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Global hypomethylation of DNA resulting from a reduction in (S-adenosyl methionine) SAM levels. SAM levels are reduced as a result of an alcohol-induced reduction in folate and the inhibition of methionine synthase. At the same time, SAH levels are increased which inhibits DNMT. Histone modification that is associated with an increase in NADH levels caused by alcohol metabolism. The increase in NADH affects SIRT1 activity, leading to gene expression or silencing. Production of ROS, which affects the expression of inflammatory genes, and acetate, which is used in extra-hepatic tissues to produce acetyl-CoA. The latter then is used in histone acetylation by HATs. These epigenetic changes resulting from chronic alcohol consumption can lead to organ pathology. Understanding the exact nature of the epigenetic changes will help design medication for the treatment or alleviation of alcohol-induced organ damage

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