Early Life Nutrition FINAL - tcm41-182859 h&s2

BMA Board of Science
Early life nutrition and lifelong health

February 2009

February 2009
Editorial board
A publication from the BMA Science and Education department and the Board of Science. Chair, Board of Science Director of Professional Activities Head of Science and Education/Project lead Authors Professor Sir Charles George Professor Vivienne Nathanson Nicky Jayesinghe Professor Mark Hanson Professor Caroline Fall Dr Sian Robinson Dr Janis Baird Luke Garland Dr Joseph Kirkman (PhD) Dr Caroline Seddon (PhD) Thom Ellinas Hilary Forrester Darshna Gohil Dr Madelaine Healey David Maynard Sarah Mills George Roycroft Richard Jones
Contributors
Editorial secretariat
(PhD)
Indexer
British Library Cataloguing-in-Publication Data. A catalogue record for this book is available from the British Library. ISBN: 978-1-905545-32-2 Cover photograph: Getty Images British Medical Association 2009 all rights reserved. No part of this publication may be reproduced, stored in a retrievable system or transmitted in any form or by any other means that be electrical, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the British Medical Association.
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Board of Science
This report was prepared under the auspices of the Board of Science of the British Medical Association, whose membership for 2008/09 was as follows: Sir Kenneth Calman Dr Peter Bennie Dr Hamish Meldrum Dr David Pickersgill Mr Tony Bourne Dr Kate Bullen Professor Sir Charles George Dr Andrew Thomson Dr Mohammad Anwar Dr JS Bamrah Mr Philip Belcher Dr Andrew Collier Dr Peter Dangerfield Dr Lucy-Jane Davis Dr Peter Maguire Dr David Sinclair Dr Dorothy Ward Dr David Wrigley Dr Richard Jarvis Professor Parveen Kumar Dr Philip Steadman Dr Ram Moorthy President, BMA Chair of the Representative Body, BMA Chair of Council Treasurer, BMA Chief Executive, BMA Deputy Chair of Council Chair, Board of Science Deputy Chair, Board of Science
(by invitation) (Co-optee) (Co-optee) (Deputy member)
Approval for publication as a BMA policy report was recommended by BMA Board of Professional Activities on 14 July 2008.
Declaration of interest
There were no competing interests with anyone involved in the research and writing of this report. For further information about the editorial secretariat or Board members please contact the Science and Education Department which holds a record of all declarations of interest: info.science@bma.org.uk
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Acknowledgements
The Association is grateful for the help provided by the BMA committees and outside experts and organisations. We would particularly like to thank: Professor Mark Hanson, Director Institute of Developmental Sciences, Director Developmental Origins of Health and Disease Division, British Heart Foundation Professor of Cardiovascular Science, University of Southampton Professor Caroline Fall, Professor of International Paediatric Epidemiology, Medical Research Council (MRC) Epidemiology Resource Centre, University of Southampton Dr Sian Robinson, Principal Research Fellow, MRC Epidemiology Resource Centre, University of Southampton Dr Janis Baird, Senior Research Fellow and Honorary Consultant in Public Health, MRC Epidemiology Resource Centre, University of Southampton Professor Alan Jackson, Director, Institute of Human Nutrition, Developmental Origins of Health and Disease Division, University of Southampton Professor Cyrus Cooper, Director of the MRC Epidemiology Resource Centre and Professor of Rheumatology at the University of Southampton Professor Keith Godfrey, MRC Epidemiology Resource Centre, University of Southampton and Centre for Developmental Origins of Health and Disease, University of Southampton Dr Tim Lobstein, Director of the Childhood Obesity Programme International Association for the Study of Obesity. Parts of the report are based on reviews by Professor Mark Hanson with Professors Gluckman or Poston. The authors are grateful to Mrs Jane Kitcher for preparation of the manuscript. Address for correspondence: Professor Mark Hanson, Institute of Developmental Sciences, Mailpoint 887, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD Tel: 02380 798421 Fax: 02380 795255 Email: m.hanson@soton.ac.uk
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About the authors

Mark Hanson MA DPhil Cert Ed FRCOG is Director of the Division of Developmental Origins of Health and Disease and British Heart Foundation Professor of Cardiovascular Science at the University of Southampton School of Medicine. He is founding Director of the Institute of Developmental Sciences at Southampton. His research concerns the ways in which the developmental environment, and especially nutrition, affects cardiovascular, metabolic and behavioural characteristics of the individual, influencing how well they respond to later challenges and the resulting risks of disease. He is much involved in promoting the public understanding of this area of biomedical science. Caroline Fall MBChB, DM, FRCP, FRCPCH is a consultant paediatrician and Professor of International Paediatric Epidemiology at the MRC Epidemiology Resource Centre, University of Southampton. Her research focuses on the effects of maternal and infant nutrition on obesity, diabetes and cardiovascular disease in later life. Sian Robinson PhD R Nutr is a Registered Nutritionist and a Principal Research Fellow at the MRC Epidemiology Resource Centre at the University of Southampton. She is responsible for the nutritional components of two large UK cohorts run by the Epidemiology Resource Centre, the Southampton Womens Survey and the Hertfordshire Cohort Study. Her principal research interests are in maternal and infant nutrition. Janis Baird MB BCh, PhD, FFPH is a Senior Research Fellow and Honorary Consultant in Public Health at the MRC Epidemiology Resource Centre, University of Southampton. Her research focuses on translating evidence of the developmental origins of health and disease into public health policy.
Abbreviations
AA AGA ALSPAC ARM BMA BMC BMI CHD CI COMA CSE DALY DDT DH DHA DNA Dnmt DXA EFNEP FSA GP HDL HIV IBFAN IFS Ig IGF IGT INCAP IQ IUGR LCPUFA LDL LGA LIDNS MRC NDNS NICE PCB PSA RB RCPCH RCT SACN SBP SD SGA UK UNICEF USA WHO WIC
Arachidonic acid Appropriate-for-gestational-age Avon Longitudinal Study of Parents and Children Annual representative meeting British Medical Association Bone mineral content Body mass index Coronary heart disease Confidence intervals Committee on Medical Aspects of Food and Nutrition Certificate of secondary education Disability adjusted life year Dichlorodiphenyl trichloroethane Department of Health Docosahexanoic acid Deoxyribonucleic acid DNA N-methyl transferase Dual-energy x-ray absorptiometry Expanded Food and Nutrition Education Programme Food Standards Agency General practitioner High-density lipoprotein Human Immunodeficiency Virus International Baby Food Action Network Infant feeding survey Immunoglobulin Insulin-like growth factors Impaired glucose tolerance Institute of Nutrition of Central American and Panama Intelligence quotient Intrauterine growth restriction Long-chain polyunsaturated fatty acids Low-density lipoprotein Large-for-gestational-age Low Income Diet and Nutrition Survey Medical Research Council National Diet and Nutrition Survey National Institute for Health and Clinical Excellence Polychlorinated biphenyls Public service agreement Representative body Royal College of Paediatrics and Child Heath Randomised controlled trial Scientific Advisory Committee on Nutrition Systolic blood pressure Standard deviation Small-for-gestational-age United Kingdom United Nations Childrens Fund United States of America World Health Organisation US Special Supplemental Nutrition Programme for Women, Infants and Children
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Glossary
Adiposity relating to, or composed of adipose tissue containing fat cells Anaemia a condition in which the number of active red blood cells and/or levels of the oxygen carrying pigment haemoglobin in the blood is reduced Atherogenic conducive to or causing atherogenesis, or the build up of fatty deposits in the arteries, which leads to cardiovascular disease Body mass index an indicator of whether a person is under- or overweight, derived from the weight of a person (in kilograms) divided by the square of their height (in metres) Cardiomyocytes cardiac muscle cells Cardiovascular disease all conditions that affect the heart and blood vessels Coeliac disease a condition in which the small intestine fails to digest and absorb food, due to a permanent sensitivity to the protein gliadin, contained in gluten Coronary heart disease heart disease caused by narrowing of the arteries that supply blood to the heart Diastolic blood pressure the pressure of the blood against the walls of the main arteries when the ventricles are relaxed and refilling Disability adjusted life year (DALY) a health gap measure that extends the concept of potential years of life lost due to premature death to include equivalent years of healthy life lost by virtue of being in states of poor health or disability Dual-energy X-ray absorptiometry a means of measuring bone mineral density Dyslipidaemia a disturbance in the amount of lipid in the blood Epigenetic please refer to Appendix 1 FTO gene a gene on chromosome 16 in humans, certain variants of which appear to correlate with obesity in humans Galactosaemia the inability to utilise the sugar galactose, leading to its accumulation within the blood Gastroenteritis the inflammation of the stomach and intestine, usually due to infection or foodpoisoning Gastro-intestinal illness illness relating to the stomach and the intestine Glycaemic index a dietary index that is used to rank carbohydrate-based foods. The index indicates the rate at which the food we eat will increase blood sugar levels Goitre swelling of the neck due to enlargement of the thyroid gland. This may be due to a lack of dietary iodine Gonadotrophin any of several hormones synthesised and released by the pituitary gland that act on the testes or ovaries to promote the production of sex hormones and either sperm or ova Hodgkins lymphoma a malignant disease of lymphatic tissue, usually characterised by painless enlargement of one or more groups of lymph nodes Homeostasis the physiological process by which the internal systems of the body are maintained at equilibrium, despite variations in external conditions Hyperinsulinaemia excessive insulin secretion Hyperphagia abnormally large intake of food Hypertension high blood pressure, above the normal range expected for a particular age group and sex In utero a Latin term meaning inside the womb, and used with reference to the fetus during pregnancy Insulin-like growth factors polypeptides with high sequence similarity to insulin, they are part of a complex system that cells use to communicate with their physiological environment and to regulate their growth and metabolism Intrauterine growth restriction a reduction in the growth of the fetus, most commonly resulting from placental dysfunction, poor maternal nutrition, or maternal smoking, and resulting in a baby that is small for gestational age.
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Ischaemic heart disease heart disease resulting from an inadequate flow of blood to the heart, caused by narrowing or blockage of the blood vessels supplying it Lymphoblastic leukaemia a type of leukaemia characterised by abnormal cells with a large nucleus and little cytoplasm present in the blood and blood forming organs Mastitis inflammation of the breast, usually caused by bacterial infection via damaged nipples Meiosis a type of cell division, consisting of two successive separations, resulting in four daughter cells, each with half the original number of chromosomes of the original cell; the process used in gamete (sperm and ova) formation Meiotic pertaining to meiosis Mitosis a type of cell division resulting in two daughter cells, genetically identical to the original cell; the process used in growth Mitotic pertaining to mitosis Neuroblastoma a malignant tumour usually of childhood, composed of embryonic nerve cells. It may originate in any part of the sympathetic nervous system Non-genomic inheritance any pattern of inheritance in which traits do not segregate in accordance with genomic factors Normoglycaemic a condition of the blood in which the blood sugar level is within normal limits Obesity refer to Appendix 2 Obesogenic factors tending to cause or produce obesity in an individual Osteoporosis the loss of bone tissue, resulting in bones which are brittle and liable to fracture Otitis media inflammation of the middle ear associated with perforations of the eardrum Overweight refer to Appendix 2 Palaeolithic pertaining to a prehistoric era distinguished by the development of the first stone tools, extending from approximately 2.5 million to around 10,000 years ago Perinatal care care relating to the period starting a few weeks before birth, including birth and a few weeks after birth Phenotype the observable characteristics of an individual resulting from the interaction between their genes and the environment Plasminogen activator inhibitor an inhibitor of enzymes that convert inactive plasminogen into the active enzyme plasmin, which digests blood clots Polymorphism a condition in which a chromosome or a genetic character occurs in more than one form, resulting in the coexistence of more than one morphological type within a population Pro-inflammatory cytokines proteins produced predominantly by activated immune cells, involved in the amplification of inflammatory reactions Rickets a disease in which bones do not harden due to a deficiency of vitamin D Statin any one of a class of pharmaceuticals that inhibit the action of an enzyme (hydroxymethylglutaryl coenzyme A reductase) involved in the production of cholesterol within the liver Stroke a sudden attack of weakness affecting one side of the body or other loss of neural function lasting at least 24 hours. It is the consequence of an interruption to the flow of blood to the brain Systolic blood pressure the pressure of the blood against the walls of the main arteries when the ventricles are contracting Teratogenic the effect of a substance, agent or process that induces the formation of developmental abnormalities in a fetus Type 1 diabetes an autoimmune disease that results in the permanent destruction of insulin producing beta cells of the pancreas Type 2 diabetes a metabolic disorder, primarily characterised by insulin resistance, relative insulin deficiency and hyperglycaemia Undernutrition inadequate nutrition from any cause von Willebrand factor a glycoprotein necessary for platelet function, abnormalities of which can result in an inherited disorder of the blood which is characterised by episodes of spontaneous bleeding similar to haemophilia
viii Early life nutrition and lifelong health
Foreword
For 175 years the BMA has promoted medicine and the allied sciences as part of its founding principle to maintain the honour and interests of the medical profession. One element of this work is to be advocates for the health of the public. In doing so we listen first to our members concerns. At the annual representative meeting (ARM) members tell us of the problems they see in the communities and patients they serve. Motions are proposed by grass roots doctors and debated at the ARM. Approximately 600 doctors form the representative body (RB), which is the democratically elected, policy-making body of the BMA. Motions passed at the ARM are usually adopted as BMA policy. A list of all BMA polices can be found at www.bma.org.uk This report was commissioned after an ARM debate in June 2007 that called on the BMAs Board of Science to recognise and promote the importance of fetal and early life nutrition and its relationship to lifelong health. The Board of Science has previously produced three reports that broadly cover childhood nutrition and exercise. Growing up in Britain: ensuring a healthy future for our children (1999) discusses child health, with a focus on nutrition rather than exercise, from conception to the age of five. Adolescent health (2003) reviews nutrition, exercise and obesity in teenagers (13-19 year olds). It serves in part to develop the 1999 report in order to cover children up to the age of 12 years. It highlights the main aspects of childhood nutrition and exercise, draws attention to the role of the clinician, and provides links to sources of further information. It also makes recommendations for tackling the obesity epidemic in the UK. Preventing childhood obesity (2005) highlights the situation with regard to childhood obesity and the impact this can have on childrens current and future health. It examines the role of healthcare professionals and the environmental barriers to change that need to be overcome or removed. This report concerns early life nutrition predominantly fetal and infant nutrition providing useful reference information and key messages for healthcare professionals. It discusses the evidence-base and draws conclusions about the ways in which the patterns of early life nutrition can be improved, and the likely consequences of such improvements. This is now of critical importance in addressing the rapid increase in the incidence of so-called lifestyle diseases such as cardiovascular disease and type 2 diabetes, which are linked to overweight and obesity. In addition there is now compelling evidence for a role of early life nutrition in setting the risk of other conditions including osteoporosis, asthma, lung 1 disease and some forms of cancer. Evidence is growing that early life nutrition can play a role in behavioural and cognitive problems in children and adolescents, and possibly even in cognitive decline and other aspects of ageing. This report from the BMA Board of Science is intended to be a useful point of reference for a wide audience, including health professionals, policy makers and members of the public. The approach of the BMA Board of Science is to provide a clear synthesis of the available research, and to develop evidence-based conclusions and recommendations for policy.
Professor Sir Charles George Chair, Board of Science

The Board of Science, a standing committee of the BMA, provides an interface between the medical profession, the Government and the public. The Board produces numerous reports containing policies for national action by Government and other organisations, with specific recommendations affecting the medical and allied professions.
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Contents
Abbreviations Glossary Foreword List of figures Executive summary Report conclusions Chapter 1: The importance of fetal and infant nutrition Nutritional transitions and patterns of chronic disease What is good nutrition? The developmental consequences of inappropriate nutrition The importance of development for later health Obesity Previous work by the BMA Conclusions Fetal nutrition: impact on development and later life Impact of fetal nutrition on health in later life: the developmental origins concept Mechanisms by which fetal nutrition affects risk of later disease Epigenetic mechanisms Maternal undernutrition and long-term outcomes in the offspring Associations between maternal obesity, diabetes, raised birth weight and adulthood disease Transgenerational effects Conclusions Infant nutrition Introduction The case for breastfeeding Current infant feeding practices Complementary feeding practices in the UK Guidelines on infant feeding Breastfeeding guidelines Maternal diet during lactation guidelines Formula feeding Complementary feeding Vitamin supplements for infants Determinants of infant weight gain and growth Recommendations about size and growth during infancy
vi vii ix xiii 1 3 5 5 7 7 8 11 13 14 15 15 19 20 21 22 22 24 25 25 26 27 34
Chapter 2:
Chapter 3:
36
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Breastfeeding and health: short- and long-term outcomes 40 Breastfeeding and later cognitive function and neurodevelopment Breastfeeding and later body composition and obesity Diabetes Blood pressure and cardiovascular disease Other cardiovascular risk factors Cancer Allergic/atopic disease Mental health Other outcomes: bone health, coeliac disease, inflammatory bowel disease Other aspects of infant diet and long-term outcomes 44 The timing of introduction of solids and later health Infant growth and long-term outcomes Conclusions 49 Chapter 4: Influences on maternal and infant nutrition and opportunities for intervention Interventions in maternal and infant nutrition a global perspective Interventions designed to improve short-term outcomes Guidelines for improving the diets of young women in the UK Influences on food choices in women Interventions to improve maternal nutrition Improving breastfeeding initiation and increasing duration of breastfeeding The WHO/UNICEF Baby Friendly Hospital Initiative Doctors role in supporting breastfeeding NICE Guidance on Breastfeeding Support for breastfeeding mothers returning to work Interventions in complementary feeding Mechanisms to address nutritional inequalities in the UK NICE guidance Healthy Start schemes Tackling the problem of obesity Conclusions
50 50 51 53 55 56
61 61
63 65 66 68 69 71 74
Appendix 1: Epigenetic processes Appendix 2: Definition of overweight Appendix 3: Current UK dietary recommendations for pregnancy Appendix 4: Infant feeding guidelines Appendix 5: The International Code on the Marketing of Breast Milk Substitutes Appendix 6: Comparison of the nutrient composition of mature human breast milk and formula References INDEX
75 77 93
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List of figures
Figure 1: Figure 2: Figure 3: Figure 4: Figure 5: Figure 6: Figure 7: Figure 8: Figure 9: Figure 10: Figure 11: Figure 12: Figure 13a and 13b: Figure 14:
Figure 15:
The human dietary transition The thrifty phenotype hypothesis Mismatch model of chronic disease Patterns of infant and childhood growth associated with later heart disease Graded effects of nutrition in development on later function The fetal supply line for nutrients Cycles of disease risk Prevalence of breastfeeding according to mothers socio-economic classification: Infant Feeding Survey 2005 Age by which solids had been introduced according to mothers socio-economic classification: Infant Feeding Survey 2005 12-month infant guidelines pattern score according to prudent diet score of the mother Mean weight and length of breastfed and formula-fed infants from birth to 18 months Cardiovascular disease mortality according to weight at one year in Hertfordshire men Height and weight scores in infancy of individuals having CHD in later life Percentage of women with prudent diet scores in lowest quarter of distribution, according to their educational attainment: 6,125 women in the Southampton Womens Survey Components of the epigenetic code
6 9 10 17 18 19 23 30 31 33 37 46 47
53 66
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Executive summary
Studies of human populations show clear links between variability in early life environment and risk of later ill health and chronic disease. A critical aspect of environment is the interaction of nutrition with other stressors. Nutrition is important in terms of its quantity and also in the balance of foods and their components, both macronutrients and micronutrients such as minerals and vitamins. An inadequate or unbalanced dietary intake can lead to malnutrition: the consequences of which embrace the range from under-weight, through the normal range to overweight. The health and other consequences of malnutrition across the entire spectrum are cause for considerable concern in all societies, especially among the poor and most economically deprived. The risk for this burden of ill health is set in train from very early life, providing opportunities for effective interventions at all ages. Future research will help identify further opportunities for effective interventions through better definition of biomarkers of risk, and underlying mechanisms. In developed societies many women consume poor quality diets, which may result in nutritional deficiencies on the one hand and overweight and obesity on the other. In developing societies maternal under-nutrition remains a major problem but maternal overweight is also of concern. Effective interventions are therefore needed to improve the nutrition of young women of childbearing age in many societies. Less healthy diets are more common among women of low educational attainment, and among women who have low incomes and who are food insecure. Both nutrition education and counselling have been shown to improve womens nutrition knowledge and behaviour. These approaches need to be increased to be effective at a population level and other interventions developed to improve the diets of young women as a matter of urgency. Our understanding of the specific mechanisms through which maternal nutrition leads to longterm effects is limited in humans, but there is strong evidence relevant to human disease from studies in animals that changing nutrition in pregnancy can produce effects on the offspring. Underlying mechanisms use developmental plasticity to produce adaptive responses to nutritional cues crossing the placenta from the mother. Some cues may even operate in the periconceptional period, before the woman knows she is pregnant. Positive steps therefore need to be taken to ensure that young people understand the importance of health and well-being before pregnancy giving attention to their diet, maintaining a healthy body weight, stopping smoking and limiting alcohol consumption. Infants are particularly vulnerable because of their immaturity and the nutritional demands of rapid growth and development. Exclusive breastfeeding is recommended for at least the first six months of life and is associated with reduced susceptibility to infection. The preferred growth associated with breastfeeding enables normal cognitive and physical development and may protect against obesity and chronic disease in adult life. Breastfeeding rates are unacceptably low in the UK and especially so among disadvantaged women. Mothers may need personal support to establish successful breastfeeding and wider society should support parents in the initiation and prolongation of the duration of breastfeeding. Interventions which educate women about the benefits and practice of breastfeeding, and which promote baby friendly policy and practice, are effective at promoting the initiation and prolonging the duration of breastfeeding. The ten steps to successful breastfeeding and the Baby Friendly Hospital Initiative guidelines should become a minimum standard of care. Action is also needed to improve the opportunities for women to breastfeed in public places and to support women who return to work to continue breastfeeding. There are wide variations in complementary feeding [weaning] practice in the UK. The influence of the timing and nutritional content of complementary feeding and the specific effects of variations in quality of complementary feeding on current and later health in countries such as the UK are still to be determined. There are wide variations in infant size, weight gain, linear growth and body
composition. There is increasing evidence that these influence the risk of developing obesity, diabetes, cardiovascular disease and other health outcomes in later life. The optimal pattern(s) of infant growth to minimise the risk of obesity, cardiovascular disease and diabetes need(s) to be determined. There is strong evidence that undernutrition (stunting or wasting) during the first two years of life leads to impaired adult cognitive, physical and economic capacity, which cannot be repaired even if nutrition improves later in childhood. Dietary patterns run in families and the diet of infants tends to be similar to that of mothers. It is likely that interventions which improve the diets of young women will also lead to improved diets for their children. The Healthy Start scheme provides support for eligible women and children through provision of food vouchers and vitamin supplements, and needs to be promoted widely. Its impact on the nutrition of mothers and young children should be evaluated at a national level. Development of future interventions highlights the need for biomarkers of poor developmental nutrition in infants and children. While there are gaps in the evidence about the long-term consequences of poor maternal and infant nutrition, and we do not as yet understand the mechanisms fully, it is clear that steps need to be taken to promote healthy diets in young women and their families, to encourage breastfeeding and the use of appropriate complementary foods.
Report conclusions
Chapter 1
Balanced nutrition during human development is of critical importance for later health and wellbeing and for reducing the risks of many chronic diseases. Unbalanced nutrition can result from diets which have either excessive or inadequate nutrient intakes. Energy dense diets can none the less be poor in micronutrients. The consequences of unbalanced nutrition at both ends of the dietary range are associated with increased risks of adult chronic disease. Humans evolved to consume a diet very different from that consumed by many people today. This makes our physiology potentially mismatched to our contemporary lifestyles, increasing the risks of ill health. During development, humans like other animals attempt to match the structure and functions of their organs and tissues to the world in which they expect to live. The prediction is based on cues from the mothers environment via the placenta and her milk. Inaccurate predictions, for example through socio-economic change leading to a nutritional transition between generations, increase mismatch and risk of disease. In addition to maternal undernutrition, the rising incidence of maternal obesity and diabetes in pregnancy will exacerbate the epidemic of chronic disease in developed societies. As low income countries develop, the cycle of diseases such as diabetes and obesity triggered by nutritional mismatch may be followed by further cycles arising from relative overnutrition during fetal and infant development.
Chapter 2
Studies of human populations show clear links between early life environment and later health and disease. While our knowledge of the specific components of maternal nutrition which produce such effects is limited in humans, experimental animal studies provide strong evidence that changing nutrition in the periconceptional period or in pregnancy can produce effects on the offspring which mimic human chronic disease. In developed societies, we know that many women consume poor quality diets, which result on the one hand in nutritional deficiencies and on the other in overweight and obesity. In developing societies, while maternal undernutrition remains a major problem, maternal overweight is also of concern. Development of future interventions will require the identification of biomarkers of poor developmental nutrition in infants and children. There is a need for better understanding of the implications of current variations in diet and nutrition for fetal development and long-term health. Positive steps need to be taken to ensure that young people understand the importance of health and wellbeing before pregnancy giving attention to their diet, optimal body weight, to stopping smoking and to limiting alcohol consumption.
Chapter 3
Infants have special nutritional requirements because of their rapid growth and development and vulnerability to infection. Optimal nutrition in infancy is essential for normal cognitive and physical development and may protect against obesity and chronic disease in adult life. Many parents need guidance to provide adequate nutrition for their children at this stage of life. Breast milk is the ideal food for babies in their first few months. Mothers need support in order to breastfeed successfully. There is consistent evidence of better childhood cognitive development, and a lower risk of several disease outcomes including obesity and diabetes, in children and adults who were breastfed rather than formula-fed. It is not known whether these effects are causal or reflect the generally healthier lifestyles of the families whose mothers choose to breastfeed.
The effects of the quality of complementary feeding on current and later health in countries such as the UK are largely unknown. There are wide variations in infant size, weight gain, linear growth and body composition. There is increasing evidence that these influence the risk of developing obesity, diabetes, cardiovascular disease and other health outcomes in later life. The optimal pattern(s) of infant weight gain in order to minimise the risk of obesity, cardiovascular disease and diabetes is, however, not yet known. There is strong evidence that undernutrition (stunting or wasting) during infancy leads to impaired adult cognitive, physical and economic capacity, even if nutrition improves later in childhood.
Chapter 4
Many young women have diets of poor quality and inadequate nutritional status. Less healthy diets are more common among women of low educational attainment, and among women who have low incomes and who are food insecure. Although evidence of effective interventions to improve the diets of young women is limited, this does not mean that the goal should not be pursued vigorously. Both nutrition education and counselling have been shown to improve womens nutrition knowledge and behaviour. Breastfeeding rates are low in the UK, and it is less common among disadvantaged women. Interventions that educate women about the benefits and practice of breastfeeding, and that promote baby friendly policies and practice, are effective at promoting the initiation and prolonging the duration of breastfeeding. Current studies of complementary feeding [weaning] show wide variations in practice in the UK. There are few studies of interventions to influence the timing and nutritional content of complementary feeding in developed countries. Infant diet is strongly linked to mothers diet suggesting that interventions to improve the diets of young women will also have direct consequences for childrens diets. Effective interventions are needed to improve the nutrition of young women of childbearing age. Such interventions may influence the way in which mothers feed their children as well as influencing the diets of women themselves. They will therefore have beneficial health effects across generations. Efforts to encourage the initiation and to prolong the duration of breastfeeding need to continue and be extended. The ten steps to successful breastfeeding and the Baby Friendly Hospital Initiative guidelines should become a minimum standard of care. Action is also needed to improve the opportunities for women to breastfeed in public places and to support continued breastfeeding in women who return to work. The Healthy Start scheme provides support for eligible women and children through provision of food vouchers and vitamin supplements, and needs to be promoted widely. Its impact on the nutrition of mothers and young children should be evaluated at a national level. Other gaps in the evidence should be addressed, including interventions to support breastfeeding mothers in the workplace and interventions to optimise the timing and content of complementary feeding.
Chapter 1: The importance of fetal and infant nutrition

Our current level of interest in the link between nutrition and health is unprecedented. Over the past century nutritional science has grown from the recognition of the properties of nutrients and their ability to prevent deficiency diseases to an understanding of the benefits of good nutrition which include the promotion and maintenance of good health and protection from disease. The definition of an optimal diet which provides a balanced supply of nutrients in sufficient amounts to support optimal metabolic function is not necessarily clear. What constitutes an appropriate balance of foods and nutrients in the diet may differ between individuals, based on their genetic makeup and previous experience. A poor, unbalanced diet has been shown in recent studies to be common in the general 2 population even in developed societies. Poor micronutrient and vitamin status, such as folate and vitamin D, occurs in many people but particularly in those of reproductive age even though their energy intakes may be sufficient. In developing countries maternal and child undernutrition is the cause of 3.5 million deaths each year, constituting 35 per cent of the burden of disease in children 3 under five years. Sub-optimal breastfeeding, especially non-exclusive breastfeeding in the first six months of life, results in 1.4 million deaths and 10 per cent of the disease burden in children 3 under five years. At the same time, there are over 300 million people around the world who are 4 obese. The effects of overnutrition are not only a concern in developed societies, living a Western lifestyle. Populations which are emerging from poverty are also at risk of the adverse effects on health caused by excesses in the diet, even in people who are not obese by Western standards. Diets which lead to over-nutrition (eg excess calories) are often micronutrient poor. Thus the possible effects of poor, unbalanced and excessive nutrition on human development need to be considered across a broad spectrum.
Key message Unbalanced nutrition can result from both inadequate and excessive dietary intakes, and both can exist at the same time in many populations. Moreover diets which lead to over-nutrition (eg excess calories) are often micronutrient poor.
Nutritional transitions and patterns of chronic disease

Human diets have changed substantially during the course of our evolution and history. Compared with current diets, the pre-agricultural hunter-gatherer diets of our Palaeolithic ancestors were based on wild animal and plant foods and were much higher in protein and lower in carbohydrate (see Figure 1).
Figure 1: The human dietary transition

Hunter-gatherer energy sources USA energy sources
65% Fruits Vegetables Nuts Honey 55% Cereal grains Milk, milk products Sugar, sweeteners Separated fats Alcohol
Lean game Wild fowl Eggs Fish Shellfish
Fruits Vegetables Legumes Nuts
17%
35%
Fatty meat Poultry Eggs Fish Shellfish 28%
A typical hunter-gatherer diet versus a typical modern USA diet. Estimated dietary components in Palaeolithic human ancestors, based in part on hunter-gatherer diets, compared with those in contemporary United States of America (USA). Note the relatively high protein and low carbohydrate content of the hunter-gatherer diet. Source: Eaton SB & Cordain L (1997) Evolutionary aspects of diet: old genes, new fuels. Nutritional changes since agriculture. World Review of Nutrition and Dietetics 81: 26-37. Modified after Cordain L, Eaton SB, Brand Miller J et al (2002) The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. European Journal of Clinical Nutrition 56: S42-52.
The introduction of agriculture 10,000 years ago permanently changed the nature of our food supply, as plants and animals were domesticated for the first time. Further dietary change followed the Industrial Revolution, which created opportunities to process foods such as grains and cereals; and the onset of global trading introduced new foods into the UK diet. Our dietary patterns have continued to evolve to the present day as new food products have become available and we are influenced by dietary trends occurring in other parts of the world. Although it is argued that this rate of change in diet from Palaeolithic times has been too fast to allow the human genome to adapt, and is linked to the rising incidence of chronic diseases,5 many of the improvements in nutrition in the UK over the last century have had an enormous beneficial impact on mortality and public health. Diseases such as goitre or rickets, which were historically associated with social deprivation and malnutrition, are now rarely seen. Improved nutrition has therefore played a role in the dramatic increase in life expectancy. Some recent trends, however, are a cause for concern, such as the increase in the sugar and salt content of the diet. These recent dietary changes have also been accompanied by reductions in physical activity, and there is considerable concern about the consequences of the combined effects of these changes on the incidence and patterns of obesity and associated diseases.
What is good nutrition?

