Location: Children's Nutrition Research Center
Title: The role of epigenetics in the developmental origins of health and diseaseAuthor
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MICHELS, KARIN - University Of California |
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GUNASEKARA, CHATHURA - Children'S Nutrition Research Center (CNRC) |
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WATERLAND, ROBERT - Children'S Nutrition Research Center (CNRC) |
Submitted to: Book Chapter
Publication Type: Book / Chapter Publication Acceptance Date: 1/1/2022 Publication Date: 4/14/2022 Citation: Michels, K.B., Gunasekara, C., Waterland, R.A. 2022. The role of epigenetics in the developmental origins of health and disease. In: Michels, K.B., editors. Epigenetic Epidemiology. 2nd Edition. Cham, Switzerland: Springer Cham. p. 123-124. DOI: https://doi.org/10.1007/978-3-030-94475-9_6 Interpretive Summary: Technical Abstract: The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that the prenatal and early postnatal environments shape the future probability of physical and mental well-being and risk of disease. A wealth of epidemiologic data document associations among maternal and infant nutrition, stress, and other exposures, and risk of chronic disease in later life including cardiovascular disease, hypertension, type 2 diabetes mellitus, obesity, neuropsychiatric disorders, and cancer. Extensive data from animal models support the biological plausibility of the DOHaD hypothesis. While the mechanisms underlying these observations remain unresolved, the DOHaD model assumes developmental plasticity, which allows adaptive regulation of embryonic, fetal, and infant development in response to nutritional and environmental perturbations. Establishment of epigenetic regulation during embryonic, fetal, and early postnatal life coincides with vulnerable ontogenic periods and provides a potential mechanism for long-lasting responses to transient environmental stimuli. In this chapter, we review recent progress in the epigenetic epidemiology of DOHaD and describe emerging approaches aimed at elucidating causal links between early environment, induced epigenetic alterations, and human disease. |