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Canadian Medical Association Journal
CMAJ - April 21, 1998 JAMC - le 21 avril 1998

Unconventional therapies for cancer: 2. Green tea

Elizabeth Kaegi, MB, ChB, MSc, on behalf of the Task Force on Alternative Therapies of the Canadian Breast Cancer Research Initiative

CMAJ 1998;158:1033-35

Dr. Kaegi was Director of Medical Affairs and Cancer Control of the National Cancer Institute of Canada and the Canadian Cancer Society, Toronto, Ont., from 1993 to 1996.

The Canadian Breast Cancer Research Initiative does not endorse the use of any particular unconventional therapy. It urges patients to evaluate all evidence carefully and to consult their caregiver in order to make thoughtful and fully informed personal decisions.

This article has been peer reviewed.

Reprint requests to: Dr. Marilyn Schneider, Director of Research, Canadian Breast Cancer Research Initiative, 200­10 Alcorn Ave., Toronto ON M4V 3B1; tel 416 961-7223; fax 416 961-4189

© 1998 Canadian Medical Association (full text / résumé)

See also:

This article continues the series that reviews the evidence for the safety and effectiveness of 6 unconventional therapies commonly used by Canadian cancer patients: Essiac, green tea, Iscador, hydrazine sulfate, vitamins A, C and E, and 714-X. Part 1 (CMAJ 1998[7]:897-902) describes the methodology used to obtain and evaluate the available information on the products and provides a summary of the findings on Essiac. Subsequent articles will cover the other products.

Annotated bibliographies that provide more detailed references for the information summarized in this series of articles are available in print from the Canadian Breast Cancer Research Initiative (CBCRI; address appears at end of article). The reference lists and the lay summaries of the findings (published in 1997) can be found on the CBCRI's Web site (www.breast.cancer.ca).

The following summary of the information on green tea adapts the lay summaries for clinicians and provides references for the key findings.

Green tea

What is it?

Each year about 2.5 million tons of tea are manufactured from the dried leaves and leaf buds of the shrub Camellia sinensis. Black tea accounts for about 78% of production and is prepared by drying and fermenting the leaves. This tea is most widely drunk in Europe, India and North America. Oolong tea, a specialty tea accounting for 2% of production, is only partly fermented and is popular in southeastern China and Japan. Green tea, which is not fermented, is made by steaming or pan-frying tea leaves and then drying them. It accounts for about 20% of world production and is mostly consumed in China and Japan, where it has been used medicinally as a stimulant and digestive remedy for about 5000 years.1

When green tea is taken for medicinal purposes, 5­10 mL of the dried herb is steeped in a cup of boiling water for about 15 minutes. The usual amount taken is 1­3 cups daily, without the addition of milk or sugar. More recently, green tea capsules have been developed for the market, but the clinical benefits of these are unknown.

Safety

No adverse effects have been reported in association with the medicinal use of green tea. However, a cup of tea, black or green, contains 10­80 mg of caffeine depending on the methods used in its production, storage and preparation. Because excess caffeine can cause nervousness, insomnia and irregularities in heart rate, pregnant women, nursing mothers and patients with cardiac problems are usually advised to limit their intake to 2 cups daily.1,2

The possible role of tea consumption in causing cancer has been explored by several researchers.3­6 However, when the International Agency for Research on Cancer (IARC) reviewed the available information in 1989, it found that there was inadequate evidence to conclude that tea drinking presented a carcinogenic risk.7

Laboratory and clinical evidence

Much of the research into the effects of green tea has focused on its potential to prevent cancer. There has been far less research into its role in the treatment of cancer.

With respect to prevention, a number of epidemiologic studies have suggested that the regular consumption of tea, particularly green tea, moderately decreases the risk of cancer, especially cancers of the upper digestive tract.8­10

There has been some laboratory research into the possible role of green tea in the treatment of cancer. However, no human studies and only limited data from animal studies were identified. In assay systems, the effects of green tea have been contradictory and inconclusive, showing both mutagenic and antimutagenic effects.4,11­13 However, several murine studies have demonstrated anticarcinogenic effects. For example, extracts of green tea applied to mouse skin have been found to inhibit the development of skin cancer in response to known skin carcinogens.14 Green tea and green tea extracts given orally or intraperitoneally have been shown to inhibit the growth of transplanted tumours14­16 and to reduce the incidence of tumours in animals exposed to carcinogenic agents.11

A few studies have reported that green tea and green tea extracts reduce the metastatic potential of cancer cells in some animal systems.17,18 These findings, together with the evidence that green tea extracts suppress chromosomal abnormalities induced by carcinogens,12 have generated some interest because they suggest that green tea plays a role in delaying the cumulative genetic damage necessary for a cell to evolve from normalcy to one with aggressive metastatic capabilities.

Constituents of green tea

Dried tea leaves are composed mainly of phytochemicals known as polyphenols (36%), principally flavonols (including catechins), flavonoids and flavondiols.9,19 The leaves also contain plant alkaloids (about 4%), including caffeine, theobromine and theophylline. Other constituents include proteins, carbohydrates, phenolic acids, minerals (including fluoride and aluminum) and fibre. Like most herbs, the precise composition of green tea varies with the geographic origin of the leaf, the time of harvest and the manufacturing process. The constituents of black tea differ from those of green tea: oxidation and fermentation of black tea alter the catechins and lower the concentration of polyphenols.

