Oral intermittent vitamin D substitution: influence of pharmaceutical form and dosage frequency on medication adherence: a randomized clinical trial

Background and aim Deficiency of vitamin D is known as a health problem all over the world and a recognized clinical complication of beta thalassemia patients. Vitamin D acts as a hormone at the nuclear receptor rendering it a beneficial medication for a number of diseases. It is believed that vitamin D is important in the modulation of the inflammation system by regulating the formation of inflammatory cytokines and immune cells. This study aimed to investigate the effect of vitamin D supplementation on the red cell indices and cytokines levels in patients with beta thalassemia major, in an open label randomized clinical trial. Patients and Methods: this study performed an open-label randomized clinical trial in patients with beta thalassemia major. Forty-six patients completed the eight weeks clinical trial and were allocated to administer oral vitamin D3 supplement of 100,000 IU every two weeks as an add-on treatment. During the study, hematological indices, serum iron, ferritin, vitamin D, calcium and inflammatory markers (interleukin-6, interleukin-2 and interleukin-10) were evaluated before (at baseline) and after vitamin D supplementation for 8 weeks. Results: Vitamin D3 supplements significantly decreases interleukin-6 levels and elevates the serum levels of anti-inflammatory cytokines IL-2 and IL-10, it also significantly reduced serum ferritin level, but it did not alter the hematological indices. Conclusion: Our results suggest that administration of vitamin D has a potential anti-inflammatory role in beta thalassemia patients and reduces serum ferritin levels, which may reduce the burdens of iron overload in thalassemia patients.

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Effects of Vitamin D3 Supplementation on Epigenetic Aging in Overweight and Obese African Americans With Suboptimal Vitamin D Status: A Randomized Clinical Trial

The Journals of Gerontology Series A ◽

10.1093/gerona/gly223 ◽

2018 ◽

Vol 74 (1) ◽

pp. 91-98 ◽

Cited By ~ 17

Author(s):

Li Chen ◽

Yanbin Dong ◽

Jigar Bhagatwala ◽

Anas Raed ◽

Ying Huang ◽

...

Keyword(s):

Clinical Trial ◽

Dna Methylation ◽

Vitamin D ◽

African Americans ◽

Randomized Clinical Trial ◽

Vitamin D3 ◽

Vitamin D Supplementation ◽

P Value ◽

Epigenetic Aging ◽

Vitamin D3 Supplementation

Abstract Background We have previously shown that vitamin D supplementation increases telomerase activity, suggesting an anti-aging effect. In this study, we aim to test the hypothesis that vitamin D supplementation would slow down epigenetic aging, a new marker of biological aging. Methods A randomized clinical trial was previously conducted among 70 overweight/obese African Americans with serum 25-hydroxyvitamin D [25(OH)D] < 50 nmol/L, who were randomly assigned into four groups of 600 IU/d, 2,000 IU/d, 4,000 IU/d of vitamin D3 supplements or placebo followed by 16-week interventions. Whole genome-wide DNA methylation analysis was conducted in 51 participants. DNA methylation ages were calculated according to the Horvath and the Hannum methods. Methylation-based age acceleration index (∆Age) is defined as the difference between DNA methylation age and chronological age in years. Mixed-effects models were used to evaluate the treatment effects. Results Fifty-one participants (aged 26.1 ± 9.3 years, 16% are male) were included in the study. After the adjustment of multi-covariates, vitamin D3 supplementation of 4,000 IU/d was associated with 1.85 years decrease in Horvath epigenetic aging compared with placebo (p value = .046), and 2,000 IU/d was associated with 1.90 years decrease in Hannum epigenetic aging (p value = .044). Serum 25(OH)D concentrations were significantly associated with decreased Horvath ∆Age only (p values = .002), regardless of treatments. Conclusions Our results suggest that vitamin D supplementation may slow down Horvath epigenetic aging. But the effect on Hannum epigenetic aging is not conclusive. Large-scale and longer duration clinical trials are needed to replicate the findings.

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