Commentary: The developmental origins of health and disease: an appreciation of the life and work of Professor David J.P. Barker, 1938-2013

Abstract

David J.P. Barker was a physician, a biologist and one of the most influential epidemiologists of our time. His ‘foetal programming hypothesis’ (‘Barker hypothesis’) transformed our thinking about the causes of diabetes, cardiovascular disease and cancer. He challenged the idea that they are explained by bad genes and unhealthy adult lifestyles, and proposed that their roots lie in the early life environment: ‘The nourishment a baby receives from its mother, and its exposure to infection after birth, determine its susceptibility to chronic disease in later life’. By permanently ‘programming’ the body’s metabolism and growth, they determine the pathologies of old age. His initially controversial, but now widely accepted, ideas have stimulated an explosion of research worldwide into early development and later disease (‘developmental origins of health and disease’ or DOHaD). David thought that ‘the poorer health of people in lower socio-economic groups or living in impoverished places is linked to neglect of the welfare of mothers and babies’. He argued that to pull back the modern epidemics of chronic disease we should prioritize the health and nutrition of girls, pregnant women and infants. David built his career in Southampton where, with Donald Acheson and Martin Gardner, the MRC Environmental Epidemiology Unit was established. He became its director in 1984. His research into the aetiology of thyroid disease, Perthes’ disease, Paget’s disease, appendicitis and chronic neurological disease led him to evidence of nutritional and infective influences in early life. He suspected that such influences caused the rapid waxing and waning of disease, for example the mysterious disappearance of rheumatic heart disease and new epidemic of coronary heart disease. The Unit’s detailed mapping of mortality (Atlas of Mortality for Selected Diseases in England and Wales, 1968-1978) led to his observation that areas with more infant mortality in 1910 had more cardiovascular deaths in 1970. He and statistician Clive Osmond confirmed strong geographical correlations between neonatal mortality and death from coronary heart disease and stroke decades later. He concluded that poor foetal nutrition was causally linked to later disease, and devoted the next three decades to a tenacious pursuit of evidence to support this. Interestingly his PhD thesis, ‘Prenatal influences and subnormal intelligence’, findings of which were published in 1966, was a harbinger of his foetal programming work. Using old birth records, he showed that people of lower birth and infant weight had more cardiovascular disease and diabetes in middle age. The latter of these papers is reprinted in this issue as part of the celebration of the centenary of the UK Medical Research Council, together with a commentary by David on his reflections on the thrifty phenotype hypothesis 20 years on. With the Helsinki Birth Cohort Group, he related patterns of childhood growth to these diseases. With colleagues in India, he showed similar relationships in developing populations. With the Dutch Hunger Winter Group in Amsterdam, he showed that exposure of mothers to famine left a legacy of ill health in their children. He collaborated with physiologists in Adelaide, Auckland and Toronto who were studying foetal development in animals, harnessing strong evidence that early life undernutrition had permanent effects on all body systems. The connections he made between the worlds of physiology and epidemiology were the forerunners of the International DOHaD Societyand congresses. There were some aspects of modern epidemiology that David disliked. He disagreed that consistency of Published by Oxford University Press on behalf of the International Epidemiological Association