Vitamin E May Increase 'Bad' Cholesterol

Study says it undoes process that destroys LDL in liver

Please note: This article was published more than one year ago. The facts and conclusions presented may have since changed and may no longer be accurate. And "More information" links may no longer work. Questions about personal health should always be referred to a physician or other health care professional.

By
HealthDay Reporter

MONDAY, May 3, 2004 (HealthDayNews) -- You've probably heard that antioxidants such as vitamin E are good for you, but new research finds antioxidants may actually help produce "bad" cholesterol.

Experiments in cells and mice indicate that oxidation is necessary to reduce the amount of low-density lipoprotein (LDL) cholesterol produced in the liver. That's why polyunsaturated fatty acids, which are oxidants, can reduce cholesterol production.

Oxidation, also called oxidant stress, is a chemical reaction of a substance with oxygen. In the body, oxidant stress releases free radicals that damage cells.

"Not all oxidant stress is bad for you," said lead researcher Dr. Edward A. Fisher, a professor of cardiovascular medicine and cell biology at New York University. "Oxidant stress also has some benefits in terms of the cardiovascular system, by decreasing the liver production of the lipoproteins that cause atherosclerosis."

"Sometimes oxidative stress is good, and sometimes it's bad," said co-researcher Dr. Kevin Jon Williams, a professor of medicine at Jefferson Medical College. For example, humans breathe oxygen because they need oxidation to convert food into energy, and oxidant stress is also how the immune system kills bacteria, he added.

Fisher's team found liver cells under oxidative stress release free radicals made by the normal conversion of polyunsaturated fatty acids to so-called lipid peroxides.

When these free radicals are released, they destroy a critical protein called ApoB100. Without ApoB, the liver cannot make LDL cholesterol, and the amount of cholesterol released into the blood is therefore substantially reduced.

The researchers found that when vitamin E was introduced to these liver cells, it prevented the destruction of ApoB, which lets the liver make more LDL cholesterol, according to their report in the May issue of the Journal of Clinical Investigation.

In large studies, "vitamin E has flunked as a protection against coronary artery disease," Fisher said. So the "blanket recommendation for the use of antioxidants, such as vitamin E, for lowering the risk of heart disease is not warranted."

However, the findings also confirm that diets rich in polyunsaturated fatty acids, such as those found in fish, can substantially reduce the amount of bad cholesterol your body makes, Fisher added.

Williams said the he would "take vitamin E supplements only in circumstances where there has been proven clinical benefit, and that is not the case in cardiovascular disease."

Dr. Ronald Krauss, director of atherosclerosis research at the Children's Hospital Oakland Research Institute, said this study shows how diet can affect blood fat levels.

"This study reminds us that even though there are number of benefits of antioxidants in the diet, we can't assume that all antioxidants will benefit all aspects of health," said Krauss, who wrote an accompanying editorial.

There may be a lack of benefit from antioxidants on blood fat levels, Krauss said. "In order to determine whether antioxidants benefit heart disease, we have to rely on clinical studies," he noted.

"The studies that have been done to date have not shown a benefit from antioxidants. Maybe this study gives us one reason for that negative result," Krauss said.

"If one wants to take advantage of antioxidants, which can have many health benefits, one should rely on eating foods that are rich in antioxidants and not rely on taking supplements to prevent heart disease," Krauss advised.

More information

The American Heart Association can tell you about cholesterol, and the National Institutes of Health has more on vitamin E.

SOURCES: Edward A. Fisher, M.D., Ph.D., professor, cardiovascular medicine and cell biology, New York University, New York City; Kevin Jon Williams, professor, medicine, Jefferson Medical College, Philadelphia; Ronald Krauss, M.D., director, atherosclerosis research, Children's Hospital Oakland Research Institute, Oakland, Calif.; May 2004 Journal of Clinical Investigation

Last Updated:

Related Articles