Abstract
(1) Introduction: vitamin D may maintain the telomere length, either directly or via the inflammation effect and/or modulating the rate of cell proliferation. Whilst results from cross-sectional studies investigating the association between 25(OH)D concentration and telomere length have been mixed, there is a dearth of data from prospective studies which have assessed these associations. This study aimed to examine the association between 25(OH)D concentration in plasma and telomere length in blood cells in very-old adults (≥85 years old) at baseline, 18 months and 36 months by controlling for related lifestyle factors. (2) Methodology: our prospective cohort study comprised 775 participants from the Newcastle 85+ Study who had 25(OH)D measurements at baseline. Plasma 25(OH)D was stratified as <25 nmol/L (low), 25–50 nmol/L (moderate) and >50 nmol/L (high). Peripheral blood mononuclear cell telomere length was measured by quantitative real-time polymerase chain reaction at baseline, 18 and 36 months from baseline. (3) Results: a positive significant association was found between 25(OH)D concentration and telomere length amongst very-old participants at baseline (95% CI = 12.0–110.3, B = 61.2 ± 5.0, p = 0.015). This association was negative at 18 months (95% CI = −59.9–−7.5, B = −33.7 ± 13.3, p = 0.012) but was non-significant at 36 months. (4) Conclusion: Circulating 25(OH)D concentration shows inconsistent relationships with telomere length over time in very-old (85+ year old) adults.
Highlights
No significant association was found between telomere length and the relative confounders from the literature, such as smoking, alcohol consumption, PA, BMI, vitamin D
No significant association was found between telomere length and the confounders when the participants were stratified by sex, except for the BMI among the women
Among the very-old in the Newcastle 85+ cohort study, 25(OH)D concentration was positively associated with telomere length at baseline
Summary
The specific deoxyribonucleic acid (DNA) protein structures, are the cap at both ends of each chromosome. Telomeres play an essential role in protecting the genome against nucleolytic destruction, recombination, repair, and interchromosomal fusion [1]. Each DNA replication causes telomere shortening and at the point when telomeres reach a critical limit, the cell undergoes senescence and/or apoptosis [2]. The enzyme telomerase plays a key role in the maintenance of telomere length [3]. Age is a well-established factor associated with telomere shortening [3,4]. Telomere length decreases at ated telomere shortening is associated with mortality and many age-associated disease such as cardiovascular diseases, type 2 diabetes mellitus (T2DM), Alzheimer’s disease [
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
