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Abstract
Response of parathyroid hormone (PTH) to vitamin D supplementation is determined by the baseline PTH level and change in vitamin D status. Conflicting reports in Blacks exist on the PTH response to vitamin D to supplementation. During 3 winters from 2007-2010, 328 healthy Blacks (median age, 51 years) living in Boston, MA were randomized into a 4-arm, double-blind trial for 3 months of placebo, 1000, 2000, or 4000 IU of vitamin D3. PTH was measured in 254 participants at baseline and at the end of vitamin D supplementation period. The differences in PTH between baseline and 3 months were 3.93 pg/mL for those receiving placebo, -3.37 pg/mL for those receiving 1000 IU/d, -6.76 pg/mL for those receiving 2000 IU/d, and -8.99 pg/mL for those receiving 4000 IU/d ( -2.98 pg/mL for each additional 1000 IU/d of vitamin D3; p<0.001). We found a significant decrease in PTH with increasing doses of vitamin D supplementation up to intakes of 4000 IU/d in Blacks. Clinical Trials.gov: NCT00585637.
Highlights
Response of parathyroid hormone (PTH) to vitamin D supplementation is determined by the baseline PTH level and change in vitamin D status
More data are needed to assess the need for vitamin D supplementation for non-skeletal outcomes and to identify potential threshold effects for non-skeletal outcomes given the current controversy about the role of PTH [13,14,15,16] and vitamin D in disease pathogenesis
We examined changes in serum PTH according to vitamin D supplementation in several ways
Summary
Response of parathyroid hormone (PTH) to vitamin D supplementation is determined by the baseline PTH level and change in vitamin D status. Conflicting reports in Blacks exist on the PTH response to vitamin D to supplementation. Blacks have significantly lower circulating 25hydroxyvitamin D [25(OH)D] and higher serum parathyroid hormone [PTH] concentrations than Whites [1, 2]. Observational and intervention studies have shown that vitamin D deficiency and high serum PTH are associated with increased risk of skeletal disease [3, 4]. Recent studies have identified an association of high PTH with increased morbidity and mortality independent of bone disease [6]. More data are needed to assess the need for vitamin D supplementation for non-skeletal outcomes and to identify potential threshold effects for non-skeletal outcomes given the current controversy about the role of PTH [13,14,15,16] and vitamin D in disease pathogenesis. Understanding the role of vitamin D supplementation on PTH homeostasis is important
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