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EDITORIAL |
1 From the Department of Medicine, Gastroenterology and Hepatology, Weill Cornell Medical College, New York, NY.
2 Supported by research grants from the National Institutes of Health (CA 29502 Clinical Nutrition Research Unit, CA 105012), American Institute for Cancer Research, Gateway for Cancer Research, Wakunaga of America Ltd, Ronald and Susan E Lynch Foundation, Edith C Blum Foundation, Rosenfeld Heart Foundation, Cremona Fund, Heisman Trophy Trust, and Filomen M D'agostino Foundation. 3 Reprints not available. Address correspondence to R Rivlin, Weill Cornell Medical College, Department of Medicine/Gastroenterology & Hepatology, 428 East 72nd Street, Suite 600, New York, NY 10021. E-mail: rivlinr{at}yahoo.com.
See corresponding article on page 257.
The use of garlic for medicinal purposes dates to antiquity. The Bible mentions garlic with regard to the Jews’ flight from Egypt. Garlic bulbs were found in tombs of the pharaohs, in Crete, and in ancient cultures throughout the world. Indeed, Hippocrates considered garlic to be a vital part of his therapeutic armamentarium (1).
Within recent years interest in garlic has grown greatly, particularly in relation to the prevention and treatment of cancer. Garlic has been found to contain a large number of potent bioactive compounds with anticancer properties, largely allylsulfide derivatives (2).
Garlic together with vitamins E and C reduced the incidence of precancerous gastric lesions in a large population in China (3). Garlic derivatives have been found to influence an increasing number of molecular mechanisms in carcinogenesis, including DNA adduct formation, scavenging of free radicals, mutagenesis, cell proliferation and differentiation, and angiogenesis (4). The growth rate of cancer cells is reduced by garlic, with cell cycle blockade that occurs particularly in the G2/M phase. Apoptosis is stimulated by garlic (5).
Diallylsulfide, a powerful garlic component, has been reported to inhibit oxidative stress caused by testosterone and to accelerate testosterone metabolism. We have postulated that in the early stages of prostate cancer, when sensitivity to testosterone is retained, the predominant effect of allium derivatives is to stimulate testosterone degradation and, in the later stages, to interfere with signal transduction (6).
Furthermore, garlic is a seleniferous plant, accumulating selenium from the soil against a concentration gradient. Selenium has many anticancer actions, particularly in control of genes involved in carcinogenesis.
The proliferation of human prostate cancer cell lines, both androgen sensitive (LNCaP) and androgen insensitive (PC-3), is inhibited by allium derivatives from garlic in a dose-dependent fashion (6). Stimulation of apoptosis has been related to inactivation of the Akt signaling axis. Rodent recipients of either androgen-sensitive or androgen-insensitive human prostate cancer cell lines show reduction in the serum concentration of prostate specific antigen.
In addition to inhibiting primary cancer, allium derivatives from garlic may further inhibit metastatic processes. In an androgen-independent prostate cancer mouse model, the water-soluble allium derivative, S-allyllmercaptocysteine, inhibited metastases to the lung and adrenal gland by 90% (7).
Despite these examples and the large base of basic research showing potent anticancer effects of various water- and fat-soluble derivatives of garlic (8), an evidence-based review in this issue of the Journal concludes that effects of garlic are only modest in reducing risk of cancer. Kim and Kwon (9) indicate that there is insufficient evidence to show any relation between garlic and cancer of the stomach, breast, lung, or endometrium. They further indicate that there is only very limited evidence of an effect of garlic on any of the gastrointestinal cancers (oral cavity, larnynx, esophagus, or colon) or the endocrine cancers (prostate and ovary) and cancer of the kidney.
How can one reconcile these divergent conclusions? To qualify as a health claim, the totality of publicly available scientific evidence (including evidence from well-designed studies) must show that such evidence truly supports the claim. In reality, the evidence-based analyses reported here and elsewhere rely largely on clinical trials with active agents and placebo controls.
The number of such trials that are considered scientifically sound in this analysis is remarkably few, and the number of subjects involved is generally small. Thus, the very strict criteria required to make a health claim may not be met by the limited number of studies conducted to date that are currently available. This article should serve as a stimulus to extend and broaden the interventional approaches to risk reduction by the use of garlic in susceptible populations, and eventually in the general public.
ACKNOWLEDGMENTS
The author received research grants from Wakunaga of America Ltd.
REFERENCES
Related articles in AJCN:
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