate for insulin
related to both waist circumference and subscapular skinfold resistance, and as assessed by whole-body glucose uptake in
thickness (Table 5), WHR and STR have also been found to be clamp studies, there is only a moderately strong correlation
independent predictors of triacylglycerol concentrations among (r = 0.65–0.70) between the 2 measurements (49).
adults (44). These associations with various fat patterns suggest Despite these limitations, our findings may have important
that it may be difficult to identify the best anthropometric index implications for the choice of skinfold-thickness or circumfer-
of fat distribution, which may also vary by outcome and popula- ence measurements in clinical and epidemiologic studies.
tion (45). It would be helpful if additional studies were per- Whereas waist circumference, which is relatively easy to meas-
formed to determine whether intraabdominal fat is the primary ure, appears to be an important correlate of concentrations of
determinant of adverse health outcomes; adequate statistical lipids and insulin among children and adolescents, triceps skin-
control of the overall degree of obesity would be important in the fold thickness and hip circumference provide little additional
analyses of these data. information about risk factors if weight and height are known.
Studies of fat patterning in children are further complicated These findings suggest that the measurement of waist circum-
by the 1) small amount of intraabdominal fat present before ference may help to identify children and adolescents with
adulthood (26, 27) and 2) the rapid changes in fat patterning that adverse concentrations of lipids and other risk factors. These
occur during growth and development (21). It is also likely that persons could then targeted for weight reduction and risk-factor
some anthropometric indexes of fat distribution among adults, surveillance.
such as WHR, may be inappropriate for children and adoles-
cents. For example, the proportionately larger increases in hip
REFERENCES
(compared with waist) circumference that we and others (20)
observed during growth may account for the low correlation 1. Vague J. The degree of masculine differentiation of obesities: a fac-
tor determining predisposition to diabetes, atherosclerosis, gout,
between WHR and intraabdominal fat among adolescents (12,
and uric calculous disease. Am J Clin Nutr 1956;4:20–34.
14, 26). Furthermore, to adequately correct for the characteristic 2. Feldman R, Sender AJ, Siegelaub AB. Difference in diabetic and
in the denominator of a ratio such as WHR, a regression of the nondiabetic fat distribution patterns by skinfold measurements. Dia-
numerator on the denominator should have a y intercept of 0 (37, betes 1969;18:478–86.
38); in contrast, the regression line in the current study was waist 3. Wei M, Gaskill SP, Haffner SM, Stern MP. Waist circumference as
316 FREEDMAN ET AL
the best predictor of noninsulin dependent diabetes mellitus 23. Després JP, Moorjani S, Lupien PJ, Tremblay A, Nadeau A,
(NIDDM) compared to body mass index, waist/hip ratio and other Bouchard C. Regional distribution of body fat, plasma lipoproteins,
anthropometric measurements in Mexican Americans—a 7-year and cardiovascular disease. Arteriosclerosis 1990;10:497–511.
prospective study. Obes Res 1997;5:16–23. 24. Björntorp P. “Portal” adipose tissue as a generator of risk factors for
4. Ducimetiere P, Richard J, Cambien F. The pattern of subcutaneous cardiovascular disease and diabetes. Arteriosclerosis 1990;10:
fat distribution in middle-aged men and the risk of coronary heart 493–6.
disease: the Paris Prospective Study. Int J Obes 1986;10:229–40. 25. Pouliot MC, Després JP, Nadeau A, et al. Visceral obesity in men.
5. Freedman DS, Williamson DF, Croft JB, Ballew C, Byers T. Body Associations with glucose tolerance, plasma insulin, and lipoprotein
fat distribution and the incidence of coronary heart disease: the levels. Diabetes 1992;41:826–34.
NHANES I Epidemiologic Follow-up Study. Am J Epidemiol 26. de Ridder CM, de Boer RW, Seidell JC, et al. Body fat distribution
1995;142:53–63. in pubertal girls quantified by magnetic resonance imaging. Int J
6. Peiris AN, Hennes MI, Evans DJ, Wilson CR, Lee MB, Kissebah Obes 1992;16:443–9.
AH. Relationship of anthropometric measurements of body fat dis- 27. Goran MI, Kaskoun M, Shuman WP. Intra-abdominal adipose tissue
tribution to metabolic profile in premenopausal women. Acta Med in young children. Int J Obes 1995;19:279–83.
Scand Suppl 1988;723:179–88.
28. Croft JB, Webber LS, Parker FC, Berenson GS. Recruitment and
7. Seidell JC, Cigolini M, Charzewska J, Ellsinger BM, Deslypere JP,
participation of children in a long-term study of cardiovascular dis-
Cruz A. Fat distribution in European men: a comparison of anthro-
ease: the Bogalusa Heart Study, 1973–1982. Am J Epidemiol 1984;
pometric measurements in relation to cardiovascular risk factors. Int
120:436–48.
J Obes Relat Metab Disord 1992;16:17–22.
29. Tanner JM. Growth at adolescence. 2nd ed. Oxford, United King-
8. Pouliot M, Després JP, Lemieux S, et al. Waist circumference and
dom: Blackwell Scientific Publications, 1962.
abdominal sagittal diameter: best simple anthropometric indexes of
30. Allain CC, Poon LS, Chan CS, Richmond W, Fu PC. Enzymatic
abdominal visceral adipose tissue accumulation and related cardio-
vascular risk in men and women. Am J Cardiol 1994;73:460–8. determination of total serum cholesterol. Clin Chem 1974;20:
9. Freedman DS, Srinivasan SR, Burke GL, et al. Relation of body fat 470–5.
31. Bucolo G, David H. Quantitative determination of serum triglyc-

