Steinberg Antioxidants and Atherosclerosis 1421 i Cells Growth and change of phenotype ARTERY WALL

T he purpose of this paper is to review briefly the strengths and weaknesses of the oxidative modification hypothesis of atherogenesis. As with any new hypothesis, there is danger that the supporting evidence, even if limited, will generate enthusiasm that runs too far and too fast. Because the hypothesis has not yet been falsified, it deserves further study. It is hoped that it will stand up to closer inspection and critical evaluation. At this time, however, it remains a hypothesis that rests primarily on in vitro data, a few in vivo rabbit studies and some epidemiological correlational data. Before a clinical trial can be rationally planned, we need to learn more about the mechanisms involved, possibly critical species differences, and the pros and cons of the several potential interventions available to test the oxidative modification hypothesis.1 It would be unfortunate if the first tests of the hypothesis were done prematurely, using inadequate intervention modalities and resulting in a false negative result. Clinical trials are expensive and time consuming; they should only be undertaken when the science base is sufficiently strong.

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