More on the Failure of Antioxidant Trials in the Prevention of Heart Attacks

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 8 No. 1 • January 2005

More on the Failure of Antioxidant Trials in the Prevention of Heart Attacks

There has been much discussion of possible reasons that many long-term trials of antioxidant vitamins E and C did not provide protection against heart attacks. For example, as reported in Reference 1 below, Vitamin E supplementation in intervention trials to prevent cardiovascular disease was found to be efficacious in two trials (CHAOS and SPACE), whereas six other trials (ATBC, GISSI, PPP, SECURE, HOPE, and VEAPS) found no benefits.1 The authors1 note that there were widely varying doses of vitamin E used in these studies and that it is not known what doses of vitamin E are necessary to suppress oxidative stress in humans. They go on to point out that, importantly, “… none of these studies incorporated measures of oxidative stress, such as measurement of F2-isoprostanes, to determine the level of oxidative stress and the ability of vitamin E [at the doses studied] to effectively lower the level of oxidative stress in the study subjects.” [Emphasis added]

“In small single human studies involving subjects with conditions associated with elevated levels of F2-isoprostanes, some have found that vitamin E supplementation reduces the production of F2-isoprostanes, whereas others have not. In healthy subjects, vitamin E has no effects on urinary F2-isoprostane concentrations at doses of up to 2000 IU/day for up to 8 weeks. Moreover, a high dose of vitamin C (2500 mg/day) had no effect on lowering F2-isoprostane levels in normal subjects but was found to be effective in suppressing isoprostane formation in smokers … What such findings suggest is that oxidative stress is a complex phenomenon that may be influenced by covariates and that appropriate selection of antioxidant(s) and dose to effectively suppress oxidative stress in specific situations is less than predictable. On the other hand, it suggests that measurements of F2-isoprostanes may provide a uniquely valuable approach to elucidate these complexities and establish effective antioxidant dose regimens that can then be formally tested in individuals with a variety of disease states to determine whether amelioration of oxidative stress mitigates manifestations of disease.” [Emphasis added; reference citations deleted from quote]

  1. Montuschi et al. Isoprostanes: markers and mediators of oxidative stress. FASEB J 18:1791-1800 (2004).

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