distribution to hyperinsulinemia in children and adolescents: the
Bogalusa Heart Study. Am J Clin Nutr 1987;46:403–10. erides by the use of enzymes. Clin Chem 1973;19:476–82.
10. Freedman DS, Srinivasan SR, Harsha DW, Webber LS, Berenson 32. Srinivasan SR, Frerichs RR, Webber LS, Berenson GS. Serum
GS. Relationship of body fat patterning to lipid and lipoprotein con- lipoprotein profile in children from a biracial community. The
centrations in children and adolescents: the Bogalusa Heart Study. Bogalusa Heart Study. Circulation 1976;54:309–18.
Am J Clin Nutr 1989;50:930–9. 33. Cleveland WS. The elements of graphing data. Monterey, CA:
11. Zwiauer KFM, Pakosta R, Mueller T, Widhalm K. Cardiovascular Wadsworth Advanced Books and Software, 1985.
risk factors in obese children in relation to weight and body fat dis- 34. Harrell FE, Lee KL, Mark DB. Multivariable prognostic models:
tribution. J Am Coll Nutr 1992;11:41S–50S. issues in developing models, evaluating assumptions and adequacy,
12. Brambilla P, Manzoni P, Sironi S, et al. Peripheral and abdominal and measuring and reducing errors. Stat Med 1996;15:361–87.
adiposity in childhood obesity. Int J Obes 1994;18:795–800. 35. Keys A, Fidanza F, Karvonen MJ, Kimura N, Taylor HL. Indices of
13. Flodmark CE, Sveger T, Nilsson-Ehle P. Waist measurement corre- relative weight and obesity. J Chronic Dis 1972;25:329–43.
lates to a potentially atherogenic lipoprotein profile in obese 12–14- 36. Venables WN, Ripley BD. Modern applied statistics with S-Plus.
year-old children. Acta Paediatr 1995;83:941–5. New York: Springer-Verlag, 1994.
14. Caprio S, Hyman LD, McCarthy S, Lange R, Bronson M, Tambor- 37. Kronmal RA. Spurious correlation and the fallacy of the ratio stan-
lane WV. Fat distribution and cardiovascular risk factors in obese dard revisited. J R Stat Soc A 1993;156:379–92.
adolescent girls: importance of the intraabdominal fat depot. Am J 38. Goran MI, Allison DB, Poehlman ET. Issues relating to normaliza-
Clin Nutr 1996;64:12–7. tion of body fat content in men and women. Int J Obes 1995;19:
15. Becque MD, Hattori KH, Katch VL, Rocchini AP. Relationship of 638–43.
fat patterning to coronary artery disease risk in obese adolescents. 39. Mueller WH, Wohlleb JC. Anatomical distribution of subcutaneous
Am J Phys Anthropol 1986;71:423–9. fat and its description by multivariate methods: how valid are prin-
16. Baumgartner RN, Siervogel RM, Chumlea WC, Roche AF. Associ- cipal components? Am J Phys Anthropol 1981;54:25–35.
ations between plasma lipoprotein cholesterols, adiposity and adi- 40. Voors AW, Webber SL, Frerichs RR, Berenson GS. Body height and
pose tissue distribution during adolescence. Int J Obes 1989;13: body mass as determinants of basal blood pressure in children—the
31–41.
Bogalusa Heart Study. Am J Epidemiol 1977;106:101–8.
17. Sangi H, Mueller WH. Which measure of body fat distribution is
41. Seidell JC, Bouchard C. Visceral fat in relation to health: is it a
best for epidemiologic research among adolescents. Am J Epi-
major culprit or simply an innocent bystander. Int J Obes 1997;21:
demiol 1991;133:870–83.
626–31.
18. Sangi H, Mueller WH, Harrist RB, Rodriguez B, Grunbaum JG,
42. Seidell JC, Cigolini M, Charzewska J, Ellsinger BM, DiBiases G.
Labarthe DR. Is body fat distribution associated with cardiovascular
Fat distribution in European women: a comparison of anthropomet-
risk factors in childhood? Ann Hum Biol 1992;19:559–79.
19. Bermingham MA, Jones E, Steinbeck K, Brock K. Plasma choles- ric measurements in relation to cardiovascular risk factors. Int J Epi-
terol and other cardiac risk factors in adolescent girls. Arch Dis demiol 1990;19:303–8.
Child 1995;73:392–7. 43. Abate N, Garg A, Peshock RM, Stray-Gundersen J, Adams-Huet B,
20. Weststrate JA, Deurenberg P, van Tinteren H. Indices of body fat Grundy SM. Relationship of generalized and regional adiposity to
distribution and adiposity in Dutch children from birth to 18 years insulin sensitivity in men with NIDDM. Diabetes 1996;45:1684–93.
of age. Int J Obes 1989;13:456–77. 44. Haffner SM, Stern MP, Hazuda HP, Pugh J, Patterson JK. Do upper-
21. Malina RM, Bouchard C. Subcutaneous fat distribution during body and centralized adiposity measure different aspects of regional
growth. In: Bouchard C, Johnston FE, eds. Fat distribution during body-fat distribution? Diabetes 1987;36:43–51.
growth and later health outcomes. New York: Alan R Liss, 1988: 45. Karter AJ, Mayer-Davis EJ, Selby JV, et al. Insulin sensitivity and
63–84. abdominal obesity in African-American, Hispanic, and non-His-
22. Berenson GS, Srinivasan SR, Cresanta JL, Foster TA, Webber LS. panic white men and women. The Insulin Resistance and Athero-
Dynamic changes of serum lipoproteins in children during adoles- sclerosis Study. Diabetes 1996;45:1547–55.
cence and sexual maturation. Am J Epidemiol 1981;113:157–70. 46. Mueller WH, Wear ML, Hanis CL, et al. Which measure of body fat
distribution is best for epidemiologic research? Am J Epidemiol 48. Mueller WH, Kaplowitz HJ. The precision of anthropometric
1991;133:858–69. assessment of body fat distribution in children. Ann Hum Biol
47. Mueller WH, Marbella A, Harrist RB, Kaplowitz HJ, Gunbaum JA, 1994;21:267–74.
Labarthe DR. Body circumferences as alternatives to skinfold measures 49. Laakso M. How good a marker is insulin level for insulin resis-
of body fat distribution in children. Ann Hum Biol 1989;16: 495–506. tance? Am J Epidemiol 1993;137:959–65.

