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Vitamin D deficiency is common among postmenopausal women. Telomere length can be a potential protective mechanism for age-related diseases. The objective of our study is to examine the association of vitamin D supplementation on leukocyte telomere length (LTL) in healthy postmenopausal women with vitamin D deficiency. The study was designed as a p...
Citations
... One randomised controlled trial (RCT) found no beneficial effect of vitamin D supplementation on telomere length; however, this study included only 102 postmenopausal women with vitamin D deficiency (<50 nmol/L) and treatment duration was short (50,000 international units/week for 8 weeks) (24). Another RCT, performed in 37 overweight African American adults (aged 19-50 years), found that supplementation with 60,000 international units (IU) of vitamin D per month for 16 weeks resulted in increased telomerase activity in peripheral blood mononuclear cells (PBMCs) (25). ...
Objectives
Observational studies have suggested that a higher 25-hydroxyvitamin D concentration may be associated with longer telomere length; however, this has not been investigated in randomised controlled trials. We conducted an ancillary study within a randomised, double-blind, placebo-controlled trial of monthly vitamin D (the D-Health Trial) for the prevention of all-cause mortality, conducted from 2014 to 2020, to assess the effect of vitamin D supplementation on telomere length (measured as the telomere to single copy gene (T/S) ratio).Design, Setting, Participants, and InterventionParticipants were Australians aged 60–84 years and we randomly selected 1,519 D-Health participants (vitamin D: n=744; placebo: n=775) for this analysis. We used quantitative polymerase chain reaction to measure the relative telomere length (T/S ratio) at 4 or 5 years after randomisation. We compared the mean T/S ratio between the vitamin D and placebo groups to assess the effect of vitamin D supplementation on relative telomere length, using a linear regression model with adjustment for age, sex, and state which were used to stratify the randomisation.ResultsThe mean T/S ratio was 0.70 for both groups (standard deviation 0.18 and 0.16 for the vitamin D and placebo groups respectively). The adjusted mean difference (vitamin D minus placebo) was −0.001 (95% CI −0.02 to 0.02). There was no effect modification by age, sex, body mass index, or predicted baseline 25-hydroxyvitamin D concentration.Conclusion
In conclusion, routinely supplementing older adults, who are largely vitamin D replete, with monthly doses of vitamin D is unlikely to influence telomere length.
... They reported that vitamin D supplementation for 12 months improved cognitive function by reducing oxidative stress regulated by increased LTL in older adults with mild cognitive impairment. In contrast, Agirbasli et al. [24] investigated the short-term effects of vitamin D supplementation on LTL in a cohort of vitamin D-deficient postmenopausal women (n = 102). The group was divided into supplementation those with oral vitamin D 3 (cholecalciferol) at a dose of 50,000 IU/week for eight weeks (n = 52) and placebo groups (n = 50). ...
Background: Shorter leukocyte telomere length (LTL) is observed in multiple age-related diseases, which are also associated with vitamin D deficiency (i.e., osteosarcopenia, neurocognitive disorders, cancer, osteoarthritis, etc.), suggesting a close association between vitamin D and LTL. In this study, we examined the relationship between vitamin D levels and LTL in older participants of the UK Biobank. Methods: Data were collected from the UK Biobank. Participants aged 60 and older (n = 148,321) were included. Baseline LTL was measured using a multiplex qPCR technique and expressed as the ratio of the telomere amplification product (T) to that of a single-copy gene (S) (T/S ratio). Serum 25-hydroxyvitamin D (25OHD) was stratified by z score and linked to LTL in a linear regression model adjusting for covariates. Results: Compared to the medium level, a low (in the range of 16.6 nmol/L, 29.7 nmol/L) or extremely low (≤16.6 nmol/L) level of serum 25OHD was associated with shorter LTL: 0.018 SD (standardized β = −0.018, 95% CI −0.033 to −0.003, p = 0.022) and 0.048 SD (standardized β = −0.048, 95% CI −0.083 to −0.014, p = 0.006), respectively. Additionally, the high serum 25OHD groups (>95.9 nmol/L) had 0.038 SD (standardized β = −0.038, 95% CI −0.072 to −0.004, p = 0.030) shorter mean LTL than the group with medium 25OHD levels. The associations above were adjusted for multiple variables. Conclusions: In this population-based study, we identified an inverted U-shape relationship between LTL and vitamin D status. Our findings could be affected by unmeasured confounders. Whether high or low vitamin D-associated shorter LTL is mechanistically related to age-related conditions remains to be elucidated.
