@article {27279,
	title = {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},
	journal = {J Gerontol A Biol Sci Med Sci},
	volume = {74},
	number = {1},
	year = {2019},
	note = {Schottker, Ben Hagen, Leonie Zhang, Yan Gao, Xin Holleczek, Bernd Gao, Xu Brenner, Hermann eng Multicenter Study Research Support, Non-U.S. Gov\&$\#$039;t J Gerontol A Biol Sci Med Sci. 2019 Jan 1;74(1):121-128. doi: 10.1093/gerona/gly253.},
	pages = {121-128},
	type = {Journal Article},
	abstract = {Background: 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. Methods: 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). Results: 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. Conclusions: 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.},
	keywords = {Aged Aging/*blood Biomarkers/blood Cause of Death/trends Dinoprost/*analogs \& derivatives/blood Epigenesis, Genetic/*genetics Epigenomics/*methods Female Follow-Up Studies Germany/epidemiology Humans Male Middle Aged Retrospective Studies Telomere/*metabolism Vitamin D/*analogs \& derivatives/blood Vitamin D Deficiency/*blood/genetics/mortality},
	issn = {1758-535X (Electronic) 1079-5006 (Linking)},
	doi = {10.1093/gerona/gly253},
	url = {https://www.ncbi.nlm.nih.gov/pubmed/30371905},
	author = {Schottker, B. and Hagen, L. and Y. Zhang and Gao, X. and Holleczek, B. and Gao, X. and Brenner, H.}
}
