In a series of experiments over the past 20 years, we have demonstrated long-term deferred effects of infant nutrition, particularly breast- as compared with formula-feeding and overfeeding as compared with normal or underfeeding, on serum HDL-cholesterol concentrations, adiposity, and atherosclerosis in the baboon, a large nonhuman primate. Low HDL-cholesterol levels and obesity are associated with accelerated progression of atherosclerosis and with increased risk of coronary heart disease in humans. We have observed other deferred effects of infant nutrition on bile acid metabolism, enzyme activities, and water and electrolyte balance, some of which may be physiologically related to HDL-cholesterol levels or to adiposity. The occurrence of these deferred effects suggests that infant nutrition may program other metabolic systems for life, and that these effects may contribute to other chronic diseases of adults. Although our understanding of the mechanisms by which infant diet regimens affect adult metabolism is meager, it is important to identify these mechanisms because they are likely to provide valuable clues to the causes and ultimately may contribute to the long-range prevention of those diseases.