Copyright © 1996 by Jack Challem, The Nutrition Reporter™
All rights reserved.
This article is from the May 1996 issue of The Nutrition Reporter™ newsletter.

In one of the most dramatic studies ever conducted on vitamin E, a team of researchers at Cambridge University found that supplements reduced the risk of non-fatal heart attacks by 77 percent. The benefits were clearly noticeable after taking the vitamin for just one year.

The double-blind, placebo-controlled study involved 2,002 patients, with an average age of 61, over 18 months. Angiography, a type of heart x-ray, confirmed that all of the patients had coronary atherosclerosis.

About half of the patients received either 400 IU or 800 IU of the natural form of the vitamin, d-alpha tocopherol, each day. The other half received dummy capsules. On average, blood levels of vitamin E rose by 49 percent among those taking 400 IU and by 88 percent among those taking 800 IU daily.

Patients taking vitamin E were one-fourth as likely to suffer a non-fatal heart attack, according to an article by Nigel G. Stephens, MRCP, and his colleagues in Lancet (March 23, 1996;347:781-6).

The findings were even more remarkable considering that the vitamin E group was generally at a high risk for "cardiovascular events." More than 37 percent had been diagnosed with serious coronary heart disease or already had triple-bypass surgery, and 24 percent had moderate or severe left ventricular dysfunction.

The researchers focused on non-fatal cases of myocardial infarction, or heart attack, because of the ability to precisely diagnose heart attacks through electrocardiography, cardiac enzyme measurements, and hospital records.

During the study, 23 of the placebo patients and 27 of the vitamin E patients died. Although deaths were slightly higher among people taking vitamin E, the researchers noted that the difference was not statistically significant and that most of the deaths occurred early in the study, before the vitamin E provided maximum benefits.

The researchers thought the vitamin E worked primarily by preventing free radical oxidative damage to cholesterol, considered a primary cause of coronary heart disease. But the study did not prove it.

"The study could not directly address the mechanism by which alpha-tocopherol reduces the risk of myocardial infarction," they wrote. "The extent of the risk reduction suggests that the benefit may be due to more than one mechanism, such as alpha-tocopherol-mediated reductions in platelet adhesion and aggregation, inhibition of vitamin-K-dependent clotting factors...and oxidised-LDL-mediated stimulation of endothelin production and inhibition of nitric oxide production. However, we believe that inhibition of oxidation is likely to exert its main effects by modification of plaque enlargement or plaque rupture."

According to the researchers, the benefits from vitamin E were greater than those from aspirin or cholesterol-lowering drugs.

The use of vitamin E in the treatment of heart disease‹which was often considered controversial‹dates back to the mid-1930s, when Evan Shute, MD, of Canada became the first physician to use the vitamin therapeutically in people.

Do Free Radicals and Antioxidants Play Roles in "Mad Cow" Disease?

It seems almost too incredible to be true, but free radicals and oxidative stress may be factors in the recent outbreak of "mad cow disease" and Creutzfelt-Jacob disease in England, two deadly neurological diseases.

According to laboratory experiments, antioxidants‹particularly vitamin E and N-acetyl cysteine‹may slow brain damage characteristic of these diseases.

In March 1996, the British government's health secretary acknowledged that bovine spongiform encephalopathy (BSE, mad cow disease) in cattle was probably the cause of the recent wave of Creutzfelt-Jacob disease in people. Within days, beef consumption plummeted, and nation after nation banned the importation of British beef.

BSE, which has been infecting large numbers of British cattle and dairy cows since the 1980s, is caused by the abnormal behavior of proteins called prions, which are neither viruses nor bacteria. The disease carves holes in the brains of animals, causing progressive and irreversible neurological degeneration. Prions also cause scrapie, a similar neurological disease in sheep, and researchers believe that the disease-causing prions were transmitted to cattle when they were fed the remains of butchered sheep as a high-protein supplement.

Since then, Creutzfelt-Jacob disease, a rare neurological disease that affects people, has increased in incidence in England. Historically, Creutzfelt-Jacob disease has struck people in their 60s. But the new strain is affecting people in their 20s, with a particularly high cluster among English dairy farmers. Although there's no definitive evidence that eating BSE-tainted meat causes Creutzfelt-Jacob disease, the link is suspected.

The disease process appears to involve microglia, a type of brain and nervous system cell that normally collects metabolic waste products from nerve tissues, according to Hans A. Kretzschmar, PhD, and his colleagues at the University of Gottingen, Germany. In recent studies, Kretzschmar found that killing microglia outright stopped the damage to brain cells, suggesting that microglia play a pivotal role in prion diseases.

So Kretzschmar focused on the behavior of microglia. In an experiment described in the journal Nature (March 28, 1996; 380:345-347), he determined that prion-stimulated microglia release large amounts of free radicals, particularly superoxide radicals and nitric oxide, which destroy normal brain cells. Another experiment by Kretzschmar showed that vitamin E and N acetyl-cysteine block this damage.

"Oxidative stress is involved in this mechanism," Kretzschmar and his colleagues wrote. "Microglia are also activated in murine [mouse] scrapie and there is evidence that microglia are stimulated by beta-amyloid [an undesirable brain protein] to produce neurotoxic agents. Microglia appear to be an important mediator of neuronal death in degenerative diseases of the brain."

Kretzschmar's findings are consistent with a growing body of research showing that free radical damage may cause other brain diseases, including Alzheimer's and Parkinson's diseases (Harman D, Age, 1995;18:97-119). In addition, the body's immune response to bacterial and viral infections releases large numbers of free radicals (Hickman P, et al., British Journal of Surgery, 1994;81:790-8).

It's conceivable that susceptibility to Creutzfelt-Jacob disease is aggravated by accumulating free radical, or oxidative, stresses. While there's no evidence vitamin E can cure BSE or Creutzfelt-Jacob disease, Kretzschmar's research points to a potential role of antioxidant therapy in slowing the disease's progression.

The information provided by Jack Challem and The Nutrition Reporter™ newsletter is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your physician.