The fetal origins of adult disease: a narrative review of the epidemiological literature

Abstract

The fetal origins of adult disease (FOAD) hypothesis suggests that risk factors from intrauterine environmental exposures affect the fetus’ development during sensitive periods, and increases the risk of specific diseases in adult life. This link was initially observed between prenatal exposures and adult coronary heart disease, but corresponding observations have later been published for a range of chronic conditions. Although the hypothesis has been praised as an essential shift in our understanding of determinants for health, the hypothesis has also been criticized on a number of accounts, both methodologically and theoretically. The aim of this paper is to critically discuss the FOAD-hypothesis, in relation to the epidemiological evidence. We conclude that much of the research literature on the FOAD-hypothesis finds support for the hypothesis. Despite this, it is still unclear if the effects are independent and what the public health relevance is. Notwithstanding the heart of the hypothesis - that environmental influences during gestation have an effect on later development - should be considered a major insight and constitutes a complement to a focus on genetic and more proximal factors (such as adult lifestyle) as causes of adult disease. As the search for determinants for disease and health continues, the FOAD-hypothesis is likely to remain an important perspective. It may however be better positioned as part of a broader life course perspective, rather than as an independent hypothesis.