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Circulation. 2003;107:926-928
doi: 10.1161/01.CIR.0000048966.26216.4C
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(Circulation. 2003;107:926.)
© 2003 American Heart Association, Inc.

Antioxidants and Atherosclerosis

Don’t Throw Out the Baby With the Bath Water

I. Jialal, MD, PhD; S. Devaraj, PhD

From the Laboratory for Atherosclerosis and Metabolic Research, UC Davis Medical Center, Sacramento, Calif.

Correspondence to Ishawarlal Jialal, MD, PhD, Laboratory for Atherosclerosis and Metabolic Research, UC Davis Medical Center, 4365 Second Ave, Research One Building, Room 3000, Sacramento, CA 95817. E-mail ishwarlal.jialal@ucdmc.ucdavis.edu


Key Words: Editorials • antioxidants • atherosclerosis


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Several lines of evidence support a role for oxidative stress and inflammation in atherogenesis. Epidemiological studies suggest that low levels of antioxidants are associated with increased risk for cardiovascular disease (CVD), and that increased intakes appear to be protective. In supplementation studies in humans, alpha-tocopherol (AT), the major form of vitamin E, decreases lipid peroxidation (low-density lipoprotein [LDL] oxidation and F2-isoprostanes) and platelet aggregation and adhesion and is antiinflammatory.1

See p 947

However, results of prospective antioxidant clinical trials have been disappointing. The Table summarizes the large prospective trials with antioxidants published to date, including the article by Salonen et al2 that appears in this issue of Circulation.


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Summary of Prospective Antioxidant Clinical Trials

Before this recent report of Salonen et al,2 there have been 10 previous studies that used various combinations of antioxidants, including AT, ascorbic acid (AA), and beta-carotene (BC) on cardiovascular events (CVE). Of the 10 studies, 3 showed a benefit with regards to the primary endpoint (Table).

In the Cambridge Heart AntiOxidant Study (CHAOS), patients received placebo or natural AT (RRR-AT) at a dose of either 400 or 800 IU/d.3 AT supplementation resulted in a significant increase in plasma AT levels and a significant 47% reduction in the primary endpoint, defined as combined endpoint of cardiovascular death and non-fatal myocardial infarction. However, there was no significant effect on cardiovascular mortality. The Secondary Prevention with Antioxidants of Cardiovascular disease in End-stage renal disease (SPACE) study4 was a double-blind, placebo-controlled, randomized, secondary prevention trial in . . . [Full Text of this Article]


Related Article:

Six-Year Effect of Combined Vitamin C and E Supplementation on Atherosclerotic Progression: The Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study
Riitta M. Salonen, Kristiina Nyyssönen, Jari Kaikkonen, Elina Porkkala-Sarataho, Sari Voutilainen, Tiina H. Rissanen, Tomi-Pekka Tuomainen, Veli-Pekka Valkonen, Ulla Ristonmaa, Hanna-Maaria Lakka, Meri Vanharanta, Jukka T. Salonen, and Henrik E. Poulsen
Circulation 2003 107: 947-953. [Abstract] [Full Text]



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