Key result
Vitamin D3 raises 25(OH)D levels but fails to improve arterial stiffness versus placebo.
Why the study?
Vitamin D deficiency is a potential cardiovascular risk factor, and few prospective studies have evaluated vitamin D supplementation effects on inflammatory and oxidative mediators of arterial stiffness.
Does vitamin D3 supplementation improve inflammatory and oxidative mediators of arterial stiffness in overweight and obese African Americans with elevated blood pressure and low vitamin D?
RCT (n=130)
Double-blind
Randomized
Yes
Does vitamin D3 supplementation improve inflammatory and oxidative mediators of arterial stiffness in overweight and obese African Americans with elevated blood pressure and low vitamin D?
Absolute Event Rate: 34.5% vs 17.2%
p-value: p=<0.001
Short-term high-dose vitamin D3 supplementation in African Americans with low vitamin D and elevated blood pressure improved biomarkers of oxidative stress and inflammation, but did not significantly improve overall arterial stiffness.
Vitamin D may reduce arterial stiffness dose-dependently in deficient overweight African Americans; leaves open effects on clinical cardiovascular outcomes.
BACKGROUND: Vitamin D deficiency has been implicated as a potential risk factor for cardiovascular disease. The high rate of vitamin D deficiency (<30 ng/ml) exhibited by African Americans may account for some of the excess prevalence of cardiovascular morbidity and mortality in this vulnerable US population. Vitamin D supplementation may reduce the risk of cardiovascular disease by ameliorating the onset and progression of arterial stiffness, a strong predictor of cardiovascular mortality, usually assessed by pulse wave velocity and augmentation index. Very few prospective studies have evaluated the effect of vitamin D supplementation on the inflammatory and oxidative stress mediators of arterial stiffness. METHOD: In a double blind randomized placebo controlled study we evaluated the effect of a monthly dose of 100,000IU of vitamin D3 for three months on the level of serum 25(OH)D, intact parathyroid hormone (PTH), urinary isoprostane, adipocyte cytokine expression and arterial stiffness among 130 overweight and obese (BMI > 25) African Americans with elevated blood pressure (130 - 150/85 - 100 mmHg) and low serum vitamin D level (10 - 25 ng/ml). RESULTS: There was a significant increase in the serum 25(OH)D levels to a mean level of 34.5 ng/ml (SD = 7.1) with the intervention (p < 0.001). The increase in 25(OH)D levels was associated with a significant decrease in the serum level of intact PTH (p = 0.02), mean urinary isoprostane (p = 0.02) and adipocyte cytokine expression. Although the increase in the 25(OH)D levels was not associated with any significant change in the Pulse Wave Velocity (PWV) in the overall study sample, it was associated with a significant decrease in the augmentation index among the participants with the highest tertile of urinary isoprostane (p = 0.007). CONCLUSION: We concluded that vitamin D supplementation increased serum 25(OH)D levels, decreased intact PTH level and the levels of select inflammatory and oxidative stress mediators of arterial stiffness. Longer term prospective studies are warranted to evaluate the effect of high dose vitamin D supplementation on arterial stiffness.
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Martins et al. (2014) conducted an RCT in Overweight and obese with elevated blood pressure and low serum vitamin D (n=130). Vitamin D3 vs. Placebo was evaluated on Serum 25(OH)D level at 12 weeks (p=<0.001). Vitamin D3 supplementation at 100,000 IU monthly for 3 months significantly increased serum 25(OH)D levels and decreased intact PTH, but did not significantly improve arterial stiffness in the overall cohort.
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