Epigenetic mechanisms underlying pathobiology of alcohol use disorder.

PURPOSE OF REVIEW

Chronic alcohol use is a worldwide problem with multifaceted consequences including multiplying medical costs and sequelae, societal effects like drunk driving and assault, and lost economic productivity. These large-scale outcomes are driven by the consumption of ethanol, a small permeable molecule that has myriad effects in the human body, particularly in the liver and brain. In this review, we have summarized effects of acute and chronic alcohol consumption on epigenetic mechanisms that may drive pathobiology of Alcohol Use Disorder (AUD) while identifying areas of need for future research.

RECENT FINDINGS

Epigenetics has emerged as an interesting field of biology at the intersection of genetics and the environment, and ethanol in particular has been identified as a potent modulator of the epigenome with various effects on DNA methylation, histone modifications, and non-coding RNAs. These changes alter chromatin dynamics and regulate gene expression that contribute to behavioral and physiological changes leading to the development of AUD psychopathology and cancer pathology.

SUMMARY

Evidence and discussion presented here from preclinical results and available translational studies have increased our knowledge of the epigenetic effects of alcohol consumption. These studies have identified targets that can be used to develop better therapies to reduce chronic alcohol abuse and mitigate its societal burden and pathophysiology.