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AWARDEES

Prof. David JP Barker, 2005 Awardee

Prof. David Barker trained as a physician at Guy's Hospital, London, and thereafter at the Queen Elizabeth Centre in Birmingham. He spent 3 years in Uganda at Makerere University, returning to Britain to join the newly founded medical school at Southampton. He is a Consultant Physician and former Director of the Medical Research Council Environmental Epidemiology Unit. Over the past twenty years he has carried out a series of studies showing that people who had low birthweights, or who were thin or stunted at birth, have high rates of coronary heart disease and the related disorders stroke, diabetes and hypertension in adult life. This has led to the hypothesis that coronary heart disease originates through undernutrition in the womb. The undernourished baby changes its structure, physiology and metabolism. These changes tend to persist through life. These findings have important implications for public health, in understanding the reasons why the incidence of so-called Western disease changes so rapidly, and why rates of these diseases differ between rich and poor people. They suggest a new strategy for the prevention of Western disease, which will focus on the nutrition of young women and their babies as well as the lifestyles of men and women in middle age.

There is now sufficient evidence for public health policies to be implemented. These include the avoidance of excessive thinness or overweight in mothers before conception; access to a balanced diet for all young women; protection of infant growth; and avoidance of overweight among young children who had small body size at birth. We will develop more effective public health action when we know more about the biological processes which underlie the associations between small size at birth and chronic disease in later life

In honour of his pioneering work within the area of diet, nutrition and chronic disease, David Barker is awarded the 2005 Danone International Prize for Nutrition.

RESEARCH WORK

SELECTED BIBLIOGRAPHY

CV

Research Work

The Barker Early Origins Hypothesis, also known as the foetal origins hypothesis or the thrifty phenotype hypothesis is founded on the concept that intrauterine growth restriction (IUGR) or foetal growth restriction -due to nutritional deprivation in early life- is an important cause of some of the most common, costly and disabling medical disorders of adult life such as coronary heart disease (CHD) and the related disorders such as hypertension and type-2 diabetes. 

Barker first put forth his hypothesis in 1986. His research group was puzzled that coronary heart disease (CHD) was the most common cause of death among certain men who otherwise had low risk characteristics, i.e., they were slim, non-smokers, and had low blood cholesterol. This suggested that the aetiology of CHD needed further exploration. It was this extensive work which led to the development and study of the “Barker Early Origins Hypothesis". Since then dozens of large-scale epidemiological and experimental studies conducted in Europe, USA, Asia and elsewhere have convincingly demonstrated a powerful link between IUGR as reflected in low birth weight and increased risk of developing chronic disease in later life.

But today there is clear evidence that also obesity, asthma and obstructive lung disease originate in utero; and emerging evidence that cancers from the breast, ovary and prostate, osteoporosis, polycystic ovary syndrome, and mental disorders including schizophrenia and depression all originate in utero. Evidence extending this list frequently appears.

The Barker hypothesis suggest a new strategy for the prevention of ‘Western’, disease, which will focus on the nutrition of girls and young women and their babies as well as the lifestyles of men and women in middle age.

According to Professor Barker public health policies should include: the avoidance of excessive thinness or overweight in mothers before conception; access to a balanced diet for girls and young women through childhood, adolescence, early adult life and pregnancy. protection of infant growth and avoidance of overweight among young children who had small body size at birth.
 

Selected Bibliography

1. Type 2 diabetes: the thrifty phenotype (2001).  Edited by Barker DJP. Oxford University Press
2. Barker DJP (2003).  The Best Start in Life.  London: Century
3. Martyn CN, Barker DJP, Osmond C. 'Mothers pelvic size, fetal growth, and death from stroke and coronary heart disease in men in the UK'. Lancet 1996;348:1264-68. 
4. Cresswell JL, Barker DJP, Osmond C, Egger P, Phillips DIW, Fraser RB. ‘Fetal growth, length of gestation, and polycystic ovaries in adult life’. Lancet 1997;350:1131-35. 
5. Ravelli ACJ, van der Meulen JHP, Michels RPJ, Osmond C, Barker DJP, Hales CN, Bleker OP. 'Glucose tolerance in adults after prenatal exposure to famine'. Lancet 1998;351:173-177. 
6. Forsen T, Eriksson J, Tuomilehto J, Reunanen A, Osmond C, Barker DJP. ‘The fetal and childhood growth of persons who develop Type 2 diabetes’. Ann Intern Med 2000;133:176-182

CV

- Professor David JP Barker (BSc, PhD, MD, FRCP, FRCOG, FRS) was trained as a physician at Guy’s Hospital in London UK, and thereafter at the Queen Elizabeth Centre in the city of Birmingham, UK.

- He spent three years working in Uganda at Markere University. Returning to Britain in 1972 he joined the newly founded medical school at Southampton University where he became Director of the MRC Environmental Epidemiology Unit.

- In the 1980s Professor Barker and his colleagues of the MRC Environmental Epidemiology Unit pioneered the idea that chronic disease in adults might have originated in foetal life. Barker’s research group was puzzled that coronary heart disease (CHD) was the most common cause of death among certain men who otherwise had low risk characteristics, i.e., they were slim, non-smokers, and had low blood cholesterol. This suggested that the aetiology of CHD needed further exploration. It was this work which led to the development and study of the “Barker Early Origins Hypothesis “ which is widely accepted today. There is also sufficient evidence for public health policies to be implemented.

- At present, DJP Barker continues his research activities on the early origins of chronic disease at the Developmental Origins of Health and Disease Division Research Centre of Southampton University, UK and at the Heart Research Centre, Oregon Health and Science University, USA .His continuing epidemiological research has three objectives:

1. Obtain more information about the way in which programmed changes in physiology and metabolism alter susceptibility to adverse influences such as obesity, high-energy diets and poor living conditions in childhood and adult life. Professor Barker and his colleagues are addressing this in studies based on population samples of 150,000 people in the UK (Hertfordshire, Sheffield and Motherwell), Finland (Helsinki), India (Mumbai), USA (Charleston, South Carolina), The Netherlands (Amsterdam) and China (Beijing).

2. Better understand how a mother’s body composition and diet influence the development of risk factors in her offspring. His group has shown that the offspring of mothers who were thin or overweight are at increased risk of cardiovascular disease and type 2 diabetes. The effect of the mother’s own body composition and glucose insulin regulation on the offspring’s growth and metabolism is studied in Mysore, South India. Because it is now presumed that events around the time of conception are important in determining foetal nutrition, Barker is undertaking a survey of 12,000 women of reproductive age in Southampton, UK (Southampton Women’s Survey) and follows foetal and childhood development in those women who become pregnant.

3. Further explore the range of diseases, which are programmed in early life such as hormonally dependent cancers, affective disorders and cognitive function.

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