Vitamin D Supplementation Does Not Reduce Blood Pressure of Premenopausal African American Women

Emerging evidence now suggests that low vitamin D status may contribute to the higher prevalence of hypertension and increased cardiovascular morbidity and mortality of African Americans. Vitamin D influences endothelial and smooth muscle cell function, mediates inflammation, and modulates the renin‐angiotensin axis. However, interventional data are limited regarding the influence of vitamin D supplementation on blood pressure and endothelial function. To further evaluate the potential of vitamin D supplementation to reduce racial blood pressure disparity, this study was undertaken to determine if vitamin D supplementation [2,000 International Units (IU) per day] for 10 weeks in premenopausal African American women would increase serum 25‐hydroxyvitamin D [25(OH)D] concentrations, reduce blood pressure, and improve endothelial function as assessed by reactive hyperemia index (RHI). Exclusion criteria included elevated blood pressure (> 140/90 mmHg), medical conditions influencing blood pressure, and regularly taking vitamin D supplements or medications that might affect endothelial function such as anti‐inflammatory medications, anti‐hypertensive medications, or daily aspirin. All statistical analyses were conducted using the IBM SPSS v2 with statistical significance set at P <.05. Wilcoxon signed rank was conducted to examine the effect of 2,0000 IU/d vitamin D supplementation on the levels of serum 25(OH)D, systolic blood pressure (SBP), diastolic blood pressure (DBP), RHI, % body fat, and body mass index (BMI) over 10 weeks. Nonparametric Spearman correlations were performed to examine the relationship of serum 25(OH)D concentrations with % body fat and BMI at baseline and after 10 weeks supplementation. Mean age of participants (n=22) was 37.7 ± 10 years and most women were overweight or obese (BMI 30.5 ± 27.9 kg/m 2 ; body fat 37.3 ± 37.4 %). Compliance assessed as the number of vitamin D pills remaining in returned supplement bottles was good (85%). Serum 25(OH)D concentrations at baseline were 22.4 ± 20.6 ng/mL indicating that 47.6% of the women were vitamin D deficient (<20 ng/mL) and only 14.3% were vitamin D sufficient (>30 ng/mL). After 10 weeks of vitamin D supplementation, serum 25(OH)D concentrations significantly increased to 36.5 ± 14.4 ng/mL (P < 0.005) and the percentage of vitamin D deficient women decreased 63%. An exact marginal homogeneity test confirmed a significant difference in vitamin D nutritional status categories between baseline and 10 weeks (P = 0.001). However, increased levels of serum 25(OH)D were not associated with significant reductions of SBP and DBP or a change of RHI (P>0.05). In addition, serum 25(OH)D concentrations were not found to be inversely correlated with % body fat which has been reported previously in some studies. In conclusion, although daily supplementation of 2,000 IU of vitamin D for 10 weeks significantly increased serum 25(OH)D concentrations, reduction of BP or change of endothelial function was not achieved in premenopausal African American women. Additional studies maybe warranted to determine if longer vitamin D supplementation helps to reduce racial blood pressure disparity in premenopausal African American women. Support or Funding Information Texas Woman's University Department of Nutrition and Food Sciences