Dietary fats, carbohydrates and vascular disease: Sri

Lankan perspectives
Mahinda Y. Abeywardena
CSIRO-Health Sciences and Nutrition, Kintore Avenue, PO Box 10041, Adelaide, SA 5000, Australia
Received: January 6, 2003; Accepted: April 22, 2003;
DOI: http://dx.doi.org/10.1016/S0021-9150(03)00157-6
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Abstract
The recent estimates for mortality from cardio and cerebrovascular diseases (CVD) for Sri Lanka524 deaths
per 100000is higher than that observed in many Western economies. However, neither an excessive total fat
intake nor an increase in the more traditional plasma lipid markers, total and LDL cholesterol (LDL-c) levels may
fully explain the increased vulnerability to CVD in this population. The average total fat intake of Sri Lankans is
25 percent of total energy (en%) and the reported total and LDL-c values are 4.9 and 2.5mmol/l, respectively.
With regard to the type of dietary fatty acids, the ratio of saturated/polyunsaturated fatty acids (PUFAs) in the
average Sri Lankan diet is 9/1 as compared with the current recommended ratio of <1/1. In spite of an
adequate total fat intake (25 en%), the relatively low intake of PUFAs in association with a high carbohydrate
diet (65 en%), appear to be resulting in similar metabolic outcomes to those of very low fat diets (VLFD, <15 en
% from fat), as reflected by high triglycerides and low HDL levels. Metabolic abnormalities including elevated
postprandial hyperlipidemia, more atherogenic lipoprotein particles, hyperglycemia with resultant
hyperinsulinemia and increased oxidative stress are likely to be more relevant in such settings. The application
of novel biomarkers for example, lipoprotein measurements in the postprandial state, LDL particle size,
estimates of endothelial dysfunction, soluble markers of inflammation and coagulability status may provide
further insight into cardiovascular disease states in populations where the dietary matrix represents high
intakes of highly digestible carbohydrates and saturated fat.

La relacin mas directa de la hipertensin arterial con el metabolismo de los

carbohidratos se presenta en el Sd. X o Sd. plurimetabolico que se define como: la
presencia concomitante de HTA con Diabetes en un paciente. La Diabetes ocasiona
una resistencia perifrica a la Insulina, que termina con la NO utilizacin de la
glucosa para la produccin de energa activando vas metabolicas "anormales" que
conducen al colesterol como fuente de energa.
Y como la activacin de estas vas se manifiesta en la HTA?

Las clulas declinan a la glucosa como

fuente para la produccin de ATP y obtendrn el sustrato de otras molculas como
el colesterol. El aumento de la degradacin del colesterol para la obtencin de
energa (ATP) genera un aumento significativo en los cidos grasos libres que en el
hgado transformarn en molculas VLDL y triglicridos (hipertrigliceridemia).
Tambin se disminuirn las HDL y se aumentarn las LDL. Todos estos productos
de la degradacin del colesterol, llevarn al organismo a un estado de estres que
supera lo tolerado en el endotelio vascular y causar un acumulo de LDL en las
paredes de las arterias (ateroesclerosis) reduciendo la luz del vaso y aumentando la
presin intravascular principio de la HTA.
Aparte de la activacin de otras vas metabolicas, la resistencia perifrica a la
Insulina contribuye a la HTA?
Si, el estado hiperinsulinemico que se presenta seguido a la resistencia, se asocia
con la hipertrofia de la clulas musculares lisa de los vasos -disminuyendo la luz- y
aumentando la sensiblidad a agentes vasoconstrictores, incidiendo en el dao al
sistema cardiovascular. Tambin tiene efectos en la reabsorcin del Na+ y agua
evitando su excrecin aumentando el volumen intravascular, volumen que no
cuenta con un buen flujo por la disminucin en la luz de los vasos sanguneos
elevando las cifras de presin arterial normales en un sistema hemostatico ptimo.

Differential effects of proteins and carbohydrates on

postprandial blood pressure-related responses.
Autores:
Teunissen-Beekman KF; Top Institute Food and Nutrition,Wageningen,The Netherlands.
Dopheide J; Top Institute Food and Nutrition,Wageningen,The Netherlands.
Geleijnse JM; Top Institute Food and Nutrition,Wageningen,The Netherlands.
Bakker SJ; Top Institute Food and Nutrition,Wageningen,The Netherlands.
Brink EJ; Top Institute Food and Nutrition,Wageningen,The Netherlands.
de Leeuw PW; Department of Medicine,Cardiovascular Research Institute Maastricht (CARIM),
Maastricht University Medical Center,Maastricht,The Netherlands.
Serroyen J; Department of Methodology & Statistics,Maastricht University,Maastricht,The

Netherlands.
van Baak MA; Top Institute Food and Nutrition,Wageningen,The Netherlands.
Fuente:
The British Journal Of Nutrition [Br J Nutr] 2014 Aug 28; Vol. 112 (4), pp. 600-8. Date of Electronic
Publication: 2014 Jun 03.
Tipo de publicacin:
Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support,
Non-U.S. Gov't
Idioma:
English
Informacin
de la
publicacin
:
Publisher: Published on behalf of the Nutrition Society by CABI Publishing Country of
Publication: England NLM ID: 0372547 Publication Model: Print-Electronic Cited
Medium: Internet ISSN: 1475-2662 (Electronic) Linking ISSN: 00071145 NLM ISO Abbreviation: Br. J.
Nutr.Subsets: MEDLINE
Nombre(s)
de la
coleccin:
Publication: <2000->: Wallingford, Oxon, UK : Published on behalf of the Nutrition Society by CABI
Publishing
Original Publication: [Cambridge, New York] Cambridge University Press.

Tr
Blood Pressure*
Meals*
Dietary Carbohydrates/*therapeutic use
Hypertension/*diet therapy
Milk Proteins/*therapeutic use
Polysaccharides/*therapeutic use
Vegetable Proteins/*therapeutic use
Body Mass Index; Cross-Over Studies; Dietary Carbohydrates/adverse effects; Dietary
Sucrose/adverse effects; Double-Blind Method; Egg Proteins, Dietary/administration & dosage; Egg
Proteins, Dietary/adverse effects; Female; Glucagon/blood; Glucagon/secretion; Glucagon-Like
Peptide 1/blood; Glucagon-Like Peptide
1/metabolism; Humans; Hypertension/blood; Hypertension/etiology; Hypertension/metabolism; Insulin/
blood; Insulin/secretion; Male; Middle Aged; Milk Proteins/administration & dosage; Nitric
Oxide/blood; Nitric
Oxide/metabolism; Overweight/physiopathology; Peas/chemistry; Polysaccharides/adverse
effects; Postprandial Period; Seeds/chemistry; Vegetable Proteins/administration & dosage
Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the
present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk
protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of
maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We
hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be
accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1)
and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight
overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and

plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and Snitrosothiols (NO(x)) were measured for 4 h. No differences were observed in TPR responses.
Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of
meals containing the other two proteins (P 001). The ingestion of the pea-protein meal induced the
highest NO(x) response (P 0006). Insulin and glucagon concentrations were lowest after the
ingestion of the egg-white-protein meal (P 0009). Postprandial BP levels were lower after the
ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P 0004),
while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than
after that of the sucrose and protein mix meals after 1-2 h (P 00001). Postprandial NO(x), GLP-1
and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of
the protein mix meal (P 0008). In conclusion, different protein and carbohydrate sources induce
different postprandial BP-related responses, which may be important for BP management. Lower
postprandial BP levels are not necessarily accompanied by higher NO(x), insulin, glucagon or GLP-1
responses