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Vitamin E, cancer, and apoptosis

Eastman Chemical Company, PO Box 1974, Kingsport, TN 37662, E-mail: andreas{at}vitaminE-factor.com
Glen Sutton, JOE 2K0, Quebec, Canada, E-mail: vos{at}health-heart.org

Dear Sir:

The suggestion in a recent article in the Journal (1) that "in heavy smokers, increased intake of ß-carotene and vitamin E was shown to increase the incidence of lung cancer" is not supported by the cited research nor by other research in the case of vitamin E. In fact, in the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study (2), on which much of the evidence in heavy smokers is based, there was no increase in lung cancer in the vitamin E group (who received 50 mg all-rac--tocopheryl acetate/d). Actually, this group experienced a significant decrease in prostate cancer of 32% (3). Furthermore, less lung cancer was found in the upper than in the lowest quartiles of baseline dietary intakes of both ß-carotene and vitamin E, a finding recently confirmed for vitamin E (4). In that study also, vitamin E was found to be more protective in younger men with fewer years of smoking (4).

It can be argued that the proposed theory (1) that antioxidants interfere with the apoptosis of cancer cells has not been proven. In contrast, the results of several studies suggest the opposite, especially for vitamin E (5, 6). Inhibition of apoptosis of other types of cells by antioxidants (7) appears to be different from the promotion of apoptosis in cancer cells. For this reason, extrapolation of findings from normal cells to cancer cells might not be appropriate.

Although it seems clear that high doses of highly bioavailable synthetic ß-carotene did not reduce lung cancer in elderly male smokers (and appeared to increase the risk), such is clearly not the case for vitamin E. Even for ß-carotene, the available epidemiologic and other data (8) strongly suggest that we should await the results of studies with lower doses, and in which vitamin E is used in combination with other antioxidants, before drawing final conclusions on the overall efficacy of vitamin E in cancer prevention (9).

REFERENCES

1. Zeisel SH. Is there a metabolic basis for dietary supplementation? Am J Clin Nutr 2000;72(suppl):507S–11S.
2. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029–35.
3. Heinonen OP, Albanes D, Virtamo J, et al. Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. J Natl Cancer Inst 1998;90:440–6.
4. Woodson K, Tangrea JA, Barrett MJ, et al. Serum alpha-tocopherol and subsequent risk of lung cancer among male smokers. J Natl Cancer Inst 1999;91:1738–43.
5. Gunawardena K, Murray DK, Meikle AW. Vitamin E and other antioxidants inhibit human prostate cancer cells through apoptosis. Prostate 2000;44:287–95.
6. McIntyre BS, Briski KP, Gapor A, Sylvester PW. Antiproliferative and apoptotic effects of tocopherols and tocotrienols on preneoplastic and neoplastic mouse mammary epithelial cells. Proc Soc Exp Biol Med 2000;224:292–301.
7. Galang N, Sasaki H, Maulik N. Apoptotic cell death during ischemia/reperfusion and its attenuation by antioxidant therapy. Toxicology 2000;148:111–8.
8. Blot W. Vitamin/mineral supplementation and cancer risk: international chemoprevention trials. Proc Soc Exp Biol Med 1997;216: 291–6.
9. Wang XD, Russell RM. Procarcinogenic and anticarcinogenic effects of beta-carotene. Nutr Rev 1999;57:263–72.

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