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13 WHY VITAMIN E DOES NOT PREVENT ATHEROSCLEROSIS.

Purpose Recent clinical trials have indicated that vitamin E does not prevent atherosclerosis, in contrast to epidemiological studies that demonstrated a beneficial effect. To clarify this controversy, we examined the effects of different dosages of vitamin E (in combination with vitamin C) on the surrogate markers of atherosclerosis. Methods Our randomized, placebo-controlled, crossover trial involved 6 males and 5 females with type 2 diabetes. Each subject participated in four study arms: placebo, low-dose (200 IU/d), medium-dose (400 IU/d), and high-dose vitamins (800 IU/d). For each study arm, the subject took the corresponding vitamins daily for 2 weeks. The clinical protocol included a day-long hospital admission, during which the subject ate a high-fat meal. Blood was drawn at multiple time points, primarily after the meal. The primary outcomes were markers of oxidative stress (oxy-LDL and intracellular glutathione), inflammation (C-reactive protein [CRP] and adiponectin), and hypercoagulation (plasminogen activator inhibitor 1 [PAI-1] and fibrinogen). Results Low-dose vitamins reduced oxy-LDL across all time points when compared to other study arms (p = .002). However, there were no differences between the four arms in intracellular glutathione (p = .89), CRP (p = .84), adiponectin (p = 1.0), PAI-1 (p = .72), and fibrinogen (p = .95). Conclusion Supplementation of low-dose vitamin E (plus C), in type 2 diabetic individuals, significantly lowered postprandial levels of oxy-LDL. However, vitamins did not alter levels of intracellular glutathione, CRP, adiponectin, PAI-1, and fibrinogen when compared to placebo. These data suggest that low-dose vitamins reduce the oxidation of LDL but do not lower inflammation and hypercoagulation. Our study may explain why vitamin E at high dosages does not prevent atherosclerosis.