Article Text

  1. A. D. Gutierrez,
  2. Gonzalez D. de Serna,
  3. I. Robinson,
  4. D. S. Schade
  1. University of New Mexico School of Medicine, Albuquerque, NM


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.

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