By Emmanuel C. Opara,
Ph.D. This is the second of a two-part
installment on the beneficial effects antioxidants may have on smokers'
health. Part 1 was published in the Nutritional News, Vol. #11, No. 7, July,
1997. Introduction Despite (1) this overwhelming evidence
of smoking-induced oxidative stress, (2) the known causative role of smoking
in the development of chronic degenerative disease, and (3) the frequently
demonstrated benefits of antioxidants in preventing these diseases, recent
findings by the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group
in Finland appear to contradict what are believed to be the established
benefits of antioxidant supplements in smokers. In the Finnish study,
investigators performed a randomized, double-blind, placebo-controlled trial
to determine whether daily supplementation with alpha-tocopherol, beta
carotene, or both would reduce the incidence of lung cancer and other
cancers. A total of 29,133 men were randomly assigned to one of four
regimens: (1) alpha-tocopherol, vitamin E, (50 mg per day) alone; (2) beta
carotene (20 mg per day) alone; (3) both alpha-tocopherol and beta carotene;
or (4) placebo. The study participants receiving these different supplement
regimens were followed for five to eight years, unless death occurred earlier
during the follow-up. At the conclusion of the trial, the
researchers found 876 new cases of cancer (3% incidence). Surprisingly, they
found no difference in the incidence of lung cancer between the two groups
who received either alpha-tocopherol or placebo. Equally unexpected were
their findings of a higher incidence of lung cancer among the men who
received beta carotene compared to those who received the placebo.
Additionally, there was no apparent benefit of combining alpha-tocopherol and
beta carotene. They did find, however, fewer cases of prostate cancer among
those who received alpha-tocopherol compared to those who did not. The
investigators concluded that "antioxidant supplements may have both
harmful as well as beneficial effects."2 The Flawed Finnish Study Because of the relatively advanced age
of the study participants and the extended period in which they had been
subjected to the smoking-induced oxidative load, it is likely that the paltry
50 mg of vitamin E that was administered was simply an inadequate dose.
Indeed, it has been suggested that the minimum dose of alpha-tocopherol
required to produce beneficial effects against oxidative stress is in excess
of 200 IU (or mg) per day.5 It is therefore not surprising that 50 mg/day of
this antioxidant was without effect. Interestingly, in contrast to the
Finnish study, it has recently been shown that red blood cells obtained from
younger smokers (mean age 30 years) who received 70 to 1050 mg/day
alpha-tocopherol for twenty weeks were significantly less susceptible to
oxidative damage after taking vitamin E than they were before taking vitamin
E.6 Furthermore, whereas beta carotene may
contribute to the overall antioxidant defense of the body, the mechanism of
its action does not appear to be through the free radical chain-breaking
reactions which involve vitamin C (ascorbate), vitamin E (tocopherol),
glutathione, selenium and the associated antioxidant enzymes.7,8 In addition,
it is believed that over-consumption of only one carotenoid (like beta
carotene) may inhibit the effectiveness of other carotenoids (like alpha and
gamma carotene, lutein, and lycopene). This is of particular significance in
view of the recent findings that subjects with the lowest blood levels of
lycopene (a carotenoid found in high levels in tomatoes) had a cancer risk about
three times higher than subjects with the highest lycopene levels.9
Consequently, it is not surprising that no positive interaction was observed
between the low doses of alpha-tocopherol and beta carotene as an isolated
nutrient as used in this study. In summary, the findings from the
Finnish study created an unwarranted controversy due to its poor design and
the erroneous conclusions arrived at by the authors. What the authors did
prove, however (but which they failed to clearly state), was that a dose of
50 mg of vitamin E per day is clearly inadequate to impart any significant
benefit to those with a significant oxidative stress load. BENEFITS OF ANTIOXIDANT SUPPLEMENTS I have already alluded to the recent
study, in which it was found that the use of 70-1050 mg/day of
alpha-tocopherol by young smokers (mean age 30 years) increased the
resistance of their red blood cells to oxidative damage.5 Furthermore, as
already pointed out, there are synergistic biochemical interactions among
certain antioxidants which participate in the chain-breaking reactions for
free radical destruction.8 Therefore, it seems advisable to use appropriate
combinations and doses of specific antioxidants, such as 400-800 IU of
vitamin E, combined with 500-5,000 mg of vitamin C per day. It is pertinent
to point out that the use of ascorbate (vitamin C) alone at the dose of 1,000
mg per day for four weeks, has been found to be effective in reducing
oxidative damage in smokers.11 Another promising supplement which
appears to have a potent role in health promotion and disease prevention is
N-acetylcysteine (NAC). This supplement is an analog of the amino acid,
cysteine, which is critically important for the formation of glutathione, the
major intra-cellular antioxidant in the body. Indeed, NAC has emerged as a
leading cancer protective agent. It has been used since 1988 in a large trial
in Europe (Euro-scan) designed to evaluate its efficacy in preventing second
primary cancers in high-risk individuals. The results of this and other studies
show that long-term daily use of 600 mg of NAC is safe and has been highly
recommended for clinical chemopreventive trials.15 Other antioxidant
supplements that have demonstrated effectiveness in reducing the damage from
smoking-associated diseases, particularly, cardiovascular disease, include
lipoic acid, fish oil, coenzyme Q10 and green tea (see part 1 of this article
for references). CONCLUSION Dr. Opara is a research professor in
the departments of Surgery and Cell Biology and a member of the Sara W.
