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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #375746

Research Project: Metabolic and Epigenetic Regulation of Nutritional Metabolism

Location: Children's Nutrition Research Center

Title: A new era for epigenetic epidemiology

Author
item GUNASEKARA, CHATHURA - Children'S Nutrition Research Center (CNRC)
item WATERLAND, ROBERT - Children'S Nutrition Research Center (CNRC)

Submitted to: Epigenomics
Publication Type: Other
Publication Acceptance Date: 10/7/2019
Publication Date: 11/15/2019
Citation: Gunasekara, C.J., Waterland, R.A. 2019. A new era for epigenetic epidemiology. Epigenomics. 11(15):1647-1649. https://doi.org/10.2217/epi-2019-0282.
DOI: https://doi.org/10.2217/epi-2019-0282

Interpretive Summary:

Technical Abstract: Methylation of CpG dinucleotides is a mitotically heritable and highly stable epigenetic mechanism fundamental to cellular differentiation. Establishment of cell type-specific DNA methylation occurs throughout embryonic, fetal and early postnatal development, and stably regulates gene expression potential throughout life. The ability of DNA methylation to stably regulate gene expression makes epigenetic and genetic etiology of disease equally plausible. Accordingly, since the first published use of the term in 2004, there has been growing interest in the field of epigenetic epidemiology, defined as the study of the associations between interindividual epigenetic variation and risk of disease. Because of its long-term stability and ability to be assayed in minute quantities of DNA, nearly all epigenetic epidemiologic studies have focused on CpG methylation. Compared with genetic epidemiology, epigenetic epidemiology presents major challenges. The inherent cell-type specificity of DNA methylationmeans that we cannot generally 'epigenotype' an individual using peripheral blood DNA, complicating large-scale population studies of most human diseases. Also, even when the 'tissue of interest' can be obtained (in a case-control design, for example), the disease process itself can induce epigenetic changes, compromising the ability to draw causal inferences.