ArticleGeroScience2026
Telomere length and appendicular lean mass over six years in older adults with overweight or obesity and metabolic syndrome: a prospective cohort study.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Telomere length (TL) has been proposed as a marker of appendicular lean mass (ALM) decline; however, longitudinal evidence remains limited. We aimed to investigate the longitudinal association between TL and 6-year trajectories of ALM. This longitudinal study included 185 older adults aged 55-75 years with overweight or obesity and metabolic syndrome at baseline. Baseline TL was assessed using a monochrome multiplex real-time quantitative PCR. ALM from the four limbs was obtained at baseline, and after 1, 3, and 6 years of follow-up using dual-energy X-ray absorptiometry. ALM was also normalized for height, total body weight, or body mass index (BMI). Baseline longer TL in continuous was associated with higher ALM (between-group difference, 0.76; 95% CI, 0.12 to 1.40) and greater lean mass in the lower limbs (between-group difference, 0.50; 95% CI, 0.02 to 0.97), ALM to height ratio (between-group difference, 0.21; 95% CI, 0.02 to 0.41), and higher ALM to BMI ratio (between-group difference, 0.02; 95% CI, 0.01 to 0.04) after 6 years. When analyzed categorically, participants with baseline TL above the median exhibited higher ALM (between-group difference, 0.62; 95% CI, 0.04 to 1.20) and greater lean mass in the lower limbs (between-group difference, 0.49; 95% CI, 0.06 to 0.92) and higher ALM to BMI ratio (between-group difference, 0.02; 95% CI, 0.01 to 0.04) compared with those below the median after 6 years. Longer baseline TL was modestly associated with more favorable long-term ALM trajectories in older adults with overweight or obesity and metabolic syndrome, although these observational findings preclude causal inference and should not be interpreted as evidence that telomere biology directly contributes to muscle aging.
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