Good nutrition implies that the bodys needs for energy and nutrients, from the macronutrients protein, carbohydrate and fats to the micronutrients such as vitamins and trace elements, are being met by the diet. The bodys needs for nutrients arise from a wide range of processes. The most immediately obvious are linked to basal metabolism such as the need for dietary fat and carbohydrate to produce energy, and thiamine (vitamin B1) in its active pyrophosphate form as a cofactor in oxidative decarboxylation of pyruvic acid and -ketoglutaric acid. Although physical activity and work require energy, the greater part of our need for dietary energy is to support basal metabolism. Nutrient intake needs to be sufficient to maintain body reserves and to replace the turnover of components such as muscle proteins that are broken down during normal function. An adequate nutrient intake is essential for immunity; nutritional status and the intake of nutrients such as n-3 polyunsaturated fatty acids, antioxidant nutrients and zinc affect immune function and the activities of the immune system may themselves have negative effects on nutritional status. Finally, nutrient requirements are increased during pregnancy, and during postnatal growth and development. The many functions of nutrients means that adequate nutrition is central to metabolic integrity, and of key importance to growth, reproductive function and the maintenance of good health.
Key message The many functions of nutrients mean that adequate nutrition is central to metabolic integrity, and of key importance to growth, reproductive function and the maintenance of good health.
Malnutrition implies that the bodys needs for nutrients are not being met; it also describes an imbalance of these constituents that can be associated with either inadequate or excessive food intake. During short periods of insufficient energy supply the body can use reserves, such as fat and glycogen in liver and muscle, and degrade some tissues to preserve its function. In the longer term, an insufficient supply of nutrients will become limiting to function. In early life an insufficient supply of nutrients will result in reduced growth and impaired development. It is noteworthy that during development these effects may be due to deficiencies in dietary constituents that are not usually essential in adult life. For example, because the fetal requirements for the non-essential amino acid glycine are large, it becomes conditionally essential in late gestation and poor nutrition 6 can produce effects of glycine insufficiency.
The developmental consequences of inappropriate nutrition

The focus of this report is on the long-term consequences for health arising from impaired growth and development in early life both in prenatal life and in early childhood. Every individual has a blue-print that is genetically determined, and that sets their growth potential; but realisation of 7 this potential is only possible if the nutrient supply during growth is adequate. Among babies born to chronically malnourished women, low birth weight is relatively common, and stunting in infancy is prevalent in communities where food supplies are insufficient. Beyond these extreme examples though, our understanding of the importance of variations in diet and nutritional status, such as those seen in the UK population, and how these impact on early development, is limited. Babies continue to be born and to survive in populations that are chronically malnourished, and nutrient supplementation studies carried out in these communities often result in small changes in 8, 9 birth size. In the past it might have been concluded that prenatal growth is largely protected from variations in maternal diet and nutritional status. We now know that variations in birth size, that we describe as being within the normal range, are predictive of disease incidence much later
in life and that this is evident even in developed communities such as the UK. Within this range, lower birth weight and impaired early growth are linked to an increased occurrence of chronic 10 conditions such as cardiovascular disease and type 2 diabetes in adult life.
The importance of development for later health

The discovery that adult chronic disease is linked to low birth weight and poor weight gain in infancy 11 led Hales and Barker, in 1992, to put forward the thrifty phenotype hypothesis (see Figure 2). The central element of the hypothesis is that fetal and infant malnutrition are important drivers of the processes leading to disease in later life. Fetal malnutrition could arise through maternal malnutrition or failure of the fetal supply line such as placental insufficiency. It was proposed that malnutrition during these periods of rapid development forced the fetus or infant to become thrifty and to prioritise limited resources to some tissues at the expense of others. Thus, brain growth would be supported, but truncal growth, the growth of skeletal muscle, the development of abdominal organs (liver, pancreas, kidneys) and some parts of the vascular tree would be deprived. It was also proposed that this altered growth led to permanent changes in the structure and physiology of many tissues, leading to reduced functional capacity in later life. This reduced capacity may not be important to individuals who continued to be poorly nourished, but disease would be triggered more readily by stressors, such as obesity, in later life. Hence if fetal and/or infant undernutrition resulted in a reduced pancreatic beta cell mass, this would be more likely to result in type 2 diabetes and the metabolic syndrome if the individual became obese in childhood or adult life.
Key message It has been known for many years that unbalanced nutrition during development can cause long-term consequences leading to permanent changes in the structure and physiology of many tissues, leading to reduced functional capacity in later life. The consequences of this for human chronic disease are now increasingly appreciated.
Figure 2: The thrifty phenotype hypothesis
Mothers development and growth impaired
Maternal malnutrition
Maternal hyperglycaemia
Other maternal/placental influences
Fetal and infant malnutrition
Changes in growth, metabolism and vasculature Hypothalamic -pituitary -adrenal axis and sympathetic system
Kidney
Pancreatic B-cells
Muscle, liver, adipose tissue
Hypertension
Renal failure
Adult B-cell function
Insulin resistance
Source: Hales & Barker (2001) The thrifty phenotype hypothesis: type 2 diabetes. British Medical Bulletin 60: 5-20.
It is now thought that the responses to fetal malnutrition not only alter key organs to ensure survival at that time, but also set in train metabolic adaptations that could improve postnatal survival. The mother in effect gives the fetus and infant a forecast of the nutrition it can expect after birth, so that its metabolism can develop to match the environment into which it is born. These adaptations 12 only become detrimental when the postnatal environment differs from that predicted. This is the reasoning behind the mismatch model of increased risk of chronic disease (see Figure 3). The use of such terms as forecast or predicted in this context does not imply that it is a conscious process. It involves fundamental processes of developmental plasticity common to many other species. The cues for such predictions come from the developmental environment and nutritional cues are of paramount importance. Development comprises critical periods in which plasticity operates over a defined period of time, and after this critical period for an organ or system has elapsed, the characteristics of the organism (their phenotype) is fixed (see Box 1). For example, the maturation of the heart muscle cells in humans is completed before birth; there is limited capacity to increase the number of cardiomyocytes postnatally and increases in cardiac muscle mass can only be achieved by hypertrophy of existing cells. This can place them at additional strain and predispose to later heart failure.
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Box 1: The impact of phenotypic adaptation on human health The period of human development is one when the individual attempts to match the structure and function of their organs and tissues to the world they expect to inhabit, particularly the future nutritional environment. These processes are unique to development and may be irreversible. It is for this reason that fetal and infant nutrition is particularly important to future health. Early interventions are not only more likely to be more efficacious in preventing disease than later interventions it is possible that later interventions may be ineffective. This is because some phenotypic attributes which confer risk of later disease are established in development. Clearly intervention to prevent them can only be made during development itself. This is why understanding the developmental processes involved and how they may be optimised during human development is an urgent priority for promoting human health.
According to the mismatch model, the risk of chronic disease will be greatest when there are extreme transitions from one nutritional environment to another, either within an individuals own lifetime or between generations. This is borne out by the high risk of disease in migrants from poor environments in developing countries to the richer environments of the West. It also emphasises that the risk will be high in populations that start from a low nutritional plane, even if the transition does not place them at a nutritional level that would be considered rich by Western standards. Hence the speed of change in developing countries experiencing economic progress is producing disease in individuals who are younger, and relatively less obese, than in the developed world. Figure 3: Mismatch model of chronic disease
Plentiful Nutritional/energy balance
Adult environment
Increasing risk of disease from unpredicted excess Healthy range
Epigenetic processes attempt to achieve match
Sparse
Optimal
Impaired Developmental environment
Source: Gluckman PD & Hanson MA (2004) Living with the past: evolution, development, and patterns of disease. Science 305: 1733-6.
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Over the course of our evolution, humans have adapted to a range of environments, including nutritional and physical activity levels. Within this range (grey zone) we should meet environmental challenges and remain healthy. Outside this range, the risk of disease increases both from inadequate and excessive nutrient/energy level (red lines). Cues from the developmental environment before birth and in infancy alter the phenotype of the person, using epigenetic processes, and hence set their adaptive range. Thus an impaired developmental environment increases the risk of disease due to a phenotype not being well matched to the environment.
Key message Ill-health can result when a person cannot respond adequately to the challenges their lifestyle presents. The settings of these responses are established in part during fetal and infant life, based on nutrition during these periods.
Obesity
Obesity is one of the most important problems of our time. The incidence is increasing rapidly all over the world. The rising levels of obesity in the UK, particularly among children, and the significant impact that this will have on the future health of the population are of concern to politicians and healthcare professionals alike. The prevalence of obesity is now so high that it is commonly referred to as an epidemic (see Box 2).
Box 2: Prevalence of overweight and obesity in the UK In England in 2003, 22 per cent of men and 23 per cent of women were obese and a 14 further 43 per cent of men and 33 per cent of women were overweight. In England in 2003, more than 2.5 million children aged two to 15 were either overweight 14 or obese. 15 In Scotland in 2003, one in five (22%) of children aged 11-12 were obese. The 2005/06 Welsh health survey reported 56 per cent of adults were classified as 16 overweight or obese; 61 per cent of men compared with 51 per cent of women. The Northern Ireland health and social wellbeing survey 2005/06 reported 59 per cent of adults were classified as overweight or obese; 64 per cent of men compared with 54 per 17 cent of women. The Scottish health survey 2003 reported 65 per cent of men and 60 per cent women were 15 classified as overweight or obese. Recent estimates suggest that without action, by 2050, 60 per cent of men, 50 per cent of women and 25 per cent of all children under-16 could be obese. The financial impact of this 18 to the NHS alone could be an additional 5.5 billion per year at current prices.
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Overweight and obesity in developing countries

Economic development and improvements in agricultural production are transforming the nutritional situation for children and adults in developing countries, although rising food prices and continued food insecurity are a concern. Undernutrition, wasting, stunting and micronutrient 3 deficiencies are still major problems in developing countries, and occurring in early life, they 19 cause long-term damage to human capital and health. Improved availability of energy-rich foods has however, enabled large numbers of people to escape from hunger. This has brought considerable benefits, but is already giving rise to obesity and obesity-related disease. Developing countries are reporting high rates of coronary heart disease (CHD) and type 2 diabetes that have appeared in one or two generations to become leading causes of morbidity and mortality. These 20 epidemics are expected to intensify. By the year 2030, the prevalence of diabetes is predicted to rise by over 100 per cent in India, China, sub-Saharan Africa, Latin America, the Caribbean and the Middle East; an increase far exceeding that in high-income countries (54%). The highest number of people with diabetes will be of working age (45-64 years) unlike developed countries, where the greatest numbers are in older age groups, and in addition diabetes in pregnancy will become a common problem. There are similar increases anticipated in hypertension, CHD and 21 21 stroke. By 2015, an estimated 20 million people will die from cardiovascular disease every year.
In the context of this report on early life nutrition, obesity is important in a number of ways. Firstly, as described, obesity arising during childhood or adult life, can unmask the effects of adaptations induced by undernutrition during fetal life or infancy. Secondly, there is good evidence that increased adiposity and/or an adverse distribution of body fat is itself an outcome of malnutrition (both undernutrition and excessive nutrition) in early life. 22 Adults who had a lower birth weight have been shown to have a higher waist circumference. Low birth weight babies born to underweight women in India are excessively adipose relative to 23 their body weight. In experimental animals, maternal undernutrition during pregnancy is 24 associated with increased adiposity in the adult offspring. The mechanisms for this phenomenon are unknown, but may arise when the correct balance of nutrients required for tissue synthesis is 25 not available, leading to energy storage as adipose tissue. Maternal obesity, another form of maternal malnutrition, also increases the adiposity of the fetus and newborn baby. This phenomenon is exacerbated further if maternal obesity is complicated by gestational diabetes, an example of fetal overnutrition in which maternal glucose, freely crossing the placenta, stimulates fetal insulin secretion and adipose tissue deposition. It is known that maternal gestational diabetes is a risk factor for early-onset type 2 diabetes in the offspring, and recent data suggest that maternal obesity alone, even in the absence of gestational diabetes, 26 increase the risks of metabolic syndrome in the offspring. A recent follow-up study of more than 9,000 women with normal glucose tolerance at initial screening, found that increasing maternal glycaemia was associated with a greater risk of obesity in the children, even amongst children of normal birth weight. Importantly, among those who fulfilled criteria for gestational diabetes, the relationship between maternal glycaemia and offspring obesity was lost if the mother received 27 treatment. Maternal obesity is an increasing problem worldwide, and it seems likely that this will contribute increasingly to the burden of diabetes in the future. Gestational diabetes is an example of how susceptibility to diabetes can be transmitted non-genetically from one generation to the next. Women who were themselves of low birth weight are at increased risk of developing 28 gestational diabetes, especially if they become obese in adult life.
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Nutrition during infancy also determines later risk of obesity. Rates of overweight and obesity are lower in people who were breastfed, although there is debate as to whether this is a causal relationship. Rapid weight gain in infancy also predicts an increased risk of obesity.
Key message The increasing incidence of obesity will have adverse consequences for the development and health of future generations.
Previous work by the BMA

The BMA recognises the importance of nutrition during early life. Before and during pregnancy it is vital that women eat healthily in order to maintain their health and for the pregnancy to develop successfully. A childs diet during infancy can also impact significantly on their health, growth and development, and on their health in adulthood. Evidence suggests that early life nutrition influences an individuals risk of adult CHD, diabetes, stroke, asthma and cancer; and has longterm effects on bone health, muscle function, immune and cognitive function and rates of ageing. These relationships may result from either under- or overnutrition in early life. The BMA publication Growing up in Britain (1999) reviews the nutritional needs of children from birth to age five and the health consequences of poor nutrition, including the effects on growth and cognitive development. It highlights the importance of breastfeeding and raises concerns about the need to increase breastfeeding rates in the UK including addressing the inequalities in breastfeeding between socio-economic groupings. This report also discusses the evidence that influences which act in fetal and infant life permanently set structures and metabolic processes in 29 the body. In particular it highlights evidence of a link between undernutrition in utero, low birth weight and later risk of CHD. Growing up in Britain makes a number of recommendations about ways in which inequalities in child health should be tackled. In relation to nutrition it states that: ensuring good standards of nutrition and advice on healthy eating for young women and their babies must be a priority for Government action with the provision of a safety net for children at nutritional risk, for example, by providing free nursery and school milk, fruit and a balanced meal. Government-led strategy should be developed to improve diets of infants and young children and help prevent anaemia, dental caries and obesity. Particular efforts should be focused on increasing breastfeeding rates and improving the quality of weaning diets; breastfeeding should be actively promoted by Government and health professionals, to employers as well as parents, and the benefits monitored. Many of the themes from the 1999 report are revisited here to establish current thinking about the relationship between early life nutrition and later health; to what degree inequalities in nutrition still exist; and what factors are influential in determining consumption patterns. Concerns about the future health of children have grown further since its publication. Public health initiatives are now focusing attention on the importance of maternal and infant nutrition, both in relation to poor and unbalanced diet and also to overnutrition. This is true in both developed counties such as the UK and also in the developing world. Further research, dissemination of the evidence and discussion of the health promotion policy necessary are urgently needed.
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Conclusions
Balanced nutrition during human development is of critical importance for later health and wellbeing and for reducing the risks of many chronic diseases. Unbalanced nutrition can result from diets which have either excessive or inadequate nutrient intakes. Energy dense diets can nonetheless be poor in micronutrients. The consequences of unbalanced nutrition at both ends of the dietary range are associated with increased risks of adult chronic disease. Humans evolved to consume a diet very different from that consumed by many people today. This makes our physiology potentially mismatched to our contemporary lifestyles, increasing the risks of ill-health. During development, humans like other animals attempt to match the structure and functions of their organs and tissues to the world in which they expect to live. The prediction is based on cues from the mothers environment via the placenta and her milk. Inaccurate predictions, for example, through socio-economic change leading to a nutritional transition between generations, increase mismatch and risk of disease. In addition to maternal undernutrition, the rising incidence of maternal obesity and diabetes in pregnancy will exacerbate the epidemic of chronic disease in developed societies. As low income countries develop, the cycle of diseases such as diabetes and obesity triggered by nutritional mismatch may be followed by further cycles arising from relative overnutrition during fetal and infant development.
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Chapter 2: Fetal nutrition: impact on development and later life

Having a nutritious diet during pregnancy helps to protect the mothers health and to control her level of weight gain. Current UK recommendations for diet before and during pregnancy are given in Appendix 3. The embryo and fetus receive all their nutrients directly from the mother; good maternal nutrition is therefore imperative for optimal prenatal development. Unbalanced nutrition will also cause metabolic and hormonal changes in the mother. In animal models this can affect the allocation of stem cells, embryonic and placental lineages, and have long-term effects on offspring growth and health. In humans, maternal diet and body composition affect the growth of the early embryo making a focus on diet before pregnancy as important as that during pregnancy. Later in gestation, when fetal growth is maximal, undernutrition leads to a range of adaptive responses such as redistribution of blood flow in the fetal body and changes in the production of 30 fetal and placental hormones which control growth. These responses may include changes in 31 placental transport function, an area of research about which we currently know relatively little. Even without changes in overall fetal body size, the growth of certain organs such as the heart and kidney can be altered. Thus even fetuses of normal birth size may have mounted adaptive responses to unbalanced nutrition and are therefore phenotypically altered. If the nutritional challenge is too great or too prolonged for these adaptive responses to cope, eventually slowing in overall fetal body growth must result, leading to low birth weight. In late gestation this growth restriction is likely to be asymmetrical, with the head being less affected than the body.
Impact of fetal nutrition on health in later life: the developmental origins concept
The developmental origins of disease concept has a long history. The seminal studies of Dorner and 32 33 colleagues linked pre- and postnatal nutrition to later risks of obesity, arteriosclerosis and 34, 35 diabetes and Gennser et al showed that blood pressure was higher in men of low birth 36 weight. Forsdahls study of Norwegian populations showed that a poor childhood environment was associated with increased chronic adult disease, even if the persons circumstances improved in 37 later years. Similarly, Lucas had proposed that detrimental influences in early life may increase risk 38 for later disease. The most well-known reports, however, are those from Barker and his colleagues in the 1980s, showing an association between low birth weight and risk of later cardiovascular disease in middle-aged men and women in the UK for whom detailed birth records 39 were available. These early papers from Barker and colleagues were followed by others showing that low birth weight was not only associated with increased risk of death from cardiovascular disease but of also hypertension, insulin resistance, type 2 diabetes, dyslipidaemia and central 40 obesity; in fact each of the criteria which define the metabolic syndrome.
Key message Low birth weight is associated with increased risk of death from cardiovascular disease, hypertension, insulin resistance, type 2 diabetes, dyslipidaemia and central obesity.
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Box 3: Fetal programming In this context the term fetal programming is widely used. It is somewhat misleading, as it implies deterministic mechanisms, similar to its original use for the genetic programme for 41 development. It suggests analogy with a computer programme which, once running, cannot be altered. There is now more use of the terms programming and reprogramming to refer to 42 the processes by which stem cells become pluripotent during embryonic life. This is in line with the original use, as it suggests switches between predetermined developmental pathways, enabling embryonic stem cells to differentiate to lung, liver, lymphocytes, etc. The use of fetal programming or programming of disease is at odds with the plastic nature of adaptive responses by the embryo, fetus and infant and also underplays the role of later environment in exacerbating the risk of disease. Developmental origins of disease, or induction of risk of disease are more accurate terms for this process.
The validity of the concept of the developmental origins of disease has been questioned because of the wide variability reported among associations between birth weight and proxy markers of 43 disease such as later blood pressure, however associations are much stronger when the outcome 44 measure is clinical disease. Interpretation is also influenced by the recognition that pregnancies in the historical cohorts occurred when nutrition and healthcare were very different from those of contemporary developed societies. The lower birth weight individuals in these cohorts, for example, would be unlikely to include very pre-term or intrauterine growth restriction (IUGR) fetuses, or the higher birth weight group to include fetuses of diabetic mothers. Another criticism has concerned the size of the associations between indices of the developmental environment 40 such as birth weight and later markers of disease. A meta-analysis suggests for example that, even if causal, a large (1kg) increase in birth weight would be associated with only a 10 to 20 per cent reduction in adult ischaemic heart disease across the population. This assumes, however, that birth weight is the exposure of interest. The hypotheses relating fetal nutrition and growth to later disease suggest that birth weight, a crude summary of fetal development, is likely to be a distant reflection of the cellular and molecular processes affected by intra-uterine environment. For disease 45 such as type 2 diabetes, childhood obesity has a large exacerbating effect. Correction for adult BMI is another area which has proved controversial. There is an association between larger size at birth and increased adult BMI (itself a strong risk factor for type 2 diabetes and cardiovascular disease). Since the associations between size at birth and adult diseases are in the opposite direction, when adjusting these associations for adult BMI the effect of small size at birth appears stronger. The interpretation of this effect is controversial; it could indicate that an adverse effect of small size at birth is revealed more clearly by removing the influence of adult BMI, or it could indicate that the key insult is the transition from being a small baby to being an obese 46 adult as in the mismatch concept (see Figure 3). It is impossible to distinguish between these two possibilities using observational data. The evidence actually suggests that both of these scenarios apply. Many studies have shown adverse effects of small size at birth on adult disease without 47-49 adjustment for BMI (see Figure 4).
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Figure 4: Patterns of infant and childhood growth associated with later heart disease
Body mass index Weight Height 0.05
COHORT
Standard deviation (z score)
-0.05
-0.1
-0.15
-0.2
-0.25 0 1 2 3 4 5 6 7 8 9 10 11 12
Age (years) Growth (shown as Z score, ie shift in standard deviation from the group mean shown as 0) in 357 boys who developed CHD from a cohort of 4,630 born in Helsinki between 1934 and 1944. Their childhood growth pattern is characterised by small size at birth, slow growth in years 0-2, then relatively greater increase in weight and BMI. Source: Eriksson JG, Forsn T, Tuomilehto J et al (2001) Early growth and coronary heart disease in later life: longitudinal study. British Medical Journal 322: 949-53
There is also clear evidence of adverse effects of excessive weight gain in childhood on adult disease risk (see Figure 5) but controversy about the effect of weight gain during infancy (see Chapter 3). Given the similarities in responses between humans and other animals in terms of adaptive responses to environmental challenges during development, it may be helpful to consider them in terms of the spectrum of effects which might be produced on theoretical grounds (see Figure 5). This is important because it shows how even a modest nutritional challenge during development might be expected to have long-term consequences, even without an effect on birth weight.
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Figure 5: Graded effects of nutrition in development on later function

Developmental disruption Reduced Predictive adaptive responses reproductive success (coping /trade-offs) Damage due to excess
Good
Later survival, health and reproductive fitness
Poor very low Nutritional plane very high
Link between the nutritional plane in development and effect on later health and fitness. Different types of effect are produced, depending on the severity of the challenge (and also its timing and duration, not shown). They can be grouped into: those where an environmental challenge is so great that it causes a disruption of development, akin to a teratogenic effect. This is rare for unbalanced nutrition a less severe challenge but one which nonetheless reduces overall fetal growth and hence birth weight. The offspring has to cope with the detrimental effects of this in later life responses to a less severe challenge, which alter the phenotype of the offspring in prediction of its later environment. Such responses are in the majority across the range of human development, and produce risk of disease when the induced phenotype is not matched to the adult environment 50 responses to overnutrition in development; this category is becoming increasingly common. Source: Gluckman PD, Hanson MA, Spencer HG et al (2005) Environmental influences during development and their later consequences for health and disease: implications for the interpretation of empirical studies. Proceedings of the Royal Society 272: 671-7.
Many studies, including those from countries other than the UK, have replicated the original association 51 between lower birth weight and death from ischaemic heart disease and also with non-fatal coronary 52 artery disease and stroke. A recent study of 13,830 men and women from the Finnish National Death 53 Register showed an association between low birth weight and all cause mortality among women. A study of 10,803 children born in Aberdeen in the 1950s has confirmed an inverse association between
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birth weight and later coronary artery disease and stroke. This is important because the 1950s was a time when environmental influences were relatively favourable for infants compared with earlier studies, and so the results may have contemporary relevance. Large cohort studies, such as that of almost 90,000 Swedish army recruits born between 1973 and 1981, also show that lower birth weight is linked to higher adulthood blood pressure and, although small in magnitude, the difference was 55 independent of socio-economic factors or familial effects. Even a small rise in blood pressure is 56 important when viewed from the perspective of risk of later disease. A recent meta-analysis of data from 198,000 individuals from 20 Nordic studies (cohorts of people born between 1910 and 1987) shows unequivocally an inverse and linear association between birth weight in males, but a U shaped relationship with females; those of a birth weight higher than 4kg having a higher systolic blood 57 pressure (SBP) in adult life. Similar confirmation of the association with low birth weight and raised SBP 58 has been derived from a British birth cohort study of 3,157 men and women born in 1946. A recent review of the literature investigating associations between low birth weight and insulin resistance shows that people who were light at birth generally have an adverse profile of later glucose and insulin metabolism, which is related to insulin resistance rather than altered insulin 59 secretion. This may be related to the development of body composition; low birth weight in the Hertfordshire cohort was associated with reduced skeletal muscle mass and increased abdominal 60 fat in adult men.
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Mechanisms by which fetal nutrition affects risk of later disease

The concept of developmental origins of health and disease has stimulated wide ranging investigations into the underlying mechanisms. These investigations have now revealed a great deal of information on the processes involved, and their operation during critical periods of development during fetal and infant life. The fetus is at the end of a long supply line for nutrient delivery from its mother (see Figure 6) so there are several points at which its nutrition might be impaired. Figure 6: The fetal supply line for nutrients Mothers diet Her body composition Metabolism Hormonal status Nutrients in maternal bloodstream
Placental barrier/transport
Placental metabolism
Nutrients in fetal bloodstream
Many processes intervene between the food consumed by the mother and the delivery of nutrients to the fetal tissues.
Delivery to developing organs and tissues
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Most of the mechanisms have been investigated using animal models. Studies in rats, mice, sheep, guinea pigs and in non-human primates all lend strong support to the developmental origins of health and disease hypothesis. Most notably, several characteristics of the offspring phenotypes arising from a range of maternal nutritional interventions, both by undernutrition and overnutrition, are shared across species. It has proved remarkably easy to demonstrate characteristics equivalent to human disease, particularly features of the metabolic syndrome, through experimental manipulation of the diet of the pregnant animal or her offspring. The effects include cardiovascular and renal dysfunction, insulin resistance, glucose intolerance, hyperphagia, 64 altered stress responses and even preference for food high in fat and sugar in the offspring. 65, 66 Adulthood adiposity has also been induced. The behavioural effects on the offspring include 67 reduced exploratory behaviour, activity levels and even impaired learning behaviour. These animal models offer the potential for investigation of mechanisms, leading to suggestions for intervention. To date the most effective interventions reported have been supplementation of a low protein diet 68, 69 70 during pregnancy in the rat with glycine or folate or treatment of the pups neonatally with 71 leptin. The adverse effects on the offspring of feeding a high fat diet in pregnancy can be 72 reduced by giving a statin to the pregnant animal in late gestation. Animal investigations reveal that the transmission of risk factors can be passed to more than just the next generation. After a nutritional challenge to animals during pregnancy effects were seen in their grand-offspring, even 73-75 without a further nutritional challenge.
61-63
Key message Unbalanced nutrition during development can lead to greater risks of chronic disease in successive generations.
One of the most striking perceptions to arise from recent experimental work in this area is that the effects of relatively modest dietary restriction or imbalance can affect offspring development and have long-term consequences for health even when they are administered to the pregnant animal in either the periconceptional period, or in early pregnancy. At this time they do not invariably 76 affect fetal growth or birth weight. They operate via effects on embryonic stem cell allocation 77 or yolk sac function, and have long-term effects on cardiovascular, endocrine and metabolic 78-82 83 function. Embryo transfer experiments also reveal long-term effects on these systems and this raises questions about the long-term consequences of assisted reproductive technologies. These observations are of general relevance because a high proportion of pregnancies are unplanned, and thus dietary and other effects can be exerted well before the woman realises that she is pregnant.
Epigenetic mechanisms
The environmental effects on the embryo referred to above suggest in particular that epigenetic processes may be involved. The processes of phenotypic induction through developmental plasticity produce integrated changes in a range of organs via epigenetic processes. The term epigenetic 84 was coined by Waddington in about 1942 to refer to the ways in which the developmental 85 environment can influence the mature phenotype. His work and that of others on developmental plasticity stemmed from observations that environmental influences during development could induce alternative phenotypes from a genotype. They establish a life-course strategy for meeting 12 the demands of the predicted later environment. This explains why impaired early nutrition produces a range of effects. These include alterations in cardiovascular and metabolic homeostasis, growth and body composition, cognitive and behavioural development, reproductive function, repair processes and longevity some of which are associated with increased risk of chronic
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diseases including cardiovascular and metabolic disease, precocious puberty, osteoporosis and some forms of cancer. Understanding the epigenetic processes thus holds the key to understanding the underlying pathophysiology and to developing approaches to early diagnosis, prevention and treatment of these diseases (see Appendix 1).
Maternal undernutrition and long-term outcomes in the offspring

