Clinic for Thoracic and Cardiovascular Surgery, Heart Center North Rhine-Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany.
J Photochem Photobiol B. 2010 Nov 3;101(2):124-9. doi: 10.1016/j.jphotobiol.2010.01.006. Epub 2010 Jan 22.
Globally, cardiovascular disease (CVD) is the number one cause of death, being responsible for approximately 30% of deaths worldwide. Urbanization and a westernized lifestyle are thought to play a major role in the development of CVD. There is accumulating evidence that vitamin D is a nonclassical risk factor for CVD. The active vitamin D metabolite, 1,25-dihydroxyvitamin D, which is synthesized from its precursor 25-hydroxyvitamin D (25[OH]D), down-regulates several negative and up-regulates various protective pathways in the heart and vasculature. First randomized trials demonstrate that vitamin D supplementation leads to vasodilatation and suppresses cardiovascular risk markers such as triglycerides and the inflammation marker tumor necrosis factor-α. Solar UV-B radiation is the major source of vitamin D for humans. Consequently, the vitamin D status is largely influenced by season, geographic latitude, daily outdoor activities, and the percentage of body surface exposed to solar UV-B. A significant proportion of individuals in Europe and North America have vitamin D concentrations in the deficiency range (25[OH]D<25 nmol/l). Available data indicate that low solar UV-B exposure and/or low 25(OH)D concentrations are associated with an increased risk of CVD. Large nonrandomized studies indicate that CVD mortality is more than twice as high in older individuals with deficient 25(OH)D concentrations compared with those individuals who have adequate 25(OH)D concentrations (>75 nmol/l). Together, experimental and epidemiological evidence does support a plausible role for improving vitamin D status in CVD prevention in the population at large. Nevertheless, future randomised clinical trials are needed to evaluate whether vitamin D is effective with respect to primary, secondary, and/or tertiary prevention of CVD.
在全球范围内，心血管疾病 (CVD) 是头号死亡原因，约占全球死亡人数的 30%。城市化和西方化的生活方式被认为是 CVD 发展的主要原因。越来越多的证据表明维生素 D 是非经典 CVD 危险因素。维生素 D 的活性代谢物 1,25-二羟维生素 D，由其前体 25-羟维生素 D（25[OH]D）合成，可下调心脏和血管中的几种负调控途径，并上调多种保护途径。首次随机试验表明，维生素 D 补充可导致血管扩张，并抑制心血管风险标志物，如甘油三酯和炎症标志物肿瘤坏死因子-α。太阳紫外线 B 辐射是人类维生素 D 的主要来源。因此，维生素 D 状况在很大程度上受季节、地理纬度、日常户外活动以及暴露于太阳紫外线 B 的体表面积百分比的影响。欧洲和北美的相当一部分人维生素 D 浓度处于不足范围（25[OH]D<25 nmol/l）。现有数据表明，低太阳紫外线 B 暴露和/或低 25(OH)D 浓度与 CVD 风险增加相关。大型非随机研究表明，与 25(OH)D 浓度充足（>75 nmol/l）的个体相比，25(OH)D 浓度不足的老年人 CVD 死亡率高出两倍以上。总之，实验和流行病学证据确实支持在一般人群中通过改善维生素 D 状态来预防 CVD 的合理作用。然而，仍需要未来的随机临床试验来评估维生素 D 是否对 CVD 的一级、二级和/或三级预防有效。
