Background
Vitamins are organic materials that are required in very minute amounts in the human body for certain critical chemical reactions to occur. (Minerals are inorganic materials that are also required for certain critical reactions to occur.) In 1922 a substance was discovered that when eliminated from the diets of rats led to infertility. This was initially called “anti-sterility factor”, and in 1925 the name was changed to vitamin E reflecting the fact that it was the fifth vitamin discovered. Vitamin E is actually a group of 8 naturally occurring compounds all referred to as tocopherols, deriving from the Greek “toc” (child) and “phero” (to bring forth) describing its role as an essential dietary substance in normal fetal and childhood development. Vitamin E is one of the four fat soluble vitamins, A, D and K being the others.
Atherosclerosis
Through a complicated process called oxidation, fats in our system, most notably LDL cholesterol, become altered and damaged and lead to deposition of these altered fatty substances on the inside of blood vessel walls. These deposits accumulate with time and eventually lead to significant blockages of the blood vessels which can limit the flow of essential blood through the vessel. This limitation of blood flow can lead to damage such as a heart attack or stroke. Because the central process to blood vessel damage is the oxidative damage to LDL cholesterol, it was hypothesized that if we could prevent that oxidation, we could prevent atherosclerosis. Vitamins B, C and E as well as the mineral selenium are all naturally occurring antioxidants. That is to say they prevent the oxidative damage to human LDL. Vitamin E also has the effect of inhibiting platelet function and decreasing the blood’s tendency to form clots. It was therefore hypothesized that these naturally occurring antioxidants (vitamin E being the most potent antioxidant) would be protective to the blood vessel and decrease and prevent atherosclerosis.
Alzheimer’s Disease
Alzheimer’s disease is the number one cause of dementia (loss of mental functioning preferentially memory function) in the U.S.A. The cause at this time is unknown but it is thought that the process of oxidation is somehow involved with the brain damage that occurs. In 1997, one small study of 341 patients with moderate Alzheimer’s Disease did show slight benefit in those patients who received 1,000 units of vitamin E twice daily for two years.
Heart Disease
With respect to heart disease, there have been 19 experimental trials involving vitamin E in over 135,000 patients. The overwhelming majority of these trials have been very disappointing. When used in high doses, greater than 400 units daily, vitamin E may actually be associated with a worsening in mortality. That is to say the patients that took high dose vitamin E actually died more often than patients that took nothing.
Cancer
There have been at least 14 randomized trials regarding vitamin E and either gastrointestinal or lung cancer. The results of these trials are uniformly disappointing in that there was no evidence that antioxidant supplementation reduced the incidence of cancer. Once again there was a slight worsening of mortality among the antioxidant recipients in some of these trials.
Recommendations
The American Heart Association and the United States Preventative Services Task Force at this time state that there is insufficient evidence to recommend the use of antioxidant vitamins for the prevention or treatment of cardiovascular disease. High dose, i.e. greater than 400 units daily, vitamin E supplementation may actually increase mortality and should probably be avoided. The use of high dose vitamin E in Alzheimer’s patients without heart disease may perhaps be beneficial and should be discussed with your physician.
We at LernerCohen Healthcare hope this has been beneficial and encourage you to discuss these issues with your physician should you have further questions or concerns.
References: Uptodate, Harrison’s Textbook of Medicine, Annals of Internal Medicine Jan 4, 2005, Lancet Oct. 2, 2004, New England Journal of Medicine 1997, New England Journal of Medicine April 14, 1994.