Newborn size is related to maternal energy balance, increasing with the mothers BMI and adiposity. Her height, and independently leg length, head circumference and birth weight, predict the babys size, suggesting that her own early nutritional biology influences how she nourishes the 86, 87 fetus. The fetal origins hypothesis proposed that maternal ill health, poverty and undernutrition 88 impair fetal and infant growth and were root causes of adult chronic disease. If this is so, indices of poor maternal nutrition would be associated with cardiovascular disease or its risk factors in the offspring. So far, unfortunately, there are only crude data available to test this. There is very little evidence concerning the effects of maternal undernutrition and nutrition in the developing world on the longer term health of the offspring. Studies in developing or historically poor countries have shown that low maternal weight, BMI or skinfold thickness in pregnancy are 89, 90 91, 92 93 associated with higher offspring blood pressure, insulin resistance and risk of CHD. Followup of people exposed to the 1944-45 Dutch Hunger Winter showed that exposure of the mother to acute famine was associated with increased cardiovascular risk in the adult offspring. Outcomes 94 varied according to the timing of famine exposure; late gestation exposure was associated with greater risk of glucose intolerance and early gestation exposure with obesity, atherogenic lipid profiles and CHD. Famine effects were independent of birth weight, suggesting that maternal undernutrition may impair adult health without reducing size at birth. The Institute of Nutrition of Central America and Panama (INCAP) trial in Guatemala (1969-77) is the only randomised trial of a nutritional intervention in which cardiovascular risk factors have been 95 measured in the adult offspring. In the original trial, pregnant women and children received one of two supplements: a high-protein, high-energy drink or a lower nutrient drink. There was no difference in birth weight between these two groups but the children of mothers who received a high-protein, high-energy drink had lower blood triglyceride and higher high-density lipid (HDL) cholesterol concentrations in adult life (profiles usually associated with better cardiovascular health). The Pune Maternal Nutrition Study was set up specifically to investigate the relationship of maternal nutrition to the childrens future risk of diabetes and heart disease. It collected prospective information on diet, workload and micronutrient status in pregnant women in rural Indian villages. At six years of age the children were thin by international standards but had a higher percentage body fat than European children. Maternal folate concentrations predicted higher insulin resistance in the child, and children born to mothers with the lowest vitamin B12 96, 97 concentrations and highest folate concentrations were the most insulin resistant. Thus an imbalance in the mother in two vitamins important in methyl group provision predicted higher adiposity and insulin resistance in the child, suggesting an important role for 1-carbon metabolism in the developmental origins of type 2 diabetes.
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Associations between maternal obesity, diabetes, raised birth weight and adulthood disease
The rising birth weight in developed countries (with the possible exception of Japan) associated with the increasing incidence of obesity in pregnancy and related gestational diabetes, also has potential for 99, 100 detrimental influences on the developing child. There is a U shaped relationship between birth weight 59, 101 and later insulin resistance and obesity, and there is now good evidence that children of women who are diabetic in pregnancy are themselves more likely to develop insulin resistance in later life and to 96 become overweight. Initially shown in the Pima Indians, a population with a very high incidence of 102 diabetes, this seems to occur in all populations. School children in Taiwan showed a similar phenomenon 103 and Indian children of gestationally diabetic mothers had increased adiposity and hyperinsulinaemia. While this may represent in part a genetically inherited disorder, studies of sibling pairs discordant for maternal diabetes show that the effect occurs only in the offspring prenatally exposed to diabetes, strongly 104, 105 suggesting a diabetic trait acquired during development. Infants of mothers with gestational diabetes 106 have a greater neonatal fat mass independent of birth weight and it is reported that a high rate of childhood metabolic syndrome (central adiposity, insulin resistance and hypertension) occurs in large-for26 gestational-age (LGA) babies born to mothers with gestational diabetes compared with appropriate-forgestational-age (AGA) babies. Importantly, the risk of metabolic syndrome is also present, but to a lesser extent, in LGA babies from normoglycaemic mothers. In a recent trial of two diets, normoglycaemic 107 mothers on a high glycaemic index diet gave birth to more LGA babies. Children of mothers with higher 27 glucose concentrations within the normal range are more adipose. Higher birth weight in normoglycaemic pregnancies is generally associated with raised adulthood BMI, and larger babies tend to become heavier adults. Although detailed investigations of the relative contributions of lean and fat mass 108, 109 have sometimes suggested that this association reflects increased lean body mass rather that fat mass, a recent study of infants from obese normoglycaemic mothers shows clear evidence of increased 110 adiposity. To date there have been few attempts to define accurately the relationship between maternal, childhood and adulthood body composition over any range of maternal BMI. Ongoing prospective longitudinal studies in contemporary cohorts such as the Avon Longitudinal Study of Parents and Children 111 112 (ALSPAC) cohort in Avon UK and the Southampton Womens Survey (SWS) will be very informative in this regard. In the latter it is already clear that mothers body composition and dietary balance before 113 pregnancy can affect fetal cardiovascular development in late gestation.
98
Key message Extremes of maternal body composition, either excessive thinness or obesity, are associated with adverse patterns of fetal and infant development leading to poorer long-term health.
Transgenerational effects
There is concern that the detrimental effects of the nutritional transition in many populations around the world will have an effect on the risk of chronic disease which will persist for several generations. Animal studies show that a dietary or glucocorticoid challenge administered in pregnancy can have effects on the metabolism, cardiovascular function and gene expression in the 74, 114 grand-offspring, even without any additional challenge in the second generation. The effects 73 can involve epigenetic changes. Similar changes have been reported in humans exposed to poor 115 nutrition during childhood development including the intriguing possibility that the effects can be transmitted through the paternal as well as the maternal line. There is now much interest in the concept that non-genomic inheritance can affect more than one successive generation, both from 75 scientific, social and medical perspectives.
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Taking a multigenerational perspective also focuses attention on the ways in which disease risk can be transmitted during periods of nutritional transition (see Figure 7). Obesity, type 2 diabetes and altered metabolism in women resulting from poor nutrition during development can result in greater glucose levels or gestational diabetes in pregnancy. This is likely to induce similar metabolic changes in their offspring. Figure 7: Cycles of disease risk
Intergenerational switching of pathways
Gestational diabetes Women malnourished Low pregnancy weight gain
Large babies
Suboptimal fetal development
Very poor postnatal environment
Enriched postnatal enviroment due to nutritional transition Obesity Insulin resistance
Stunting
Material morbidity
Premature death and morbidity
Cycles of disease risk can involve more than one generation. Women who are malnourished or who have sub-optimal body composition and weight gain in pregnancy are more likely to have offspring with stunting and premature death and morbidity (left part of diagram). This becomes a self-perpetuating cycle. Their offspring are at higher risk of cardiovascular and metabolic disease, especially if socio-economic transition or migration gives access to high fat and glycaemic index food and reduced physical activity. Women of this generation are more likely to develop gestational diabetes and to have offspring which in turn are also at risk of obesity and diabetes. This process, which may involve different mechanisms from the first, nonetheless produces another cycle of disease. Source: Gluckman PD & Hanson MA (2005) Metabolic disease: evolutionary, developmental and transgenerational influences. In: Hornstra G, Uauy R, Yang X (eds) The Impact of maternal nutrition on the offspring. Nestle Nutrition workshop series: Pediatric program. Switzerland: Karger.
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Conclusions
Studies of human populations show clear links between early life environment and later health and disease. While our knowledge of the specific components of maternal nutrition which produce such effects is limited in humans, experimental animal studies provide strong evidence that changing nutrition in the periconceptional period or in pregnancy can produce effects on the offspring which mimic human chronic disease. In developed societies, we know that many women consume poor quality diets, which results on the one hand in nutritional deficiencies and on the other in overweight and obesity. In developing societies, while maternal undernutrition remains a major problem, maternal overweight is also of concern. Development of future interventions will require the identification of biomarkers of poor developmental nutrition in infants and children. There is a need for better understanding of the implications of current variations in diet and nutrition for fetal development and long-term health. Positive steps need to be taken to ensure that young people understand the importance of health and wellbeing before pregnancy giving attention to their diet, optimal body weight, to stopping smoking and to limiting alcohol consumption.
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Chapter 3: Infant nutrition
Introduction
Infancy refers to the first one to two years after birth. It is a period of rapid growth in weight, length and brain size and rapid social, cognitive and motor development. These changes carry high nutritional needs at a time of total dependence on carers who may have little knowledge about nutrition or the special requirements of infancy. During the first 12 months of life, the infant must make a transition from a milk-only diet to one containing the diversity of foods eaten by the rest of the family. Good nutrition is essential for the infant to maintain and develop its immature immune defences as it meets pathogens for the first time. Patterns of weight gain and growth, and nutritional experience, in infancy can have long-term effects on health (see page 40).
Key Message Infancy is a period of high nutrient requirements, to support rapid growth (including brain growth) and critical social, cognitive and motor development.
Breast milk is the ideal food for newborn babies and currently in the UK, exclusive breastfeeding is recommended until the age of six months. Other (often termed complementary) foods are then introduced and gradually increased in variety and quantity. It is not known what constitutes the 116 ideal diet during this transition but there are well-established guidelines on nutrient requirements 117, 118 and on foods and feeding practice. In the UK, there are wide variations in infant feeding practices and in how closely parents follow these guidelines (see page 31). For discussion on the contraindications to breastfeeding see page 35. In all populations infancy is a period of relatively high mortality. The infant mortality rate (IMR) in England and Wales (five per 1,000 live births in 2006) has fallen continuously for the past 100 119 years (14.3 in 1976; 105 in 1910). Just over half the deaths are neonatal and related to 120 congenital abnormalities, low birth weight and pre-term birth. There are marked regional differences in IMR. In 2006, it was highest, 6.4, in the West Midlands and lowest, 4.0, in South 121 West England. There are also strong social class differentials. It is not known to what extent these inequalities have a nutritional basis.
Developing country perspective on infant nutrition

Infant undernutrition is a huge problem in developing countries. It is estimated that 178 million (32%) children under five years are stunted, 55 million are wasted, and micronutrient 3 deficiencies are widespread and frequently multiple. Undernutrition causes three million deaths among children under the age of five in developing countries every year. Infancy is the period when growth commonly starts to falter and it is difficult to reverse stunting after the 122 age of two years. The main causes are inadequate food (energy, animal protein and micronutrients) and high rates of infection. Sub-optimal breastfeeding and poor quality 123 complementary foods are key factors. Efforts to improve nutrition in developing countries should focus on pregnant women and infants to get the maximum benefits for growth, 124, 125 development, health and later economic productivity.
25
The case for breastfeeding

All current guidelines, including those from the Department of Health (DH), recommend exclusive breastfeeding for newborns and for the first six months of infancy. Breast milk provides all the nutrients required at this age in a form that is hygienic and easy to digest. The protein, carbohydrate and fat profiles are unique to breast milk and differ in many ways from other animal 126 milks. Breast milk also contains a range of bioactive components, including anti-microbial and 126, 127 anti-inflammatory factors, digestive enzymes, hormones and growth factors. Anti-microbial agents include leucocytes, secretory immunoglobulin (Ig)A, IgM and IgG antibodies, oligosaccharides, lysozyme, lactoferrin, lipids, fatty acids and mucins. Growth factors are thought to be important for gut maturation. Lactoferrin is one of several specific binders in human milk that greatly increase the bioavailability of micronutrients.
Key message All current guidelines, including those from DH, recommend exclusive breastfeeding for the first six months after birth.
The volume and composition of breast milk vary with the stage of lactation, within each individual 126 feed, and with maternal nutritional status. Recent research in animals has shown that reduced 128 fetal growth caused by placental insufficiency can impair the quality and quantity of breast milk. Colostrum, produced during the first few days is low in volume and nutrient content but high in anti-microbial factors. Volume and nutrient content reach a peak, in mature breast milk, several weeks after birth. The mothers macronutrient intakes do not have much influence on milk composition, but her diet does affect the long-chain fatty acid and vitamin content of her milk. Breastfed infants have more control over the flow of milk than bottle-fed infants. Breastfeeding is therefore often described as an ideal supply and demand regulation system. The feeding behaviour of the baby and the quality of the breast milk change with time in a way that may prevent overfeeding, teach the infant how to recognise satiety signals, and regulate energy intake differently from formula-fed infants. The role of leptin in breast milk may be of particular importance in the early development of both adipose tissue and appetite regulatory systems in the infant, and ultimately on propensity to obesity in later life. A recent study showed that administration of physiological levels of leptin to 129 suckling rats caused a significantly lower body weight in adulthood. Observational studies have 130 shown that breastfeeding is associated with lower rates of childhood obesity. Bearing in mind the absence of leptin in formula milk, this may have important implications for the prevention of obesity in children and in adults.
26
Current infant feeding practices

The national Infant feeding survey (IFS) is conducted every five years; the latest data are from 131 2005 (see Box 4). These reports provide a wealth of information about variations in feeding practice, factors that influence the type of milk and duration of milk feeding. They also detail trends in feeding over time. Exclusive breastfeeding is recommended up to the age of six months in the UK. The IFS shows, however, that less than 1 per cent of mothers are exclusively breastfeeding at six months. Current guidelines are to introduce solid foods from six months, to provide a varied diet that includes starchy foods, fruit and vegetables and meat and fish, and to encourage the use of home-prepared rather than commercial baby foods (see Appendix 4).
Box 4: The UK Infant feeding survey 2005 findings on breastfeeding Initial breastfeeding rates in 2005 had increased since 2000 (78% in England, 70% in Scotland, 67% in Wales, and 63% in Northern Ireland). Only 48 per cent of mothers were breastfeeding at six weeks and 25 per cent at six months. 45 per cent were breastfeeding exclusively at one week, 21 per cent at six weeks, 7 per cent at four months and <1 per cent at six months. Three-quarters of mothers had given their baby milk other than breast milk by six weeks, and 92 per cent by six months. Just under half of all mothers who had prepared powdered infant formula in the last seven days had not followed the instructions properly, for example by not using cooled 131 boiled water.
Breastfeeding rates in the UK are much lower than in many European countries for example, more than 90 per cent of babies in a nationally representative sample studied in Norway were 132 breastfed from birth, and high rates were still present at one, four and six months. The IFS shows that there are strong relationships between the mothers socio-economic status and educational attainment and breastfeeding prevalence these factors are associated with both initiation rates and breastfeeding duration (see Figure 8). In the UK Gateshead Millennium Baby Study (1999-2000) 84 per cent of mothers with higher education initiated breastfeeding compared 133 with 25 per cent of mothers with no educational qualifications. Percentages still breastfeeding at four months were 49 per cent and seven per cent. There were also strong negative associations with Townsend score, a measure of deprivation based on residential postcode.
Key message Breastfeeding rates in the UK are much lower than in many European countries. Less than 1 per cent of mothers in the UK are exclusively breastfeeding at six months.
27
Box 5: Reasons why mothers do not breastfeed or cease breastfeeding early A recent focus group study in the UK suggested further detail of the reasons women may not breastfeed or why they stop breastfeeding early. These were as follows. The attitude of other people women felt that breastfeeding in public was unacceptable and embarrassing, while bottle-feeding was accepted by everybody and in all places. A lack of places to breastfeed out of sight restricted womens ability to get out of the house. This may be a bigger issue for low-income women, who may not have the option of breastfeeding in the car. Some women reported breastfeeding in public toilets as the only option. Women wished that cafs and shops could provide places to breastfeed with some privacy. Attitudes of family and friends some women said that even family and friends found it repulsive to be in the same room when they were breastfeeding. Some grandparents thought it excluded them from having the chance to feed the new baby. It was clear that the opinion of family and friends was a stronger influence than that of health practitioners. Lack of knowledge women vaguely knew that breastfeeding was supposed to be beneficial, but they could not name any benefits, and were not convinced about them. In the study only one woman had learnt at school about benefits of breastfeeding; most did not hear about it until they were pregnant. Feeding was not well covered in antenatal classes. Lack of professional support women experienced difficulty in trying to establish breastfeeding but were unwilling to bother the midwife. Bottle feeding seemed easier. Experience breastfeeding seemed difficult and painful, and many women experienced problems ranging from getting the baby latched on, sore nipples, and disturbed sleep. Women, especially adolescents, complained of a lack of freedom to travel/socialise/work. Worry about babys weight gain women said that health visitors were always worried about weight gain. Although some women in this study mentioned the benefits of breastfeeding including feelings of wellbeing and relaxation during feeds, convenience (less washing up), and less expense, it is clear that there are significant barriers for women in the UK which impact on their choice to breastfeed.
Source: McFadden A & Toole G (2006) Exploring womens views of breastfeeding: a focus group study within an area with high levels of socio-economic deprivation. Maternal & Child Nutrition 2: 156-68.
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Box 6: Reasons given by mothers for stopping breastfeeding by duration of breastfeeding Babys age when breastfeeding ceased Less than 1 week 1 week, less than 2 weeks 2 weeks, less than 6 weeks 6 weeks, less than 4 months 4 months, 6 months, All mothers giving up less than less than 6 months 9 months
Percentage (%) of mothers who stopped breastfeeding Why stopped breastfeeding Insufficient milk Baby rejected breast Painful breasts/nipples Took too long/tiring Mother was ill Domestic reasons Returned to work/college Too stressful Baby ill Baby could not be fed by others Did not like breastfeeding Breastfed for as long as intended More settled on formula Baby not gaining weight Teething/biting All Stage 3 mothers who stopped breastfeeding during survey period 26 34 24 11 8 4 1 7 6 1 2 1 1 * 41 21 29 17 11 7 7 7 5 5 1 2 1 53 17 17 19 9 9 1 6 5 4 4 1 2 2 48 13 9 19 8 10 8 4 3 6 1 4 4 6 37 11 1 5 5 3 15 3 2 4 1 10 8 4 3 195 24 16 2 5 5 2 22 1 1 3 * 6 3 3 14 727 39 20 14 14 8 7 7 5 4 4 3 3 3 3 2 4827
1143
351
1087
1284
Includes some cases where mothers breastfeeding duration not known Code introduced at later Stages * Percentage less than 0.5% Percentages do not add to 100% as some mothers gave more than one answer Source: Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The Information Centre.
29
Figure 8: Prevalence of breastfeeding according to mothers socio-economic classification: Infant Feeding Survey 2005
100
% of mothers breastfeeding
Managerial & professional Intermediate Routine & manual
80
60
40
20
0 Birth 2 4 Months Source: Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The Information Centre. 6 8 10
Developing country perspective on breastfeeding

As in the UK, breastfeeding rates are sub-optimal in most developing countries. Although more than 95 per cent of babies overall receive some breastfeeding, rates of exclusive breastfeeding are only 50 per cent on average up to the age of two months, and 20 to 30 per cent from two 3 to five months.
3
Complementary feeding practices in the UK

In comparison with milk feeding in UK infants, current variations in complementary feeding practice and the weaning diet are less well documented. Some information on weaning practice is collected in the IFS (see Box 7).
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Box 7: The UK Infant feeding survey 2005 findings on complementary feeding In 2005, mothers were introducing solid foods later than in the 2000 survey (51% by four months compared with 85% by four months respectively). Very few women (2%) followed DH guidance to delay weaning onto solid foods until six months. Babies given solid foods between four and six months were much more likely to be fed commercially-prepared foods (85%) than home-prepared foods (51%). Most mothers (92%) avoided the use of salt completely in the diets of their babies. The proportion of mothers avoiding the use of salt increased between 2000 and 2005 (33% to 51%), rises were also seen in the proportion avoiding nuts (30% to 48%) and honey 131 (6% to 13%); a greater awareness of food allergies was a key reason for this change.
The IFS showed that in 2005, although there was a decline in prevalence of very early introduction of solid foods since 2000, most infants had been introduced to solid foods before the recommended 131 age of six months. The main reasons given for the introduction of solid foods before three months were that the baby was not satisfied with milk alone, or the mothers experience with a previous baby. Early introduction of solid foods was more common in younger mothers, and among mothers of lower socio-economic status and lower educational attainment (see Figure 9). Figure 9: Age by which solids had been introduced according to mothers socio-economic classification: Infant Feeding Survey 2005
100
Managerial & professional Intermediate Routine & manual
80
60 % 40 20
0 Birth 1 2 3 Months Source: Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The Information Centre. 4 5 6 7
31
Among working mothers, delaying return to work until at least six months was associated with 131 later introduction of solid foods. The nature of the weaning diet varied by mothers socio-economic status. When compared with other women, mothers in managerial/professional occupations were more likely to feed their infants cooked vegetables and fruit, rice and pasta, and meat and fish, and less likely to provide 131 regular servings of sweets, biscuits and savoury snacks. There are two large cohort studies of UK infants in which variations in complementary feeding and weaning practice and dietary intakes have been assessed: ALSPAC and the Southampton Womens Survey (SWS). The ALSPAC study collected dietary data using three-day diet diaries for over 1,000 135, 136 infants born in 1991-92. At eight months, 34 per cent of the infants had not eaten any fruit and 25 per cent had not eaten vegetables in the three-day study period, while 26 per cent of the infants had eaten chocolate. At 18 months, 16 per cent of the children had not eaten fruit and 8 per cent had not eaten vegetables in the three-day period but 63 per cent of the children had eaten chocolate and 66 per cent had eaten savoury snacks. Although intakes of most nutrients were above the reference nutrient intakes (considered adequate for 97% of children), vitamin D intakes were low at both ages, and iron intakes were low at 18 months. The ALSPAC study also showed that at 18 months, the most common container for drinks was a trainer cup. Eighty-six per cent of children had at least one drink from a trainer cup over a 24-hour period, 64 per cent of children were given at least one drink in a bottle, and 10 per cent solely used a bottle. Use of a bottle was more common among children who had not been breastfed, 137 who had older siblings, and who had mothers who smoked. Children being fed milk in a bottle consumed greater volumes when compared with children given milk in a cup; this was particularly marked for the children only fed by bottle. A wide variety of drinks were given at this age, including low calorie squashes (48%), tea and coffee (17%), and fizzy drinks (7%). Maternal education was the most important factor associated with the types of drinks consumed at this age more highly educated mothers gave their children fruit juices more often, whereas women with low levels of educational attainment were more likely to give their children tea, coffee and soft drinks. Seventeen per cent of children whose mothers had Certificate of Secondary Education (CSE) qualifications or less were given fizzy drinks over a 24-hour period. More recently the dietary patterns of 1,434 infants born to women in the SWS between 1999-2003 138 were reported. The most important pattern of diet identified at both six months and 12 months of age was consistent with current infant feeding guidance, and was characterised by high consumption of vegetables, fruit, meat and fish, and other home-prepared foods. This dietary pattern was labelled the infant guidelines pattern. Infants who had high scores for this pattern of feeding were also more likely to have been breastfed. A number of factors, including a range of maternal and family characteristics were considered as influences on the infants pattern scores. At both ages the key determinant of the nature of the infant diet was the quality of the mothers diet. Infants whose mothers had high prudent diet scores and healthier dietary patterns, 139 characterised by high intakes of fruits and vegetables, and wholemeal bread, were more likely to have a comparable diet, and were fed in accordance with infant feeding guidelines. Conversely, mothers who had low prudent diet scores and whose diets were characterised by high intakes of white bread and chips, added sugar and full-fat dairy products, were less likely to provide a diet for their infant that conformed with infant feeding guidance (see Figure 10). The influence of mothers dietary pattern on her infants diet was independent of a range of other factors, including her educational attainment and smoking status.
32
Key message In comparison with milk feeding, less attention has been given to the introduction of nutritious weaning foods. It is known that the quality of the weaning diet for UK infants is strongly influenced by the socio-economic status and educational attainment of the mother.
Figure 10: 12-month infant guidelines pattern score according to prudent diet score of the mother
P<0.001
1 12 month infant guidelines score
0.5
-0.5
-1 to -1 to -0.5 to 0 to 0.5 to 1 >1
Mothers prudent diet score Source: Robinson S, Marriott L, Poole J et al (2007) Dietary patterns in infancy: the importance of maternal and family influences on feeding practice. British Journal of Nutrition 98: 1029-37.
Childrens diets and food preferences have been shown to be influenced by their food 140-142 environment, and by the eating behaviours of their parents. The SWS provided evidence that influences of the food environment on childrens diet operate very early as soon as infants start to eat solid food. The findings also suggest that interventions to change mothers diets will have direct consequences for the diets of their children.
Key message Influences of the food environment including maternal diet operate very early on childrens diets, from weaning onwards. Interventions to change mothers diets will have direct consequences for the diets of their children.
33
Developing country perspective on complementary feeding

Poor-quality complementary feeds are the norm for infants in disadvantaged families and a major cause of infant stunting. Programmes to support breastfeeding, promote better complementary feeding and supply micronutrient supplements, are some of the most effective 123 measures that could be taken to reduce undernutrition in these countries.
Guidelines on infant feeding Breastfeeding guidelines

In 2003, the World Health Organisation (WHO) recommended that all babies should be exclusively breastfed for the first six months of life (the previous recommendation was four to six months). Thereafter complementary feeding should be introduced, with breastfeeding continuing as long as possible up to two years. The evidence underlying the advice to extend exclusive breastfeeding from four to six months is persuasive in developing countries, but less so for high-income 143-145 countries. Breastfed babies, even in high-income countries, experience significantly fewer 146 episodes of gastro-intestinal and respiratory infection. Benefits to the mother of breastfeeding include convenience, less expense, a faster return to pre-pregnant weight, delayed onset of 147 ovulation, and possibly long-term protection against breast and ovarian cancer.
Key message Breastfed babies, even in high-income countries, experience significantly fewer episodes of gastro-intestinal and respiratory infection compared with formula-fed babies.
The National Service Framework for Children, Young People and Maternity Services highlights the importance of breastfeeding, and recognises that it is a skill that needs to be taught and supported. The DH produces a booklet for health professionals on how best to do this entitled 148 Good practice and innovation in breastfeeding. More recently NICE have produced guidance on improving the nutrition of pregnant and lactating mothers from lower socio-economic groups as a way of targeting those most in need of advice and support.
149
Maternal diet during lactation guidelines

For most women in the UK, a normal healthy diet is adequate to support breastfeeding. The Food 150 Standards Agency (FSA) provides specific dietary advice for lactating mothers. Vitamin D supplements (10 micrograms daily) are recommended. Mothers are advised that fish is good for their own health and for the development of the baby, but to limit the intake of oily fish to two portions per week because of mercury levels. If there is a family history of peanut allergy, women 150 are advised to avoid eating peanuts during lactation.
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Developing country perspective on maternal diet during lactation

Maternal micronutrient deficiency during lactation (especially for the B vitamins, vitamin A and 151 iodine) can lead to low levels in breast milk. Even undernourished mothers in developing countries can, however, usually breastfeed successfully, and milk quality appears to be largely 126 unimpaired.
Box 8: Contraindications for breastfeeding There are some circumstances in which breast milk can contain harmful agents, such as HIV, environmental pollutants (eg dichlorodiphenyl trichloroethane (DDT), polychlorinated biphenyls (PCBs), dioxins, radiation), stimulants (caffeine, nicotine), drugs and food allergens. The few contraindications to breastfeeding include galactosaemia in the infant, psychotropic drug abuse by the mother and active maternal tuberculosis. In the UK, HIV-positive women are advised not to breastfeed because of a risk of transmission to the baby. This advice is not appropriate in countries where the risks of bottle-feeding are high, especially because of the lack of clean safe water, and outweigh the risk of HIV infection. Some therapeutic drugs are contraindicated during lactation or require monitoring: antineoplastic drugs and radioactive substances, retinoids, iodides, lithium, phenindione, tetracyclines, chloramphenicol and amiodarone. Drugs commonly used by UK mothers during lactation include analgesics, antibiotics and antidepressants and for most of these, concentrations in breast milk are too low to cause problems. 152 The British National Formulary (BNF) has a section on safety of drugs during breastfeeding. 153,154 Several reviews have also been published concerning this topic.
Formula feeding
If mothers cannot or choose not to breastfeed, there is a range of commercially available formula milks designed as total substitutes for breast milk during the babys first year. They are the only safe alternatives to breast milk and infants can grow and develop normally on these feeds. The 155 content of infant formula is tightly regulated. There is an international code, legally binding in the UK, governing its marketing, to prevent mothers from being encouraged to formula-feed (see Appendix 5). Formula milk has changed considerably over the past 70 years and there are frequently new compositional changes. Standard formula is based on skimmed cows milk, with whey protein, vegetable oil and extra vitamins and minerals added to bring the composition closer to human milk. Formula does not contain most of the bioactive factors present in human milk, the protein content is higher and different in quality, and the concentrations of most vitamins are higher (see Appendix 6). Several specific additives, which are present in breast milk but low in cows milk, have been 156, 157 introduced to some formula milks recently and may be unfamiliar to many professionals. These include amino acids such as taurine; long-chain polyunsaturated fatty acids (LCPUFAs) such as docosahexanoic acid (DHA); oligosaccharides; and pre-formed nucleotides. Docosahexanoic acid is a major constituent of neuronal cell membranes and there is some evidence that newborns, especially pre-term babies, cannot synthesise adequate quantities for optimal brain development, although this theory is controversial. Oligosaccharides are analogous to cell surface receptors for pathogens and are thought to inhibit the pathogenicity of bacteria. In infant formula they are
35
known as prebiotics (distinct from probiotics or so-called friendly bacteria, which are not currently added to formula). Pre-formed nucleotides are thought to be required for the growth of rapidly dividing cells in bone marrow and intestinal epithelium, and also to enhance beneficial intestinal bacterial growth. There is currently no strong evidence that these additives have health benefits.
Complementary feeding
Complementary feeding is the term used for the introduction of foods other than milk (sometimes called weaning foods or solids). It is recommended that complementary feeds are introduced from the age of six months onwards, and that infants progress onto the same foods as the rest of the family by around one year. The optimal diet for infants at this stage is not known, and is certainly not innate knowledge for parents. Detailed guidelines are available on suitable foods at every stage (see Appendix 4). Key recommendations are a varied diet, adequate energy density, high-quality (preferably animal) protein sources, and fresh fruit and vegetables.
Vitamin supplements for infants

