Associations between alcohol use and accelerated biological ageing

摘要: Abstract Background Harmful alcohol use is a leading cause of premature death, and associated with age-related disease. Ageing highly variable between individuals, may deviate from chronological ageing, suggesting that biomarkers biological ageing (based on DNA methylation or brain structural measures) be clinically relevant. Here, we investigated the relationships phenotypes both age estimates. Methods First, using data UK Biobank Generation Scotland, tested association consumption (units/week) hazardous (AUDIT scores), accelerated epigenetic in 20,258 8,051 respectively. Second, used Mendelian randomization to test for causal effect levels disorder (AUD) ageing. Results Alcohol showed consistent positive higher predicted (AUDIT-C: β=0.053, p=3.16×10−13; AUDIT-P: β=0.052, p=1.6×10−13; total AUDIT score: β=0.062, p=5.52×10−16; units/week: β=0.078, p=2.20×10−16), GrimAge (Units/week: p=1.48×10− 7) PhenoAge β=0.077, p=2.18×10−10). analyses revealed some evidence AUD (β=0.272, p=0.044), no Conclusions We provide phenotypic linking There possible age, but not any other alcohol-related trait acceleration. Future studies investigating mechanisms associating are warranted.