Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women

Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programme d changes may he the origins of a number of diseases in later life, includi ng coronary heart disease, hypertension and noninsulin-dependent diabetes. We review epidemiologic studies in which the incidence of these diseases ha s been related to the recorded, early growth of individuals, while consider ing factors in the adult lifestyle, such as obesity and socioeconomic statu s. We discuss possible mechanisms. For hypertension these mechanisms includ e placentation, maternal blood pressure, fetal undernutrition: childhood gr owth, activation of the renin-angiotensin system, renal structure, programm ing of the hypothalamic-pituitary-adrenal axis, vascular structure, and sym pathetic nervous activity. For noninsulin-dependent diabetes we discuss mec hanisms concerning both insulin resistance and insulin deficiency. We inclu de a review of evidence for the programming of serum cholesterol and clotti ng factor concentrations. We address the timing of critical windows for cor onary heart disease, reviewing studies that allow assessment of the relativ e importance of fetal, infant, and childhood growth. We argue for a researc h strategy that combines clinical, animal, and epidemiological studies.