Advice in the UK is that healthy breastfed infants under six months do not require supplements 117 provided the mother has adequate vitamin status. If there is any doubt about this, supplements should start at one month. From six months, infants receiving breast milk as their main drink should have vitamin A and D supplements, but these are not required by infants on formula-milk, which is fortified with vitamins. Pre-term infants are a special case and require supplements from birth. Between one and five years, it is recommended that all children have vitamin A and D supplements unless their diet is diverse and plentiful and there is good exposure to sunlight. There are many 152, 158 preparations available. Supplementary vitamins are available free for families receiving certain benefits under the Healthy Start scheme, and all families can buy these preparations.
Developing country perspective on complementary feeding

Infants in developing countries are at increased risk of undernutrition after six months, when breast milk alone is no longer nutritionally adequate but complementary foods are frequently of 3, 159 159 very low nutritional quality. The WHO has developed guidelines for infant feeding which are suitable for use in all countries (see Appendix 4). Educational interventions and supplementation programmes, designed to improve the quality of complementary feeding, have been shown to 123 reduce or prevent stunting in vulnerable infants.
Determinants of infant weight gain and growth

A characteristic of the healthy infant is rapid, though also rapidly decelerating, weight gain and linear growth, but the factors which determine these processes and the relative accrual of lean and fat body mass are still poorly understood. Given adequate postnatal nutrition, babies who experienced intra-uterine growth restriction due to placental insufficiency, small maternal size, maternal undernutrition or smoking tend to show catch-up weight gain and growth, while macrosomic babies of mothers with gestational diabetes catch-down. Early postnatal growth rates therefore 160 compensate for intra-uterine restriction or enhancement of growth. Boys gain weight and grow slightly faster than girls in early infancy. Weight gain and growth are modified by the type of feed used. Formula-fed babies gain weight and length faster than breastfed babies after the age of three 160-162 to four months (see Figure 11). Small-for-gestational-age (SGA) babies grow faster on enriched 163 than on standard formula. Infant feeding is largely demand-driven in that mothers tend to offer feeds when the baby appears to want them, and appetite is likely to be one of the factors influencing weight gain. Recurrent infections are a major cause of poor infant weight gain and growth in developing countries.
36
Figure 11: Mean weight and length of breastfed and formula-fed infants from birth to 18 months
Breastfed Formula-fed
80
Girls
12
Girls
10 70 Length (cm) Weight (kg) 60 4 50 0 2 4 6 8 10 12 14 16 18 Age (months) Breastfed Formula-fed 80 8
2 0 2 4 6 8 10 12 14 16 18 Age (months)
Boys
12
Boys
10 70 Length (cm) Weight (kg) 60 4 50 0 2 4 6 8 10 12 14 16 18 Age (months) 8
2 0 2 4 6 8 10 12 14 16 18 Age (months)
Source: Dewey KG, Heinig MJ, Nommsen LA et al (1992) Growth of breastfed and formula-fed infants from 0 to 18 months: the DARLING study. Pediatrics 89: 1035-41.
37
Karlberg described postnatal growth in three distinct phases infancy, childhood and puberty. During infancy the fetal growth hormones, such as insulin and the insulin-like growth factors (IGFs) play a more important role than growth hormone. From six to 12 months, growth hormone starts to have a significant effect on growth and becomes the main endocrine growth regulator during childhood. Nutritional status, especially during infancy, interacts with these hormones, and both circulating IGF-1 concentrations and receptors are reduced in undernutrition. Thyroid hormone is required for normal infant growth. In early infancy, gonadotrophin concentrations are high, and testosterone concentrations in boys are raised; they fall over the first six postnatal months to very low levels that persist until the onset of puberty. There may be mild elevation of oestrogen concentrations in girls in the neonatal period. The reasons for differences in weight gain and growth between breastfed and formula-fed babies are not known. Formula milk contains more protein than breast milk, which may alter growth factor concentrations. The greater control that the infant exerts over the flow of milk, and the supply and demand interaction between infant and mother, may influence appetite, satiety and energy intake differently from formula-fed babies. Inadequate growth is often a reason for mothers deciding that they have insufficient milk, and changing to formula feeding (see pages 28 and 29). There are also numerous social factors influencing parents infant feeding choices. This complex interplay between biological and societal influences makes it difficult to disentangle the 165 factors that control infant growth.
164
Key message Inadequate growth is often a reason for mothers mistakenly deciding that they have insufficient milk, and changing to formula feeding.
Recommendations about size and growth during infancy

Growth monitoring is one of the prime activities of health visitors and doctors looking after infants in the UK. The aims are to detect inadequate weight gain or growth (failure to thrive), which may indicate illness or problems with feeding or diet, or excessive weight gain. Research suggests that it 166 is important to parents that their child is normal in size or growth and a belief that an infant is not gaining weight normally is one of the commonest reasons mothers give for stopping breastfeeding. The growth charts currently in general use in the UK are based on the 1990 UK 167-169 reference data. These came from a study of fetal growth in white Caucasian pregnancies in London, and Cambridge infants taking part in a study of the effects of infant feeding practices on growth. In 2006, the WHO launched a new growth reference, which is now recommended for use 170 worldwide. There were a number of reasons for developing the new reference. Formula-fed 162 infants gain weight more rapidly after the first four to six months than breastfed infants and studies had shown that the weight gain pattern of breastfed infants deviated considerably from 171 most current reference data. An optimal reference was considered to be that based exclusively on breastfed infants. Infants from all ethnic groups can grow equally well, given an optimal environment and adequate nutrition, and a unified standard would have benefits for comparing data from different populations. The WHO has defined the new reference as a standard rather than a reference, ie a description of how children should grow. The infants from which it was derived lived in conditions favourable to child growth: they were singletons born at full-term without major neonatal morbidity; had no known health or environmental constraints to growth;
38
the mothers were willing to breastfeed exclusively for at least four months continuing until 12 months, and to introduce complementary feeds by six months; and none were smokers. The data were collected using standardised techniques in the USA, Oman, Norway, Brazil, Ghana and India in 1997-2003. One concern about the generalisability of these standards is the wide international variation in birth weight. Mean maternal height and birth weight in Oman and India were much lower than in Norway and the USA, indicating maternal constraint on fetal growth in these developing countries, which is also likely to be associated with effects on postnatal growth, 172 inducing more rapid catch-up growth.
Box 9: Comment on the WHO infant growth reference standard The most interesting thing about the study that gave rise to these standards is that despite being based on very diverse populations around the globe, they produced very similar growth curves, indicating that genetics plays a very small part in determining growth rates compared with environmental factors which were optimised for this study healthy pregnancy, good mother and child nutrition, no smoking, full breastfeeding etc. Tim Lobstein, Director Childhood Obesity Research Programme
A joint expert group from SACN and the Royal College of Paediatrics and Child Heath (RCPCH) 172 met to consider the routine use of the WHO standards in the UK. They concluded that UK infants would appear large at birth and show apparent marked catch-down growth during the first few weeks, which could discourage mothers from breastfeeding. Using the WHO standards would, however, reduce the number of UK infants showing weight faltering, and thus being classified as underweight, after four months. They found little difference in length between the UK 1990 and WHO references at any age, and there was convergence of weight in the two references from around two years onwards. The group advised adoption of the WHO Growth Standard for routine use from two weeks to 24 months, while retaining the UK 1990 reference from 24 months onwards. Since the WHO reference population did not include pre-term infants, the UK 1990 reference would also need to be retained for these infants. They recommended piloting of the new charts, training for health professionals, and a well-planned communications strategy preceding implementation. It is not clear when all this will happen, but it is unlikely that the standard will be in general use before 2009.
Key message Infant growth-charts currently in general use in the UK (based on 1990 UK reference data) are now considered inadequate because weight gain patterns of breastfed infants deviate considerably from such data. Old growth charts should be replaced by the 2006 WHO new growth reference based exclusively on breastfed babies for assessing all infants aged between two weeks and 24 months.
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Breastfeeding and health: short- and long-term outcomes

Even in developed countries, with modern breast milk substitutes and easy access to clean water for preparation, breastfeeding is associated with fewer infections, especially gastroenteritis and respiratory 173-177 173 infection, and possibly otitis media. In one UK study, babies who were fully or partially breastfed for 13 weeks or more were seven to 17 per cent less likely to have a gastro-intestinal illness and were 70 per cent less likely to be admitted to hospital with gastro-intestinal illness. Significant reductions in gastro-intestinal illness in this group were found up to one year of age. McCance and Widdowson demonstrated in animals over 40 years ago that early postnatal nutrition 178, 179 has long-term effects. They showed that by manipulating litter size at birth, rat pups could be transiently overfed or underfed during lactation; reducing the litter size resulted in more rapid early growth and larger adult size. Later overfeeding did not have this effect, suggesting that there is a critical period within which postnatal nutrition permanently influences growth and body composition. Most research into long-term effects of infant feeding in humans has compared rates of various health outcomes between children or adults who were breastfed or formula-fed. Despite a wealth of literature, there is still much that we do not know. The ability to combine infant feeding data with adult outcomes means that a dataset must be quite old, dating back to when bottle feeds were very different from those in use today. Information about feeding is usually sparse, recording whether or not a baby was initially breastfed, and sometimes the duration of breastfeeding and/or the age at which solids were introduced. Collating evidence across studies can be difficult because of the different ways of describing infant feeding. There is no information in these studies on the quality and quantity of breast or bottle milk. A major problem in interpreting these studies is that of confounding. A mothers choice to breastfeed is related to many other factors that could influence the later health of the child, especially her socio-economic status and education (see page 30). These influences change with time. Adjusting for these factors, to isolate the biological effects of early feeding, is an imperfect science. Randomised trials would be helpful, but it is clearly impossible to randomise healthy babies to be 180 breastfed or formula-fed. A recent trial in Belarus in which mothers attending different health clinics were randomised to receive or not receive intensive breastfeeding education and support, leading to greatly increased rates of breastfeeding in the former group, is likely to yield useful data. Lucas and colleagues have carried out randomised trials of different infant feeds among babies born pre-term or SGA (see page 41). The ongoing European Childhood Obesity Project is carrying out a series of randomised trials in babies whose mothers have decided to bottle-feed, testing the effects of different 181 protein intakes from formula milk.
Developing country perspective on breastfeeding and health

Breastfeeding is a lifesaver in developing countries, where formula feeds are often by necessity made with unsterile water and fed from unsterile bottles and teats. A recent review estimated relative risks for diarrhoea incidence and mortality under six months at 3.0 (95% confidence interval (CI) 1.3 to 7.0) and 4.6 (95% CI 1.8 to 11.8) for partially breastfed infants and 3.7 (95% CI 1.7 to 7.9) and 10.5 (95% CI 2.8 to 39.6) for non-breastfed infants, compared with exclusively 3 breastfed babies. Estimates for pneumonia incidence and mortality were 2.5 (95% CI 0.2 to 27.2) and 2.5 (95% CI 1.0 to 6.0) in partially breastfed infants and 2.1 (95% CI 0.2 to 22.6) and 15.1 (95% CI 0.6 to 373.8) in non-breastfed infants. The same review estimated that sub-optimal breastfeeding causes 1.4 million preventable deaths (12% of under-five deaths in developing countries) and 43 million disability adjusted life years (DALYs).
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Breastfeeding and later cognitive function and neurodevelopment

A large number of studies have compared neurodevelopmental scores and visual function between 182-184 children who were breastfed and those who were formula fed. A consistent message is that at all ages children who were breastfed score an average two to eight developmental quotient points higher and/or have better visual function. Several studies report dose-response effects with duration of breastfeeding. The size of these effects is small, and unlikely to make a difference to an individual child, although on a population scale they could be important. The issue of confounding is especially important for cognitive outcomes, because mothers who breastfeed tend to be more affluent and better educated than women who formula-feed. In a large recent study, it was shown that the mothers intelligence quotient (IQ) predicted her likelihood of breastfeeding 185 even more strongly than these factors. A one standard deviation advantage in maternal IQ more than doubled the odds of breastfeeding. Before adjustment, breastfeeding was associated with an increase of around four points in childhood cognitive ability, but when adjusted for a range of confounders including maternal IQ, the effect was non-significant (+0.5 points, 95% confidence interval -0.2 to +1.2). There are however, plausible biological reasons for better cognitive development in breastfed babies. The close contact and interaction between mother and baby may enable more visual, social and motor stimulation in early infancy. Constituents of breast milk could favour brain development. The LCPUFAs, DHA and arachidonic acid (AA) are required in large quantities in the developing brain and retina. They have not been added to formula milk until recently (~2002 onwards) and are not present in all formulas. DHA can however, be synthesised from precursors in formula, and there are only small differences in brain DHA content between breastfed and formula-fed infants. It is not yet known how important these differences are in functional terms. They may be more important in pre-term babies, since accumulation of DHA in the fetal brain occurs mainly in the last trimester of pregnancy. Randomised studies in pre-term infants, comparing banked breast milk with pre-term formula (both given by nasogastric tube) showed that breastfed infants had an eight 186 point IQ advantage at eight years, even after adjustment for confounding factors.
Key message There is consistent evidence of better cognitive function in children who were breastfed. There is controversy as to whether this is a direct effect, or the result of confounding resulting from the fact that mothers who are more intelligent and/or better educated are more likely to breastfeed.
Breastfeeding and later body composition and obesity

There are several recent systematic reviews of studies comparing indices of obesity between 187-190 children and adults who were breastfed or formula-fed. BMI, which does not distinguish between fat and lean body mass, was the main outcome in most studies, but some used specific measures of adiposity such as skinfold thickness or dual-energy x-ray absorptiometry (DXA) measurements. Breastfeeding is associated with a lower mean BMI in later life in most studies. The difference is 2 189 2 small (-0.04 kg/m [95% CI 0.05 to -0.02]) but the lower incidence of obesity (BMI >30 kg/m ) 188 is more impressive (odds ratio [OR] 0.87 [95% CI 0.85 to 0.89]). Several studies have shown a dose-response relationship, with longer duration of breastfeeding associated with lower rates of obesity. Again, there are major confounding issues, because the choice to breastfeed is associated
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with less obesogenic family characteristics. A recent study showed however, that fat mass assessed using DXA at age nine to 10 years was inversely related to the duration of breastfeeding and this association, although attenuated, was robust to adjustment for a range of confounding 192 factors. On the other hand, there were no differences in skinfold thickness at six years of age 180 between children in the two arms of the Belarus trial. Mechanisms that could protect breastfed babies from later obesity include aspects of the feeding process or particular constituents of breast milk. As already mentioned, breastfed infants may learn to regulate their energy intake more effectively. Breastfed babies grow more slowly in infancy than formula-fed babies, which may be protective. Constituents of milk, such as protein, may influence 127, 193 body composition through effects on hormones such as insulin and IGF-1.
191, 192
Key message Breastfeeding is associated with a lower mean BMI in later life, and a longer duration of breastfeeding is associated with lower rates of obesity. Breastfed babies grow more slowly in infancy than formula-fed babies, which may be protective against the later development of obesity. There is also evidence that breastfeeding is associated with a lower risk of both type 1 and type 2 diabetes and some forms of cancer, and lower LDL-cholesterol concentrations in childhood and adulthood.
Diabetes
Type 1 diabetes is an auto-immune disease in which antibodies are formed against components of the pancreatic beta cells, leading to insulin secretory failure. It usually presents in childhood or adolescence. Case-control studies have shown a 30 to 50 per cent reduced risk of type 1 diabetes in children who were breastfed, but more evidence is required in this area. It has been suggested that the avoidance of cows milk formula is important rather than breastfeeding per se, because there is structural similarity between bovine albumin and beta cell surface proteins, and children 194 presenting with type 1 diabetes have elevated antibodies to bovine albumin. Type 2 diabetes is a common disease and, until recently, usually presents in middle-to-old age. It is strongly associated with obesity, and the underlying cause is insulin resistance, which imposes an increased demand for insulin that eventually exhausts the pancreatic beta cells. The obesity epidemic in Western countries has led to increasing numbers of children presenting with type 2 diabetes. It has been estimated that there could be 1,400 children with type 2 diabetes and 195 20,000 with pre-diabetes (impaired glucose tolerance (IGT)) undetected in the UK. There is some evidence that breastfeeding protects against the risk of developing type 2 diabetes in later life, possibly through effects on adiposity. A meta-analysis of seven studies showed a reduced risk in six 196 (overall OR 0.61; 95% CI 0.44 to 0.85; p=0.003). This was little changed after adjusting for confounding factors (maternal size, birth weight, parental diabetes, socio-economic status and adult body size).
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Blood pressure and cardiovascular disease

There were no differences in blood pressure at six years of age between children in the two arms of 180 197, 198 the Belarus trial. Two recent systematic reviews found that breastfeeding was associated with a small reduction in blood pressure of 1-1.5 mmHg (systolic) and 0.5 mmHg (diastolic) in observational studies. Effect estimates were lower after adjusting for confounding. Although small in individual terms, an effect of this size at a population level could translate into significant reductions in hypertension and CHD. A meta-analysis of the few studies that have related infant feeding to cardiovascular disease found no evidence of a lower incidence in men and women who were 199 breastfed. There was some evidence that prolonged breastfeeding (for more than a year) was associated with a small increase in adult cardiovascular disease mortality in this analysis, and with 200 increased arterial stiffness in one other cohort study.
Other cardiovascular risk factors

There are few data for other risk factors such as serum lipid concentrations and inflammatory markers. A meta-analysis found that breastfed babies have higher serum cholesterol and low-density lipid (LDL) cholesterol concentrations in infancy itself (probably because of the higher cholesterol content in breast milk) but concentrations were lower in adult life by -0.18 mmol/l (CI -0.3 to -0.06). This difference would 201 be associated with an approximate 10 per cent reduction in CHD risk. Consistent with these findings, in a follow up study of pre-term infants randomly assigned to banked breast milk or pre-term formula, 202 children in the former group had lower LDL cholesterol and apolipoprotein B concentrations. A recent study of 8,000 members of the 1958 UK birth cohort, whose infant feeding was recalled by the mother at seven years, and in which it was possible to adjust for confounding factors, showed that a longer duration of breastfeeding was associated with lower plasma fibrinogen, plasminogen activator inhibitor 203 and von Willebrand factor, although the effects were small.
Cancer
Higher birth weight and taller adult height are associated with an increased risk of some cancers, 19 suggesting effects of nutrition in early life. This may reflect exposure to hormones promoting early growth. A recent meta-analysis suggested reduced rates of pre-menopausal breast cancer among women who were breastfed in infancy, but found no evidence of an effect on overall cancer incidence 204 or other specific adult cancers. There may be small reductions in some childhood cancers, including 205 acute lymphoblastic leukaemia, Hodgkins lymphoma, and neuroblastoma, but data are limited.
Allergic/atopic disease
The incidence of allergic disease in infancy and childhood (wheezy bronchitis, asthma and atopic dermatitis or eczema) has increased recently in many Western countries including the UK. Several studies have suggested a protective effect of breastfeeding, but systematic reviews show that the findings are inconsistent. Infants at high risk because of a family history of allergic disease do seem to 206 benefit from exclusive breastfeeding for three to four months. Soya-based formula does not protect against atopic disease, but there is some evidence that hydrolysed formulas are protective compared 206 with formula containing intact bovine protein.
Mental health
One of the proposed benefits of breastfeeding is increased bonding between mother and baby, and an increased sense of security that could promote psychosocial resilience and reduce mental illness. This is a remarkably poorly studied outcome. Fergusson found no evidence of better psychosocial adjustment 207 in adolescents who were breastfed, while another small study suggested lower anxiety levels in 208 response to parental separation in breastfed children.
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Other outcomes: bone health, coeliac disease, inflammatory bowel disease

Breastfed infants, consistent with their smaller size, have lower bone mineral content (BMC) than formula-fed infants. The calcium and phosphate content of formula has been shown to influence 209 BMC during infancy in randomised intervention studies. There are, however, no data on longterm outcomes such as adult bone density or fracture risk. A systematic review found consistent evidence from six case-control studies that longer duration of breastfeeding, and breastfeeding at the time of introduction of gluten containing foods, protected 210 against the later development of coeliac disease. There is inconclusive evidence of protection 194 against inflammatory bowel disease.
Other aspects of infant diet and long-term outcomes

There are very few studies relating long-term outcomes to other aspects of infant diet, for example effects of different formulas, the age at which solids were started, the type and quality of complementary feeds, and the use of micronutrient supplements. Lucas and Singhal have followed up children who took part in a series of randomised trials of 202, 211-213 different formula feeds as babies born pre-term or SGA. Among pre-terms those who received banked breast milk had the lowest blood pressures and 32-33 split proinsulin concentrations (an indicator of insulin resistance) at 13-16 years. Those fed enriched pre-term formula had the highest, and those fed standard formula had intermediate levels. Term SGA babies fed standard formula had lower diastolic blood pressures at six to eight years than those fed enriched formula. The macronutrient balance of the infant diet may be important. Higher protein intakes in late 193, 214 infancy have been associated with greater adiposity in childhood. Another study suggested that animal protein (especially dairy protein), but not vegetable protein, was linked to later 215 adiposity. The INCAP trial in Guatemala, randomised villages to receive one of two supplements for mothers and children: high-protein, high-energy drink (protein 6.4 g/100ml, energy 900 kcal/l) or a lower nutrient drink (energy 330 kcal/l, no protein). Both contained multiple micronutrients. People who received high-nutrient drink in utero (through their mother) and/or infancy (either through their mothers breast milk or by direct intake) had lower adult triglyceride concentrations 95 and higher HDL cholesterol concentrations. Evidence linking the early introduction of solid feeds to allergic disease (eczema, asthma, and 216 217, 218 others) and obesity in childhood is inconclusive.
The timing of introduction of solids and later health

It has been suggested that introducing certain foods too early or too late during infancy increases the risk of developing food allergies and atopy (eczema and wheezing). The evidence base is not strong. In the UK it is recommended that certain foods are never introduced before six months (see Appendix 4). Symptoms of food allergy and intolerance in infancy can be obvious (facial swelling, urticaria) or non-specific (coryza, wheezing, vomiting, diarrhoea, colic, blood in the stools). The commonest allergies are to cows milk protein, egg, soya, wheat, nuts and shellfish. Diagnosis is based on history, skin prick testing, the measurement of food-specific IgE antibodies, patch tests, and food 219, 220 challenge testing. The latter should be carried out using a blinded format, and placebo controls.
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There is little evidence that adding probiotics (live non-pathogenic bacteria that colonise the gut) or prebiotics (nondigestible food components such as oligosaccharides that stimulate the growth of 221, 222 non-pathogenic bacteria in the gut) to infant feeds reduces later food allergy/intolerance.
Infant growth and long-term outcomes

There is strong and consistent evidence that undernutrition in infancy is associated with permanent adverse effects on growth and development. In a recent analysis of young adults from five developing countries, stunting and/or underweight at the age of two years were associated with 19 reduced adult height, fewer years of attained schooling and lower adult income or assets. Among women, undernutrition in infancy was associated with lower birth weight in the next generation. These relationships remained after adjustment for childhood socio-economic status and parental education, suggesting that they were related to infant undernutrition, rather than simply a reflection of continuing disadvantage in later life. A literature review also found consistent evidence of impaired cognitive ability in children who had been undernourished (stunted or 19 wasted) in infancy.
Key message There is strong and consistent evidence that poor weight gain and growth during infancy are associated with permanent stunting and cognitive impairment, resulting in fewer years of attained education, and lower adult productivity and earning capacity.
The relationship of infant size and growth to later health outcomes in well-nourished populations is currently unclear and controversial. This is partly because of a paucity of data. Cohort studies old enough to hold data on both infant size and adult disease are few. In a recent systematic review relating size in infancy to the 12 diseases accounting for the highest burden of disease (ischaemic heart disease, stroke, depression, lung cancer, road traffic accidents, alcohol abuse, dementia, chronic obstructive lung disease, suicide, breast cancer and diabetes (split into type 1 and type 2)) 223 only 19 good quality studies, relating to 10 of the disease outcomes, were found. The highest number of studies for a single disease was seven for type 1 diabetes, a disease with its onset mainly in childhood. Three of these seven studies showed a positive association between infant weight or BMI and type 1 diabetes risk. This is consistent with the data described previously showing a lower risk of type 1 diabetes in children who were breastfed (see page 42). Several studies of cardiovascular risk factors in children have shown higher blood pressure in those 224, 225 who gained more weight during infancy. In non-randomised analyses of Lucass infant feeding trials, SGA babies who gained more weight between birth and nine months had higher diastolic 213 blood pressure in childhood and pre-term babies who gained more weight in the first two weeks 202, 212 had higher 32-33 split proinsulin concentrations and LDL/HDL ratios at 13-16 years. Greater weight gain in infancy is consistently associated with higher BMI, and in some but not all studies 19, 226-228 with greater adiposity, in later childhood and in adult life. These studies have led to the 229 Growth Acceleration Hypothesis, which suggests that rapid weight gain in infancy, as well as in later childhood, is a risk factor for later cardiovascular disease. In marked contrast to these data, retrospective studies of adult cohorts suggest benefits of infant weight gain. In the Hertfordshire cohort, men with a higher weight at one year had lower 47, 230, 231 cardiovascular disease mortality (see Figure 12) and were less likely to have impaired 232 glucose tolerance or type 2 diabetes. Men and women in Finland who developed CHD or type 2
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diabetes were significantly lighter, thinner and shorter than average in infancy. In the New Delhi 231, 234 birth cohort in India, lower weight at one year predicted an increased risk of IGT or type 2 diabetes. Figure 12: Cardiovascular disease mortality according to weight at one year in Hertfordshire men
231, 233
140 120 Standardised mortality ratio 100 80 60 40 20 0 -18 -19 -20 -21 -22 -23 -24 -25 -26 -27
Weight at 1 year (pounds) Source: Osmond C, Barker DJP, Winter PD et al (1993) Early growth and death from cardiovascular disease in women. British Medical Journal 307: 1519-24.
Two of these three adult cohort studies had data on weight and BMI gain in childhood and 233, 234 adolescence as well as in infancy. Men and women with CHD or diabetes were light and thin as infants but gained weight more rapidly than average in later childhood (see Figure 13a and b) suggesting that infant weight gain and childhood weight gain may have completely different effects on later disease risk. There was no evidence that increased height at any stage of childhood was associated with adverse outcomes in adult life. The reasons for the different findings in the adult and childrens studies are not known. One possibility is that the rapid infant weight gain seen in the Hertfordshire, Finland and Delhi babies reflected healthy weight gain in predominantly breastfed babies, whereas the rapid weight gain seen in recent studies of children reflected the effects of predominant formula feeding. Recent data suggest that breastfeeding attenuates the 235 effect of rapid infant growth on adiposity at the age of two years.
Key message While the long-term effects of rapid weight gain in infancy require further research, there is clear evidence that excessive weight gain in childhood and adolescence is associated with an increased risk of adult obesity, type 2 diabetes and cardiovascular disease.
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Figure 13a and 13b: Height and weight scores in infancy of individuals having CHD in later life
Height BMI Weight 0.3 Z-score 0.2
Boys
0.1 COHORT 0
-0.1
-0.2
-0.3 0 6 12 Age (months) 18 2 4 6 8 10
Age (years)
Height BMI Weight
0.3 Z-score 0.2
Girls
0.1 COHORT 0
-0.1
-0.2
-0.3 0 6 12 Age (months) 18 2 4 6 8 10
Age (years)
Mean standard deviation (SD) scores for height, weight and body mass index in infancy (up to two years) and from two to 11 years after birth among boys and girls who had CHD as adults. The dotted line at zero represents the average for the whole cohort. Source: Barker DJP, Osmond C, Forsen TJ et al (2005) Trajectories of growth among children who have coronary events as adults. New England Journal of Medicine 353: 1802-9.
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There is another paradox in the data from the older cohorts, which needs to be investigated. High BMI is a risk factor for cardiovascular disease and diabetes, but the relationships of infant weight gain to adult BMI and to adult disease are in opposite directions. The key to understanding this may be to obtain better information about body composition in infancy. The Delhi study showed that infant BMI gain was more strongly related to adult lean mass than to adult adiposity, while 19, 236 BMI gain in later childhood was strongly related to adult adiposity. Infant weight gain in 237 Hertfordshire was associated with taller adult height and bone mineral content, which would also be associated with greater lean mass.
Key message Several studies of cardiovascular risk factors in children have shown higher blood pressure in those who gained more weight during infancy. On the other hand, studies of adults have shown a lower risk of cardiovascular disease and type 2 diabetes in those who gained more weight during infancy. These apparently paradoxical findings need to be investigated further.
There remain many unanswered questions. Most people would agree that normal infant weight gain should be protected, but should it be actively promoted or should catch-up or rapid weight gain be actively prevented? Is the answer to this question the same in all populations? And how modifiable, in any case, is the weight gain of a healthy well-nourished and demanding infant? These are important questions, because infancy is an accessible stage of life when optimal nutrition could have lifelong benefits. In developing countries, paediatricians generally try to promote catch-up weight gain and linear growth in small babies. There is good evidence that this reduces infant mortality, improves growth and development and has lasting benefits on education 3, 125, 238 and work attainment. In more affluent countries such as the UK, getting infant nutrition right is likely to be an important element of efforts to prevent obesity and common causes of death and disability such as cardiovascular disease and diabetes.
Key message Getting infant nutrition right has lasting benefits for growth and development, and is important in the prevention of obesity and chronic disease in adult life.
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Conclusions
Infants have special nutritional requirements because of their rapid growth and development and vulnerability to infection. Optimal nutrition in infancy is essential for normal cognitive and physical development and may protect against obesity and chronic disease in adult life. Many parents need guidance to provide adequate nutrition for their children at this stage of life. Breast milk is the ideal food for babies in their first few months. Mothers need support in order to breastfeed successfully. There is consistent evidence of better childhood cognitive development, and a lower risk of several disease outcomes, including obesity and diabetes, in children and adults who were breastfed rather than formula-fed. It is not known whether these effects are causal or reflect the generally healthier lifestyles of the families whose mothers choose to breastfeed. The effects of the quality of complementary feeding on current and later health in countries such as the UK are largely unknown. There are wide variations in infant size, weight gain, linear growth and body composition. There is increasing evidence that these influence the risk of developing obesity, diabetes, cardiovascular disease and other health outcomes in later life. The optimal pattern(s) of infant weight gain in order to minimise the risk of obesity, cardiovascular disease and diabetes is however, not yet known. There is strong evidence that undernutrition (stunting or wasting) during infancy leads to impaired adult cognitive, physical and economic capacity, even if nutrition improves later in childhood.
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Chapter 4: Influences on maternal and infant nutrition and opportunities for intervention
Interventions in maternal and infant nutrition a global perspective
In May 2004, WHO published a report, Global strategy on diet, physical activity and health which stated that A life-course perspective is essential for the prevention and control of noncommunicable diseases. This approach starts with maternal health and prenatal nutrition, pregnancy outcomes, exclusive breastfeeding for six months, and child and adolescent health. It reaches children at schools, adults at worksites and other settings, and the elderly and encourages a healthy diet and regular physical activity from youth into old age. This was followed 240 by the WHO report Promoting optimal fetal development: report of a technical consultation. Its recommendations included initiatives to: prolong the interval between menarche and first pregnancy (> four years) improve maternal nutrition prior to conception (BMI and micronutrient status) optimise weight gain and nutrition during pregnancy reduce malaria, HIV and smoking promote breastfeeding develop strategies to avoid gross mismatch between the developmental environment and childhood nutritional environment. In March 2006, the World Bank produced a report entitled Repositioning nutrition as central to 124 development, which stated The emphasis of any programmes to combat poor nutrition should target pregnant women and children under two years of age. This formed part of the World Banks attempt to calculate the cost of a poor start to life. This was based on the savings gained from moving an infant from a low birth weight (<2500g) to a normal (>2500g) category, under the headings of: reduced infant mortality reduced neonatal care reduced costs of infant/child illness productivity gain from reduced stunting productivity gain from increased ability reduction in costs of chronic diseases intergenerational benefits. The total saving was $510 (US) for each low birth weight prevented. This is recognised to be an under-estimate and work is now ongoing to amend it to take into account newer perceptions. Additional factors that may increase the estimate include the fact that the risk of noncommunicable disease is graded across the normal birth weight range and is not just a consequence of birth weight below 2500g, and that disease risk is also associated with high birthweight. Chronic non-communicable diseases now start earlier in life in many populations and the effects can be passed across more than one generation. The discount model, which assesses the relative saving on later poor health by investing in preventative measures, may be too simple for calculating the real cost-benefit relation. Notwithstanding the need to obtain new estimates of the cost, influential economists agree that human development offers a very important time over 241 which to intervene to promote later health.
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Interventions designed to improve short-term outcomes

