PROF BLOG
Simon Langley-Evans Professor of Human Nutrition, University of Nottingham
Simon has 25 years’ experience in nutrition research, with expertise in maternal and infant nutrition. He is Chair in Human Nutrition and Head of School of Biosciences at the University of Nottingham and is the Editor-inChief of The Journal of Human Nutrition and Dietetics.
42
EARLY ORIGINS OF DISEASE: YOU ARE WHAT YOU EAT, BUT ALSO WHAT YOUR MOTHER ATE! Obesity and the conditions it causes - Type 2 diabetes and cardiovascular disease - are a major threat to the health of populations all over the world. It is estimated that there are already 400 million people with diabetes and that by 2040 the global total will be over 600 million. Action is needed to manage and prevent this rapidly developing health crisis. Our understanding of the causes of obesity and related disorders has long centred on the fact that adult diet and lifestyle plays a major role in determining risk. We are all familiar with the phrase ‘you are what you eat’, but we should also bear in mind that what our mothers and even our grandmothers ate has a significant bearing on our health.1 The first clues that this is the case came from studies which followed up men and women who had been born in the 1920s and 30s and considered whether their health in their 60s and 70s might be related to the environment that they had experienced before birth. These studies showed that being of low birth weight, but still within the normal range, was associated with greater risk of Type-2 diabetes, the metabolic syndrome, high blood pressure and death from coronary heart disease. Other measures of size and shape at birth were also related to later disease, with thinness at birth being predictive of insulin resistance and diabetes. In short, to be born small and thin appears to predispose to major disease many decades later. Measurements of anthropometry at birth are a simple proxy for the nutritional exposure of the foetus during key periods of growth and development. Low birth weight and thinness at birth are generally, but not always, associated with undernutrition, whilst higher birth weights (>4kg) are
www.NHDmag.com June 2017 - Issue 125
often observed with maternal obesity. More direct evidence that maternal nutrition during pregnancy influences disease patterns in offspring has come from follow-ups of the Dutch Famine of 1944-45. Adults whose mothers were caught by this famine during pregnancy (at its’ peak the daily ration was just 600kcal) show increased prevalence of obesity in early adulthood, Type-2 diabetes and coronary heart disease. More recent studies have confirmed these early observations. For example, blood pressure in four-year-old children is related to the fat and carbohydrate intakes of their mothers during pregnancy.2 Such work has reinforced the studies of historical cohorts that gave rise to the developmental origins of health and disease hypothesis (DoHaD). Essentially, the DoHaD concept is that factors experienced during early development permanently shape or ‘programme’ long-term physiology and metabolic functions. Such factors include maternal nutrition, smoking, infection and psychological trauma. Although there are problems associated with linking current disease states to events that occurred 50 to 60 years ago, with no direct measurements of maternal nutrition, we know from experimental studies with animals that both maternal undernutrition (low protein, micronutrient restriction) and maternal obesity during pregnancy has lasting effects on disease
Are disease processes associated with ageing already in motion?
Human foetus at 20 weeks gestation.
risk in offspring. For example, offspring of rats and mice fed a low protein diet develop high blood pressure, atherosclerosis, insulin resistance and live shorter lives.1 Some of these effects persist across two or even three generations. Maternal nutritional status in pregnancy plays a key role in setting the structure and hence the later function of organs, such as the kidney and the pancreas. In animals, both iron deficiency and protein restriction reduce the number of nephrons in the kidney and this makes the development of renal disease more likely. The time frame in which health and disease is programmed goes beyond pregnancy and continues into childhood. There are many reports that breastfed infants are less prone to obesity and related disorders than those who are formula fed. Reports also suggest a higher IQ and reduced risk of atopic conditions. Growth in childhood is also important. A study of women born in Helsinki in the 1930s showed that those who went on to develop coronary heart disease as adults had been born smaller than average and remained so until aged four to five years. They had then gained weight more rapidly, such that, by the age of 11, their BMIs were higher than average. Studies of this
nature tell us that the factors that contribute to disease in adult life are complex and are a combination of genetic inheritance, early life programming and adult lifestyle. In effect, our risk of disease at any stage of life is a product of our cumulative experiences across the whole lifespan from the moment of conception. The link between maternal diet and longterm health poses a challenge for public health policy. Most current health promotion activities which focus on diet and health have a onesize-fits-all approach, so, for example, we are all encouraged to reduce salt consumption and consume at least five portions of fruit and vegetables a day. When thinking about obesity and health we focus most heavily on promoting health messages to adolescents and adults. If part of our fate is set before we are born, then are these policies and interventions appropriate? Should we adopt a more personalised approach based on experiences in foetal life or infancy? At the moment it may be too early to tell, but we can be certain that optimising maternal weight and diet before and during pregnancy is of huge importance. The message that ‘you are what your mother ate’ needs to be widely publicised and promoted.
References 1 Langley-Evans SC (2015). Nutrition in early life and the programming of adult disease: a review. J Hum Nutr Diet. 28 (Suppl 1), 1-14 2 Normia J, Laitinen K, Isolauri E, Poussa T, Jaakkola J and Ojala T (2013). Impact of intrauterine and post-natal nutritional determinants on blood pressure at four years of age. J Hum Nutr. Diet. 26, 544-552
You can read more Prof Blogs from Simon Langley-Evans in the Student zone at www.NHDmag.com
www.NHDmag.com June 2017 - Issue 125
43