Bone Abstracts

There is wide variation in the dose-response to oral vitamin D and the increment in plasma 25(OH)D decreases per unit vitamin D given. We hypothesised that this is related to increased 25(OH)D catabolism as reflected in 25OHD half-life (25(OH)D₃ t_1/2).

Design: 25(OH)D₃ t_1/2 was measured with a stable isotope (SI) technique in older (70y+) men and women in the UK during winter before (n=47; 0kIU) or after 9–10 months of supplementation (n=20, 24, 22 for 12k, 24k or 48k IU Vitamin D₃/month, respectively). Plasma concentrations of the SI of 25(OH)D, 25(OH)D and 24,25(OH)₂D were measured by LC-MS-MS and 1,25(OH)₂D by RIA.

Results: Plasma 25(OH)D₃ t_1/2 did not significantly differ before and after supplementation (P=0.35) and between groups with no apparent dose-response (ANOVA for group difference P=0.05); mean(S.E.M.) was 20.3(0.45), 22.6(1.1), 20.6 (0.65) and 19.8(0.58) days for 0, 12, 24 and 48kIU, respectively. Vitamin D supplementation was associated with a significantly higher plasma 25(OH)D [49(3.7), 73(5.2), 77(3.1) and 97(4.7) nmol/l; P<0.0001] and 24,25(OH)₂D [3.1(0.33), 7.1(0.61), 7.1(0.36) and 9.0(0.57) nmol/; P<0.0001] for 0, 12, 24 and 48kIU, respectively. Plasma 1,25(OH)₂D concentrations were (geometric mean(95%CI)): 123(69-220), 125(68-234), 145(88-241) and 143(98-210) pmol/L (P=0.04). Chromatograms showed a significant increase in the ratio between the peak intensity of respectively 25(OH)D and 24,25(OH)₂D and 2 yet unidentified peaks with the same MRMs of these two compounds but with different retention times.

Conclusions: Plasma 25(OH)D₃ t_1/2 was not influenced by vitamin D supplementation, despite higher plasma 25(OH)D and 24,25(OH)₂D concentrations. This suggests that, in contrast to previous assumptions, 25(OH)D₃ t_1/2 may be closely regulated and mechanisms other than 25- and 24,25-hydroxylation may be involved in the increased clearance of vitamin D at a high oral supply.