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The developmental origins hypothesis proposes that undernutrition during early development is associated with an increased type 2 diabetes risk in adulthood. We investigated the association between undernutrition during childhood and young adulthood and type 2 diabetes in adulthood. We studied 7,837 women from ProspectEPIC (European Prospective Investigation Into Cancer and Nutrition) who were exposed to the 1944-1945 Dutch famine when they were between age 0 and 21 years. We used Cox proportional hazards regression models to explore the effect of famine on the risk of subsequent type 2 diabetes in adulthood. We adjusted for potential confounders, including age at famine exposure, smoking, and level of education. Self-reported famine exposure during childhood and young adulthood was associated with an increased type 2 diabetes risk in a dose-dependent manner. In those who reported moderate famine exposure, the age-adjusted type 2 diabetes hazard ratio (HR) was 1.36 (95% CI [1.09-1.70]); in those who reported severe famine exposure, the age-adjusted HR was 1.64 (1.26-2.14) relative to unexposed women. These effects did not change after adjustment for confounders. This study provides the first direct evidence, using individual famine exposure data, that a short period of moderate or severe undernutrition during postnatal development increases type 2 diabetes risk in adulthood. Diabetes 61:2255-2260, 2012
Diabetes is a major health problem; ~330 million people suffer from type 2 diabetes worldwide (1,2). The developmental origins of health and disease hypothesis proposes that type 2 diabetes originates in early life (3). It postulates that disturbed growth as a result of undernutrition during important periods of growth and development, including fetal life, infancy, and childhood, results in early adaptations in structure and function of the body (4). These adaptations may be beneficial for short-term survival but can also increase the risk of chronic diseases, including type 2 diabetes, in the long-term.
A substantial body of evidence is available on long-term health outcomes of suboptimal conditions during fetal life. Since body size at birth is a marker of fetal growth rate and a reflection of the fetal environment, such research focuses on associations between body size at birth and chronic diseases in adult life. A systematic review of the evidence of 31 studies shows an inverse association between birth weight and the risk of type 2...