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Letter to the Editor |
University of California, Davis Department of Internal Medicine CCRBM, 1121 Surge I Davis, CA 95616 E-mail: avandervliet{at}ucdavis.edu
The proposal by Horrobin that antioxidants may have both antitumorigenic and tumor-growth-promoting properties raises an interesting additional antioxidant paradox that I did not discuss in my editorial (1). As mentioned, products of lipid oxidation can selectively kill tumor cells, and antioxidants can prevent the formation of such tumoricidal products. Thus, it appears possible that the growth of undetected preexisting cancers, which may be more prevalent in high-risk subjects (eg, smokers), might be promoted rather than inhibited by antioxidant nutrients such as vitamin E. However, this notion should be interpreted with caution and in the proper context.
First, the procarcinogenic effects of antioxidants observed in the large clinical trials I discussed in my editorial were attributed to ß-carotene, not to vitamin E (2). In fact, there is no evidence in humans that supplementation with vitamin E promotes cancer, and long-term vitamin E supplementation was actually found to reduce the incidence of and mortality from prostate cancer in smokers (3). Thus, it is unclear how the study by Lhuillery et al (4), in which tumor growth was enhanced in rats that were fed vitamin E–rich, high-fat diets, relates to human cancer. In addition, vitamin E also appears to protect against cardiovascular disease (5, 6). Although results from clinical trials are not quite as conclusive, again, there is no evidence of any adverse effects of vitamin E supplementation in human subjects. Thus, I think it unwise to promote the idea that antioxidant micronutrient consumption or supplementation might be disadvantageous in high-risk groups (eg, smokers) and to discourage the public (and especially these high-risk groups) from consuming these micronutrients at recommended amounts (7).
Second, I reemphasize that generalizations regarding the prooxidant or antioxidant properties of carotenoids and of vitamins C and E are inappropriate because they disregard other well-known properties of these micronutrients, eg, cell differentiation and growth regulation. Given the multiple properties of these antioxidants, it is naive to presume that these different classes of micronutrients have similar biological actions, even though they all have antioxidant properties. In fact, there is no conclusive evidence of the in vivo antioxidant activity of carotenoids, and the prooxidant or anticarcinogenic properties of these micronutrients are most likely unrelated to their presumed antioxidant properties. Similarly, recent studies indicate that the protective actions of vitamin E against atherogenesis may be independent of its antioxidant activity (6). Thus, the term "antioxidant paradox" is somewhat misleading because it wrongly implies that the biological actions of these micronutrients are always related to their prooxidant or antioxidant effects. Clearly, this is not the case.
Overall, it is unwise to encourage subjects at high risk of cancer (eg, heavy smokers) to consume high-fat diets, which are relatively deficient in antioxidants, because the association between such diets and cardiovascular disease is well established. However, I still believe there is too little knowledge available to strongly advocate antioxidant micronutrient supplementation beyond what is available from a balanced diet.
REFERENCES
-tocopherol and ß-carotene: incidence and mortality in a controlled trial. J Natl Cancer Inst 1998;90:440–6.-tocopherol transfer protein and vitamin E. Proc Natl Acad Sci U S A 2000;97:13830–4.
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