Many trials have tested the effect of nutritional supplementation in the mother (usually started in mid-late pregnancy) on birth weight. Few have assessed the effect of pre-conceptional supplementation on fetal growth but there are ongoing trials aimed at doing this. In an early trial in the Gambia, a high-energy biscuit for severely undernourished pregnant women increased birth weight by more than 130g, but most trials of energy and protein supplementation have shown 8 only small increases in birth weight (around 50g overall). The same is true of multiple
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micronutrient supplementation trials. Birth weight is a crude measure of fetal development, and may under-estimate effects on specific fetal tissues and organs. The Gambia high-energy biscuit trial, and a recent trial of multiple micronutrient supplementation in Indonesian mothers, reported 242 243 reduced infant mortality but opposing results were found in two earlier trials in Nepal. More measurements of functional outcomes such as growth and risk factors for later disease are required in such trials.
Developing country perspective

The BMA report Improving the health of the worlds poor (2007), highlights the persisting problems of poverty and undernutrition in many developing countries and its effects on maternal, fetal and infant health. Young women often have little control over family finances and food purchases, and come last in the family hierarchy in terms of access to food. Babies born to undernourished women are more likely to be born pre-term and/or be growth restricted. Sub-optimal breastfeeding practices and poor-quality complementary feeding frequently follow and set the infant on course to becoming a stunted child, with impaired physical development and cognitive ability. An especially adverse situation, in terms of adult health, comes from poor nutrition in early life followed by obesity in later life. This combination is increasingly common in developing countries and carries a high risk of adult 19 hypertension, diabetes and cardiovascular disease. Of the eight United Nations Millennium Development Goals, Numbers 1 (Eradicate extreme poverty and hunger), 4 (Reduce child mortality) and 5 (Improve maternal health) directly relate to the issues discussed in this report. In addition Number 2 (Achieve universal primary education), and 3 (promote gender equality and empower women) are related goals. While progress towards these is being made, it is likely that many of them will not be met by the target year of 2015.
Guidelines for improving the diets of young women in the UK

There have been consistent dietary messages to adults over many years to encourage consumption of fruit and vegetables, starchy foods and oily fish, and to limit consumption of dietary fat, salt and added sugar. The recommendations for a healthy diet were based on evidence of the role of diet 244, 245 in the aetiology of cardiovascular disease and some cancers, and recently specific advice on 246-248 oily fish consumption, salt and vitamin D intakes has been updated. Dietary guidelines are comparable across the developed world. Current UK advice is depicted in the Eatwell plate 249 model. While this advice may be widely understood, the most recent National Diet and Nutrition Survey (NDNS) shows that many adults do not comply with these dietary guidelines, and that the 2, 250, 251 diets of young adults may be a particular cause for concern (see Box 10).
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Box 10: The diets of young people: findings from the National diet and nutrition survey When compared with older adults, young men and women in the NDNS were more likely to consume fast foods, savoury snacks, and carbonated soft drinks, and less likely to eat wholemeal bread, whole grain cereals and oily fish. Although fruit and vegetable consumption was below the target of five daily servings for many adults, consumption was particularly low among young adults (1.3 and 1.6 servings per day in men and women aged 19 to 24 years respectively). In comparison with older age groups in the NDNS, younger men and women obtained the largest proportion of food energy from non-milk extrinsic sugars and had the lowest intakes of dietary fibre (non-starch polysaccharides), vitamin A, riboflavin, folate, vitamin D, iron, calcium, magnesium and zinc.
These findings show that poor quality diets are common among young people in the UK raising the possibility that, for many young women, current patterns of diet and nutritional status could impact on their ability to meet the nutrient needs of future pregnancies. There are currently few specific dietary recommendations for pregnancy (see Appendix 3). The most consistent dietary message to pregnant women in the UK is to increase folate intake before conception, and recent data show widespread awareness of the need for adequate folate status in 131 pregnancy. Among mothers studied in the Health survey for England in 2002 who had planned their pregnancy, more than half (55%) reported taking dietary supplements or changing their diet prior to pregnancy to increase folate intake. Of mothers who increased their folate intake before conception, 61 per cent reported that they had done so at least three months before becoming pregnant. Use of folic acid supplements was uneven, however, and was less common among women of lower social status. The value of recommendations for preconception supplementation 252 with folic acid may be limited due to the high rates of unplanned pregnancies in the UK.
Key message Poor quality diets are common among young people in the UK raising the possibility that, for many young women, current patterns of diet and nutritional status could impact on their ability to meet the nutrient needs of future pregnancies.
Apart from these specific recommendations for pregnancy, young women are encouraged to comply with general healthy eating advice before and during pregnancy. Given that so many young women do not follow current guidance, it is clear that it is not sufficient just to popularise dietary messages. To achieve change in dietary behaviours, the influences on food choice need to be considered and understood.
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Influences on food choices in women

A vast array of factors influence food choice. They include cultural, social and environmental factors, as well as knowledge and understanding of the role of food in health and disease. In a recent study of 6,125 women aged 20 to 34 years living in Southampton, compliance with current healthy 139 eating recommendations was described using a score for a prudent dietary pattern. Women with high scores had diets characterised by a high consumption of fruits, vegetables and wholemeal bread while women with low scores had diets characterised by a high consumption of white bread and chips, added sugar and full-fat dairy products. The most important influence on the prudent diet score was the educational attainment of the woman, such that lower scores were much more common among women with few educational qualifications (see Figure 14). This influence was far more important than any other factor considered, including the womans social class, the deprivation score of her neighbourhood, or whether she was in receipt of financial benefits. Figure 14: Percentage of women with prudent diet scores in lowest quarter of distribution, according to their educational attainment: 6,125 women in the Southampton Womens Survey
60 Proportion with low prudent diet score (%)
50
40
30
20
10
0 none CSE O-level A-level HND degree
Source: Robinson S, Crozier SR, Borland SE et al (2004) Impact of educational attainment on the quality of young womens diets. European Journal of Clinical Nutrition 58: 1174-80.
Although cost is a recognised barrier to eating healthily the less prudent diets observed in this study did not seem to be simply a result of lower income. The relationship between income and diet is complex. The low income diet and nutrition survey (LIDNS) published in 2007 yielded a positive view of the diets of people living on low incomes in the UK, since in comparison with the general population, the types and quantities of many foods 254 eaten and patterns of nutrient intake were similar. Consumption of fruit and vegetables by lowincome participants however, was lower, and consumption of soft drinks, processed meats, whole milk and sugar was greater. Food security was also assessed in this study; 39 per cent of the lowincome population reported that they had been worried that their food would run out before they got money to buy more in the past year and 36 per cent said that they could not afford to eat
253
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balanced meals. Although the diets of children in food insecure households were comparable with those of children in food secure households, this was not the case for women. Women in food insecure households had typically less healthy diets, with lower consumption of fruit, wholemeal 255 bread, meat and meat dishes and fish and fish dishes. Drewnowski and Specter describe an inverse relationship between the energy density of foods and energy cost so that high-fat energy-dense diets may be more affordable than prudent diets based on lean meats, fish and fresh fruit and vegetables. This may partly explain the link between food insecurity and greater levels of 256 obesity observed in some studies, particularly among women.
Key message Educational attainment is a key influence on the quality of young womens diets.
While a number of studies have examined the associations between diet and socio-demographic factors, there are important environmental and contextual influences on food choice that are less commonly considered. These include: the effects of the physical environment, such as the distance between home and shops that may determine the accessibility and affordability of foods, and the ability to store and cook food at home the nature of the contexts within which food is bought and eaten that may impact directly on purchasing patterns and foods consumed structural differences in families and households that define the nature of shared meals the wider influences of food advertising and the promotion of foods. Increases in fruit and vegetable consumption have been observed following the building of new 257 superstores in areas of poor retail provision, and purchasing patterns of confectionery can be 258 changed by altering its location in a cafeteria. Interventions to change aspects of the food environment, so that consumers are encouraged to choose healthier foods, may offer important opportunities to achieve change in eating habits. The choice of foods eaten is influenced by individual factors. Some of these have been extensively researched with a view to predicting and understanding food choices. They include variations in personal taste preferences, differences in knowledge, attitudes and beliefs as well as psychological factors such as matters of control and self-esteem. There are complex interactions between socio-demographic, environmental and individual influences that act to determine food choice and these influences must also underlie the reasons why current dietary recommendations are not met. To address the dietary and nutritional inequalities that exist across the general population we need to identify the primary influences on food choice. With this understanding, effective interventions can be defined to achieve dietary change.
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Interventions to improve maternal nutrition

Box 11: Comment on nutritional intervention in women living in poverty In the UK the health and wellbeing of millions of women are influenced by living in poverty. Food choices, dietary intake and feeding behaviour are far from optimal among poorer women, and this situation is reflected in higher rates of diet-related morbidity and mortality well beyond maternal and child health considerations. Interventions to change diet need to take account of the factors that influence household economic status and should be integrated at policy, community and individual level. There is a dearth of research on effective interventions in this subgroup of the population from within the UK, although there are some encouraging United States (US) examples to draw on in terms of possible intervention approaches. Lack of evidence does not mean that policy work should be delayed. It is recognised that engaging with hard to reach groups of women is a challenge for intervention implementation and evaluation, and it is essential that policy work should be evaluated for its ability to engage with target groups as well as 259 for behavioural change and health outcomes. Professor Annie Anderson, Professor of Food Chioce University of Dundee (2007)
A systematic review of interventions that aimed to improve diet in women who were pregnant or of childbearing age suggested that interventions that included elements of education or 260 counselling, support and empowerment can improve nutrition knowledge and behaviour. Much of the existing evidence on interventions to improve maternal nutrition comes from evaluation of the federally funded US health programmes. These include the US Special Supplemental Nutrition Programme for Women, Infants and Children (WIC) and the Expanded Food and Nutrition Education Programme (EFNEP) both of which focus on people from disadvantaged backgrounds. Evaluation suggests that the WIC programme which combines food supplementation, nutrition counselling and referral to health and social services, can lead to improvement in maternal diet 261 during pregnancy, increased maternal weight gain and increased breastfeeding rates. 262 WIC programmes have also been effective at increasing fruit and vegetable consumption. EFNEP, which aims to give low-income families food knowledge and skills and to bring about dietary behaviour change through practical sessions delivered by peers, has been shown to 263 improve food practices among recipients. Evaluation of smaller-scale intervention programmes within the UK has also suggested that imparting food knowledge and skills to women from disadvantaged backgrounds has the potential to improve diet in this group. The Cookwell project, set in eight urban communities in Scotland aims to improve diet in areas of social deprivation by delivering food skills sessions each week over a seven-week period: in a study of 113 adults living in areas of social deprivation, 88 per cent of whom were women, the intervention led to early increases in fruit consumption and at six months follow-up there was a significant increase in the proportion of subjects who reported confidence in following recipes and cooking from basic 264 ingredients.
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Key messages US programmes which combine food supplementation, nutrition counselling, cookery skills and referral to health and social services, can lead to an improvement in maternal diet during pregnancy and to increased breastfeeding rates.
Two recent systematic reviews have considered the effectiveness of interventions which aim to increase fruit and vegetable consumption in adults and the findings of both have relevance for women of childbearing age. The first focused on community interventions that were effective in 265 increasing fruit and vegetable consumption in people aged four years and over. Fifteen studies, all of which were based in the USA, were included in the review. Four trials were specifically targeted at parents with young children. The most effective interventions gave clear messages about the benefits of fruit and vegetables, were intensive and used multiple strategies delivered over a prolonged period of time, and involved families as a group in the intervention. The second, and more recent, systematic review collated evidence from the published and grey literature 266 relating to programmes that promote fruit and vegetable consumption in adults. Forty-four studies were reviewed, with over 70 per cent set in the USA and around 16 per cent in Europe. Consistent positive effects were seen in studies involving face-to-face education or counselling. A more recent US intervention study of 269 adults from low-income backgrounds evaluated the impact of the Sisters in health nutrition education programme which aimed to increase fruit and 267 vegetable consumption among low-income groups. The intervention, which involved peer-led small group sessions to teach cooking skills and provide social support, led to significant improvements in fruit and vegetable intake at the end of the intervention programme.
Key message There is limited evidence of interventions that are effective in improving maternal nutrition. There is, however, some evidence that interventions that include elements of education or counselling can bring about improvements in nutrition knowledge and behaviour.
Improving breastfeeding initiation and increasing duration of breastfeeding

Women surveyed in the most recent IFS were asked about their experience of breastfeeding; 73 per cent of the women who initiated breastfeeding, but who gave up in the survey period, said 131 that they would have preferred to have continued to breastfeed for longer. The most common reason given for stopping breastfeeding was insufficient milk. Stopping breastfeeding within two weeks of birth was associated with rejection of the breast, or painful breasts; in later months, returning to work or college was also associated with stopping breastfeeding. Interventions that educate women about the benefits and practice of breastfeeding are effective at increasing breastfeeding initiation. A recent Cochrane systematic review of seven randomised controlled trials (RCTs) of 1,388 women demonstrated that interventions based on one-to-one 268 health education and support are effective at increasing initiation rates. Overall, the relative likelihood of breastfeeding initiation was 1.59 (95% CI 1.25 to 1.88) in the group who received educational interventions compared with those who received routine care. A further systematic review based on non-randomised controlled trials as well as RCTs has suggested that peer support
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may be effective in improving breastfeeding initiation rates in women from disadvantaged 261 backgrounds. One community-based controlled trial, considered in the review, was carried out over a two-year period in two socially deprived communities in Glasgow, Scotland. One of the communities received peer counselling from trained lay breastfeeding counsellors who were resident within the community. A second trial set in Chicago, USA evaluated the effectiveness of a hospital-based breastfeeding peer counsellor programme delivered to women who expressed an interest in breastfeeding. Both studies demonstrated improved initiation rates in women who had expressed an interest in breastfeeding, suggesting that peer-counselling programmes can be effective at encouraging women who would like to breastfeed to follow through with their decision. There is also good evidence that appropriate support for breastfeeding mothers can prolong the duration of breastfeeding. A Cochrane systematic review updated in November 2006, based on 34 trials of 29,385 mother-infant pairs, showed that all forms of extra support together were associated with an increase in duration of any (includes partial and exclusive) breastfeeding the 269 relative likelihood of stopping breastfeeding before six months was 0.91 (95% CI 0.86 to 0.96). Additional professional support (over and above standard care) was effective in prolonging any breastfeeding but its effect on exclusive breastfeeding was unclear. Additional support from trained lay people was effective in prolonging exclusive breastfeeding while its effect on duration of any breastfeeding was unclear. Exclusive breastfeeding was significantly prolonged with use of WHO/United Nations Childrens Fund (UNICEF) Baby Friendly Hospital Initiative training for professionals. Overall, the relative likelihood of stopping exclusive breastfeeding during the study period considered was 0.69 (95% CI 0.52 to 0.91) in the six RCTs using the WHO/UNICEF training.
Key message Interventions that educate women about the benefits and practice of breastfeeding are effective at increasing breastfeeding initiation. Appropriate support for breastfeeding mothers can prolong the duration of breastfeeding.
The WHO/UNICEF Baby Friendly Hospital Initiative

The Baby Friendly Hospital Initiative is a worldwide programme of the WHO and UNICEF. It was launched in 1992 to encourage maternity hospitals to implement the Ten steps to successful breastfeeding (see Box 12) and to practise in accordance with the International Code of Marketing of Breast Milk Substitutes (Appendix 5). Hospitals are encouraged to introduce a breastfeeding policy, educate staff to implement the policy according to role and introduce practices which promote, protect and support breastfeeding. External assessment can then lead to accreditation for those facilities implementing the standards effectively. In the UK, the Initiative has been expanded to include community healthcare facilities. Accreditation of universities which introduce approved education for breastfeeding into their preregistration courses for midwives and health visitors has also been introduced.
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Key message Baby Friendly accredited programmes worldwide encourage hospitals and community healthcare facilities to promote breastfeeding and provide the training for healthcare practitioners. They have been shown to prolong exclusive breastfeeding. NICE guidance recommends that the WHO/UNICEF Baby Friendly Hospital Initiative should be implemented as routine practice.
Data from the Millennium Cohort Study of 18,819 children born in the year 2000 found that mothers delivering in Baby Friendly accredited hospitals are 10 per cent more likely to initiate breastfeeding (after adjustment for confounding variables) than those who deliver in nonaccredited units. The study found that Baby Friendly hospital accreditation is not associated with 270 an increase in breastfeeding at one month of age. Data on all babies (n=464,246) born between 1995 and 2002 in Scottish maternity units with more than 50 births per year show that babies born in Baby Friendly hospitals are 28 per cent more likely to be exclusively breastfed at seven days postnatal age than babies born in other hospitals. Breastfeeding rates increased faster in the Baby Friendly hospitals: an 11.39 per cent 271 (95% 10.35 to 12.43) rise compared with 7.97 per cent (95% 7.21to 8.73) in other units. A cluster randomised controlled trial among 17,046 mother-infant pairs in Belarus found that implementing the Baby Friendly Hospital Initiative significantly increased the duration and exclusivity of breastfeeding and decreased the risk of gastro-intestinal tract infection and of atopic eczema in the first year of life. Infants from Baby Friendly hospitals were significantly more likely than control infants to be breastfed to any degree at 12 months (19.7% vs 11.4%; adjusted OR 0.47; 95% CI 0.32, 0.69), were more likely to be exclusively breastfed at three months (43.3% vs 6.4%; P<.001) and at six months (7.9% vs 0.6%; P =.01), and had a significant reduction in the risk of one or more gastro-intestinal tract infections (OR, 0.60; 95% CI, 0.40 to 0.91) and of atopic eczema (OR, 0.54; 272 95% CI, 0.31 to 0.95).
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Box 12: Ten steps to successful breastfeeding 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Have a written breastfeeding policy that is routinely communicated to all healthcare staff Train all health care staff in the skills necessary to implement this policy Inform all pregnant women about the benefits and management of breastfeeding Help mothers initiate breastfeeding soon after birth Show mothers how to breastfeed and how to maintain lactation if they are separated from their infants Give newborn infants no food or drink other than breast milk unless medically indicated Practice rooming-in and allow mothers and infants to stay together 24 hours a day Encourage breastfeeding on demand Give no artificial teats or pacifiers (also called dummies or soothers) to breastfeeding infants Foster the establishment of breastfeeding support groups and refer others to them on discharge from the hospital or clinic.
Source: www.babyfriendly.org.uk
Doctors role in supporting breastfeeding

In common with all other health professional groups in the UK, doctors require education to enable them to implement the WHO/UNICEF standards effectively. Paediatricians and obstetricians require an understanding of the role of breastfeeding in improving the health of mothers and babies. Paediatricians also require an understanding of the normal neonatal adaptation to intermittent feeding after delivery, how poor practice can lead to excessive weight loss in breastfed babies and how this can be avoided, and how to protect safety and breastfeeding when caring for babies who are reluctant to feed after delivery or who are jaundiced or at risk of hypoglycaemia. It is recognised that in the UK hospital doctors are not the primary caregivers for breastfeeding and therefore it is not considered necessary for their education to include clinical skills in supporting breastfeeding. The requirement to educate general practitioners (GPs) to implement the breastfeeding policy has been a source of confusion ever since the initiative was launched. GPs in the UK have a limited role in supporting breastfeeding. Their role requires them to have a basic understanding of how breastfeeding works, a knowledge of how to treat common breast conditions (mastitis, thrush etc), access a reliable reference source for prescribing drugs for breastfeeding mothers and refer mothers to the most appropriate professional for breastfeeding help and support (particularly when a baby is failing to thrive).
Key message GPs can have a significant effect on whether or not mothers give up breastfeeding when experiencing health problems. Baby Friendly programmes show GPs how they can support the continuation of breastfeeding in such circumstances.
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Teaching packs for Paediatricians and GPs are available from the UNICEF UK Baby Friendly Initiative www.babyfriendly.org.uk
NICE Guidance on Breastfeeding

Recent guidance from the NICE gives evidence-based recommendations relating to the promotion 177 of breastfeeding initiation and duration. The guidance was formulated through the integration of published scientific literature with practitioner expertise and experience obtained during a national consultation exercise with professionals working in areas that could have an impact on maternal and child nutrition. These included hospitals, primary care trusts and social services. The consultation exercise focused on areas of deprivation. The guidance recommends that the WHO/UNICEF UK Baby Friendly Initiative should be implemented as routine practice. An appropriate range of educational and support programmes should be routinely delivered by health professionals and peer supporters. These include antenatal breastfeeding education combined with peer support programmes to increase breastfeeding initiation and duration among women from disadvantaged backgrounds. Other recommendations include avoidance of routine hospital practices that might lead to separation of mother and infant since these have been shown to be harmful to breastfeeding rates. The guidance also states the importance of encouraging mothers to breastfeed on demand in order to encourage breast milk production and prevent breast engorgement and mastitis. Early skin-to-skin contact has also been shown to be effective in increasing the initiation and duration of breastfeeding. A Cochrane review updated in 2007, 273 considered the findings of 30 studies of 1,925 mother-infant pairs. Early skin-to-skin contact had positive effects on breastfeeding initiation (odds ratio of initiation was 1.82, 95% CI 1.08 to 3.07) and breastfeeding duration (weighted mean difference in duration was 42.55 days, 95% CI 1.69 to 86.79).
Support for breastfeeding mothers returning to work

In the UK the proportion of women in employment has increased considerably in recent years and about 50 per cent of women with pre-school children are in paid work outside the home. Working mothers often return to work early after having a baby and can have difficulty maintaining breastfeeding if not supported by their employers. This may discourage working mothers from breastfeeding at all. Recent findings from the Millennium cohort study demonstrated that women who were employed full-time were less likely to initiate breastfeeding than mothers who were not 274 employed rate ratio was 0.92 (95% CI 0.89 to 0.96) after adjustment for confounding factors. Strategies to support working mothers to continue with breastfeeding are needed. A recent Cochrane review to identify workplace interventions to promote breastfeeding, found no published 275 RCTs of relevance. This represents an important gap in the evidence given the rapid increase in maternal employment in recent years.
Key message Strategies are needed to support working mothers to continue with breastfeeding.
Interventions that educate women about the benefits and practice of breastfeeding and that promote baby friendly policy and practice are effective at promoting the initiation and prolonging the duration of breastfeeding. There are still some important gaps in the evidence, however, and studies are needed to look for effective ways of supporting breastfeeding in the workplace.
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Interventions in complementary feeding

There is little evidence relating to interventions that aim to influence the timing and nutritional content of complementary feeding in developed country settings. One study of WIC participants suggested that peer-delivered educational interventions can be effective in reducing inappropriate 276 early introduction of solid foods. The study was based on 181 adolescent mothers who were shown a videotape made by a peer-group of black adolescent mothers which challenged the barriers to following infant feeding guidance. The intervention was delivered as part of a homevisiting programme and assessed in a RCT. Mothers who were part of the intervention group were significantly more likely to introduce their babies to solid foods later and were more likely to report accurate knowledge of the optimal timing for the introduction of complementary food. A recent RCT set in Germany assessed the effect on infant diet of dietary counselling derived from food277 based guidelines for infant nutrition. The study found that more intensive telephone counselling was more effective than less intensive counselling or written information alone in improving adherence to infant feeding guidance (assessed by food-based and meal-based dietary scores). The authors suggested that face-to-face counselling may have even greater positive effects on infant feeding practices. In developing countries where tackling infant undernutrition is the primary focus of intervention, there is evidence that educational interventions, combined with food support in 123 countries that are food insecure are effective in improving infant nutrient intake and growth.
Mechanisms to address nutritional inequalities in the UK

Inequalities in the nutrition of young women and their children in the UK (see Box 13) can have long-term health consequences. Although evidence of successful interventions to address these inequalities may be limited, we already have a sufficiently clear understanding of the effects of early disadvantage to make the nutritional needs of mothers and their children a priority.
Box 13: Inequalities in maternal and infant nutrition Women of lower educational attainment are more likely to have diets of poor quality than 139 other women. Consumption of fruit and vegetables is lower in low income groups in the UK while 254 consumption of soft drinks, processed meats, whole milk and sugar is higher. Many people with low incomes in the UK are food insecure, and food insecurity in women 254 is associated with poorer diets. 131 Breastfeeding rates are lower in mothers from disadvantaged backgrounds. Early introduction of solids is more common in young mothers and mothers of lower 131 socio-economic status. Compliance with infant feeding guidance to provide a diet based on fruits, vegetables and 138 home-prepared foods is strongly associated with the quality of the mothers own diet.
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NICE guidance
National policy will influence the nutrition of women of childbearing age and their children. Recent public health programme guidance from NICE on maternal and child nutrition endorses existing 278 policy on nutritional recommendations for pregnant and pre-pregnant women and for infants. The guidance strongly reinforces and builds on the previous evidence-based guidance from NICE 177 on the promotion of breastfeeding, and recommends that all staff involved in the care of pregnant or breastfeeding women have the appropriate knowledge and skills to support and advise women about breastfeeding. Recent cross-government policy to tackle obesity also highlights the importance of breastfeeding and improved childhood nutrition in the prevention 279 of obesity.
Healthy Start schemes

National programmes introduced within the UK to address inequalities in the health of young women and children may have an important impact on nutrition. The Healthy Start scheme was introduced in 2005, following a review of the Welfare Foods Scheme in 2000 by the Committee on Medical Aspects of Food and Nutrition (COMA). The review recommended that pregnant women should be given vouchers for a wider range of foods, and identified the need for health professionals to give general dietary advice during pregnancy, emphasising the importance of breastfeeding. The aim of Healthy Start is to reduce inequalities in nutrition for women and children. The scheme provides food support, professional advice and support to pregnant women and mothers of young babies and children from disadvantaged backgrounds. Like the Welfare Foods Scheme before it, food support comes in the form of vouchers to buy milk and infant formula and provision of vitamin supplements. As recommended by COMA, however, there is greater flexibility within the Healthy Start scheme allowing the vouchers to be used to buy fruit and vegetables. Early evaluation of the scheme in Devon and Cornwall suggested that women who were recipients of Healthy Start were buying more fruit and vegetables than they were before 280 the scheme began. Further follow-up will be needed to confirm whether these beneficial effects on fruit and vegetable uptake are observed on a wider scale and maintained in the longer term. The evaluation did not examine overall uptake of the scheme nor were any nutritional outcomes measured. A survey of health professionals was also carried out: interviews with a small sample of health visitors and midwives suggested that most professionals interviewed were aware of the scheme and how to apply it. Knowledge about some elements of the scheme remained low, however, and the authors of the evaluation concluded that coverage of training to prepare for Healthy Start had been somewhat patchy. Evaluation at national level is needed to assess uptake of the scheme and to examine its impact on the nutrition of women and young children. Other public health programmes that are directed at families with young children including Sure Start Childrens Centres, also have the potential to bring about improvements in maternal nutrition and infant feeding practices. Although national policy may influence maternal and child nutrition, the central importance of the family should also be recognised. A womans diet before and during pregnancy, and her views on breastfeeding and weaning will be influenced by her partner, friends and family. Clear and consistent guidance for families on the benefits of healthy eating is needed, particularly to explain the long-term consequences for their children of early diet and nutrition. In the future it needs to be ensured that all professionals who care for pregnant women and their families have appropriate knowledge and skills to provide this guidance.
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Tackling the problem of obesity

