The reported failure of vitamin E to prevent heart attacks may be due to underdosing, according to a new study conducted by researchers at the Vanderbilt University, Nashville, Tennessee, USA. The findings, published in the on-line edition of Free Radical Biology and Medicine, suggest that, in earlier studies the doses used were not high enough to have a significant antioxidant effect. In fact, no studies have ever conclusively demonstrated the dose at which vitamin E can be considered an antioxidant drug, the researchers report.
Oxidative stress occurs when reactive molecules called free radicals attack and damage cellular proteins, lipids and DNA. Epidemiological data and animal studies suggested that antioxidants like vitamins E and C, as well as beta-carotene, might protect against heart attack in those at risk. However, Jason Morrow, one of the investigators on the Vanderbilt study, noted that, "short of a couple of studies, there was no benefit in terms of prevention of cardiovascular events and deaths."
These results caused many to discount vitamin E supplementation as a cardioprotective treatment, but the US team suspected that the studies had been poorly designed. All of the trials simply gave a dose of vitamin E and looked for end points such as heart attack occurrence. But the US team found a critical piece of information missing. "All of these studies were designed in a way that they never assessed the ability of the dose of vitamin E tested to effectively reduce oxidant stress," Prof Morrow said.
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