Heart Disease

Health |

The latest research findings appear to have turned the tables on our once high hopes for vitamin E. Now it looks increasingly unlikely that this antioxidant vitamin is a “magic bullet” that by itself can put a dent in heart disease.

The Heart Outcomes Prevention Evaluation (HOPE) trial found that natural vitamin E (d-alpha-tocopherol) at a dose of 400 IU daily did not reduce the number of heart attacks, strokes, or deaths from heart disease any more than placebo.93 The details of this well-designed double-blind trial were published in the January 20, 2000, issue of The New England Journal of Medicine. The trial, lasting an average of 4.5 years, followed over 9,000 men and women who had existing heart disease or were at high risk for it.

We already knew that vitamin E supplements (50 IU synthetic) didn’t work for heart disease in smokers,94,95,96 but that could be readily explained away: Perhaps vitamin E, especially in that relatively small dose, could not overcome the damaging effects of smoking.

The Cambridge Heart Antioxidant Study (CHAOS) trial,97 published in 1996, is what really had gotten our hopes up. In that trial, people with existing heart disease who took natural vitamin E (400 IU or 800 IU daily) had substantially fewer nonfatal heart attacks compared to the placebo group after about 1.5 years. Even so, and this may resonate with the latest findings, heart-related deaths were not reduced in the vitamin E group. Furthermore, it has been suggested that possible flaws in the design of this trial might make its findings questionable.

Large observational studies in both men and women found substantial benefits for vitamin E (100 IU).98,99,100 One observational study of 11,178 people aged 67 to 105 years found good results from combining vitamins E and C.101 Those who were taking vitamin E supplements at the beginning of the study had a 34% lower risk of death from heart disease than those who were not. Vitamin C supplements alone did not seem to make a difference, but the combination of vitamins E and C boosted the risk reduction to 53%. Long-term use of vitamin E granted an even stronger risk reduction of 63%. By their nature, though, observational studies cannot fully control for lifestyle factors, so it is possible that people taking vitamin E might also eat better and exercise more, which would influence the results.

So where does all this leave us? Experts uncomfortable with abandoning vitamin E have wondered whether it could be that vitamin E supplements exert a benefit in people who do not already have heart disease or are at low risk for it. Or, perhaps it takes vitamin E longer to exert a clinical benefit than the follow-up period of the studies. Realistically, though, there is no real evidence that this is true.

It might be that we just can’t expect vitamin E—or perhaps any other single nutrient—to carry the full burden alone. The antioxidants are a package deal in nature. This group of nutrients, including vitamins E, A, C, selenium, and others, may work best as a team in nature’s finely tuned botanical orchestra. The fact that lone vitamin E supplementation appears not to be the magic bullet we had hoped for hints that it might be better to take a balanced, comprehensive array of nutrients rather than depending on high doses of a few key nutrients to carry the load. We will be eagerly awaiting the outcome of ongoing trials of vitamin E combined with other antioxidants.

In addition, vitamin E itself is present in several forms in food, and some researchers believe that this mixture may work best and that perhaps taking too much of one form of vitamin E may blunt the effect of the others.