Study shows antioxidant takes no bite out of atherosclerosis in healthy people
LOS ANGELES, Sept. 17-Despite its early promise, taking vitamin E does not appear to slow the progression of atherosclerosis in healthy people, according to researchers from the USC Atherosclerosis Research Unit and colleagues.
Many believe that atherosclerosis, the thickening of artery walls that can lead to heart attack and stroke, results from oxidative damage to tissue in the artery wall caused by fats in the blood.
Epidemiological studies had supported the idea that vitamin E protected against atherosclerosis by fighting oxidative damage, but results from the Vitamin E Atherosclerosis Prevention Study call that into doubt, researchers report in the Sept. 17 issue of Circulation.
"The study showed that vitamin E could reduce the oxidation of LDL cholesterol-the so-called bad cholesterol-in the blood, but that didn't translate into a slower progression of atherosclerosis," says Howard N. Hodis, M.D., professor of medicine and preventive medicine at the Keck School of Medicine of USC and the study's lead author.
More than 300 healthy men and women age 40 or older enrolled in the study, and each took either a daily dose of 400 international units of vitamin E or a placebo. (Drugstore vitamin E supplements typically range from 50 I.U. to 1,000 I.U.) They visited the clinic every six months for three years, and investigators measured the intima-media thickness of their carotid arteries on each visit through ultrasound.
After three years, participants who took the vitamin E showed significantly less oxidized LDL in the blood, but had comparable progression of atherosclerosis to those who took no vitamin E.
"This means there's either something wrong with the hypothesis about oxidative damage and atherosclerosis, or we haven't found the right clinical trial to prove it," says Hodis, director of the USC Atherosclerosis Research Unit.
The study parallels findings from other recent randomized controlled trials.
It might come down to finding a specific group of patients who benefit, Hodis says. Antioxidant therapy might work better for people in their 20s, rather than those in their 40s and above, for example. Or perhaps it might only help high-risk patients, such as those with diabetes. A recent study showed that patients with existing heart disease and kidney disease who took vitamin E had fewer heart attacks than those who took a placebo, he adds.
Perhaps vitamin E might help those who have low levels of vitamins in their blood. "It may be that in epidemiological studies showing a benefit from vitamin E, participants didn't have high vitamin E levels to begin with, so supplementing this vitamin up to a point might help," Hodis says. "It may be that after that point, it provides no additional benefit."
Also, though vitamin E clearly acts as an anti-oxidant within the blood, it may not have the same effects within the tissue of the artery wall, where it would be most important, Hodis says. Its mechanisms need further study.
Vitamin E showed no negative health effects in the study.
For now, Hodis says, the best advice for healthy people who want to slow down atherosclerosis is to eat right, maintain healthy blood pressure and exercise. Lipid-lowering drugs prescribed by a physician also can help reduce the risk of heart attacks and strokes.
"We don't want to throw vitamin E out with the bath water," Hodis says. "But we do want to reflect, rethink and figure out where to go next."
The study was supported by a grant from the National Institute on Aging and Hoffmann-La Roche Inc. Investigators in the study came from the Keck School of Medicine of USC, the USC School of Pharmacy, Kaiser Permanente Medical Center in Los Angeles and the Jet Propulsion Laboratory and Caltech.
Howard N. Hodis, Wendy J. Mack, Laurie LaBree, Peter R. Mahrer, Alex Sevanian, Chao-ran Liu, Ci-hua Liu, Juliana Hwang, Robert H. Selzer and Stanley P. Azen, "Alpha-Tocopherol Supplementation in Healthy Individuals Reduces LDL Oxidation but not Atherosclerosis," Circulation. Vol. 106, No. 12, Sept. 17, 2002.