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Excesso de peso (pré-obesidade + obesidade) Obesidade por

Fonte: DGS, 2017

• Diagnóstico da obesidade, etapas:

➡Plotagem do IMC na curva de IMC

➡Diagnóstico de acordo com pontos de corte

Exames Laboratoriais Sobrepeso versus obesidade

OGTT p = 0,3917 ( bicaudal) n.s.

Colesterol total p = 0,3387 ( bicaudal), n.s.

LDL-colesterol p = 0,3206 (bicaudal), n.s.

Sinaliza para SNS

Atingido percentual necessário

Reduz deposição de gordura Início da puberdade

Ponto médio entre

Anexo 9 - Distribuição em percentis da circunferência abdominal segundo gênero e idade

• 50% do tecido adiposo encontra-se no sub-cutâneo

– Estimar o percentual de gordura corporal

– Avaliar a distribuição da gordura corporal

Muito baixo 8-9 7 - 11

Meninos e meninas (abaixo de 18 anos, Lohman TG, 1987)

• Resistência: Medida de oposição pura ao fluxo de corrente

• Reactância: Oposição ao fluxo de corrente causado pela

Preparo para BIA

• Evitar período pré menstrual

Excesso de adiposidade corporal

Obesidade sem Resistência Obesidade Metabólica

Sindrômica Epigenética Induzida Clássica

Ag. Infecciosos Somática

% gordura (BIA) 37%

Colesterol total 202

• Menino, 12 anos, busca atendimento encaminhado pelo

% gordura (BIA) 37%

Colesterol total 202

% GORDURA % GORDURA Peso 72 kg

• Menino, 12 anos, busca atendimento encaminhado pelo

% gordura (BIA) 37%

Colesterol total 202

% gordura (BIA) 37%

Colesterol total 202

Excesso de adiposidade corporal

Obesidade sem Resistência Obesidade Metabólica

Sindrômica Epigenética Induzida Clássica

Ag. Infecciosos Somática

% gordura (BIA) 37%

Glicemia 92 •Obesidade induzida por fármaco

Anexo 19 – Valores do perfil lipídico de crianças

Nogueira-de-Almeida et al, 2016, Rev. Medicina USP, 49:504-510

98 36 Manual de Orientação – Departamento de Nutrologia

Boys Girls Total

50% 44,1% 39,2% 42,7% 40,5%

Nogueira-de-Almeida et al, 2016, Rev. Medicina USP, 49:504-510

Resistência Periférica à Insulina

50% 57,6% 57,8%

Resistência Periférica à Insulina

Cuartero et al; An Pediatr.2007;66:481-90 - Vol. 66 Núm.5

Doença Gordurosa Hepática Não Alcoólica

• O padrão-ouro de diagnóstico da lesão hepática é a biópsia

Circ. Abdominal 89,5

Pressão arterial 125 / 84

Glicemia 86 Qual o diagnóstico?

Colesterol total 161

Menina de 9 anos e 11 meses, com Caso Clínico 3

Pressão arterial 125 / 84

Circ. Abdominal 89,5