Research Paper Volume 15, Issue 20 pp 10938—10971
Alcohol consumption and epigenetic age acceleration across human adulthood
- 1 Department of Biostatistics, Boston University School of Public Health, Boston, MA 02118, USA
- 2 Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
- 3 Population Sciences Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
- 4 Framingham Heart Study, Framingham, MA 01702, USA
- 5 Nutrition Epidemiology and Data Science, Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA 02111, USA
Received: May 21, 2023 Accepted: October 4, 2023 Published: October 26, 2023
https://doi.org/10.18632/aging.205153How to Cite
Copyright: © 2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The alcohol-associated biological aging remains to be studied across adulthood. We conducted linear regression analyses to investigate the associations between alcohol consumption and two DNA methylation-based biological age acceleration metrics in 3823 Framingham Heart Study participants (24–92 years and 53.8% women) adjusting for covariates. We also investigated whether the two epigenetic aging metrics mediated the association of alcohol consumption with hypertension. We found that higher long-term average alcohol consumption was significantly associated with biological age acceleration assessed by GrimAge acceleration (GAA) and PhenoAge acceleration (PAA) in middle-aged (45–64 years, n = 1866) and older (65–92 years, n = 1267) participants while not in young participants (24–44 years, n = 690). For example, one additional standard drink of alcohol (~14 grams of ethanol per day) was associated with a 0.71 ± 0.15-year (p = 2.1e-6) and 0.60 ± 0.18-year (p = 7.5e-4) increase in PAA in middle-aged and older participants, respectively, but the association was not significant in young participants (p = 0.23). One additional standard serving of liquor (~14 grams of ethanol) was associated with a greater increase in GAA (0.82-year, p = 4.8e-4) and PAA (1.45-year, p = 7.4e-5) than beer (GAA: 0.45-year, p = 5.2e-4; PAA: 0.48-year, p = 0.02) and wine (GAA: 0.51-year, p = 0.02; PAA: 0.91-year, p = 0.008) in middle-aged participant group. We observed that up to 28% of the association between alcohol consumption and hypertension was mediated by GAA or PAA in the pooled sample. Our findings suggest that alcohol consumption is associated with greater biological aging quantified by epigenetic aging metrics, which may mediate the association of alcohol consumption with quantitative traits, such as hypertension.
Abbreviations
FHS: Framingham Heart Study; DNAm: DNA methylation; EAA: epigenetic age acceleration; IEAA: intrinsic epigenetic age acceleration; EEAA: extrinsic epigenetic age acceleration; EAASkinBlood: epigenetic age acceleration with skin and blood clock; GAA: GrimAge acceleration; PAA: PhenoAge acceleration; CVD: cardiovascular disease; WBC: white blood cell; GDF 15: growth differentiation factor 15; CRP: C-reactive protein; ROS: reactive oxygen species; BMI: body mass index; PAI: physical activity index; SV: surrogate variable.