Early-life growth patterns predict subsequent disease risk. The ontogenetic development of body composition appears to play a key role in such associations, but details have only recently begun to emerge. Studies in diverse populations consistently associate birthweight with subsequent lean mass. Associations with subsequent adiposity show less consistency, and may be gender-specific, while associations between infant weight gain and subsequent body composition appear to differ systematically between industrialised and developing countries. Existing evidence suggests two primary pathways whereby the body composition development contributes to disease risk. First, poor growth during fetal life and infancy appears permanently to constrain lean mass, thereby constraining metabolic capacity to tolerate a rich diet. Second, rapid catch-up growth and childhood weight gain appear to divert energy disproportionately to adipose issue, particularly in the abdomen, thereby increasing metabolic load. These complementary processes may account for disease risk being greatest in those born small who subsequently become large.