Public Release: 

Cutting the risk of coronary disease - start before birth says UK doctor

European Society of Human Reproduction and Embryology

Lausanne, Switzerland: Modest improvements in foetal and infant growth would lead to substantial falls in disease rates in later life, an international conference in reproductive medicine heard today (Monday 2 July).

Professor David Barker told the European Society of Human Reproduction and Embryology that prevention of conditions such as coronary heart disease, stroke, non-insulin dependent diabetes and high blood pressure might ultimately depend on changing the body composition and diets of young women and preventing imbalances between pre and postnatal growth in children.

Professor Barker, who is Director of the UK's Medical Research Council Environmental Epidemiology Unit at Southampton University, is an exponent of foetal origin hypothesis, which proposes that these diseases originate through adaptations that the foetus and infant make when they are undernourished.

The adaptations included diversion of oxygenated blood away from the trunk to the brain, alterations in the hormonal systems that regulate growth and maturation and in body composition.

Professor Barker said that, among men, the highest death rates from coronary heart disease were in those who were thin at birth and at one year but whose weight gain accelerated in childhood so that they had an above average body mass. Death from coronary heart disease may therefore be a consequence of poor prenatal or infant nutrition followed by improved nutrition in early childhood.

"The amount of fat in the body in relation to muscle may explain the increased risk. Boys who were thin at birth will always have comparatively fewer muscle cells because the numbers of muscle cells are determined before birth. Rapid weight gain may lead to a body with a high proportion of fat in relation to muscle and we know that is unhealthy in later life."

Other patterns of foetal and childhood growth were associated with the later development of stroke, non-insulin dependent diabetes and high blood pressure and the patterns differed between men and women. But, common to them all, was a period of reduced early growth followed by a period of accelerated growth.

"The persisting changes in the body's structure and function that are associated with reduced early growth alter the body's responses to adverse biological and social influences in later life."

Professor Barker said that findings from his recent study of the hospital admission or death from coronary heart disease of over 5,500 Finnish men born between 1934 and 1944 showed that if none of the men had been thin at birth and if they had all reached average height and weight at one year, the numbers who developed coronary heart disease might have been halved.

Nor was foetal origins hypothesis a condition limited to the developed world, he said. In India, where there was a rising epidemic of coronary heart disease, the condition was similarly associated with low birth weight and short body length, followed by accelerated weight gain.

"Our findings add to the evidence that protection of foetal and infant growth is a key area in strategies for primary prevention of coronary heart disease. Further benefit will come from preventing rapid weight gain after infancy in boys who were thin at birth."

A number of maternal influences that programme the foetus had now been identified, he said, including the mother's body composition before and during pregnancy and her diet in pregnancy.

Foetal growth was usually limited by the nutrients and oxygen received from the mother and that depended on the mother's body stores of nutrients, what she ate and the transfer of nutrients across the placenta. A mother's body size before pregnancy was the most important determinant of the size of her baby.

"Simple calculations show that quite modest improvement in foetal and infant growth would lead to substantial falls in disease rates. So we need to be thinking about changing the body composition and diets of young women and preventing imbalances between pre and postnatal growth among today's children if we want to reduce the toll from coronary heart disease and other chronic life-threatening conditions."

Abstract no: O-002

###

Further information:
Margaret Willson, information officer, Tel: 44-0-1536-772181, Mobile: 07973-853347, or Emma Mason, information officer, Tel: 44-0-1376-563090, Mobile: 07711-296986 Email: m.willson@mwcommunications.org.uk, or Email: wordmason@aol.com.

Press Office: (Sunday 1 July -Wednesday 4 July)
Margaret Willson, Emma Mason, Janet Blümli, Tel: 41-21-643-33-33 or 41-21-643-33-32 or 41-21-643-33-23, Fax: 41-21-643-33-28.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.