... They reported that vitamin D supplementation for 12 months improved cognitive function by reducing oxidative stress regulated by increased LTL in older adults with mild cognitive impairment. In contrast, Agirbasli et al. [23] investigated the short-term effects of vitamin D supplementation on LTL in a cohort of vitamin D-deficient postmenopausal women (n = 102). The group was divided into supplementation those with oral vitamin D3 (cholecalciferol) at a dose of 50,000 IU/week for eight weeks (n = 52) and placebo groups (n = 50). ...
Background: Shorter leukocyte telomere length (LTL) is observed in multiple age-related diseases, which are also associated with vitamin D deficiency (i.e., osteosarcopenia, neurocognitive disorders, cancer, osteoarthritis, etc.), which suggests a close association. In this study, we examined the relationship between vitamin D levels and LTL in older participants of the UK Biobank. Methods: Data were collected from the UK Biobank. Participants aged 60 and older (n=148,321) were included. Baseline LTL was measured using a multiplex qPCR technique and expressed as the ratio of the telomere amplification product (T) to that of a single-copy gene (S) (T/S ratio). Se-rum 25-hydroxyvitamin D (25OHD) was stratified by z score and linked to LTL in a linear regression model adjusting for covariates. Results: Compared to the medium level, a low (in the range of 16.6 nmol/L, 29.7 nmol/L) or extremely low (≤ 16.6 nmol/L) level of serum 25OHD was associated with shorter LTL: 0.018 SD (standardized β= -0.018, 95% CI -0.033 to -0.003, P=0.022) and 0.048 SD (standardized β= -0.048, 95% CI -0.083 to -0.014, P=0.006), respectively. Additionally, the high serum 25OHD groups (> 95.9 nmol/L) had 0.038 SD (standardized β= -0.038, 95% CI -0.072 to -0.004, P=0.030) shorter mean LTL than the group with medium 25OHD levels. The associations above were adjusted for multiple variables. Conclusion: In this population-based study, we identified an inverted U-shape relationship between LTL and vitamin D status. Whether high or low vitamin D-associated shorter LTL is mechanistically related to age-related conditions remains to be elucidated.
Each cell controls when and how its genes must be expressed for proper function. Every function in a cell is driven by signaling molecules through various regulatory cascades. Different cells in a multicellular organism may express very different sets of genes, even though they contain the same DNA. The set of genes expressed in a cell determines the set of proteins and functional RNAs it contains, giving it its unique properties. Malfunction in gene expression harms the cell and can lead to the development of various disease conditions. Use of rapid high-throughput gene expression profiling unravels the complexity of human disease at various levels. Peripheral blood mononuclear cells (PBMC) have been used frequently to understand gene expression homeostasis in various disease conditions. However, more studies are required to validate whether PBMC gene expression patterns accurately reflect the expression of other cells or tissues. Vitamin D, which is responsible for a multitude of health consequences, is also an immune modulatory hormone with major biological activities in the innate and adaptive immune systems. Vitamin D exerts its diverse biological effects in target tissues by regulating gene expression and its deficiency, is recognized as a public health problem worldwide. Understanding the genetic factors that affect vitamin D has the potential benefit that it will make it easier to identify individuals who require supplementation. Different technological advances in gene expression can be used to identify and assess the severity of disease and aid in the development of novel therapeutic interventions. This review focuses on different gene expression approaches and various clinical studies of vitamin D to investigate the role of gene expression in identifying the molecular signature of the disease.
