A 16-Week Randomized Clinical Trial of 2000 International Units Daily Vitamin D3 Supplementation in Black Youth: 25-Hydroxyvitamin D, Adiposity, and Arterial Stiffness

Context: Vitamin D insufficiency/deficiency is commonly observed in black youth. Objective: The aim was to determine 25-hydroxyvitamin D[25(OH)D] in response to 2000 IU vitamin D supplementation over time; to evaluate the relation between 25(OH)D concentrations and total body fat mass by dual-energy x-ray absorptiometry; and to determine whether vitamin D supplementation improves arterial stiffness measured by pulse wave velocity (PWV). Design: We conducted a randomized, blinded, controlled clinical trial. Setting and Participants: Forty-nine normotensive black boys and girls, aged 16.3 +/- 1.4 yr, were randomly assigned to either the control group (400 IU/d; n = 24) or the experimental group (2000 IU/d; n = 25). Results: Plasma 25(OH)D values at baseline and at 4, 8, and 16 wk were 34.0 +/- 10.6, 44.9 +/- 9.4, 51.2 +/- 11.1, and 59.8 +/- 18.2 nmol/liter, respectively, for the control group; and 33.1 +/- 8.7, 55.0 +/- 11.8, 70.9 +/- 22.0, and 85.7 +/- 30.1 nmol/liter, respectively, for the experimental group. The experimental group vs. the control group reached significantly higher 25(OH)D concentrations at 8 and 16 wk, respectively. Partial correlation analyses indicated that total body fat mass at baseline was significantly and inversely associated with 25(OH)D concentrations in response to the 2000-IU supplement across time. Furthermore, carotid-femoral PWV increased from baseline (5.38 +/- 0.53 m/sec) to posttest (5.71 +/- 0.75 m/sec) in the control group (P = 0.016), whereas in the experimental group carotid-femoral PWV decreased from baseline (5.41 +/- 0.73 m/sec) to posttest (5.33 +/- 0.79 m/sec) (P = 0.031). Conclusion: Daily 2000 IU vitamin D supplementation may be effective in optimizing vitamin D status and counteracting the progression of aortic stiffness in black youth. Plasma 25(OH)D concentrations in response to the 2000 IU/d supplementation are negatively modulated by adiposity. (J Clin Endocrinol Metab 95: 4584-4591, 2010)