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
From the study on this page
"The curves were estimated with a Cox proportional hazards regression model adjusted for chronological age, sex, BMI, education, smoking behaviour, physical activity, history of cancer and history of CVD"
Mortality starts with:
People die sooner if they have low vitamin D
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Items in both categories Genetics and Mortality are listed here:
- Vitamin D appears to keep telomeres long (longer life) – Jan 2021
- Live longer if have more than 40 ng of Vitamin D (gene analysis of 10,500 people) – Jan 2019
- Telomeres in boys were 2.5% longer if 9 ng higher vitamin D – July 2018
- 5.8 X more likely to die in 15 year followup if low vitamin D and poor methylation – July 2018
- Increased mortality associated with low vitamin D genes – Nov 2014
PDF is available free at Sci-Hub 10.1093/gerona/gly253
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.
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