Less likely to die early if have a good level of vitamin D
Serum 25-hydroxyvitamin D levels as an ageing marker. Strong associations with age and all-cause mortality independent from telomere length, epigenetic age acceleration and 8-isoprostane levels
The Journals of Gerontology: Series A, gly253, https://doi.org/10.1093/gerona/gly253
Ben Schöttker, PhD Leonie Hagen Yan Zhang, PhD Xīn Gào, MSc Bernd Holleczek, PhD Xu Gao, PhD Hermann Brenner, MD
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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 ageing 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 ageing markers leukocyte telomere length, 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 leukocyte telomere length nor epigenetic age acceleration. The association of 25(OH)D quartiles with mortality was almost unchanged after adjusting for all ageing markers (1.6-fold increased mortality in bottom quartile compared to top quartile). All ageing markers were independent mortality predictors and subjects with unfavorable values for 4, 3, 2 and 1 ageing 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 ageing marker because it is linearly associated with age and an independent mortality predictor. Mechanisms linking vitamin D to healthy ageing are unique and can neither be fully explained by ageing of the epigenome, loss of telomeres or anti-oxidative effects of vitamin D metabolites.