期刊
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
卷 74, 期 1, 页码 121-128出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/gly253
关键词
Biomarkers; Epidemiology; Longevity; Successful aging
资金
- German Research Foundation [SCHO 1545/3-1]
- German Cancer Aid [108250, 108426]
- Saarland state Ministry for Social Affairs, Health, Women and Family Affairs
- Baden-Wurttemberg state Ministry of Science, Research and Arts
- Federal Ministry of Education and Research
- Federal Ministry of Family Affairs, Senior Citizens, Women and Youth
A strong association of serum 25-hydroxyvitamin-D levels (25(OH)D) with all-cause mortality has been shown previously and 25(OH)D could be a useful aging marker. The analysis was performed in a population-based, cohort study from Germany with 9,940 participants, aged 5074 years at baseline. A general linear model was used to assess associations of 25(OH)D levels with chronological age and the aging markers leukocyte telomere length (LTL), epigenetic age acceleration, and 8-isoprostane levels. A multivariate Cox regression model was applied to explore the independent and combined associations of these biomarkers with all-cause mortality (2,204 deaths occurred during a median follow-up of 14.3 years). On average, study participants lost 2.9 nmol/L 25(OH)D each 10 years of age. Increasing 25(OH)D levels were significantly associated with decreasing levels of 8-isoprostane levels but neither with LTL nor epigenetic age acceleration. The association of 25(OH)D quartiles with mortality was almost unchanged after adjusting for all aging markers (1.6-fold increased mortality in bottom quartile compared with top quartile). All aging markers were independent mortality predictors and subjects with unfavorable values for 4, 3, 2, and 1 aging marker(s) had 4.3-, 2.9-, 2.2, and 1.4-fold increased mortality, respectively. The 25(OH)D level can be regarded as an aging marker because it is linearly associated with age and an independent mortality predictor. Mechanisms linking vitamin D to healthy aging are unique and can neither be fully explained by aging of the epigenome, loss of telomeres, or antioxidative effects of vitamin D metabolites.
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