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Assessing the impact of alcohol consumption on biological age is important for understanding alcohol use-related comorbidities and mortality. Evidence shows that monocyte plays a critical role in both alcohol-induced pathophysiology and aging process. In this study, we developed a new monocyte-based DNA
methylation clock (MonoDNAmAge) that was benchmarked by using epigenetic age acceleration (EAA) in HIV infection. The MonoDNAmAge showed a significant age acceleration for HIV infection adjusting for confounding factors. More importantly, we found a non-linear relationship between MonoDNAmAge and
alcohol consumption in independent cohorts (N=2,242). Heavy consumption increased EAA up to 1.60 years while light consumption decreased EAA to 2.66 years. These results were corroborated by the four established epigenetic clocks. The results, for the first time, highlight the complex effects of alcohol consumption on monocyte epigenetic age and provide new insights on alcohol consumption-related biological aging.
Furthermore, the monocyte clock we developed can be applied to measure monocyte-related diseases or traits for future studies.