Nutrition in early life, a critical period for human development, can have long-term effects on health in adulthood. Supporting evidence comes from epidemiological studies, animal models and experimental interventions in human subjects. The mechanism is proposed to operate through nutritional influences on growth. Substantial evidence now supports the hypothesis that 'accelerated' or too fast infant growth increases the propensity to the major components of the metabolic syndrome (glucose intolerance, obesity, raised blood pressure and dyslipidaemia), the clustering of risk factors that predispose to cardiovascular morbidity and mortality. The association between infant growth and these risk factors is strong, consistent, shows a dose-response effect and is biologically plausible. Moreover, experimental data from prospective randomised controlled trials strongly support a causal link between infant growth and later risk factors for atherosclerosis. Evidence that infant growth affects the development of atherosclerosis therefore suggests that the primary prevention of CVD should begin from as early as the first few months of life. The present review considers this evidence, the underlying mechanisms involved and its implications for public health.