That's certainly been the case with vitamin E. Some human studies have shown this antioxidant to play a protective role in cardiovascular disease, while other studies have shown it to have no effect at all. So the question on many consumers' minds is, Should I increase my vitamin E intake or not?

Scientists at Southwest Foundation for Biomedical Research (SFBR) don't have a definitive answer to that question yet, but their research with baboons has shed light on why human studies have been contradictory and why the answer isn't as clear cut as one would hope. In fact, the answer might be yes to one individual and no to another.

In the September issue of The American Journal of Clinical Nutrition, SFBR scientists explain their findings from a study with 250 baboons on a diet with equal levels of dietary fat and cholesterol but varying degrees of vitamin E concentration.

What we found was that vitamin E had a significant effect on cardiovascular disease risk factors, but those effects went in opposite directions. Some of the effects were positive, and some were negative, said Dr. David Rainwater, a scientist in the SFBR Department of Genetics and the lead author on the paper. This leads us to believe that the discrepancies in human studies are due to which effect is emphasized in the group of people studied.

Rainwater explained that the baboons that consumed higher levels of vitamin E had lower levels of oxidized LDL cholesterol. Oxidized LDL is believed to be a major player in terms of promoting atherosclerosis (the build up of fatty plaques in the arteries) and in cardiovascular disease in general, he said. So in this way, vitamin E was shown to play a protective role.

However, findings about vitamin E's effect on HDL, the good cholesterol, were contradictory. Higher levels of vitamin E in the diet increased levels of apolipoprotein A-1 (apo A-1), which helps HDL remain soluble in the blood. On the other hand, it decreased the average particle size of HDL.

And that is a bad thing, because a decrease in the size of HDL particles is generally associated with an increase in atherosclerosis, said Rainwater. So we found that vitamin E is exerting two different effects on HDL properties, one positive and one negative with respect to heart disease.

While the contradictory results are frustrating, the problem might not be so much with vitamin E as it is with our genes. This scientific investigation further revealed that vitamin E's positive influence on apo A-1 levels were not genetically influenced, but genes do appear to play a role in the negative effect vitamin E can have on HDL particle size.

So although this study doesn't give us a definite answer about whether or not everyone should increase their vitamin E intake, it does help explain the reason for the controversy over dietary vitamin E and its influence on cardiovascular disease, said Rainwater.

It also tells us that vitamin E might be beneficial to some individuals and not to others depending upon their genetic makeup. That means we need to conduct further investigations to find the genes involved.

Other scientists contributing to this investigation were Drs. Michael Mahaney and John L. VandeBerg with SFBR and the Southwest National Primate Research Center; and Dr. Xing Li Wang with Baylor College of Medicine in Houston.

Research funding was provided by the National Heart, Lung and Blood Institute (NHLBI) and the National Center for Research Resources (NCRR), both part of the National Institutes of Health.

Southwest Foundation for Biomedical Research is one of the leading independent biomedical research institutions in the United States, dedicated to advancing human health through innovative biomedical research. It is recognized within scientific and academic communities worldwide for the quality of its basic research into the nature, causes, preventions, and treatments for disease. SFBR's staff of more than 75 doctoral-level scientists conducts nearly 200 major research projects, with marked success in the areas of genetics, neonatal development, metabolic disorders and infectious diseases.

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