Stedman Center for Nutritional Studies at Duke University Medical Center in
Durham, NC. He received his Ph.D. degree in Medical Biochemistry from the
University of London in England and did his postdoctoral training in
Endocrinology and Metabolism at the Mayo Clinic in Rochester, MN. He
subsequently worked as an investigator at the National Institutes of Health
in Bethesda, M.D., before his present employment at Duke. Dr. Opara has
written well over 100 scientific publications. References: 1. Cross CE, Traber MG. Cigarette smoking and antioxidant
vitamins: the smoke screen continues to clear but has a way to go. Am J
Clin Nutr, 1997, 65:562-563. 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 Eng J Med. 1994,
330:1029-1035. 3. Lang CA, Naryshkin S, Schneider DL, Mills BJ, Lindeman RD.
Low blood glutathione levels in healthy aging adults. J Lab Clin Med,
1992, 120: 720-725. 4. Vega JA, Cavallotti C, Collier WL, De Vincentis G,
Rossodivita I, Amenta F. Changes in glutathione content and localization in
rat heart as a function of age. Mechanisms of Aging and Dev, 1992,
64: 37-48. 5. Jialal I, Fuller CJ, Huet BA. The effect of
alpha-tocopherol supplementation on LDL oxidation. A dose-response study. Arterioscler
Thromb Vasc Biol, 1995, 15: 190-198. 6. Brown KM, Morrice PC, Duthie GD. Erythrocyte vitamin E and
ascorbate concentrations in relation to erythrocyte peroxidation in smokers
and nonsmokers: dose response to vitamin E supplementation. Am J Clin
Nutr, 1997, 65:496-502. 7. Halliwell B. Free radicals, antioxidants, and human
disease: curiosity, cause, or consequence? Lancet, 1994, 344:
721-724. 8. Machlin LJ, Bendich A. Free radical tissue damage:
protective role of antioxidant nutrients. FASEB J, 1987, 1: 441-445. 9. Ford, J.G. Nutrient in tomatoes is found to lower an
individual's risk of lung cancer. Presentation at 1997 Annual meeting of
the American Association for Cancer Research, reported in: 10. Reilly M, Delanty N, Lawson JA, Fitzgerald GA. Modulation
of oxidant stress in vivo in chronic cigarette smokers. Circulation,
1996, 94: 19-25. 11. Fuller CJ, Grundy SM, Norkus EP, Jialal I. Effect of
ascorbate supplementation on low density lipoprotein oxidation in smokers. Atherosclerosis,
1996, 119: 139-150. 12. Lane JD, Opara EC, Rose JE, Behm F. Quitting smoking
raises whole blood glutathione. Physiol Behav, 1996, 60: 1379-1381. 13. Brown AJ. Acute effects of smoking cessation on
antioxidant status. J Nutr Biochem, 1996, 7: 29-39. 14. Handelman GJ, Packer L, Cross CE. Destruction of
tocopherols, carotenoids, and retinol in human plasma by cigarette smoke. Am
J Clin Nutr, 1996, 63: 559-565. 15. van Zandwijk N. N-Acetylcysteine (NAC) and glutathione
(GSH): antioxidant and chemopreventive properties, with special reference
to lung cancer. J Cell Biochem, 1995, Suppl 22: 24-32. |
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