The DH has set targets to address obesity. The public service agreement (PSA), established in 2007 has the aim by 2020 we will have reduced the proportion of overweight and obese children to 14 2000 levels. The Government Office for Science through the Foresight programme has developed 18 a strategic approach to address the problem. In terms of chronic disease prevention, it appears that addressing infant nutrition could impact on these relatively short-term targets, and it would be very important in influencing the incidence of chronic disease in the longer term. Some research shows that weight gain even in the first few 226, 227, 281 weeks of life is related to childhood obesity. The BMA policy report Preventing childhood obesity (2005) raises concerns at the rising levels of 282 childhood obesity and poor nutritional quality of diets of children and adolescents. The report discusses those factors contributing to the rise in obesity and highlights the responsibilities of individuals in addressing obesity, and of policy makers to provide an environment which is less obesogenic. The importance of infant feeding is noted and the protective effect of breastfeeding on childhood obesity is discussed. A primary theme of this work focuses on enabling parents and carers, as well as children, to make healthy choices through effective education and information provision which is consistent and free from adverse influences which encourage unhealthy food choices. Recent follow up work to this report has concentrated on: improving school food and food education in school lobbying for restrictions on the advertising of foods high in fat, salt and sugar to children supporting and encouraging adoption of traffic light front-of-pack signposting. The Foresight project Tackling obesities: future choices was announced in 2005. The BMA was a key stakeholder and had an input particularly focused on systems mapping and scenario building. 283 The outcomes report was published in October 2007 and examines the scientific evidence base from across a wide range of disciplines in order to understand the relationships and importance of key factors influencing obesity. Using this evidence it aims to identify effective interventions, predict how obesity might change in the future and identify the most effective responses. As well as the final report, this project produced a series of reviews of the current science and models for future trends of obesity and policy options and the impacts on health. The Foresight report argued for a life-course approach to prevention and emphasised that society would have to be prepared to measure success over longer timeframes than currently. A specific recommendation was the promotion and implementation of a programme of early interventions at birth or in infancy.
Key message Improving infant nutrition could be very important in influencing the incidence of chronic disease in the longer term.
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Box 14: Governments obesity strategy In January 2008, the Cross-Government Obesity Unit published its strategy for England, to address the rising prevalence of obesity. This strategy recognises the importance of promoting childrens health and wellbeing. It encompasses a range of recommendations that include promotion of breastfeeding, further investment in the Healthy Schools Programme, and the promotion of a culture of healthy eating. Through the development of a Healthy Food Code of Good Practice, the Government aims to work with industry and other stakeholders to develop a single approach to food labelling, to rebalance the advertising and marketing of foods that are high in fat, salt or sugar to children, and to promote the consumption of healthy foods, particularly fruit and vegetables. As part of the Code, all food businesses will work with the Foods Standards Agency (FSA), DH and other stakeholders to deliver a single set of key healthy eating messages.
In November 2007, the BMA hosted a stakeholder event on food labelling. Invited representatives from health-related organisations and the food industry came together to discuss ways in which healthy eating messages can be reinforced through advice about nutrition and food labelling. The group agreed a position statement, which is available on the BMA website, (see Box 15).
Box 15: A BMA food labelling statement January 2008 The British Medical Association (BMA) has a long-term interest in the health of the public and believes that the increase in the frequency of obesity is a cause for great concern. While tackling obesity requires commitment to a multi-faceted approach, there is a particular need to change dietary behaviour. The BMA considers improved and consistent food labelling to be an important mechanism for enabling consumers to make informed dietary choices. The BMA believes that the food and drink industry should implement a standardised, consistent approach to food labelling. This approach should be based upon the traffic light front of pack labelling recommended by the FSA. In order to increase the nutritional information available to consumers we propose that the labelling should also include Guideline Daily Amount (GDA) information. The BMA also recognises that public awareness should be raised about the health benefits of micronutrients. This could be done in the form of in-store leaflets explaining the benefits of healthy food choices and stating which foods are rich in which micronutrients.
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Conclusions
Many young women have diets of poor quality and inadequate nutritional status. Less healthy diets are more common among women of low educational attainment, and among women who have low income and who are food insecure. Although evidence of effective interventions to improve the diets of young women is limited, this does not mean that the goal should not be pursued vigorously. Both nutrition education and counselling have been shown to improve womens nutrition knowledge and behaviour. Breastfeeding rates are low in the UK, and it is less common among disadvantaged women. Interventions that educate women about the benefits and practice of breastfeeding, and that promote baby friendly policies and practice, are effective at promoting the initiation and prolonging the duration of breastfeeding. Current studies of complementary feeding show wide variations in practice in the UK. There are few studies of interventions to influence the timing and nutritional content of complementary feeding in developed countries. Infant diet is strongly linked to mothers diet suggesting that interventions to improve the diets of young women will also have direct consequences for childrens diets. Effective interventions are needed to improve the nutrition of young women of childbearing age. Such interventions may influence the way in which mothers feed their children as well as influencing the diets of women themselves. They will therefore have beneficial health effects across generations. Efforts to encourage the initiation and to prolong the duration of breastfeeding need to continue and be extended. The ten steps to successful breastfeeding and the Baby Friendly Hospital Initiative guidelines should become a minimum standard of care. Action is also needed to improve the opportunities for women to breastfeed in public places and to support continued breastfeeding in women who return to work. The Healthy Start scheme provides support for eligible women and children through provision of food vouchers and vitamin supplements, and needs to be promoted widely. Its impact on the nutrition of mothers and young children should be evaluated at a national level. Other gaps in the evidence should be addressed including interventions to support breastfeeding mothers in the workplace and interventions to optimise the timing and content of complementary feeding.
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Appendix 1: Epigenetic processes
In addition to the sequence of nucleotide bases which comprise the genetic code, and which are inherited from the parents (the genotype) the characteristics of an individual (their phenotype) are affected by epigenetic processes, which alter the ways in which genes are switched on and off. Epigenetic processes do not affect the DNA sequence, but do alter gene expression. Epigenetic changes occur during development and can be affected by the environment before and after birth. Figure 15: Components of the epigenetic code
Me
The two main compoments of the epigenetic code
Me
Me
DNA methylation Methyl marks added to certain DNA bases repress gene activity.
Me
Histone tails
Histone modification A combination of different molecules can attach to the tails of proteins called histones. These alter the activity of the DNA wrapped around them.
Histones
Chromosomes
Diagram of chromosome being unravelled to show deoxyribonucleic acid (DNA) wrapped around histone protein cores to form nucleosomes. Protruding histone tails are subject to a range of chemical modification which can alter structure and make genomic DNA more accessible to transcription. CG base pairs of the DNA can also be modified by methylation, which silences transcription. Thus these processes can affect gene expression, and hence development and phenotypic characteristics, without altering the genomic DNA code itself. Source: Qui J (2006) Epigenetics: unfinished symphony. Nature 441: 143-5.
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Epigenetic inheritance is defined as biological processes that regulate mitotically or meiotically 284 heritable changes in gene expression without altering the DNA sequence. Of particular relevance is methylation of specific CpG dinucleotides in gene promoters and alterations in DNA packaging in nucleosomes arising from chemical modifications of the chromatin histone core around which DNA wraps. The histone modifications include acetylation, methylation, ubiquitination, and phosphorylation. Other changes may involve other DNA associated proteins. Recently microRNAs which affect DNA transcription and mRNA stability and translation into proteins have been 285 implicated as a further mechanism for inherited epigenetic effects, including those transmitted via the paternal line. Epigenetic mechanisms are widely implicated in cancer. In this situation the changes can be 287 modified by alteration of methyl group metabolism. This suggests a mechanism by which folate 288 and methyl donor status during development may operate. Gene promoter methylation is 289 290, 291 important for asymmetrical silencing of imprinted genes and retrotransposons. They also play a critical role in a range of developmental processes. With the exception of imprinted genes, widespread removal of epigenetic marks occurs following fertilisation when maternal and paternal genomes undergo extensive demethylation to ensure pluripotency of the developing embryonic 292, 293 cells. This is followed by de novo methylation just prior to implantation. About 70 per cent of CpGs are methylated, mainly in repressive heterochromatin regions and in repetitive sequences 294 such as retrotransposable elements. DNA methylation also plays a key role in cell differentiation by silencing the expression of specific genes during the development and differentiation of individual tissues. For some genes there also appear to be gradations of promoter demethylation associated with developmental changes in the role of the gene product. Changes in methylation which are associated with cell differentiation and functional changes are established at different times during development of the embryo. The pattern of DNA methylation is copied during mitosis by DNA methyltransferase (Dnmt) -1 activity. This provides an epigenetic memory of patterns of gene regulation and hence cell function, which are established during development and which are 292 passed to the adult. Environmental challenges at different times during development may induce stable changes in cell function, which persist in the adult organism. They may produce different phenotypic outcomes and in humans differential risk of disease.
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Appendix 2: Definition of overweight
World Health Organisation classifications of BMI

BMI values are age-independent and the same for both sexes. It may not, however, correspond to the same degree of fatness in different populations due, in part, to different body proportions. The health risks associated with increasing BMI are continuous and the interpretation of BMI gradings in relation to risk may differ for different populations.
Classification
BMI (kg/m2) Principal cut-off points Additional cut-off points <18.50 <16.00 16.00 - 16.99 17.00 - 18.49 18.50 - 24.99 25.00 25.00 - 29.99 30.00 30.00 - 34-99 35.00 - 39.99 40.00 <18.50 <16.00 16.00 - 16.99 17.00 - 18.49 18.50 23.00 25.00 25.00 27.50 30.00 30.00 32.50 35.00 37.50 40.00 22.99 24.99 27.49 29.99 32.49 34.99 37.49 39.99
Underweight Severe thinness Moderate thinness Mild thinness Normal range Overweight Pre-obese Obese Obese class I Obese class II Obese class III
Source: World Health Organisation. Global Database on Body Mass Index: an interactive surveillance tool for monitoring nutrition transition. www.who.int/bmi
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Appendix 3: Current UK dietary recommendations for pregnancy

Before pregnancy
A healthy diet is important at any time but particularly when planning a pregnancy. The Eatwell 249 plate makes healthy eating easier. Try to eat: plenty of fruit and vegetables aim for at least five portions a day plenty of starchy foods some milk and dairy foods some meat, fish, eggs and other non-dairy sources of protein just a small amount of foods and drinks high in fat and/or sugar. A 400 g folic acid supplement should be taken daily from the time contraception is stopped until the 12th week of pregnancy. Women who have previously had a baby with neural tube defects, or who are taking medication for diabetes, epilepsy or coeliac disease should take a 5mg supplement. DH guidelines on the consumption of alcohol state that women trying to conceive should avoid drinking alcohol, but if they do choose to drink, to minimise the risk to the baby, they should not drink more than one to two units of alcohol once or twice a week and should not get drunk.
During pregnancy
A healthy diet is important in pregnancy. There is no need to eat for two its the quality not the quantity of the diet thats important. Try to eat a variety of foods including: plenty of fruit and vegetables aim for at least five portions a day plenty of starchy foods plenty of iron-rich foods such as red meat, pulses, bread, green vegetables, and foods rich in vitamin C that will help the iron to be absorbed milk and dairy foods these contain calcium foods rich in protein such as lean meat, chicken and fish (aim for at least two portions of fish each week including one of oily fish), eggs and pulses fibre-rich foods such as wholegrain bread and cereals. Cut down on foods and drinks high in fat and/or sugar such as cakes and biscuits. A 400 g folic acid supplement should be taken daily until the 12th week of pregnancy. Women who have previously had a baby with neural tube defects, or who are taking medication for diabetes, epilepsy or coeliac disease should take a 5mg supplement. A 10 g vitamin D supplement should be taken throughout pregnancy. Do not take dietary supplements that contain vitamin A such as fish liver oils, and avoid liver and liver-containing products. Caffeine-containing drinks should be consumed in moderation to limit caffeine intake to less than 200mg a day (equivalent to two mugs of instant coffee, two mugs of tea or five cans of cola). Avoid pat, certain cheeses and raw or partially cooked eggs, shellfish and meats, and unpasteurised milk. DH guidelines on the consumption of alcohol state that pregnant women should avoid drinking alcohol but if they do choose to drink, to minimise the risk to the baby they should not drink more than one to two units of alcohol once or twice a week and should not get drunk. The BMA believe that the only sensible message for women who are pregnant must be complete abstinence from alcohol.
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www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_074920 www.eatwell.gov.uk/agesandstages/pregnancy/?lang=en http://units.nhs.uk/pregnancy.html
Vegetarianism and veganism

It is possible for vegetarians and vegans (people who eat no animal products at all, including dairy products) to be adequately nourished for successful pregnancy and lactation, but they need to be knowledgeable about nutrition and plan their diet carefully. For vegans, there is a high risk of deficient intakes of micronutrients such as vitamin B12, iodine, calcium, vitamin D and omega-3 fatty acids. There are reports of neurological deficits in children born to vitamin B12 deficient vegan mothers. Vegan mothers should therefore take vitamin B12 supplements, as this micronutrient is found only in foods of animal origin. The high levels of vitamin B12 found in some algae and seaweeds (eg spirulina) are not bio-active. For the other micronutrients listed above, supplements must be taken, or fortified foods (eg many soya milks are fortified with calcium) or specific foods sources included in the diet (eg kelp seaweed for iodine, or flaxseed for omega-3 fatty acids). 295 296 Good advice can be found on the websites of the Vegetarian Society and Vegan Society.
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Appendix 4: Infant feeding guidelines
World Health Organisation
159
UK Food Standards Agency
118
Breastfeeding: Practice exclusive breastfeeding from birth to six months, and introduce complementary foods at six months while continuing to breastfeed on-demand until two years of age or beyond.
Breastfeeding: Breastfeeding is best and provides all the nutrients a baby needs for the first six months. Continue exclusive breastfeeding for six months. The longer breastfeeding continues, the greater the benefits. Formula feeds: Infant formula is the only alternative to breastfeeding until one year. Cows milk-based formula is best. Follow-on formula can be used from six months but is not essential. Other types of formula should be used only on medical advice: Hydrolysed protein formula may be useful in cases of cows milk allergy. Soya formula is an alternative but may also be allergenic. Goats milk formula is not suitable for babies. Other drinks: Water is the best alternative drink to milk. Breastfed babies dont need any until they start solids. Under six months use tap water, boiled and cooled. Some bottled water has a mineral content too high for babies. Others are suitable (labelled accordingly). Bottled water should be boiled too. Fruit juices are a source of vitamin C but reduce the babys appetite for milk and can cause tooth decay; avoid before six months. After that use diluted (one in 10 with boiled water) in a feeding cup, at mealtimes only. Squashes, fizzy drinks, flavoured milk, juice drinks, tea and coffee are not suitable for infants. Starting complementary feeds: Solids can be started from six months and gradually increased in amount and variety so that by twelve months, solid foods are the main part of the diet, with breast or formula milk making up the balance.
Formula feeds: Not recommended all babies should be breastfed. WHO has recently developed guidelines for the nonbreastfed baby (partly for use by HIV-positive 297 women).
Other drinks: Avoid giving drinks with low nutrient value, such as tea, coffee and sugary drinks such as soda. Limit the amount of juice offered so as to avoid displacing more nutrient-rich foods. Increase fluid intake during illness.
Starting complementary feeds: Start at six months with small amounts of food and increase as the child gets older while maintaining frequent breastfeeding. Energy needs from complementary foods in developing countries are ~200 kcal/day at six to eight months, 300 kcal/day at nine to 11 months, and 550 kcal/day at 12-23 months. In industrialised countries these estimates are 130, 310 and 580 kcal/day because of differences in average breast milk intake.
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Progress with complementary feeds: Gradually increase food consistency and variety, adapting to the infants requirements and abilities. Infants can eat pureed, mashed and semi-solid foods beginning at six months, by eight months finger foods, by 12 months the same types of food as the rest of the family, keeping in mind the need for nutrientdense foods. Avoid foods that may cause choking such as nuts, grapes, raw carrots. Increase the number of times the child is fed complementary foods as he/she gets older. For the average infant complementary foods should be provided two to three times/day at six to eight months and three to four times/day at nine to 24 months. Additional nutritious snacks (pieces of fruit or bread or chapatti with nut paste) may be offered one to two times/day. If the energy density or amount of food per meal is low, or the child is no longer breastfed, more frequent meals may be required. Feed a variety of foods to ensure that nutrient needs are met. Meat, poultry, fish, eggs and vitamin A-rich foods should be eaten daily or as often as possible. Provide diets with adequate fat content. After illness, encourage the child to eat more than usual. Vegetarian diets cannot meet nutrient needs at this age unless nutrient supplements or fortified products are used.
Progress with complementary feeds: Start with a teaspoon of smooth vegetable pure (carrot, parsnip, potato, yam) or fruit pure (banana, cooked apple, pear or mango) or cereal (not wheat-based) such as baby rice, sago, maize, corn meal or millet, given with the babys usual milk (breast or formula) at one feed in the day. Gradually increase the amount within one feed, and then progress to two and three feeds per day. React to the babys appetite, giving more if wanted. Solids can include full-fat cows milk products (yoghurt, fromage frais, cheese sauce). Give cereals once a day. Use home-cooked foods mashed, sieved, or pured. Introduce pured red meat, poultry, fish or eggs, or pured beans or pulses (lentils, hummus) at least once a day. Serve starchy foods (potatoes, yams, rice or bread) two to three times/day, and fruit and vegetables as finger foods at two or more meals/day. As the baby continues to develop, use foods with a thicker and lumpier texture to encourage chewing, even before teeth emerge. Give finger foods (toast, bread, breadsticks, pitta bread or chapatti, peeled apple, banana, carrot sticks, or cubes of cheese). Avoid sweet biscuits and rusks. Later, start minced or chopped meals and fruit between meals. When the baby is mobile (crawling and walking) increase the amount of food. Use full-fat dairy products; low fat is sensible for adults but not babies. If the family is vegetarian, use pulses (such as red lentils, beans or chickpeas) or tofu as protein sources. Vitamin C in fruit and vegetables helps iron absorption, so include these at mealtimes.
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Do not force: Feed slowly and patiently; encourage but do not force. If children refuse foods, experiment with different foods, tastes, textures and methods of encouragement. Minimise distractions during meals. Feeding times are periods of learning and love talk to children during feeding, with eye to eye contact. Food safety: Practice good hygiene. Wash hands before food preparation. Store foods safely. Serving immediately after preparation, using clean utensils and serving dishes. Avoid using feeding bottles, which are difficult to keep clean. To be avoided: No specific guidelines
Do not force: Go at the babys pace. Allow plenty of time for feeding and to allow the baby to learn to swallow solids. Dont rush or force feed. Most babies know when theyve had enough to eat. Offer a wide variety of foods to avoid choosiness later on.
Food safety: Heat only what the baby will want. Do not reheat previously warmed food. Heat food thoroughly and allow it to cool. Do not refreeze food thats been warmed or previously frozen. Everything for feeding the baby needs to be really clean. To be avoided: Added salt: Babies under a year should have less than 1g salt per day. Dont add salt to cooked foods. Limit high-salt foods (cheese, bacon, sausages, processed foods, pasta sauces, breakfast cereal). Avoid sugar and honey: Sweeten stewed sour fruit like rhubarb with mashed banana, breast or formula milk. Dont use honey until after one year as it may contain harmful bacteria. Some foods can cause allergic reactions in some babies. If a family history of coeliac disease, consult a doctor before using wheat, rye or barley-based foods. Nuts and seeds including peanuts, peanut butter and other nut spreads. Dont give whole peanuts to children under five years old because they can cause choking.
Vitamin-mineral supplements: Use fortified complementary foods or vitamin-mineral supplements as needed. Starting ordinary cows milk: No specific guidelines.
Vitamin-mineral supplements: No specific guidelines. See DH guidelines in text.
Starting ordinary cows milk: Full-fat cows milk not suitable as a drink until one year. Semi-skimmed milk not suitable as a drink until two years. Skimmed milk not suitable until five years.
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Appendix 5: The International Code on the Marketing of Breast Milk Substitutes

