Whayne Thomas F
Professor of Medicine (Cardiology), Gill Heart Institute, University of Kentucky, Lexington, KY.
Int J Angiol. 2011 Jun;20(2):63-72. doi: 10.1055/s-0031-1279679.
Vitamin D deficiency is prevalent in the United States. Understanding any relationship between this deficiency and cardiovascular disease is essential. Vitamin D, as used, refers to both D(2) and D(3); both are present in over-the-counter supplements, whereas D(2) is the prescription product in the United States. In the liver, both D(2) and D(3) are converted to 25-hydroxyvitamin D, the major circulating metabolite that is measured to assess activity. The actual active form at a cellular level is 1,25-dihydroxyvitamin D; however, it does not correlate well with overall activity. Estimated vitamin D deficiency is, at times, more than 50%. Despite absence of placebo-controlled randomized trials, much information associates vitamin D deficiency with cardiovascular risk and supports benefit from vitamin D supplementation. There are also reports that explain how this benefit from vitamin D may occur. Vitamin D appears to cause only minimal changes in low- and high-density lipoprotein levels. Therefore, any cardiovascular benefit that may exist from vitamin D probably has an explanation other than an effect on levels of these lipoproteins. There is more association of vitamin D deficiency with metabolic syndrome components such as an increase in blood pressure, elevated plasma triglycerides, and impaired insulin metabolism. Possible documentation of cardiovascular benefit from vitamin D includes some evidence for endothelial stabilization and decreased inflammation in arteries. If the clinician decides that recommendation of vitamin D supplementation is warranted, it is reassuring that toxicity is rare. Furthermore, this toxicity involves doses exceeding those of most clinical trials and mainly has involved hypercalcemia. Vitamin D supplementation is easy and can be taken as a dose of 2000 IU daily on an indefinite basis. In 1997, the Food and Nutrition Board of the U.S. Institute of Medicine considered this the safe tolerable upper limit, but this is not based on current evidence. Some practitioners, especially endocrinologists, recommend vitamin D at a dose of 50,000 IU per week for 8 weeks, repeated if necessary to achieve a normal level of vitamin D. It appears appropriate to assess low vitamin D as a possible cardiovascular risk factor, but potential benefit of supplementation must be weighed against the current absence of definitive outcomes studies.
维生素D缺乏在美国很普遍。了解这种缺乏与心血管疾病之间的任何关系至关重要。本文中使用的维生素D是指D(2)和D(3)；两者都存在于非处方补充剂中，而在美国，D(2)是处方药。在肝脏中，D(2)和D(3)都会转化为25-羟基维生素D，这是用于评估活性的主要循环代谢物。细胞水平上的实际活性形式是1,25-二羟基维生素D；然而，它与总体活性的相关性并不好。估计维生素D缺乏率有时超过50%。尽管缺乏安慰剂对照的随机试验，但许多信息将维生素D缺乏与心血管风险联系起来，并支持补充维生素D有益。也有报告解释了维生素D的这种益处可能是如何产生的。维生素D似乎只会引起低密度和高密度脂蛋白水平的微小变化。因此，维生素D可能存在的任何心血管益处可能有其他解释，而不是对这些脂蛋白水平的影响。维生素D缺乏与代谢综合征的组成部分，如血压升高、血浆甘油三酯升高和胰岛素代谢受损，有更多关联。维生素D对心血管有益的可能证据包括一些内皮稳定和动脉炎症减轻的证据。如果临床医生决定有必要推荐补充维生素D，令人放心的是毒性很罕见。此外，这种毒性涉及超过大多数临床试验的剂量，主要涉及高钙血症。补充维生素D很容易，可以无限期地每天服用2000国际单位的剂量。1997年，美国医学研究所食品和营养委员会认为这是安全可耐受的上限，但这并非基于当前证据。一些从业者，尤其是内分泌学家，建议每周服用50000国际单位的维生素D，持续8周，如有必要可重复服用以达到正常的维生素D水平。将低维生素D评估为可能的心血管危险因素似乎是合适的，但补充维生素D的潜在益处必须与目前缺乏确定性结果研究的情况相权衡。
