Boucher Barbara J
Queen Mary University of London; Centre for Diabetes; Bart's & The London School of Medicine & Dentistry; London, UK.
Dermatoendocrinol. 2012 Apr 1;4(2):212-24. doi: 10.4161/derm.20012.
Review of the evidence on hypovitaminosis D as a risk factor for metabolic syndrome and its sequelae, T2DM and CVD, suggests long-term vitamin D repletion could reduce these risks. There is mechanistic evidence for protective effects for MetS and the balance of evidence, (cross-sectional and prospective), supports this postulate. Much of the data so far available from randomized controlled trials is weakened by inadequate power, low vitamin D dosages, starting supplementation too late in life or after MetS disorders have developed or, most importantly, by non-inclusion of many recognizable confounders. On balance, therefore, maintenance of US 2010 recommended intakes for bone protection has the potential to prove protective for MetS. Supplementation has been shown to increase survival in patients with cardiac disorders; whether higher doses would provide useful protection for apparently healthy people in the general population awaits the outcomes of ongoing randomized-controlled trials that, it is hoped, will prove or disprove causality for hypovitaminosis D in MetS and its long-term ill-effects.
对维生素D缺乏作为代谢综合征及其后遗症、2型糖尿病和心血管疾病风险因素的证据进行回顾表明,长期补充维生素D可降低这些风险。有机制证据表明维生素D对代谢综合征具有保护作用,且现有证据(横断面研究和前瞻性研究)支持这一假设。目前随机对照试验提供的许多数据因效力不足、维生素D剂量低、在生命后期或代谢综合征疾病发展后才开始补充,或者最重要的是未纳入许多可识别的混杂因素而受到削弱。因此,总体而言,维持美国2010年推荐的用于骨骼保护的摄入量有可能对代谢综合征起到保护作用。补充维生素D已被证明可提高心脏病患者的生存率;更高剂量是否能为普通人群中看似健康的人提供有效保护,有待正在进行的随机对照试验的结果,希望这些试验能证明或反驳维生素D缺乏与代谢综合征及其长期不良影响之间的因果关系。