Can antioxidants ease the onset of atherosclerosis?
the progression of atherosclerosis in healthy people, according to
researchers in the United States.
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 in the US.
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 17 September 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," said Howard N. Hodis, 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 aged 40 or older enrolled in the study, and each took either a daily dose of 400 international units of vitamin E or a placebo (chemist 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 oxidised 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," added Hodis.
The study parallels findings from other recent randomised controlled trials, Hodis writes. It might come down to finding a specific group of patients who benefit, he added. 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, Hodis continued.
He suggest that 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 said. "It may be that after that point, it provides no additional benefit."
Although vitamin E clearly acts as an antioxidant within the blood, it may not have the same effects within the tissue of the artery wall, where it would be most important. As such, Hodis is calling for further study into its mechanisms.
Hodis stressed that 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 doctor can also help to reduce the risk of heart attacks and strokes.
"We don't want to throw vitamin E out with the bath water," said Hodis. "But we do want to reflect, rethink and figure out where to go next."
Full findings of the "Alpha-Tocopherol Supplementation in Healthy Individuals Reduces LDL Oxidation but not Atherosclerosis," study are published in the 17 September issue of Circulation (Vol. 106, No. 12).
