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000143318 0247_ $$2doi$$a10.1093/gerona/gly253
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000143318 0247_ $$2ISSN$$a1758-535X
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000143318 1001_ $$0P:(DE-He78)c67a12496b8aac150c0eef888d808d46$$aSchöttker, Ben$$b0$$eFirst author$$udkfz
000143318 245__ $$aSerum 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.
000143318 260__ $$aOxford [u.a.]$$bOxford Univ. Pr.$$c2019
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000143318 520__ $$aA 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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000143318 7001_ $$0P:(DE-HGF)0$$aHagen, Leonie$$b1
000143318 7001_ $$0P:(DE-He78)6a8f87626cb610618a60d742677284cd$$aZhang, Yan$$b2$$udkfz
000143318 7001_ $$0P:(DE-He78)8218df9f6f41792399cd3a29b587e4e7$$aGào, Xin$$b3$$udkfz
000143318 7001_ $$aHolleczek, Bernd$$b4
000143318 7001_ $$0P:(DE-He78)0c11091f5d6e883a9b6029e4ccea5d5c$$aGao, Xu$$b5$$udkfz
000143318 7001_ $$0P:(DE-He78)90d5535ff896e70eed81f4a4f6f22ae2$$aBrenner, Hermann$$b6$$eLast author$$udkfz
000143318 773__ $$0PERI:(DE-600)2043927-1$$a10.1093/gerona/gly253$$gVol. 74, no. 1, p. 121 - 128$$n1$$p121 - 128$$tThe journals of gerontology / A Biological sciences, medical sciences Series A$$v74$$x1758-535X$$y2019
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