Abstract
The Developmental Origins of Health and Disease (DOHaD) hypothesis suggests that the prenatal and early postnatal environments shape the future probability of physical and mental wellbeing and risk of disease. A wealth of epidemiologic data supports the associations between maternal malnutrition, intrauterine growth retardation, and birthweight, and the risk of chronic disease including cardiovascular disease, hypertension, type 2 diabetes mellitus, obesity, neuropsychiatric disorders, and cancer. While the mechanisms underlying these observations remain unresolved, the DOHaD model assumes a developmental plasticity that allows adaptive regulation of the embryonic, fetal, and/or early postnatal metabolism in response to nutritional and environmental perturbations. Establishment of the epigenome coincides with vulnerable phases in development and provides one potential mechanism for long-lasting responses to transient environmental stimuli. Future studies in epigenetic epidemiology will seek to understand the role of various epigenetic mechanisms in DOHaD.
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