Gutierrez Absalon D, de Serna Daniela Gonzalez, Robinson Irina, Schade David S
University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Metabolism. 2009 Apr;58(4):469-78. doi: 10.1016/j.metabol.2008.11.003.
Vitamin E has been studied extensively in the prevention of atherosclerosis. Cross-sectional population studies as well as randomized controlled intervention trials have demonstrated conflicting results. A recent meta-analysis of these trials has emphasized the ineffectiveness of vitamin E in atherosclerosis prevention, with a possibility of harm at higher dosages. However, vitamin E has several isomers, with the alpha form being available via dietary supplements and the gamma form being available via dietary foodstuffs. The gamma form of vitamin E demonstrates several superior properties (such as trapping reactive nitrogen species and detoxifying nitrogen dioxide) compared with alpha vitamin E. All clinical trials have used the alpha isomer, with little concern that this isomer of vitamin E may actually suppress the gamma isomer of vitamin E. We undertook a dose-response study in volunteers with type 2 diabetes mellitus to include all the dosages of alpha vitamin E that have been used in cardiovascular prevention trials to determine the effect of alpha vitamin E on gamma vitamin E. We also assessed the effect of alpha vitamin E on several traditional markers of atherosclerotic risk. We added vitamin C to the vitamin E because several clinical trials included this vitamin to enhance the antioxidant effects of alpha vitamin E. Volunteers received, in randomized order for a 2-week period, one of the following vitamin dosage arms: (1) no vitamins, (2) low-dose supplemental vitamins E plus C, (3) medium-dose supplemental vitamins E plus C, and (4) high-dose supplemental vitamins E plus C. Blood levels of both alpha and gamma vitamin E were measured as well as surrogate markers of oxidative stress, hypercoagulation, and inflammation during a high-fat atherogenic meal (to increase the ambient oxidative stress level during the study). The results demonstrate that alpha vitamin E levels increased in proportion to the dose administered. However, at every dose of alpha vitamin E, gamma vitamin E concentration was significantly suppressed. No beneficial changes in surrogate markers of atherosclerosis were observed, consistent with the negative results of prospective clinical trials using alpha vitamin E. Our results suggest that all prospective cardiovascular clinical trials that used vitamin E supplementation actually suppressed the beneficial antioxidant gamma isomer of vitamin E. No beneficial effects on several potential cardiovascular risk factors were observed, even when the vitamin E was supplemented with vitamin C. If a standardized preparation of gamma vitamin E (without the alpha isomer) becomes available, the effects of gamma vitamin E on atherosclerotic risk will warrant additional studies.
维生素E在动脉粥样硬化预防方面已得到广泛研究。横断面人群研究以及随机对照干预试验得出了相互矛盾的结果。最近对这些试验的一项荟萃分析强调了维生素E在预防动脉粥样硬化方面无效,且高剂量时可能有害。然而,维生素E有几种异构体,α型可通过膳食补充剂获得,γ型可通过食物获得。与α型维生素E相比,γ型维生素E具有几种优越的特性(如捕获活性氮物种和使二氧化氮解毒)。所有临床试验都使用了α异构体,几乎没有人担心这种维生素E异构体实际上可能会抑制维生素E的γ异构体。我们对2型糖尿病志愿者进行了一项剂量反应研究,纳入了心血管预防试验中使用过的所有α型维生素E剂量,以确定α型维生素E对γ型维生素E的影响。我们还评估了α型维生素E对几种传统动脉粥样硬化风险标志物的影响。我们在维生素E中添加了维生素C,因为一些临床试验加入这种维生素以增强α型维生素E的抗氧化作用。志愿者在2周内按随机顺序接受以下维生素剂量组之一:(1)不服用维生素;(2)低剂量补充维生素E加C;(3)中剂量补充维生素E加C;(4)高剂量补充维生素E加C。在高脂致动脉粥样硬化餐期间(以增加研究期间的环境氧化应激水平)测量α和γ维生素E的血液水平以及氧化应激、高凝和炎症的替代标志物。结果表明,α型维生素E水平随给药剂量成比例增加。然而,在每一个α型维生素E剂量下,γ型维生素E浓度均被显著抑制。未观察到动脉粥样硬化替代标志物的有益变化,这与使用α型维生素E的前瞻性临床试验的阴性结果一致。我们的结果表明,所有使用维生素E补充剂的前瞻性心血管临床试验实际上都抑制了维生素E有益的抗氧化γ异构体。即使维生素E与维生素C一起补充,也未观察到对几种潜在心血管危险因素的有益影响。如果有不含α异构体的标准化γ型维生素E制剂,γ型维生素E对动脉粥样硬化风险的影响将值得进一步研究。