Close relationships exist between patterns of intra-uterine growth and the risk of ischaemic heart disease, hypertension, diabetes, insulin-resistance syndrome, obesity and some cancers later in life. Earlier studies placed emphasis on low birth weight and reduced growth, but it is now clear that disproportions in early growth are of great importance. Disproportion may be identified as disproportions of fetal and placental growth (and the risk of high blood pressure), or in head circumference, length and weight. It is hypothesized that the availability of nutrients at different times during gestation, by interacting with the maternal and fetal hormonal profile, predisposes to different patterns of growth. The same interaction programmes critical metabolic functions and determines the metabolic capacity at all later ages. People who were exposed to severe undernutrition during the Dutch hunger winter showed increased adiposity if the exposure was during early pregnancy, but decreased adiposity if the exposure was during late pregnancy. In men born in the UK, those with evidence of retarded fetal growth had significantly greater waist/hip circumference ratios for any given body mass index (the ratio fell with increasing weight at one year of age). In Mexican-Americans and non-Hispanic Caucasian Americans, people in the lowest third of birth weight had more truncal fat than those in the highest third. Offspring of rats exposed to marginally reduced protein intakes during pregnancy manifest a similar pattern of growth and metabolic change to that seen in humans, with perturbations of appetite and body fat patterning. Studies in rats suggest that programming of the hypothalamus, especially the hypothalamic-pituitary-adrenal axis might be the mechanism through which these changes are brought about.