Vitamin E Helps Heart Only in High Doses

Research has found that vitamin E, despite being an antioxidant, does not provide any help in the prevention of heart attacks. Now a new study by researchers at Vanderbilt University Medical Center has found that this reported failure of vitamin E might be on account of lack of proper dosage.

When highly reactive molecules known as free radicals go on a rampage and attack cellular proteins, lipids (fats) and DNA, a condition known as oxidative stress or oxidant injury arises. The free radicals are normally byproducts of normal metabolism and present in our body at all times. However, in certain disease states such as heart disease, they are produced in excess and cause damage.

Epidemiological data and animal studies have found that antioxidant compounds such as vitamin E, vitamin C and beta-carotene can shield people who are at risk of heart attack from the action of these free radicals. However, certain other controlled clinical trials of vitamin E found that there is little or no benefit to be gained from this antioxidant.

Now Dr. Jack Roberts and colleagues claim that most of these studies were flawed. According to them, the studies did not use sufficiently high doses of vitamin E to be able to observe any significant antioxidant effect. In their opinion, none of the studies have conclusively found an ideal dose at which vitamin E can be considered an effective antioxidant drug.

“Multiple human trials looking at the effect of vitamin E supplementation on coronary events and atherosclerosis have all failed,” said Dr. Roberts, the T. Edwin Rogers Professor of Pharmacology, Professor of Medicine, and lead author on the study.
“We’re talking about trials that examined quite high doses,” added Dr. Jason Morrow, F. Tremaine Billings Professor of Medicine & Pharmacology and chief of the Division of Clinical Pharmacology. “Short of a couple of studies, there was no benefit in terms of prevention of cardiovascular events and deaths.”

The failure of the studies to find vitamin E effective in protecting the heart led many doctors to refrain from prescribing vitamin E supplements as treatment for heart disease. Dr. Morrow and Dr. Roberts however felt that there was something lacking in the studies in the sense that all of them just administered a dose of vitamin E to subjects and then checked for end results such as occurrences of heart attacks.

They felt that there was something crucial missing in the way the trials were conducted. “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,” Dr. Morrow said. The researchers hypothesized that results of the earlier trials were bound to be flawed if they did not determine if the dose of vitamin E administered was enough to exert any antioxidant effects.

To confirm their hypothesis, the study team used a different approach to checking the effects of vitamin E. They developed an assay to measure F2-isoprostanes. This measure, said Dr. Roberts, “has been independently validated as the best measure of oxidative stress status in vivo.” Using this assay they arrived at the best antioxidant dose of vitamin-E.

For doing this, the researchers first administered very high doses of vitamin E – 3200 IU/day to check how long it took for the antioxidant to suppress oxidative stress in patients at risk for cardiovascular disease. Despite the dose being more than 100 times the recommended daily intake of vitamin E, the researchers were surprised to find that the process took nearly 16 weeks.

3200 IU/day was also nearly four times higher than doses used in most of the earlier trials to achieve maximum suppression of F2-isoprostane formation. The researchers then administered varying doses of vitamin E (0, 100, 200, 400, 800, 1600 and 3200 IU/day) to a group of patients with similar cardiovascular risk factors. The period of study was kept at 16-weeks again to allow them to find the minimum effective dose.

The researchers found that 1600 IU/day of vitamin E was the minimum necessary to bring about an effective reduction in oxidative stress. This figure was still double of what was used in most of the earlier clinical trials.

“It was clear that large doses – and doses in excess of what all clinical studies had used – were necessary,” Dr. Morrow said. “Even with this massive dose of vitamin E, you only observe a 50% reduction in F2- isoprostanes,” added Dr. Roberts. “So in my opinion, vitamin E is not the spiffy antioxidant everybody thinks it is – it’s a pretty poor antioxidant.”

Because the long-term safety of such high doses is unknown, “we are not touting taking vitamin E in large doses,” Dr. Morrow said. “We are saying that, in the design of clinical trials, one needs to have good surrogate biochemical markers.”

Based on their findings, which have been published online in Free Radical Biology and Medicine, the researchers suggest the incorporation of measures such as F2-isoprostane into future studies that involve antioxidants in prevention of atherosclerosis.

And since oxidative stress has been linked to numerous other diseases, including Alzheimer’s disease, Dr. Morrow suggests that F2-isoprostane measurement “really ought to be incorporated into studies assessing disease prevention by antioxidants in general.”

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