Epigenetic clocks use DNA methylation to estimate biological age. Whether body composition and physical activity are associated with these clocks is not well understood. Using blood samples collected at enrollment (2003–2009) from 2,758 women in the nationwide Sister Study, we calculated six epigenetic age acceleration metrics using four epigenetic clocks (Hannum, Horvath, PhenoAge, GrimAge). Recreational physical activity was self-reported and adiposity measures were assessed by medical examiners (body mass index [BMI], waist-to-hip ratio [WtH], waist circumference). In cross-sectional analyses, all adiposity measures were associated with epigenetic age acceleration. The strongest association was for BMI and PhenoAgeAccel, a measure of biological age that correlates with chronic disease (BMI≥35.0 vs 18.5–25: β=3.15 years, 95% CI: 2.41, 3.90; P-trend<0.001). In a mutually-adjusted model, BMI and WtH ratio were both associated with PhenoAgeAccel (BMI≥35.0 vs 18.5–24.9: β=2.69 years, 95% CI: 1.90, 3.48; P-trend<0.001; Quartile 4 vs 1 WtH: β=1.00 years, 95% CI: 0.34, 1.65; P-trend<0.001). After adjustment, physical activity was only associated with GrimAgeAccel (Quartile 4 vs 1: β=−0.42 years, 95% CI: −0.70, −0.14; P-trend=0.001). Physical activity attenuated the waist circumference associations with PhenoAgeAccel and GrimAgeAccel. Excess adiposity was associated with epigenetic age acceleration; physical activity may attenuate associations with waist circumference.
Epigenetic age acceleration is considered a measure of biological aging based on genome-wide patterns of DNA methylation. Although age acceleration has been associated with incidence of diseases and death, less is known about how it is related to lifestyle behaviors. Among 2,316 women, we evaluate associations between self-reported alcohol consumption and various metrics of epigenetic age acceleration. Recent average alcohol consumption was defined as the mean number of drinks consumed per week within the past year; lifetime average consumption was estimated as the mean number of drinks per year drinking. Whole blood genome-wide DNA methylation was measured with HumanMethylation450 BeadChips and used to assess four epigenetic clocks (Hannum, Horvath, PhenoAge, GrimAge) and their corresponding metrics of epigenetic age acceleration (Hannum AgeAccel, Horvath AgeAccel, PhenoAgeAccel, GrimAgeAccel). Although alcohol consumption showed little association with most age acceleration metrics, both lifetime and recent average consumption measures were positively associated with GrimAgeAccel (lifetime, per additional 135 drinks/year: β=0.30 years, 95% CI: 0.11, 0.48, p=0.002; recent, per additional 5 drinks/week: β=0.19 years, 95% CI: 0.01, 0.37, p=0.04). In a mutually adjusted model, only average lifetime alcohol consumption remained associated with GrimAgeAccel (lifetime, per additional 135 drinks/year: β=0.27 years, 95% CI: 0.04, 0.50, p=0.02; recent, per 5 additional drinks/week: β=0.05 years, 95% CI: -0.16, 0.26, p=0.64). Although alcohol use does not appear to be strongly associated with biological age measured by most epigenetic clocks, lifetime average consumption is associated with higher biological age assessed by the GrimAge epigenetic clock.
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