TY  - JOUR
AU  - Schöttker, Ben
AU  - Hagen, Leonie
AU  - Zhang, Yan
AU  - Gào, Xin
AU  - Holleczek, Bernd
AU  - Gao, Xu
AU  - Brenner, Hermann
TI  - 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.
JO  - The journals of gerontology / A Biological sciences, medical sciences Series A
VL  - 74
IS  - 1
SN  - 1758-535X
CY  - Oxford [u.a.]
PB  - Oxford Univ. Pr.
M1  - DKFZ-2019-00908
SP  - 121 - 128
PY  - 2019
AB  - 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.
LB  - PUB:(DE-HGF)16
C6  - pmid:30371905
DO  - DOI:10.1093/gerona/gly253
UR  - https://inrepo02.dkfz.de/record/143318
ER  -