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| 024 | 7 | _ | |a 10.1093/gerona/gly253 |2 doi |
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| 024 | 7 | _ | |a 1758-535X |2 ISSN |
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| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 570 |
| 100 | 1 | _ | |a Schöttker, Ben |0 P:(DE-He78)c67a12496b8aac150c0eef888d808d46 |b 0 |e First author |u dkfz |
| 245 | _ | _ | |a Serum 25-Hydroxyvitamin D Levels as an Aging Marker: Strong Associations With Age and All-Cause Mortality Independent From Telomere Length, Epigenetic Age Acceleration, and 8-Isoprostane Levels. |
| 260 | _ | _ | |a Oxford [u.a.] |c 2019 |b Oxford Univ. Pr. |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a 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 50-74 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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| 700 | 1 | _ | |a Hagen, Leonie |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Zhang, Yan |0 P:(DE-He78)6a8f87626cb610618a60d742677284cd |b 2 |u dkfz |
| 700 | 1 | _ | |a Gào, Xin |0 P:(DE-He78)8218df9f6f41792399cd3a29b587e4e7 |b 3 |u dkfz |
| 700 | 1 | _ | |a Holleczek, Bernd |b 4 |
| 700 | 1 | _ | |a Gao, Xu |0 P:(DE-He78)0c11091f5d6e883a9b6029e4ccea5d5c |b 5 |u dkfz |
| 700 | 1 | _ | |a Brenner, Hermann |0 P:(DE-He78)90d5535ff896e70eed81f4a4f6f22ae2 |b 6 |e Last author |u dkfz |
| 773 | _ | _ | |a 10.1093/gerona/gly253 |g Vol. 74, no. 1, p. 121 - 128 |0 PERI:(DE-600)2043927-1 |n 1 |p 121 - 128 |t The journals of gerontology / A Biological sciences, medical sciences Series A |v 74 |y 2019 |x 1758-535X |
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