uwinsymposium.org

It has long been known that smokers are at a much higher risk for developing heart disease than are nonsmokers. Some smokers hope that taking antioxidant vitamins, such as vitamin E, can reduce their risk of smoking-related heart trouble.

However, research reported in the February 2000 issue of the Journal of the American College of Cardiology suggests that while very high doses of vitamin E may be helpful in improving short-term changes in artery function after smoking, it cannot reverse established blood vessel abnormalities in smokers.

Smokers’ arteries are more likely to develop fatty deposits, or atherosclerosis, and become less elastic than arteries of nonsmokers. One aspect of arterial function that worsens with smoking is dilation, or expansion, of the arteries when blood flow through them increases. Smoking appears to decrease an artery’s ability to widen when necessary. Such a lack of arterial dilation could lead to diminished blood flow to the heart. If it continues, a heart attack might result.

The researchers, from the Universities of Innsbruck and Vienna, Austria, studied the arterial dilation of 22 healthy young men, with an average age of 27, who smoked about a pack of cigarettes per day. Eleven of the men took a high dose vitamin E supplement (600 International Units) every day for four weeks; 11 others took an inactive compound for the same period. These groups were also compared with a matched group of 11 healthy nonsmokers.

To measure arterial function, the researchers used a blood pressure cuff to compress each subject’s brachial artery, a large artery in the upper arm, and then released the pressure. Normal response to such manipulation is a widening, or dilation, of the artery after the pressure is removed. The widening was measured by an ultrasound technique, which produced an image of the artery.

Before the study began, the investigators measured the dilation response of the brachial arteries of both smokers and nonsmokers. They found that the smokers’ arteries did not expand to the same degree as did the arteries of nonsmokers.

After four weeks of high-dose vitamin E supplementation, the subjects were examined again — at least two hours after they had smoked a cigarette. In these tests, there was no difference between the arterial responses of smokers who had taken vitamin E supplements and smokers who had not.

The arterial responses were measured again 20 minutes after the smokers had smoked a cigarette, and in this case, vitamin E did seem to affect arterial dilation. In smokers who had taken vitamin E, the arterial dilation was more normal than in the smokers who had taken the placebo pills.

The authors interpreted these results as indicating that four weeks of vitamin E supplementation could not reverse the chronic arterial dysfunction that accompanies cigarette smoking. They did note that there seemed to be “a partially beneficial effect of vitamin E supplementation. … it prevented the transient further impairment of vasodilatation after acute smoking.”

“The potentially beneficial effect of high doses of vitamin E on arterial widening in smokers is so short-lived as to be a nonfactor,” commented Dr. David Kritchevsky, institute professor at the Wistar Institute in Philadelphia. “If smokers want to preserve their blood vessels and heart, the best way to accomplish this is by quitting smoking. It can’t be done with a pill. The best way to get vitamin E is from the grocery, or the cheap pharmacy,” he added.

It should be noted that the level of vitamin E supplementation in this study — 600 International Units — was quite high compared to the dietary amount recommended for healthy adults, which is 12 to 15 International Units per day.

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