The code was established by WHO in 1981 and has been modified by subsequent World Health Assembly resolutions. The essential elements are as follows. The Code forbids direct contacts between commercial representatives and medical personnel, mothers or pregnant women. Baby food companies may not distribute free or discounted samples of formula in hospitals and other health premises. Advertisements for baby foods must not target parents of infants younger than six months. There should be no promotional distribution of dummies (pacifiers), bottles or teats. Manufacturers of breast milk substitutes may not distribute promotional gifts to health workers, and information produced for health professionals should be strictly factual and based on scientific studies. Images of mothers and children are not allowed on packaging. Information on labels must be printed in easy to understand terms in the local language. Certain words, such as motherly, cannot be used. The labels must state that breastfeeding is the best way of feeding babies and that a substitute should only be used after consultation with health professionals. The Code has no legal power unless it is incorporated into national legislatures (as in the UK). Many developing countries have no effective legislation. The Code was initiated in response to aggressive marketing of formula in developing countries in the 1970s and 80s. Code violations are monitored by the International Baby Food Action Network (IBFAN) (www.ibfan.org); according to IBFAN, violations are much less common but are still occurring.
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Appendix 6: Comparison of the nutrient composition of mature human breast milk and formula
Mature breast milk Energy (kcal) (kJ) Protein (g/l) Casein (%) -lactalbumin (%) Lactoferrin (%) Secretory IgA (%) Lysozyme Fat (g/l) Saturated fat (%) DHA (%) Carbohydrate (g/l) Vitamins A ( g Re/l) carotene ( g Re/l) B1 (mg/l) B2 (mg/l) B3 (mg/l) B6 (mg/l) B12 ( g/l) Folic acid ( g/l) Biotin ( g/l) Pantothenic acid (mg/l) C (mg/l) D ( g/l) E (mg/l) K ( g/l) Minerals and trace elements Sodium (mg/l) Potassium (mg/l) Calcium (mg/l) Phosphorus (mg/l) Ca/P ratio Iron (mg/l) Zinc (mg/l) Iodine ( g/l) Copper ( g/l) Selenium ( g/l) Magnesium (mg/l) Other Cholesterol (mmol/l) Taurine (mg/l) 670-700 2800-3000 10-13 35-40 22-33 10-15 10-15 1-4 38-42 42 0.07-1.0 69-74 600 24 0.1-0.2 0.3-0.4 1.5-2.0 0.1 0.1-0.3 50-52 7.6 2.0-2.6 38-43 0.1-0.4 2.0-3.5 15 150-160 550-600 300-360 140-155 1.7-1.8 0.5-0.8 3-4 30-70 384-400 10-30 29-40 163 40-54 Breast milk substitutes or first milks* 670-700 2800-2950 14-14.5 40-43 16 0 0 0 35-38 40-45 0.2-0.5 70-75 540-820 35-42 0.4-1.0 0.6-1.5 6.9-9.0 0.4-0.6 1.4-2.1 34-160 10-20 2.3-3.0 69-90 10-14 5-13 27-67 160-170 570-740 390-510 240-290 1.4-2.0 5-8 3-6 45-100 330-420 10-15 45-52 0 47-67 Follow-on Formula* 670-700 2800-2950 18-19 78-80 na 0 0 0 33-34 na varies 74-81 650-800 25-43 0.4-1.0 1.0-1.5 6.5-9.0 0.4-0.6 1.6-2.0 70-150 20-30 3.0-3.6 80-140 11-19 5-11 29-67 200-300 850-900 720-900 480-530 1.2-1.7 12-3 4-9 100-120 410-600 15 65-70 0 50
* The composition of formula milk is presented as the range present in four leading brands each of cows milk-based first and follow-on preparations information supplied by the manufacturers (date 31 January 2008). Breast milk varies in composition and therefore the values provided are approximate; information on the composition of breast milk was obtained from 126, 127, 298-301 several sources. na in the table indicates that the authors of this study were unable to find the relevant data. Source: Hamosh 2001, Prentice 1996, Williams 1998, Behrman 1987, Golden 2000.
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References
1. 2. 3. 4. 5. 6. 7.
8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.
25.
Gluckman PD & Hanson MA (eds) (2006) Developmental origins of health and disease. Cambridge: Cambridge University Press. Henderson L, Gregory J & Swan G (2002) The national diet & nutrition survey: adults aged 19 to 64 years. Volume 1. London: The Stationery Office. Black RE, Allen LH, Bhutta ZA et al (2008) Maternal and child undernutrition: global and regional exposures and health consequences. Lancet 371: 243-60. International Obesity Task Force. The global epidemic. www.iotf.org/intro/global.htm Cordain L, Eaton SB, Sebastian A et al (2005) Origins and evolution of the Western diet: health implications for the 21st century. American Journal of Clinical Nutrition 81: 341-54. Jackson AA (1991) The glycine story. European Journal of Clinical Nutrition 45: 59-65. Jackson AA (1996) Perinatal nutrition: the impact on postnatal growth and development. In: Gluckman PD & Heymann MA (eds) Pediatrics and perinatalogy: the scientific basis. London: Arnold. Kramer MS & Kakuma R (2003) Energy and protein intake in pregnancy. Cochrane Database of Systematic Reviews CD000032. Haider BA & Bhutta ZA (2006) Multiple-micronutrient supplementation for women during pregnancy. Cochrane Database of Systematic Reviews CD004905. Barker DJP (1998) Mothers, babies and health in later life. London: Churchill Livingstone. Hales CN & Barker DJP (2001) The thrifty phenotype hypothesis. British Medical Bulletin 60: 5-20. Gluckman PD & Hanson MA (2004) Living with the past: evolution, development, and patterns of disease. Science 305: 1733-6. Gluckman PD & Hanson MA (2006) Mismatch why our world no longer fits our bodies. Oxford: Oxford University Press. Department of Health (2006) Forecasting obesity to 2010. London: Department of Health. Scottish Executive (2005) The Scottish health survey 2003. Edinburgh: Scottish Executive. Office for National Statistics (2007) Welsh health survey 2005/06. Cardiff: Welsh Assembly Government. Northern Ireland Statistics and Research Agency (2007) Northern Ireland health and social wellbeing survey 2005/06. Belfast: Northern Ireland Statistics and Research Agency. Government Office for Science (2007) Tackling obesity: future choices summary of key messages. London: Department for Innovation, Universities and Skills. Victora CG, Adair L, Fall C et al (2008) Maternal and child undernutrition: consequences for adult health and human capital. Lancet 371: 340-57. Wild S, Roglic G, Green A et al (2004) Global prevalence of diabetes; estimates for the year 2000 and projections for 2030. Diabetes Care 27: 1047-53. World Health Organisation (2005) Cardiovascular disease prevention and control: translating evidence into action. Geneva: World Health Organisation. Rogers I (2005) Birth weight and obesity and fat distribution in later life; a review. Birth Defects Research Part A: Clinical and Molecular Teratology 73: 485-6. Yajnik CS, Fall CHD, Coyaji KJ et al (2003) Neonatal anthropometry: the thin-fat Indian baby; the Pune Maternal Nutrition Study. International Journal of Obesity 27: 173-80. Vickers MH, Breier BH & Cutfield WS (2000) Fetal origins of hyperphagia, obesity, and hypertension and postnatal amplification by hypercaloric nutrition. American Journal of Physiology Endocrinology and Metabolism 279: E83-7. Jackson AA & Wootton SA (1989) The energy requirements of growth and catch-up growth. In: Schurch B & Scrimshaw NS (eds) Activity, energy expenditure and energy requirements of infants and children international dietary energy consultancy group. Cambridge, Massachusetts: International Dietary Energy Consultancy Group.
77
26.
27. 28.
29. 30. 31.
32. 33.
34. 35.
36. 37.
38. 39. 40. 41. 42. 43.
44. 45. 46.
Boney CM, Verma A, Tucker R et al (2005) Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus. Pediatrics 115: e290-6. Hillier TA, Mullen JA & Pedula KL (2007) Childhood obesity and metabolic imprinting. The ongoing effects of maternal hyperglycemia. Diabetes Care 30: 2287-92. Williams MA, Emanuel I, Kimpo C et al (1999) A population-based cohort study of the relation between maternal birthweight and risk of gestational diabetes mellitus in four racial/ethnic groups. Paediatric and Perinatal Epidemiology 14: 378-80. British Medical Association (1999) Growing up in Britain: ensuring a healthy future for our children. London: British Medical Association. Hoet JJ & Hanson MA (1999) Intrauterine nutrition: its importance during critical periods for cardiovascular and endocrine development. Journal of Physiology 514: 617-27. Myatt L & Roberts V (2006) Placental mechanisms and developmental origins of health and disease. In: Gluckman PD & Hanson MA (eds) Developmental origins of health and disease. Cambridge: Cambridge University Press. Drner G (1973) Possible significance of prenatal and-or perinatal nutrition for the pathogenesis of obesity. Acta Biologica et Medica Germanica 30: K19-22. Drner G, Haller H & Leonhardt W (1973) Possible significance of pre- and/or early postnatal nutrition in the pathogenesis of arteriosclerosis. Acta Biologica et Medica Germanica 31: K31-5. Drner G & Mohnike A (1973) Possible significance of pre- and/or early postnatal nutrition in the pathogenesis of diabetes mellitus. Acta Biologica et Medica Germanica 31: K7-10. Drner G, Plagemann A & Reinagel H (1987) Familial diabetes aggregation in type 1 diabetics: gestational diabetes an apparent risk factor for increased diabetes susceptibility in the offspring. Experimental and Clinical Endocrinology 89: 84-90. Gennser G, Rymark P & Isberg PE (1988) Low birth weight and risk of high blood pressure in adulthood. British Medical Journal 28: 1498-500. Forsdahl A (1978) Living conditions in childhood and subsequent development of risk factors for arteriosclerotic heart disease. The cardiovascular survey in Finnmark 1974-75. Journal of Epidemiology and Community Health 32: 34-7. Singhal A & Lucas A (2004) Early origins of cardiovascular disease: is there a unifying hypothesis? Lancet 363: 1642-5. Barker DJ & Osmond C (1986) Infant mortality, childhood nutrition and ischaemic heart disease in England and Wales. Lancet 1: 1077-81. Huxley R, Owen CG, Whincup PH et al (2007) Is birth weight a risk factor for ischemic heart disease in later life? American Journal of Clinical Nutrition 85: 1244-50. Jacob F & Monod J (1961) Genetic regulatory mechanisms in the synthesis of proteins. Journal of Molecular Biology 3: 318-56. Nowacki M, Vijayan V, Zhou Y et al (2008) RNA-mediated epigenetic programming of a genome-rearrangement pathway. Nature 451: 153-8. Huxley R, Neil A & Collins R (2002) Unravelling the fetal origins hypothesis: is there really an inverse association between birth weight and subsequent blood pressure? Lancet 360: 659-65. Curhan GC, Chertow GM, Willett WC et al (1996) Birth weight and adult hypertension and obesity in women. Circulation 94: 1310-5. Whincup PH, Cook DG, Adshead F et al (1997) Childhood size is more strongly related than size at birth to glucose and insulin levels in 10-11-year-old children. Diabetologia 40: 319-26. Lucas A, Fewtrell MS & Cole TJ (1999) Fetal origins of adult disease the hypothesis revisited. British Medical Journal 319: 245-9.
78
47. 48. 49. 50.
51.
52. 53.
54.
55.
56. 57.
58.
59. 60.
61. 62. 63.
64.
65.
Osmond C, Barker DJP, Winter PD et al (1993) Early growth and death from cardiovascular disease in women. British Medical Journal 307: 1519-24. Barker DJP, Osmond C, Forsen TJ et al (2005) Trajectories of growth among children who have coronary events as adults. New England Journal of Medicine 353: 1802-9. Eriksson JG, Forsen T, Tuomilehto HJ et al (2001) Early growth and coronary heart disease in later life: longitudinal study. British Medical Journal 322: 949-53. Gluckman PD, Hanson MA, Spencer HG et al (2005) Environmental influences during development and their later consequences for health and disease: implications for the interpretation of empirical studies. Proceedings of the Royal Society 272: 671-7. Koupilova I, Leon DA, McKeigue PM et al (1999) Is the effect of birth weight on cardiovascular mortality mediated through high blood pressure? Journal of Hypertension 17: 19-25. Rich-Edwards J, Stampfer MJ, Manson JE et al (1997) Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. British Medical Journal 315: 396-400. Kajantie E, Osmond C, Barker D et al (2005) Size at birth as a predictor of mortality in adulthood: a follow-up study of 350,000 person-years. International Journal of Epidemiology 34: 655-63. Lawlor DA, Ronalds G & Clark H (2005) Birth weight is inversely associated with incident coronary heart disease and stroke among individuals born in the 1950s: findings from the Aberdeen Children of the 1950s prospective cohort study. Circulation 112: 1414-8. Bergvall N, Iliadou A, Tuvemo T et al (2005) Birth characteristics and risk of high systolic blood pressure in early adulthood: socio-economic factors and familial effects. Epidemiology 16: 635-40. Vasan RS, Pencine MJ, Cobain M et al (2005) Estimated risks for developing obesity in the Framingham Study. Annals of Internal Medicine 143: 473-80. Gamborg M, Byberg L, Rasmussen F et al (2007) Birth weight and systolic blood pressure in adolescence and adulthood: meta-regression and analysis of sex- and age-specific results from 20 Nordic studies. American Journal of Epidemiology 166: 634-45. Hardy R, Wadsworth ME, Langenberg C et al (2004) Birth weight, childhood growth and blood pressure at 43 years in a British birth cohort. International Journal of Epidemiology 33: 121-9. Newsome CA, Shiell AW, Fall CHD et al (2003) Is birth weight related to later glucose and insulin metabolism? A systematic review. Diabetic Medicine 20: 339-48. Kensara OA, Wootton SA, Phillips DI et al (2005) Fetal programming of body composition: relation between birth weight and body composition measured with dual-energy x-ray absorptiometry and anthropometric methods in older Englishmen. American Journal of Clinical Nutrition 82: 980-7. Bertram CE & Hanson MA (2001) Animal models and programming of the metabolic syndrome. British Medical Bulletin 60: 103-21. McMillen IC & Robinson JS (2005) Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. Physiological Reviews 85: 571-633. Armitage J, Taylor P & Poston L (2005) Experimental models of developmental programming; consequences of exposure to an energy rich diet during development. Journal of Physiology 565: 3-8. Bayol SA, Farrington SJ & Stickland NC (2007) A maternal junk food diet in pregnancy and lactation promotes an exacerbated taste for junk food and a greater propensity for obesity in rat offspring. British Journal of Nutrition 98: 843-51. Samuelsson A-M, Matthews PA, Argenton M et al (2008) Diet induced obesity in female mice leads to offspring hyperphagia, adiposity, hypertension and insulin resistance: a novel murine model of developmental programming. Hypertension 51: 383-92.
79
66. 67.
68.
69. 70.
71. 72.
73.
74.
75. 76.
77.
78.
79.
80.
81.
82.
Vickers MH (2007) Developmental programming and adult obesity: the role of leptin. Current Opinion in Endocrinology, Diabetes and Obesity 14: 17-22. Vickers MH, Breier BH, McCarthy D et al (2003) Sedentary behaviour during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition. American Journal of Physiology 285: R271-3. Jackson AA, Dunn RL, Marchand MC et al (2002) Increased systolic blood pressure in rats induced by a maternal low-protein diet is reversed by dietary supplementation with glycine. Clinical Science 103: 633-9. Brawley L, Torrens C, Anthony FW et al (2004) Glycine rectifies vascular dysfunction induced by dietary protein imbalance during pregnancy. Journal of Physiology 554: 497-504. Torrens C, Brawley L, Anthony FW et al (2006) Folate supplementation during pregnancy improves offspring cardiovascular dysfunction induced by protein restriction. Hypertension 47: 982-7. Vickers MH, Gluckman PD, Coveny AH et al (2005) Neonatal leptin treatment reverses developmental programming. Endocrinology 146: 4211-6. Elahi MM, Cagampang FR, Anthony FW et al (2008) Statin treatment in hypercholesterolemic pregnant mice reduces cardiovascular risk factors in their offspring. Hypertension 51: 1-2. Burdge GC, Slater-Jefferies J, Torrens C et al (2007) Dietary protein restriction of pregnant rats in the F0 generation induces altered methylation of hepatic gene promoters in the adult male offspring in the F1 and F2 generations. British Journal of Nutrition 97: 435-9. Torrens C, Anthony FW, Poston L et al (2008). Transmission of raised blood pressure and endothelial dysfunction induced to the F2 generation induced by maternal protein restriction in the F0, in the absence of dietary challenge in the F1 generation. British Journal of Nutrition 100: 760-6. Gluckman PD, Hanson MA & Beedle AS (2007) Non-genomic transgenerational inheritance of disease risk. BioEssays 29: 145-54. Kwong WY, Wild AE, Roberts P et al (2000) Maternal undernutrition during the preimplantation period of rat development causes blastocyst abnormalities and programming of postnatal hypertension. Development 127: 4195-202. Watkins AJ, Ursell E & Panton R (2008) Adaptive responses by mouse early embryos to maternal diet protect fetal growth and predispose to adult onset disease. Biology of Reproduction 87: 299-306. Edwards LJ & McMillen IC (2002) Periconceptional nutrition programs development of the cardiovascular system in the fetal sheep. American Journal of Physiology Regulatory, Integrative and Comparative Physiology 283: R669-79. Gardner DS, Van Bon BWM, Dandrea J et al (2006) Effect of periconceptional undernutrition and gender on hypothalamic-pituitary-adrenal axis function in young adult sheep. Journal of Endocrinology 190: 203-12. Cleal JK, Poore KR, Boullin JP et al (2007) Mismatched pre- and postnatal nutrition leads to cardiovascular dysfunction and altered renal function in adulthood. Proceedings of the National Academy of Sciences 104: 9529-33. Rumball CWH, Harding JE, Oliver MH et al (2008) Effects of twin pregnancy and periconceptional undernutrition on maternal metabolism, fetal growth and glucose-insulin axis function in ovine pregnancy. Journal of Physiology 586: 1399-411. Poore KR, Cleal JK, Newman JP et al (2007) Nutritional challenges during development induce sex-specific changes in glucose homeostasis in the adult sheep. American Journal of Physiology Endocrinology and Metabolism 292: E32-9.
80
83.
84. 85. 86. 87. 88. 89. 90. 91.
92. 93. 94.
95.
96.
97.
98. 99. 100. 101. 102.
103.
104.
Watkins AJ, Platt D, Papenbrock T et al (2007) Mouse embryo culture induces changes in postnatal phenotype including raised systolic blood pressure. Proceedings of the National Academy of Sciences of the United States of America 104: 5449-54. Van Speybroeck L (2002) From epigenesis to epigenetics. The case of CH Waddington. Annals of the New York Academy of Sciences 981: 61-81. Schmalhausen IL (1949) Factors of evolution. New York: Blakiston (McGraw-Hill). Leary SD, Smith GD, Rogers IS et al (2006) Smoking during pregnancy and offspring fat and lean mass in childhood. Obesity 14: 2284-93. Martin RM, Smith GD, Frankel S et al (2004) Parents growth in childhood and the birth weight of their offspring. Epidemiology 15: 308-16. Barker DJP (1995) The fetal origins of coronary heart disease. British Medical Journal 311: 171-4. Adair LS, Kuzawa BBA & Borja J (2001) Maternal energy stores and diet composition during pregnancy program adolescent blood pressure. Circulation 104: 1034-9. Godfrey KM, Forrester T, Barker DJP et al (1994) Maternal nutritional status in pregnancy and blood pressure in childhood. British Journal of Obstetrics and Gynaecology 101: 398-403. Jie M, Law C, Zhang K-L et al (2000) Effects of infant birth weight and maternal body mass index in pregnancy on components of the Insulin Resistance Syndrome in China. Annals of Internal Medicine 132: 253-60. Erikksson JG, Forsen T, Tuomilhehto J et al (2002) Effects of size at birth and childhood growth on the insulin resistance syndrome in elderly individuals. Diabetologia 45: 342-8. Stein C, Fall CHD, Kumaran K et al (1996) Fetal growth and coronary heart disease in South India. Lancet 348: 1269-73. Roseboom TJ, van der Meulen J, Ravelli ACJ et al (2001) Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview. Molecular and Cellular Endocrinology 185: 93-8. Stein AD, Wang M & Ramirez-Zea M (2006) Exposure to a nutrition supplementation intervention in early childhood and risk factors for cardiovascular disease in adulthood: evidence from Guatemala. American Journal of Epidemiology 164: 1160-70. Drner G & Plagemann A (1994) Perinatal hyperinsulinism as possible predisposing factor for diabetes mellitus, obesity and enhanced cardiovascular risk in later life. Hormonal and Metabolic Research 26: 213-21. Yajnik CS, Deshpande SS, Jackson AA et al (2008) Vitamin B12 and folate concentrations during pregnancy and insulin resistance in the offspring: the Pune Maternal Nutrition Study. Diabetologia 51: 29-38. Gluckman PD, Yap Seng C, Fukuoka H et al (2007) Low birthweight and subsequent obesity in Japan. Lancet 369: 1081-2. Catalano P (2003) Obesity and pregnancy the propagation of a vicious cycle? Journal of Clinical Endocrinology and Metabolism 88: 3505-6. Oken E & Gillman MW (2003) Fetal origins of obesity. Obesity Research 11: 496-506. Rich-Edward JW, Colditz GA, Stampfer MJ et al (1999) Birthweight and the risk of type 2 diabetes in adult women. Annals of Internal Medicine 130: 278-84. Wei J-N, Sung F-C, Li C-Y et al (2003) Low birth weight and high birth weight infants are both at an increased risk to have type 2 diabetes among schoolchildren in Taiwan. Diabetes Care 26: 343-8. Krishnaveni GV, Hill JC, Leary S et al (2005) Anthropometry, glucose tolerance and insulin concentrations in Indian children: relationships to maternal glucose and insulin concentrations during pregnancy. Diabetes Care 28: 2919-25. Dabelea D, Hanson RL, Lindsay RS et al (2000) Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity. A study of discordant sibships. Diabetes 49: 2208-11.
81
105.
106.
107. 108.
109.
110.
111.
112. 113. 114.
115. 116.
117.
118. 119. 120. 121.
122. 123. 124.
Dabelea D & Pettitt DJ (2001) Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. Journal of Pediatric Endocrinology and Metabolism 14: 1085-91. Catalano PM, Thomas A, Huston-Presley L et al (2003) Increased fetal adiposity: a very sensitive marker of abnormal in utero development. American Journal of Obstetrics and Gynaecology 189: 1698-704. Moses RG, Luebcke M, Davis WS et al (2006) Effect of a low-glycemic-index diet during pregnancy on obstetric outcomes. American Journal of Clinical Nutrition 84: 807-12. Singhal A, Wells J, Cole TJ et al (2003) Programming of lean body mass: a link between birth weight, obesity and cardiovascular disease? American Journal of Clinical Nutrition 77: 726-30. Sayer AA, Syddall HE & Dennison EM (2004) Birth weight, weight at 1 y of age, and body composition in older men: findings from the Hertfordshire Cohort Study. American Journal of Clinical Nutrition 80: 199-203. Sewell MF, Huston-Presley L & Super DM (2006) Increased neonatal fat mass, not lean body mass, is associated with maternal obesity. American Journal of Obstetrics and Gynecology 195: 110-3. Ness AR (2004) The Avon Longitudinal Study of Parents and Children (ALSPAC) a resource for the study of the environmental determinants of childhood obesity. European Journal of Endocrinology 151: U141-9. Inskip H, Godfrey KM, Robinson SM et al (2006) Cohort profile: the Southampton Womens Survey. International Journal of Epidemiology 35: 42-8. Haugen G, Hanson M, Kieerud T et al (2005) Fetal liver-sparing cardiovascular adaptations linked to mothers slimness and diet. Circulation Research 96: 12-4. Drake AJ, Walker BR & Seckle JR (2005) Intergenerational consequences of fetal programming by in utero exposure to flucocorticoids in rats. American Journal of Physiology Regulatory, Integrative and Comparative Physiology 288: R34-8. Kaati G, Bygren LO, Pembrey M et al (2007) Transgenerational response to nutrition, early life circumstances and longevity. European Journal of Human Genetics 15: 784-90. Department of Health (1999) Dietary reference values for food energy and nutrients for the United Kingdom: report of the Panel on Dietary Reference Values of the Committee on Medical Aspects of Food Policy. London: The Stationery Office. Department of Health (1994) Weaning and the weaning diet: report of the Working Group on the Weaning Diet of the Committee on Medical Aspects of Food Policy. London: The Stationery Office. Food Standards Agency. Weaning your baby. www.eatwell.gov.uk/agesandstages/baby/weaning Office for National Statistics (2007) Health statistics quarterly 35: infant and perinatal mortality 2006: health areas, England and Wales. London: Office for National Statistics. Ananth CV & Platt RW (2004) Reexamining the effects of gestational age, fetal growth and maternal smoking on neonatal mortality. BioMed Central Pregnancy and Childbirth 4: 22. Maher J & Macfarlane A (2004) Inequalities in infant mortality: trends by social class, registration status, mothers age and birth weight, England and Wales, 1976. Health Statistics Quarterly 24: 14-22. Shrimpton R, Victora CG, de Onis M et al (2001) Worldwide timing of growth faltering; implications for nutritional interventions. Pediatrics 107: E75. Bhutta ZA, Ahmed T, Black RE et al (2008) What works? Interventions for maternal and child undernutritrion and survival. Lancet 371: 417-40. The World Bank (2006) Repositioning nutrition as central to development; a strategy for large-scale action. Washington DC: The World Bank.
82
125. 126. 127. 128.
129. 130. 131. 132.
133. 134.
135.
136.
137.
138. 139. 140. 141. 142. 143.
144. 145. 146.
Hoddinot J, Maluccio JA, Behrman JR et al (2008) Effect of a nutrition intervention during early childhood on economic productivity in Guatemala adults. Lancet 371: 411-6. Prentice A (1996) Constituents of human milk. Food and Nutrition Bulletin 17. Hamosh M (2001) Bioactive factors in human milk. Pediatric Clinics of North America 48: 69-86. ODowd R, Kent JC, Moseley JM et al (2007) The effects of uteroplacental insufficiency and reduced litter size on mammary function and postnatal offspring growth. American Journal of Physiology Regulatory, Integrative and Comparative Physiology 294: R539-48. Pico C, Oliver P, Sanchez J et al (2007) The intake of physiological doses of leptin during lactation in rats prevents obesity in later life. International Journal of Obesity 31: 1199-209. Armstrong J & Reilly JJ (2002) Breastfeeding and lowering the risk of childhood obesity. Lancet 359: 2003-4. Bolling K, Grant C, Hamlyn B et al (2007) Infant feeding survey 2005. London: The Information Centre. Lande B, Anderson LF, Baerug A et al (2003) Infant feeding practices and associated factors in the first six months of life: the Norwegian Infant Nutrition Survey. Acta Paediatrica 92: 152-61. Wright CM, Parkinson K & Scott J (2006) Breastfeeding in a UK urban context: who breastfeeds, for how long and does it matter? Public Health Nutrition 9: 686-91. McFadden A & Toole G (2006) Exploring womens views of breastfeeding: a focus group study within an area with high levels of socio-economic deprivation. Maternal and Child Nutrition 2: 156-68. Cowin I & Emmett P (2000) Diet in a group of 18-month-old children in South West England, and comparison with the results of a national survey. Journal of Human Nutrition & Dietetics 13: 87-100. Noble S, Emmett P and the ALSPAC team (2001) Food and nutrient intakes in a cohort of 8-month old infants in the South West of England in 1993. European Journal of Clinical Nutrition 55: 698-707. Northstone K, Rogers I, Emmett P et al (2002) Drinks consumed by 18-month-old children: are current recommendations being followed? European Journal of Clinical Nutrition 56: 236-44. Robinson S, Marriott L, Poole J et al (2007) Dietary patterns in infancy: the importance of maternal and family influences on feeding practice. British Journal of Nutrition 98: 1029-37. Robinson S, Crozier SR, Borland SE et al (2004) Impact of educational attainment on the quality of young womens diets. European Journal of Clinical Nutrition 58: 1174-80. Oliveria SA, Ellison RC, Moore LL et al (1992) Parent-child relationships in nutrient intake: the Framingham Childrens Study. American Journal of Clinical Nutrition 56: 593-8. Birch LL & Fisher JO (1998) Development of eating behaviors among children and adolescents. Pediatrics 101: 539-49. Vereecken CA, Keukelier E & Maes L (2004) Influence of mothers educational level on food parenting practices and food habits of young children. Appetite 43: 93-103. Fewtrell MS, Morgan JB, Duggan C et al (2007) Optimal duration of exclusive breastfeeding: what is the evidence to support current recommendations. American Journal of Clinical Nutrition 85: 635S-8S. Reilly JJ & Wells JCK (2005) Duration of breast-feeding: introduction of complementary feeding may be necessary before 6 months of age. British Journal of Nutrition 94: 869-72. Raiten DJ, Kalhan SC & Hay WW (2007) Maternal nutrition and optimal infant feeding practices: executive summary. American Journal of Clinical Nutrition 85: 577S-83S. Kramer M & Kakuma R (2004) The optimal duration of breast feeding; a systematic review. Advances in Experimental Biology 554: 63-77.
83
147.
148. 149.
150. 151. 152.
153. 154. 155. 156. 157.
158. 159.
160.
161. 162. 163. 164. 165. 166. 167. 168.
Collaborative Group on Hormonal Factors in Breast Cancer (2002) Breast cancer and breastfeeding: collaborative reanalysis of individual data from 47 epidemiological studies in 30 countries, including 50,302 women with breast cancer and 96,973 women without the disease. Lancet 360: 187-95. Department of Health (2004) Good practice and innovation in breastfeeding. London: Department of Health. National Institute for Health and Clinical Excellence (2008) Improving the nutrition of pregnant and breastfeeding women and children in low income households: NICE Public Health Guidance 11. Food Standards Agency. Breastfeeding your baby. www.eatwell.gov/agesandstages/baby/breastfeed Allen L (2005) Multiple micronutrients in pregnancy and lactation; an overview. American Journal of Clinical Nutrition 81: 1206S-12S. British Medical Association and Royal Pharmaceutical Society of Great Britain (2008) British National Formulary 2008. London: British Medical Association and Royal Pharmaceutical Society of Great Britain. Ilett KF & Kristensen JH (2005) Drug use and breastfeeding. Expert Opinion 4: 745-68. Anderson PO, Pochop SL & Manoquerra AS (2003) Adverse drug reactions in breast fed infants; less than imagined. Clinical Pediatrics 42: 325-40. HM Government (1995) The infant formula and follow-on formula regulations 1995. London: The Stationery Office. Koletzko B, Aggett PJ, Bindels JG et al (1998) Growth, development and differentiation: a functional food science approach. British Journal of Nutrition 80: S5-S45. Koletzko B, Lien E, Agostini C et al (2008) The roles of long-chain polyunsaturated fatty acids in pregnancy, lactation and infancy: a review of current knowledge and consensus recommendations. Journal of Perinatal Medicine 36: 5-14. Royal College of Paediatrics and Child Health (1999) Medicines for children. London: Royal College of Paediatrics and Child Health. Daelmans B, Martines J, & Saadeh R (eds) (2003) Special issue based on a World Health Organization expert consultation on complementary feeding. Food and Nutrition Bulletin 24: 1-134. Ong KK, Preece MA, Emmett PM et al (2002) Size at birth and early childhood growth in relation to maternal smoking, parity and infant breastfeeding: longitudinal birth cohort study and analysis. Pediatric Research 52: 863-7. Kramer M, Guo T, Platt RW et al (2004) Feeding effects on growth in infancy. Journal of Pediatrics 145: 600-5. Dewey KG, Heinig MJ, Nommsen LA et al (1992) Growth of breastfed and formula-fed infants from 0 to 18 months: the DARLING study. Pediatrics 89: 1035-41. Fewtrell MS, Morley R & Abbott RA (2001) Catch up growth in small-for-gestational-age term infants: a randomised trial. American Journal of Clinical Nutrition 74: 516-23. Karlberg J, Engstrom I, Karleberg P et al (1987) Analysis of linear growth using a mathematical model. I. From birth to three years. Acta Paediatrica Scandinavica 76: 478-88. Law C (2005) Early growth and chronic disease: a public health overview. Maternal and Child Nutrition 1: 169-76. Lucas P, Arai L, Baird J et al (2007) A systematic review of lay views on infant size and growth. Archives of Disease in Childhood 92: 120-7. Freeman JV, Cole TJ, Chinn S et al (1995) Cross sectional stature and weight reference curves for the UK, 1990. Archives of Disease in Childhood 73: 17-24. Cole TJ, Freeman JV & Preece MA (1995) Body mass index reference curves for the UK, 1990. Archives of Disease in Childhood 73: 25-9.
84
169. 170.
171.
172. 173. 174. 175. 176. 177.
178. 179. 180.
181. 182. 183. 184. 185. 186. 187.
188.
189.
190.
www.childgrowthfoundation.org World Health Organisation (2006) WHO child growth standards: length/height-for-age, weight-for-age, weight-for-length, weight-for-height and body mass index-for-age. Geneva: World Health Organisation. Dewey KG, Peerson JM, Brown KH et al (1995) Growth of breastfed infants deviates from current reference data: a pooled analysis of US, Canadian and European datasets. Pediatrics 96: 495-503. Scientific Advisory Committee on Nutrition & Royal College of Paediatrics and Child Health (2007) Application of WHO growth standards in the UK. London: The Stationery Office. Howie PW, Forsyth JS, Ogston SA et al (1990) Protective effect of breastfeeding against infection. British Medical Journal 300: 11-6. Cunningham AS, Jelliffe DB & Jelliffe EFP (1991) Breastfeeding and health in the 1980s: a global epidemiologic review. Journal of Pediatrics 118: 659-66. Forsyth JS (1995) The relationship between breastfeeding and infant health and development. Proceedings of the Nutrition Society 54: 407-18. American Academy of Pediatrics (1997) Breastfeeding and the use of human milk. Pediatrics 100: 1035-9. Dyson L, Renfrew M, McFadden A et al (2006) Promotion of breastfeeding initiation and duration; evidence into practice briefing. London: National Institute for Health and Clinical Excellence. McCance RA (1962) Food, growth and time. Lancet II: 621-6. Ashwell M (1993) McCance and Widdowson; a scientific partnership of 60 years. London: British Nutrition Foundation. Kramer MS, Matush L, Vanilovich I et al (2007) Effects of prolonged and exclusive breastfeeding on child height, weight, adiposity, and blood pressure at age 6.5 years: evidence from a large randomised trial. American Journal of Clinical Nutrition 86: 1717-21. Koletzko B (2006) Long-term consequences of early feeding on later obesity risk. Nestl Nutrition Workshop Series: Pediatric Program 58: 1-18. Villalpando S & Hamosh M (1998) Early and late effects of breastfeeding: does breastfeeding really matter? Biology of the Neonate 74: 177-91. Reynolds A (2001) Breastfeeding and brain development. Pediatric Clinics of North America 48: 159-71. Jain A, Concato J & Leventhal JM (2002) How good is the evidence linking breastfeeding and intelligence? Pediatrics 109: 1044-53. Der G, Batty GD & Deary IJ (2006) Effect of breastfeeding on intelligence in children; prospective study, sibling pairs analysis and meta-analysis. British Medical Journal 333: 929-30. Lucas A, Morley R & Isaacs E (2001) Nutrition and mental development. Nutrition Reviews 59: S24-33. Arenz S, Ruckerl R, Koletzko B et al (2004) Breastfeeding and childhood obesity a systematic review. International Journal of Obesity and Related Metabolic Disorders 28: 1247-56. Owen CG, Martin RM, Whincup PH et al (2005) Effect of infant feeding on the risk of obesity across the life course: a quantitative review of published evidence. Pediatrics 115: 1367-77. Owen CG, Martin RM, Whincup PH et al (2005) The effect of breastfeeding on mean body mass index throughout life: a quantitative review of published and unpublished observational evidence. American Journal of Clinical Nutrition 82: 1298-1307. Harder T, Bergmann R, Kallischnigg G et al (2005) Duration of breastfeeding and risk of overweight: a meta-analysis. American Journal of Epidemiology 162: 397-403.
