Public release date: 22-Aug-2007
Nashville (Tenn.) – The reported failure of vitamin E to prevent heart attacks may be due to underdosing, according to a new study by investigators at Vanderbilt University Medical Center.
The findings, published early online in Free Radical Biology and Medicine, suggest that these earlier studies all had a fundamental flaw – the doses used weren’t 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.
Epidemiological data and animal studies suggested that antioxidant compounds like vitamin E, vitamin C and beta-carotene might offer some protection against heart attack in individuals at risk.
But subsequent controlled clinical trials of vitamin E – which showed little to no benefit from the vitamin – stymied that hope.
These results caused many to discount vitamin E supplementation as a cardioprotective treatment, but Morrow and Roberts 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 Morrow and Roberts 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,” Morrow said.
In the new study, Morrow and Roberts determined the optimum antioxidant dose of vitamin E using an assay they developed to measure compounds formed by oxidative stress processes, called F2-isoprostanes. This measure, said Roberts, “has been independently validated as the best measure of oxidative stress status in vivo.”
The researchers first determined how long it took for a very high dose of vitamin E – 3200 IU/day – to suppress oxidative stress in individuals at risk for cardiovascular disease.
To their surprise, it took 16 weeks for this dose – which is more than 100 times the recommended daily intake and about four times higher than doses used in most previous clinical studies – to maximally suppress F2-isoprostane formation.
In another group with similar cardiovascular risk factors, the researchers administered varying doses (0, 100, 200, 400, 800, 1600, and 3200 IU/day) over the 16-week period to find the minimum effective dose.
They found that it was necessary to give at least 1600 IU per day to cause a significant reduction in oxidative stress – twice that used in some of the previous clinical trials.
Ralph’s Note- Since Vitamin E is Fat Soluble, they should now measure this marker in individuals who have been consuming Vitamin E for much longer durations.