Effect of Vitamin D3 Supplementation in Black and in White Children: A Randomized, Placebo-Controlled Trial.
What this study found
Vitamin D3 1000 IU/day safely increased serum 25(OH)D, but it did not produce an overall improvement in PTH or bone-turnover markers. In Black children, 25(OH)D rose from 16.6 Ϯ 7.4 to 24.2 Ϯ 7.4 ng/mL at 6 months; in White children, it rose from 23.5 Ϯ 6.0 to 29.2 Ϯ 7.0 ng/mL. PTH changed little in either group, and osteocalcin and C-telopeptide showed no consistent overall benefit, although race-specific changes were observed. No hypercalcemia occurred. The 25(OH)D-PTH relationship was linear without a clear plateau, and mean 25(OH)D still did not reach 30 ng/mL.
- Study & population
- Randomized, double-blind, placebo-controlled trial in healthy Black and White children aged 8 to 14 years from the Pittsburgh area who were not taking vitamin supplements.
- Intervention
- Children received oral vitamin D3, 1000 IU once daily as a tablet for 6 months, compared with placebo in race-stratified randomized arms.
- Key limitation
- The intervention was short term and involved a modest number of healthy children from one geographic region, which limits generalizability.
Original abstract
CONTEXT Dosages of vitamin D necessary to prevent or treat vitamin D deficiency in children remain to be clarified. OBJECTIVE To determine the effects of vitamin D3 1000 IU/d on serum 25-hydroxyvitamin D [25(OH)D], PTH, and markers of bone turnover (osteocalcin and collagen type 1 cross-linked C-telopeptide) in black children and white children, and to explore whether there is a threshold level of 25(OH)D associated with maximal suppression of serum PTH concentration. DESIGN Healthy 8- to 14-year-old Pittsburgh-area black (n = 84) and white (n = 73) children not receiving vitamin supplements, enrolled from October through March from 2008 through 2011, were randomized to vitamin D3 1000 IU or placebo daily for 6 months. RESULTS The mean baseline concentration of 25(OH)D was <20 ng/mL in both the vitamin D-supplemented group and the placebo group (19.8 ± 7.6 and 18.8 ± 6.9 ng/mL, respectively). The mean concentration was higher in the supplemented group than in the placebo group at 2 months (26.4 ± 8.1 vs 18.9 ± 8.1 ng/mL; P < .0001) and also at 6 months (26.7 ± 7.6 vs 22.4 ± 7.3; P = .003), after adjusting for baseline 25(OH)D, race, gender, pubertal status, dietary vitamin D intake, body mass index, and sunlight exposure. Increases were only significant in black children, when examined by race. The association between 25(OH)D and PTH concentrations was inverse and linear, without evidence of a plateau. Overall, vitamin D supplementation had no effect on PTH and bone turnover. CONCLUSIONS Vitamin D3 supplementation with 1000 IU/d in children with mean baseline 25(OH)D concentration <20 ng/mL effectively raised their mean 25(OH)D concentration to ≥20 ng/mL but failed to reach 30 ng/mL. Vitamin D supplementation had no effect on PTH concentrations.