The nutritional basis of the fetal origins of adult disease

Abstract

Epidemiological observations linking size at birth with the risk of adult disease have now been extensively replicated and are widely accepted. It is hypothesized that such observations are the result of programming events in fetal life leading both to altered birth size and to permanent changes in structure and function which predispose to disease in adult life. Programming is a well-established biological phenomenon and there is good experimental evidence that nutrition can be an important and probably central programming stimulus. However, clear distinctions need to be drawn between maternal nutrition and size at birth on the one hand, and between fetal nutrition and fetal growth on the other. Maternal nutrition may bear little or no relationship to size at birth, but fetal nutrition is critically important in fetal growth. Many common assumptions about the relationship between body proportions and prenatal physiological events lack a sound experimental basis. Furthermore, important species differences in physiology, metabolism, placental structure and function necessitate cautious interpretation of animal experiments in their application to human situations. Details of these nutritional influences are likely to be very species dependent. Despite these caveats, it is clear that altered fetal nutrition can influence both fetal growth and later disease risk. There is indeed a nutritional basis for the fetal origins of adult disease.