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@ARTICLE{Schttker:143318,
      author       = {B. Schöttker$^*$ and L. Hagen$^*$ and Y. Zhang$^*$ and X.
                      Gào$^*$ and B. Holleczek and X. Gao$^*$ and H. Brenner$^*$},
      title        = {{S}erum 25-{H}ydroxyvitamin {D} {L}evels as an {A}ging
                      {M}arker: {S}trong {A}ssociations {W}ith {A}ge and
                      {A}ll-{C}ause {M}ortality {I}ndependent {F}rom {T}elomere
                      {L}ength, {E}pigenetic {A}ge {A}cceleration, and
                      8-{I}soprostane {L}evels.},
      journal      = {The journals of gerontology / A Biological sciences,
                      medical sciences Series A},
      volume       = {74},
      number       = {1},
      issn         = {1758-535X},
      address      = {Oxford [u.a.]},
      publisher    = {Oxford Univ. Pr.},
      reportid     = {DKFZ-2019-00908},
      pages        = {121 - 128},
      year         = {2019},
      abstract     = {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.},
      cin          = {C070},
      ddc          = {570},
      cid          = {I:(DE-He78)C070-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30371905},
      doi          = {10.1093/gerona/gly253},
      url          = {https://inrepo02.dkfz.de/record/143318},
}