Does early growth affect long-term risk factors for cardiovascular disease?

Abstract

The concept that early growth and nutrition have long-term biological effects is based on extensive studies in animals dating from the 1930s. More recently, compelling evidence for a long-term influence, or programming effect, of growth has also emerged in humans. 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 dyslipidemia), the clustering of risk factors which 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 randomized controlled trials strongly support a causal link between infant growth and later cardiovascular risk factors. These observations suggest therefore that the primary prevention of cardiovascular disease could 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.