85
191.
192.
193.
194. 195. 196.
197.
198.
199.
200. 201. 202. 203. 204.
205. 206.
207. 208. 209.
Baker JL, Michaelsen KF, Sorensen TI et al (2007) High prepregnant body mass index is associated with early termination of full and any breastfeeding in Danish women. American Journal of Clinical Nutrition 86: 404-11. Toschke AM, Martin RM, von Kries R et al (2007) Infant feeding method and obesity: body mass index and dual X-ray absorptiometry measurements at 9-10 y of age from the Avon Longitudinal Study of Parents and Children (ALSPAC). American Journal of Clinical Nutrition 85: 1578-85. Rolland-Cachera MF, Deheeger M, Akrout M et al (1995) Influence of macronutrients on adiposity development: a follow up study of nutrition and growth from 10 months to 8 years of age. International Journal of Obesity Related Metabolic Disorders 19: 573-8. British Paediatric Association (1994) Is breastfeeding beneficial in the UK? Archives of Disease in Childhood 71: 376-80. Lobstein T & Leach R (2004) Diabetes may be undetected in many children in the UK. British Medical Journal 328: 1261-2. Owen CG, Martin RM, Whincup PH et al (2006) Does breastfeeding influence the risk of type 2 diabetes in later life? A quantitative analysis of published evidence. American Journal of Clinical Nutrition 84: 1043-54. Owen CG, Whincup PH, Gilg JA et al (2003) Effect of breastfeeding in infancy on blood pressure in later life: systematic review and meta-analysis. British Medical Journal 327: 1189-95. Martin RM, Gunnell D & Davey Smith G (2005) Breastfeeding in infancy and blood pressure in later life; systematic review and meta-analysis. American Journal of Epidemiology 161: 15-26. Martin RM, Davey Smith G, Mantani P et al (2004) Breastfeeding and cardiovascular mortality: the Boyd Orr cohort and a systematic review with meta-analysis. European Heart Journal 25: 778-86. Leeson CP, Kattenhorn M, Deanfield JE et al (2001) Duration of breastfeeding and arterial distensibility in early adult life: population based study. British Medical Journal 322: 643-7. Owen CG, Whincup PH, Odoki K et al (2002) Infant feeding and blood cholesterol: a study in adolescents and a systematic review. Pediatrics 110: 597-608. Singhal A, Cole TJ & Fewtrell M (2004) Breastmilk feeding and lipoprotein profile in adolescents born preterm: follow up of a prospective randomised trial. Lancet 363: 1571-8. Rudnicka AR, Owen CG & Strachan DP (2007) The effect of breastfeeding on cardiorespiratory risk factors in adult life. Pediatrics 119: 1107-15. Martin RM, Middleton N & Gunnell D (2005) Breast-feeding and cancer; the Boyd Orr cohort and systematic review with meta-analysis. Journal of the National Cancer Institute 97: 1446-57. Martin RM, Gunnell D, Owen CG et al (2005) Breast-feeding and childhood cancer; a systematic review with meta-analysis. International Journal of Cancer 117: 1020-31. Greer FR, Sicherer SH, Burks AW et al (2008) Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 121: 183-91. Fergusson DM & Woodward LF (1999) Breast feeding and later psychosocial adjustment. Paediatric & Perinatal Epidemiology 13: 144-57. Montgomery SM, Ehlin A & Sacker A (2006) Breastfeeding and resilience against psychosocial stress. Archives of Disease in Childhood 91: 990-4. Specker B (2004) Nutrition influences bone development from infancy through toddler years. Journal of Nutrition 134: 691S-5S.
86
210.
211. 212. 213.
214. 215.
216.
217. 218.
219.
220.
221. 222. 223.
224. 225. 226. 227. 228. 229.
Akobeng AK, Ramanan AV, Buchan I et al (2006) Effect of breastfeeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies. Archives of Disease in Childhood 91: 39-43. Singhal A, Cole TJ & Lucas A (2001) Early nutrition in preterm infants and later blood pressure: two cohorts after randomised trials. Lancet 357: 413-9. Singhal A, Fewtrell M, Cole TJ et al (2003) Low nutrient intake and early growth for later insulin resistance in adolescents born pre-term. Lancet 361: 1089-97. Singhal A, Cole TJ, Fewtrell M et al (2007) Promotion of faster weight gain in infants born small for gestational age: is there an adverse effect on later blood pressure? Circulation 115: 213-20. Scaglioni S, Agostoni C, Notaris RD et al (2000) Early macronutrient intake and overweight at five years of age. International Journal of Obesity Related Metabolic Disorders 24: 777-81. Gunther AL, Remer T, Kroke A et al (2007) Early protein intake and later obesity risk: which protein sources at which time points throughout infancy and childhood are important for body mass index and body fat percentage at 7 y of age? American Journal of Clinical Nutrition 86: 1765-72. Tarini BA, Carroll AE, Sox CM et al (2006) Systematic review of the relationship between early introduction of solid foods to infants and the development of allergic disease. Archives of Pediatrics and Adolescent Medicine 160: 502-7. Reilly JJ, Armstron J & Dorosty AR (2005) Early life risk factors for obesity in childhood: cohort study. British Medical Journal 330: 1357-63. Wilson AC, Forsyth JS, Greene SA et al (1998) Relation of infant diet to childhood health: seven year follow up of cohort of children in Dundee infant feeding survey. British Medical Journal 316: 21-5. Niggemann B & Bayer K (2007) Diagnosis of food allergy in children: toward a standardization of food challenge. Journal of Pediatric Gastroenterology and Nutrition 45: 399-404. Vandenplas Y, Koletzko S, Isolauri E et al (2007) Guidelines for the diagnosis and management of cows milk protein allergy in infants. Archives of Disease in Childhood 92: 902-8. Osborn DA & Sinn JK (2007) Prebiotics in infants for prevention of allergic disease and food hypersensitivity. Cochrane Database of Systematic Reviews CD006474. Osborn DA & Sinn JK (2007) Probiotics in infants for prevention of allergic disease and food hypersensitivity. Cochrane Database of Systematic Reviews CD006475. Fisher DJ, Baird J & Payne L (2006) Are infant size and growth related to burden of disease in adulthood? A systematic review of literature. International Journal of Epidemiology 35: 1196-210. Horta BL, Barros FC, Victora CG et al (2003) Early and late growth and blood pressure in adolescence. Journal of Epidemiology and Community Health 57: 226-30. Belfort MB, Rifas-Shiman SL, Rich-Edwards J et al (2007) Size at birth, infant growth and blood pressure at three years of age. Journal of Pediatrics 151: 670-4. Monteiro POA & Victora CG (2005) Rapid growth in infancy and childhood and obesity in later life a systematic review. Obesity Reviews 6: 143-54. Baird J, Fisher D, Lucas P et al (2005) Being big or growing fast: systematic review of size and growth in infancy and later obesity. British Medical Journal 331: 929-31. Stettler N (2007) Nature and strength of epidemiological evidence for origins of childhood and adulthood obesity in the first year of life. International Journal of Obesity 31: 1035-43. Singhal A & Lanigan J (2007) Breastfeeding, early growth and later obesity. Obesity Reviews 8 (suppl 1): 51-4.
87
230. 231. 232. 233. 234.
235.
236.
237. 238. 239. 240. 241.
242.
243. 244.
245.
246. 247. 248. 249. 250.
Barker DJP, Osmond C, Winter PDW et al (1989) Weight in infancy and death from ischaemic heart disease. Lancet 2: 577-80. Osmond C, Cooper C, Sayer AA et al (2007) Infant growth and risk of chronic disease in adult life. Early Human Development 83: S65. Hales CN, Barker DJP, Clark PMS et al (1991) Fetal and infant growth and impaired glucose tolerance at age 64. British Medical Journal 303: 1019-22. Eriksson JG, Forsen T, Tuomilehto J et al (2003) Early adiposity rebound in childhood and risk of type 2 diabetes in adult life. Diabetologia 46:190-4. Bhargava SK, Sachdev HPS, Fall CHD et al (2004) Relation of serial changes in childhood body mass index to impaired glucose tolerance in young adulthood. New England Journal of Medicine 350: 865-75. Karaolis-Danckert N, Gunther ALB, Kroke A et al (2007) How early dietary factors modify the effect of rapid weight gain in infancy on subsequent body composition development in term children whose birth weight was appropriate for gestational age. American Journal of Clinical Nutrition 86: 1700-8. Sachdev HPS, Fall CHD, Osmond C et al (2005) Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood; the New Delhi birth cohort. American Journal of Clinical Nutrition 82: 456-66. Cooper C, Fall C, Egger P et al (1997) Growth in infancy and bone mass in later life. Annals of the Rheumatic Diseases 56: 17-21. Victora C, Barros FC, Horta BL et al (2001) Short-term benefits of catch-up growth for small-for-gestational-age infants. International Journal of Epidemiology 30: 1325-30. World Health Organisation (2004) Global strategy on diet, physical activity and health. Geneva: World Health Organisation. World Health Organisation (2006) Promoting optimal fetal development: report of a technical consultation. Geneva: World Health Organisation. Heckman JJ (2007) Economics of health and mortality special feature: the economics, technology, and neuroscience of human capability formation. Proceedings of the National Academy of Science USA 104: 13250-5. Shankar AH, Jahari AB & Sebayang SK et al (2008) Effect of maternal multiple micronutrient supplementation on fetal loss and infant death in Indonesia: a double-blind cluster-randomised trial. Lancet 371: 215-27. Christian P, Osrin D & Manandhar DS et al (2005) Antenatal micronutrient supplements in Nepal. Lancet 366: 711-2. Department of Health (1994) Nutritional aspects of cardiovascular disease: report of the Cardiovascular Review Group, Committee on Medical Aspects of Food Policy. London: The Stationery Office. Department of Health (1998) Nutritional aspects of the development of cancer: report of the Working Group on Diet and Cancer of the Committee on Medical Aspects of Food and Nutrition Policy. London: The Stationery Office. Scientific Advisory Committee on Nutrition (2003) Salt and health. London: The Stationery Office. Scientific Advisory Committee on Nutrition (2004) Advice on fish consumption: benefits and risks. London: The Stationery Office. Scientific Advisory Committee on Nutrition (2007) Update on vitamin D. London: The Stationery Office. Food Standards Agency. The eatwell plate. www.eatwell.gov.uk/healthydiet/eatwellplate Henderson L, Irving K, Gregory J et al (2003) The national diet & nutrition survey: adults aged 19 to 64 years. Volume 3. London: The Stationery Office.
88
251. 252. 253. 254. 255. 256.
257. 258.
259. 260.
261.
262. 263.
264.
265.
266.
267.
268. 269. 270.
Henderson L, Gregory J & Swan G (2003) The national diet & nutrition survey: adults aged 19 to 64 years. Volume 2. London: The Stationery Office. Scientific Advisory Committee on Nutrition (2006) Folate and disease prevention. London: The Stationery Office. Kearney JM & McElhone S (1999) Perceived barriers in trying to eat healthier results of a pan-EU consumer attitudinal survey. British Journal of Nutrition 81: S133-7. Nelson M, Erens B, Bates B et al (2007) Low income diet and nutrition survey. London: The Stationery Office. Drewnowski A & Specter SE (2004) Poverty and obesity: the role of energy density and energy costs. American Journal of Clinical Nutrition 79: 6-16. Dinour LM, Bergen D & Yeh MC (2007) The food insecurity-obesity paradox: a review of the literature and the role food stamps may play. Journal of the American Dietetic Association 107: 1952-61. Wrigley N, Warm D, Margetts B et al (2002). Assessing the impact of improved retail access on diet in a food desert: a preliminary report. Urban Studies 39: 2061-82. Meiselman HL (2006) The role of context in food choice, food acceptance and food consumption. In: Shepherd R & Raats M (eds) The psychology of food choice. Oxford: CAB International. Anderson A (2007) Nutrition interventions in women in low-income groups in the UK. Proceedings of the Nutrition Society 66: 25-32. Van Teijlingen ER, Wilson BJ, Barry N et al (1998) Effectiveness of interventions to promote healthy eating in pregnant women and women of childbearing age: a review. London: Health Education Authority. Fairbank L, OMeara S, Renfrew MJ et al (2000) A systematic review to evaluate the effectiveness of interventions to promote the initiation of breastfeeding. London: Health Technology Assessment NHS R&D HTA Programme. Havas S, Anliker J, Damron D et al (1998). Final results of the Maryland WIC 5-a-day program. American Journal of Public Health 88:1161-7. Arnold CG & Sobal J (2000) Food practices and nutrition knowledge after graduation from the Expanded Food and Nutrition Education Program (EFNEP). Journal of Nutrition Education 32: 130-9. Wrieden WL, Anderson AS, Longbottom PJ et al (2007) The impact of community-based food skills intervention on cooking confidence, food preparation methods and dietary choices an exploratory trial. Public Health Nutrition 10: 203-11. Ciliska D, Miles E, OBrien MA et al (1999) The effectiveness of community interventions to increase fruit and vegetable consumption in people four years of age and older. Ontario: Ontario Ministry of Health. Pomerleau J, Lock K, Knai C et al (2005) Interventions designed to increase adult fruit and vegetable intake can be effective: a systematic review of literature. Journal of Nutrition 135: 2486-95. Devine CM, Farrell TJ & Hartman R (2005) Sisters in health: experiential program emphasizing social interaction increases fruit and vegetable intake among low income adults. Journal of Nutrition Education and Behavior 37:265-70. Dyson L, McCormick F & Renfrew MJ (2005) Interventions for promoting the initiation of breastfeeding. Cochrane Database of Systematic Reviews CD001688. Britton C, McCormick FM, Renfrew MJ et al (2007) Support for breastfeeding mothers. Cochrane Database of Systematic Reviews CD001141. Bartington S, Griffiths L, Tate A et al (2006) Are breastfeeding rates higher among mothers delivering in Baby Friendly accredited maternity units in the UK? International Journal of Epidemiology 35: 1178-86.
89
271.
272.
273. 274.
275.
276. 277.
278. 279. 280. 281.
282. 283. 284. 285. 286. 287. 288. 289. 290. 291. 292. 293.
Broadfoot M, Britten J & Tappin DM (2005) The Baby Friendly Hospital Initiative and breastfeeding rates in Scotland. Archives of Disease in Childhood Fetal and Neonatal Edition 90: F114-6. Kramer MS, Chalmers B, Hodnett ED et al (2001) Promotion of breastfeeding intervention trial (PROBIT). A randomized trial in the Republic of Belarus. Journal of the American Medical Assocation 285: 413-20. Moore ER, Anderson GC, Bergman N (2007) Early skin-to-skin contact for mothers and their healthy newborn infants. Cochrane Database of Systematic Reviews CD003519. Hawkins SS, Griffiths LJ, Dezateux C et al (2007) Maternal employment and breast-feeding initiation: findings from the Millennium Cohort Study. Paediatric & Perinatal Epidemiology 21: 242-7. Abdulwadud OA & Snow ME (2007) Interventions in the workplace to support breastfeeding for women in employment. Cochrane Database of Systematic Reviews CD006177. Black MM, Siegel EH, Abel Y et al (2001) Home and videotape intervention delays early complementary feeding among adolescent mothers. Pediatrics 107: E67. Koehler S, Sichert-Hellert W & Kersting M (2007) Measuring the effects of nutritional counselling on total infant diet in a randomised controlled intervention trial. Journal of Pediatric Gastroenterology and Nutrition 45: 106-13. National Institute for Health and Clinical Excellence (2008) Maternal and child nutrition. London: National Institute for Health and Clinical Excellence. HM Government (2008) Healthy weight, healthy lives: a cross government strategy for England. London: HM Government. Hills D, Child C, Jungle K et al (2006) Healthy Start: rapid evaluation of early impact on beneficiaries, health professionals, retailers and contactors. London: Department of Health. Stettler E, Stallings VA, Troxel AB et al (2005) Weight gain in the first week of life and overweight in adulthood: a cohort study of European American subjects fed infant formula. Circulation 111: 1897-903. British Medical Association (2005) Preventing childhood obesity. London: British Medical Association. Government Office for Science (2007) Tackling obesity: future choices outcomes report. London: Department for Innovation, Universities and Skills. Jablonka E & Lamb MJ (2005) Evolution in four dimensions: genetic, epigenetic, behavioral and symbolic variation in the history of life. Cambridge: MIT Press. Rassoulzadegan M, Grandjean V, Gounon P et al (2007) Inheritance of an epigenetic change in the mouse: a new role for RNA. Biochemical Society Transactions 35: 623-5. Laird PW (2005) Cancer epigenetics. Human Molecular Genetics 14: R65-76. Cho E, Willett WC, Colditz GA et al (2007) Dietary choline and betaine and the risk of distal colorectal adenoma in women. Journal of the National Cancer Institute 99: 1224-31. Godfrey KM, Lillycrop KA, Burdge G et al (2007). Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease. Pediatric Research 61: 5R-10R. Li E, Beard C & Jaenisch R (1993) Role for DNA methylation in genomic imprinting. Nature 366: 362-5. Walsh CP, Chaillet JR & Bestor TH (1998) Transcription of IAP endogenous retroviruses is constrained by cytosine methylation. Nature Genetics 20: 116-7. Waterland RA & Jirtle RL (2003) Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Molecular and Cellular Biology 23: 5293-300. Bird A (2001) DNA methylation patterns and epigenetic memory. Genes & Development 16: 6. Reik W, Dean W & Walter J (2001) Epigenetic reprogramming in mammalian development. Science 293: 1089-93.
90
294.
295. 296. 297.
298. 299. 300. 301.
Yoder JA, Soman NS & Verdine GL (1997) DNA (cytosine-5)-methyltransferases in mouse cells and tissues. Studies with a mechanism-based probe. Journal of Molecular Biology 270: 385-95. www.vegsoc.org www.vegansociety.com Dewey K, Cohen RJ & Rollins NC (2004) WHO technical background paper: feeding of nonbreastfed infants from 6-24 months of age in developing countries. Food and Nutrition Bulletin 25: 377-402. Williams AF (1998) Infant feeding. In: Campbell AGM, McIntosh N (eds) Forfar and Arneils textbook of paediatrics. New York: Churchill Livingstone. Behrman RE, Vaughan VC & Nelson WE (eds) (1997) Nelson textbook of pediatrics. 13th edition. Philadelphia: WB Saunders. Golden BE (2000) Infancy, childhood and adolescence. In: Garrow JS, James WPT & Ralph A (eds) Human nutrition and dietetics. 10th Edition. Edinburgh: Churchill Livingstone. McCance RA, Widdowson EM, Holland B et al (1991) The composition of foods 5th edition. London: Royal Society of Chemistry and Ministry of Agriculture, Fisheries and Food.
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92
Index
A
AA see arachidonic acid adiposity 3, 12, 20 adolescence 28, 42, 46, 50, 61, 63 Adolescent health (2003) ix advertising 54, 63, 74 AGA see appropriate for gestational age agriculture 6, 12 albumin 42 alcohol 1, 3, 6, 24, 45, 69 allergic diseases 43, 44-5, 71 ALSPAC see Avon Longitudinal Study of Parents and Children amino acids 7, 35 analgesics 35 animal models 1, 12, 15, 20, 22, 26, 40 anorexia nervosa 1 antibiotics 35 antidepressants 35 appetite 26, 36, 38, 42, 71, 72 appropriate for gestational age (AGA) 22 arachidonic acid (AA) 41 asthma 13, 43, 44 atopic dermatitis 43, 44, 57 Avon Longitudinal Study of Parents and Children (ALSPAC) 22, 32
B
baby foods see complementary feeding Baby Friendly Hospital Initiative 1, 57-9, 60 Barker concept see thrifty phenotype hypothesis basal metabolism 7 Belarus 40, 42, 43, 58 birth weight see also low birth weight cancer risk 43 disease in adults 16, 18, 19, 21, 42, 43 growth standards 39 maternal dietary supplementation 50-1 maternal obesity and 22 blood pressure breast feeding and 43, 44 infant weight gain and 45, 48 low birth weight and 15, 16, 19 maternal weight and 21 BMA see British Medical Association body mass index (BMI) breast feeding and adult BMI 41, 42 infant weight and adult BMI 16, 17, 22, 45, 48 infant weight and adult disease 46, 47, 48 WHO definition 68
93
bone mineral content (BMC) 3, 13, 44, 48 brain development 8, 25, 35, 41 breast cancers 43, 45 breast feeding advantages 26, 40-4 at work 60 blood pressure and 4, 43 bone health and 3, 13, 44, 48 cancers and 43, 45 CHD and 13, 43 coeliac disease 44 cognitive development and 41 confounding 40, 41-2, 42, 43 contraindications 25 CVD and 42 developed countries 40 developing countries 30, 40 diabetes and 42 doctors role 59-60 gastrointestinal diseases and 44 guidelines 27, 34, 71-4 improving initiation and duration 56-60 obesity in adults and 13, 41-2 prevalence 13, 27 reasons for avoidance 28, 29, 38, 56 social class and 5, 27, 30, 41 ten steps to successful breastfeeding 57, 59 weight gain in children 42 weight gain in infants 36, 37, 38 WHO guidelines 34 breast milk 25, 60, 71 contaminants 35 nutrient composition 26, 35, 41, 42, 43, 75 British Medical Association (BMA) Adolescent health (2003) ix food labelling statement 64 Growing up in Britain: ensuring a healthy future for our children (1999) ix 13 Improving the health of the worlds poor (2007) 51 Preventing childhood obesity (2005) ix 63 British National Formulary (BNF) 35 bronchitis 43
C
caffeine 32, 35, 36, 69, 71 calcium 44, 52, 69, 70 cancers breast feeding 35, 43 epigenetic mechanisms 67 infant diet and 13
94
carbohydrates see also cereals 3 hunter-gatherer diets 5-6 cardiovascular diseases (CVD) breast feeding and 43 child growth and adult CVD 45-6 developed countries 7-8 developing countries 12 low birth weight and 15 micronutrient feeding in infancy 21, 44 women 46 catch-up infant weight gain 36, 39, 46, 48 cereals see also carbohydrates 6, 44, 53, 72 CHD see coronary heart diseases child growth CHD in adults 17, 47 phases 38 chronic diseases 15, 21, 22 mismatch model 9, 10, 11 nutritional transitions 5-7 coeliac disease breast feeding and 44, 69 infant diet 73 coffee 32, 69, 71 cognitive development breast feeding 41 infant diet and 13, 45 colostrum 26 Committee on Medical Aspects of Food and Nutrition (COMA) 62 complementary feeding 5, 44 developing countries 25, 34, 36, 51 guidelines 36, 39, 71-2 initiatives 61 UK practice 30-4 conclusions 3-4 confounding 40, 41-2, 42, 43, 58, 60 Cookwell Project 55 coronary heart diseases (CHD) breast feeding 13, 43 child growth and adult CHD 17, 47 developing countries 12, 21 infant and child growth 21 infant diet and 13, 16 low birth weight and 18 maternal diet and 21 cost benefit analysis 50 cows milk see also dairy food 35, 42, 44, 71, 72, 73
95
D
dairy food see also cows milk; eggs 44, 53, 69, 70, 72 deoxyribonucleic acid (DNA) 66-7 Department of Health (DH) alcohol guidelines 69 Good practice and innovation in breastfeeding 26, 34 obesity targets 63 dermatitis 43, 44 developed countries 21 developing countries breast feeding 5, 30, 34, 40 chronic diseases in 10 complementary feeding 34, 36, 61 Improving the health of the worlds poor (2007) 51 infant diet 25, 50-1 maternal diet 21, 35, 50-1 obesity 12-13 developmental origins concept 8-9, 15-19 developmental plasticity 1, 9, 16 diabetes see gestational diabetes; pre-diabetes; type 1 diabetes; type 2 diabetes discount model 50 DNA see deoxyribonucleic acid (DNA) DNA N-methyl transferase (Dnmt) 67 docosahexanoic acid (DHA) 35, 41 doctors role in supporting breastfeeding 59-60
E
Eatwell plate 51, 69 educational attainment breastfeeding in women and 27, 40, 41, 45 complementary feeding 31, 32, 36 diet in women 53 eggs see also dairy food 6, 42, 44, 69, 72, 73 embryo environmental effects 19-20 epigenetic mechanisms 20-1 energy balance with nutrition 10-11 density/cost of food 54, 72 food sources 6, 7 England infant mortality 25 obesity 11 epigenetic mechanisms 10, 11, 20-1, 66-7 European Childhood Obesity Project 40 evolution 5-6, 10 exercise 3, 6, 50 Expanded Food and Nutrition Education Programme (EFNEP) 55
96
F
families attitudes to breast feeding 28 influence on food choice 2, 54, 55, 56, 62 feeding behaviour infant 26, 32, 36 maternal 53-4 fetal growth breast milk and 26 hormones 38 menarche and 50 fetal nutrition 15-24 fetal origins concept 21 fetal programming 16 fetal supply mechanisms 19-20 finger foods 72 fish see also seafood 34, 44, 51, 54 fizzy drinks 32, 53, 71 folate deficiency 5, 20, 21, 52, 67, 68 food choice see feeding behaviour food labelling 64 food safety 73 food security 12, 53-4 food skills 55, 56 Food Standards Agency (FSA) infant feeding guidelines 71-4 maternal diet guidelines 34-5, 64 Foresight Project, Tackling obesities: future choices 63 formula milk advertising 35, 74 composition 35-6 guidelines 71-4 long-term outcomes 44 neurodevelopment 41 nutrient composition 75 weight gain in infants 36, 37, 38 fruit consumption by infants 32, 71, 72 consumption by women 51, 52, 53-4, 56, 69 Healthy Start scheme 62
97
G
galactosaemia 35 Gambia 50-1 gastrointestinal tract 8, 36 breastfeeding and 34, 40, 57 Gateshead Millennium Baby Study (1999-2000) 27 general practitioners (GPs), breastfeeding policy 59-60 gestational diabetes 12, 22, 36 Global strategy on diet, physical therapy and health 50 gluten 44, 73 glycaemic index 3, 22, 23 glycine insufficiency 7 goats milk 71 goitre 6 Good practice and innovation in breastfeeding 26, 34 grains see cereals Growing up in Britain: ensuring a healthy future for our children (1999) ix 1-2, 13 Growth Acceleration Hypothesis 45 growth hormones 38 Guatemala 21, 44
H
Healthy Start scheme 2, 36, 62 heart diseases see coronary heart diseases (CHD) heart muscle cells 9 high-density lipids (HDL) 21, 44, 45 HIV 35, 50, 71 honey 6, 31, 73 hunter-gatherer diets 5-6 hypertension 9, 12, 15, 22, 51
I
IFS see under infant feeding immunity 7, 13 Improving the health of the worlds poor (2007) 51 INCAP see Institute of Nutrition of Central America and Panama income, diet in women 53-6 India 21 inequalities in health 13, 61-2 infant diet 13, 25-49 adult obesity and 13, 16, 63 developing countries 25, 51 effect of maternal diet 32-3, 33 global perspective 50-1 guidelines 27, 71-4 long-term outcomes 43-9 pre-term infants 44 vitamin supplements 36
98
infant feeding appetite 26, 36, 42 behaviour 32, 33, 36, 73 Infant feeding survey (2005) 3, 27, 30, 31 infant growth adult health and 17, 45-8 charts 38-9 determinants 36-9 height and adult CVD 47 infant mortality 25, 40 infant weight determinants 36-9 health in adults 12, 15-19, 22, 46 optimal gain 48, 49 rapid gain 13, 48 Repositioning nutrition as central to development 50 waist circumference in adults 12 inflammatory bowel diseases 44 Institute of Nutrition of Central America and Panama (INCAP) 21, 44 insulin infant growth and 21, 38 low birth weight and 15, 19 intelligence quotient (IQ) 41 intrauterine growth restriction (IUGR) 16, 36 iodine 6, 35, 70, 75 ischaemic heart diseases see coronary heart diseases
J
Japan 22
L
large for gestational age (LGA) 22 leptin 20, 26 long-chain polyunsaturated fatty acids (LCPUFAs) 7, 70 brain development 41 in breast milk 26, 35 low birth weight see also birth weight health in adults 15-19 Repositioning nutrition as central to development 50 waist circumference in adults 12 Low income diet and nutrition survey 53-4
99
M
maternal diet CHD in adults 21 diabetes in adults 21 effect on fetus 19-20, 21 effect on infant diet 32-3, 33 food choice 53-4 global perspective 50-1 guidelines during lactation 34-5 guidelines during pregnancy 69-70 improvement interventions 55-6 obesity in adults 12 WHO report 50 maternal obesity birth weight and 22 fetal adiposity and 12 maternal-child relations 41 breast feeding and 43, 60 meat see protein menarche 50 mental health, breast feeding and 43, 60 metabolic integrity 7 metabolic syndrome 20 micronutrients for mothers 34, 51 in obesity 5 supplements in infants 44 vegetarianism and veganism 70 middle classes see social class migrants 10 milk see breast milk; cows milk Millennium Cohort Study 58, 60 mismatch model 9, 10, 11, 16 mortality 6 infant 25, 40 muscle growth 8, 13
N
National Diet and Nutrition Survey (NDNS) 51-2 National Institute for Health and Clinical Excellence (NICE) guidance on breastfeeding 34, 60 nutritional policy 62 Netherlands 21 neurodevelopment 35, 41 NICE see National Institute for Health and Clinical Excellence Northern Ireland 11 Norway 15, 19 nucleotides 35-6
100
nutrition inequalities 61-2 plane 18 what is good nutrition? 7 nuts 6, 31, 34, 44, 72, 73
O
obesity developing countries 12-13 European Childhood Obesity Project 40 infant birth weight and 16 intervention programmes 63 prevalence 11, 12 UK government strategy 63, 64 WHO definition 68 oestrogen 38 oligosaccharides 26, 35-6, 45 optimal infant weight gain 48, 49 otitis media 40 ovarian cancers 34 overnutrition 5, 13, 18, 20
P
paediatricians, breastfeeding policy 59-60 pancreas 8, 9, 42 peanuts 34, 73 physical activity see exercise plasticity 1, 9, 16 pre-diabetes 42 pre-formed nucleotides 35-6 pre-term infants 16, 35, 36, 39, 40, 41, 44, 45 prebiotics 35-6, 45 pregnancy, dietary guidelines 69-70 Preventing childhood obesity (2005) ix 63 probiotics 45 professional classes see social class Promoting optimal fetal development 50 protein allergy and 44 consumption by women 69 in eggs 42 in formula milk 38, 44 hunter-gatherer diets 5-6 prudent diet 32, 33, 53 psychotropic drugs 35 puberty 38 Pune Maternal Nutrition Study 21
101
R
rapid infant weight gain 13, 48 Repositioning nutrition as central to development 50 respiratory infections, breastfeeding and 34, 40 retinal development 41 rickets 6 Royal College of Paediatrics and Child Health (RCPCH) 39
S
salt 6, 31, 51, 73 Scientific Advisory Committee on Nutrition (SACN) 34, 39 Scotland Baby Friendly Hospitals survey 58 birth weight and CHD 18-19 breast feeding initiation project 57 Cookwell Project 55 obesity 11 seafood see also fish 69 allergy and 44 separation of mother from infant 60 sex factors 36, 37 shops 54 skin-to-skin contact 60 small-for-gestational-age (SGA) infants 36, 44 smoking 32, 35 social class breast feeding 5, 27, 30 complementary feeding 31-2 diet in women 53 infant mortality 25 solid foods see complementary feeding Southampton Womens Survey 22, 32, 53 soya 43, 44, 71 Special Supplemental Nutrition Programme for Women, Infants and Children (WIC) 55, 61 stroke 12, 13, 19-20, 45 sugars 6, 20, 32, 51, 53, 61, 69, 71, 73 sunlight 36 Sure Start 62 Sweden 19
T
Tackling obesities: future choices 63 taurine 35, 75 tea 32, 71 testosterone 38 thrifty phenotype hypothesis 8, 9 thyroid hormones 38
102
timing of introducing foods 31, 44-5 trainer cups 32 transgenerational effects 22-3 tuberculosis 35 type 1 diabetes breast feeding 42 in children of mothers with gestational diabetes 22 developing countries 21, 22 infant diet and 13, 45 type 2 diabetes developed countries 7-8, 12 developing countries 12, 21, 22, 42, 46 fetal development and 8, 12 infant diet and 13, 45 low birth weight and 15 obesity and 42
U
UK Gateshead Millennium Baby Study 27 United Nations, Millennium development goals 51 United States diet 6 nutritional intervention programmes 55, 56, 61 unpasteurised foods 69
V
vegetables consumption by women 51, 53-4, 61, 69, 72 consumption intervention programmes 55-6, 64 in diet 6, 51-2 Healthy Start scheme 62 infant diet 27, 32, 36, 44, 72 vegetarianism and veganism 70, 72 vitamin A infant diet 72 supplements 36, 69 vitamin B 7, 21, 35, 70 vitamin D deficiency 5, 69 infant diet 32 maternal diet 51 supplements 34, 36, 69 vegetarianism and veganism 70 vitamin supplements infants 36, 73 maternal to improve fetal development 50-1, 69
103
W
Wales infant mortality 25 obesity 11 water (drinking) 71 weaning see complementary feeding Welfare Foods scheme 62 women breastfeeding initiatives 56-60 complementary feeding initiatives 61 CVD in 46 guidelines to improve diet 51-2 nutrition intervention programmes 55-6 work 32, 60 working classes see social class World Bank, Repositioning nutrition as central to development 50 World Health Organization BMI definition 68 breast milk substitutes marketing guidelines 74 breastfeeding guidelines 34 Global strategy on diet, physical therapy and health 50 infant feeding guidelines 71-4 infant growth charts 38-9 Promoting optimal fetal development 50 World Health Organization/UNICEF Baby Friendly Hospital Initiative 57-9 doctors role 59-60 NICE recommendations 60
Y
young people 1, 51-2
Z
zinc 7, 52, 75
104
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BMA Board of Science, British Medical Association, BMA House, Tavistock Square, London, WC1H 9JP www.bma.org.uk British Medical Association, 2009
CODE: BMA 49484 /AB / SCIENCE & EDUCATION/ 02.09
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BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

(by invitation) (Co-optee) (Co-optee) (Deputy member)

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

About the authors

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

BMA Board of Science

Professor Sir Charles George Chair, Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Early life nutrition and lifelong health

BMA Board of Science

Chapter 1: The importance of fetal and infant nutrition

Nutritional transitions and patterns of chronic disease

Early life nutrition and lifelong health

BMA Board of Science

Figure 1: The human dietary transition

Lean game Wild fowl Eggs Fish Shellfish

Fruits Vegetables Legumes Nuts

Fatty meat Poultry Eggs Fish Shellfish 28%

Early life nutrition and lifelong health

BMA Board of Science

What is good nutrition?

The developmental consequences of inappropriate nutrition

Early life nutrition and lifelong health

BMA Board of Science

The importance of development for later health

Early life nutrition and lifelong health

BMA Board of Science

Figure 2: The thrifty phenotype hypothesis

Mothers development and growth impaired

Other maternal/placental influences