The emerging field of behavioral epigenetics is producing a growing body of evidence that early life experience and social exposure can alter the way by which genes are marked with DNA methylation. We hypothesize that changes in DNA methylation as well as other epigenetic markers could generate stable phenotypes. Early life adversity appears to result in altered DNA methylation of genes in the brain and peripheral tissues, and these changes are associated with adverse phenotypic changes. Although the data are still sparse, early epigenetic studies have provided a proof of principle that experiences and the environment leave marks on genes, and thus suggest molecular and physical mechanisms for the epidemiological concept of gene-environment interaction. The main attraction of DNA methylation for type I (TI) translational prevention science is the fact that, different from genetic changes that are inherited from our ancestors, DNA methylation is potentially preventable and reversible and, therefore, there is a prospect of epigenetically targeted interventions. In addition, DNA methylation markers might provide an objective tool for assessing effects of early adverse experience on individual risks as well as providing objective measures of progress of an intervention. In spite of this great potential promise of the emerging field of social and translational epigenetics, many practical challenges remain that must be addressed before behavioral epigenetics could become translational epigenetics.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4807203PMC
http://dx.doi.org/10.1007/s13142-016-0387-7DOI Listing

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