Accelerated epigenetic aging and shorter DNA methylation-based telomere length in sarcopenic obesity: an exploratory pilot study.

BACKGROUND

Sarcopenic obesity (SO), defined as the coexistence of excess fat mass and low muscle mass/function, has been linked to adverse outcomes. Epigenetic alterations are central hallmarks of aging. Evaluating how obesity, sarcopenia, and SO are related to epigenetic aging biomarkers may provide insights into cellular aging and disease risk.

METHODS

In this cross-sectional study, 30 older women were classified into the control, obesity, sarcopenia, and SO groups and underwent anthropometry measurements, body composition analysis, and handgrip strength. Blood DNA methylation (DNAm) biomarkers were used to estimate eight epigenetic clocks (Horvath, Hannum, DNAmTL, PhenoAge, GrimAge, GrimAge2, Zhang, and FitAge) and to calculate intrinsic and extrinsic epigenetic age acceleration (IEAA and EEAA). Associations were tested with Bayesian linear and quantile regressions, adjusted for age and HOMA-IR.

RESULTS

SO was associated with higher EEAA, DNAmFitAge, and Hannum clock estimates, and shorter DNAmTL in both models. Obesity showed positive associations with these clocks in adjusted models and higher quantiles.

CONCLUSIONS

SO is associated with accelerated aging and shorter DNAmTL. Obesity contributes to biological aging, whereas sarcopenia without obesity does not. These findings suggest that excess adiposity combined with low muscle mass may worsen age-related decline, although the small sample size should be considered.