Vitamin E – Small Risk, Big Consequencesby Jennifer Gibson, PharmD | March 16, 2011
Many people supplement their diets with natural or synthetic vitamin E with the hope of preventing cardiovascular disease, dementia, cancer and other health conditions. But, recent evidence has shown virtually no widespread benefit of vitamin E supplementation. Moreover, vitamin E may actually increase the risk of stroke.
Vitamin E is a fat-soluble antioxidant, readily available in many foods: wheat germ, seeds and nuts, green leafy vegetables, tomatoes, pumpkin, sweet potatoes, blue crab, rockfish, mangoes, olives, avocadoes, and many more. The recommended daily intake of vitamin E for most adults is 15 mg/day. A vitamin E deficiency is rare.
A meta-analysis published in the British Medical Journal evaluated nine randomized, placebo-controlled trials that included a total of more than 100,000 patients taking vitamin E supplements for at least one year. The study reports that vitamin E supplementation does not affect overall stroke risk. In fact, vitamin E was associated with a significant 10% reduction in ischemic stroke. Overall, one ischemic stroke is prevented for every 476 people taking vitamin E for one year, equivalent to 21 strokes per 10,000 patients.
However, the most alarming finding is that the same study reports that the risk of hemorrhagic stroke increased by 22% with vitamin E supplementation. One additional hemorrhagic stroke will occur for every 1250 patients taking vitamin E for one year, equivalent to 8 strokes per 10,000 patients. Hemorrhagic strokes account for approximately 10% of all strokes, but lead to significant morbidity and mortality. Within 30 days of experiencing a hemorrhagic stroke, 40% to 80% of patients will die. Of those who survive, only 20% will regain functional independence.
Risk factors for hemorrhagic stroke include male gender, smoking, hypertension, advanced age, African American race, obesity, and high cholesterol. Unfortunately, this is the very group of people in whom prevention of cardiovascular and other diseases with vitamin E would be of the most interest. Other studies have already shown an increased risk of stroke among these specific populations related to vitamin E supplementation. Among men receiving 400 IU of vitamin E daily, the risk of hemorrhagic stroke increased significantly. Also, among men who were smokers, supplements as low as 50 mg vitamin E daily (approximately 110 IU) increased the risk of stroke. Among patients with a variety of chronic diseases, doses of 400 IU daily or higher increased all-cause mortality. (In healthy patients, other studies have shown no affect on all-cause mortality.)
The mechanism by which vitamin E increases stroke risk is unclear, but it is likely related to the fact that vitamin E inhibits platelet function and interferes with vitamin K-dependent clotting factors. Vitamin E should be consumed as part of every healthy, balanced diet, but supplementation should likely not be advised except for specific medical conditions under the advice of a health care professional. While the risk of hemorrhagic stroke is still small, the consequences are devastating. With no proven benefit of vitamin E supplementation, the risks should discourage its indiscriminate use.
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