School of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK.
Department of Medicine, University of Auckland, Auckland, New Zealand.
J Bone Miner Res. 2018 Aug;33(8):1464-1469. doi: 10.1002/jbmr.3442. Epub 2018 Jun 15.
Most trials of vitamin D supplementation have shown no benefits on bone mineral density (BMD), although severe vitamin D deficiency causes osteomalacia, which is associated with profound BMD deficits. Recently, the ViDA-BMD study from New Zealand demonstrated a threshold of baseline 25-hydroxyvitamin D (25OHD; 30 nmol/L) below which vitamin D supplementation did benefit BMD. We have now reexamined data from a similar trial in Aberdeen to determine whether a baseline 25OHD threshold of 30 nmol/L is also observed in that database. The Aberdeen study recruited 305 postmenopausal women in late winter and randomized them to receive placebo, vitamin D 400 IU/d, or vitamin D 1000 IU/d over 1 year. As previously reported, BMD loss at the hip was reduced by vitamin D 1000 IU/d only, and there was no significant treatment effect of either dose at the lumbar spine. In the present analysis, when the trial participants were grouped according to whether their baseline 25OHD was ≤30 nmol/L or above this threshold, significant treatment effects were apparent at both the spine and hip in those with baseline 25OHD ≤30 nmol/L, but no significant effects were apparent in those with baseline 25OHD above this level. There was evidence of a similar threshold for effects on parathyroid hormone, but no groups showed changes in bone turnover markers during the study. It is concluded that vitamin D supplements only increase bone density in adults with nadir 25OHD ≤30 nmol/L. This moves us further toward a trial-based definition of vitamin D deficiency in adults with adequate calcium intakes and suggests that supplement use should be targeted accordingly. Future trials of vitamin D supplementation should focus on individuals with 25OHD concentrations in this range. © 2018 American Society for Bone and Mineral Research.
大多数维生素 D 补充试验并未显示对骨密度 (BMD) 有任何益处，尽管严重的维生素 D 缺乏会导致佝偻病，这与严重的 BMD 缺乏有关。最近，新西兰的 ViDA-BMD 研究表明，基线 25-羟维生素 D (25OHD；30 nmol/L) 低于该水平时，维生素 D 补充可有益于 BMD。我们现在重新检查了阿伯丁类似试验的数据，以确定在该数据库中是否也观察到基线 25OHD 阈值为 30 nmol/L。阿伯丁研究招募了 305 名绝经后妇女，于隆冬季节入组，并将她们随机分配接受安慰剂、维生素 D 400 IU/d 或维生素 D 1000 IU/d 治疗，为期 1 年。如先前报道，仅维生素 D 1000 IU/d 可减少髋部 BMD 丢失，且腰椎的任何剂量均无显著治疗效果。在本次分析中，当根据基线 25OHD 是否≤30 nmol/L 或高于该阈值将试验参与者分组时，在基线 25OHD≤30 nmol/L 的患者中，脊柱和髋部均出现明显的治疗效果，但在基线 25OHD 高于该水平的患者中，未见明显效果。甲状旁腺激素的作用也存在类似的阈值，但在研究期间，没有任何组的骨转换标志物发生变化。结论是，维生素 D 补充剂仅可增加 25OHD 最低值≤30 nmol/L 的成年人的骨密度。这使我们更接近于在摄入足够钙的成年人中根据试验来定义维生素 D 缺乏症，并表明应相应地针对性地使用补充剂。未来的维生素 D 补充试验应集中在该范围内的 25OHD 浓度的个体上。 © 2018 美国骨矿研究学会。
