Childhood socioeconomic circumstances and cause-specific mortality in adulthood: systematic review and interpretation.

Abstract

There is convincing evidence that exposures acting across the life course influence adult health outcomes (1–3). Lifecourse epidemiology examines a range of potential processes through which exposures acting at different stages of life can, singly or in combination, influence disease risk (table 1) (4). In the critical period model, an exposure acting at a specific time has long-lasting effects on the structure or function of the body. The fetal origins hypothesis, in its original formulation, took this approach (5). Other examples of processes where outcomes appear to depend upon the time window during which an exposure acts are limb development (in relation to maternal thalidomide use); infection with hepatitis B and risk of adulthood liver cancer (with very early postnatal infection being most implicated); and environmental lead exposure, which results in serious neurodevelopmental deficits only if occurring in infancy and childhood (3). However, the influence of exposures acting during critical periods of susceptibility may be modified by later life exposures. This is the case for the associations of birth weight with coronary heart disease, high blood pressure, and insulin resistance, where associations are stronger (or only evident) among those who become obese during adolescence or adulthood (6–8).