Research suggests that it is the polyphenols in green tea that are responsible for its chemopreventive effect.19­21 Some animal studies have also shown that extracts of tea catechins injected intraperitoneally cause implanted breast and prostatic tumours to decrease in size.22 With respect to anticarcinogenic activity, the catechin in green tea that has generated the most interest is a potent, naturally occuring antioxidant, epigallocatechin gallate (EGCG). The mechanism of action of EGCG and other similar substances is uncertain, but they may function in several ways: by acting as antioxidants, by inhibiting enzymes involved in cell replication and DNA synthesis, by interfering with cell-to-cell adhesion, or by inhibiting some of the intracellular communication pathways required for cell division.16,20,21,23­28

Conclusion

Moderate consumption of green tea appears safe. There is some evidence that green tea may prevent the occurrence of some forms of cancer, but the mechanisms of action of its specific constituents are poorly understood. Preliminary evidence exists of the potential effectiveness of green tea as a treatment of cancer. Further research into the effects of green tea and some of its constituents would be worthwhile.

This article reports some of the work carried out by the Task Force on Alternative Therapies of the Canadian Breast Cancer Research Initiative (CBCRI). The CBCRI is the main funder of breast cancer research in Canada and was established in 1993 as a consortium of the Canadian Cancer Society (CCS), the National Cancer Institute of Canada (NCIC) — which also serves as the administrative home of the CBCRI — and the federal government (through the participation of the Medical Research Council of Canada and the National Health Research and Development Programme). In addition to the author, a number of other CBCRI staff worked on the project, including Dr. Carmen Tamayo (research associate), Ms. Rebecca McDonald and Ms. Jess Merber. Others contributed to the reviews of specific agents. The task force was chaired by Ms. Donna Cappon. Dr. Kaegi was the Director of Medical Affairs and Cancer Control for the CCS and the NCIC and staff partner with the task force.

References

  1. Chow K, Kramer I. All the tea in China. San Francisco: China Books and Periodicals; 1990.
  2. Tea Council of Canada. Tea consumption and related health benefits. Toronto: The Council; Spring 1994.
  3. Kapadia GJ, Paul BD, Chung EB, Ghosh B, Pradhan SN. Carcinogenicity of Camellia sinensis (tea) and some tannin-containing folk medicinal herbs administered subcutaneously in rats. J Natl Cancer Inst 1976;57(1):207-9.
  4. Nagao M, Takahashi Y, Yamanaka H, Sugimura T. Mutagens in coffee and tea. Mutat Res 1979;68:101-6.
  5. Kinlen LJ, Willows AN, Goldblatt P, Yudkin J. Tea consumption and cancer. Br J Cancer 1988;58(3):397-401.
  6. Tewes FJ, Koo LC, Meisgen TJ, Rylander R. Lung cancer risk and mutagenicity of tea. Environ Res 1990;52(1):23-33.
  7. Tea [review]. IARC Monogr Eval Carcinog Risks Hum 1991;51:207-71.
  8. Gao YT, McLaughlin JK, Blot WJ, Ji BT, Dai Q, Fraumeni JF Jr. Reduced risk of esophageal cancer associated with green tea consumption. J Natl Cancer Inst 1994;86(11):855-8.
  9. Weisburger JH. Introduction: physiological and pharmacological effects of Camellia sinensis (tea): first international symposium. Prev Med 1992;21:329-30.
  10. Yang CS, Wang ZY. Tea and cancer. J Natl Cancer Inst 1993;85(13):1038-49.
  11. Jain AK, Shimoi K, Nakamura Y, Kada T, Hara Y, Tomita I. Crude tea extracts decrease the mutagenic activity of N-methyl-N´-nitro-N-nitrosoguanidine in vitro and in intragastric tract of rats. Mutat Res 1989;210:1-8.
  12. Ito Y, Ohnishi S, Fujie K. Chromosome aberrations induced by aflatoxin B1 in rat bone marrow cells in vivo and their suppression by green tea. Mutat Res 1989;222:253-61.
  13. Wang ZY, Cheng SJ, Zhou ZC, Athar M, Khan WA, Bickers DR, et al. Antimutagenic activity of green tea polyphenols. Mutat Res 1989;223:273-85.
  14. Huang MT, Ho CT, Wang ZY, Ferraro T, Finnegan-Olive T, Lou YR, et al. Inhibitory effect of topical application of a green tea polyphenol fraction on tumor initiation and promotion in mouse skin. Carcinogenesis 1992;13(6):947-54.
  15. Oguni I, Nasu K, Yamamoto S, Nomura T. On the antitumor activity of fresh green tea leaf. Agric Biol Chem 1988;52(7):1879-80.
  16. Wang ZY, Huang MT, Ho CT, Chang R, Ma W, Ferraro T, et al. Inhibitory effect of green tea on the growth of established skin papillomas in mice. Cancer Res 1992;52:6657-65.
  17. Taniguchi S, Fujiki H, Kobayashi H, Go H, Miyado K, Sadano H, et al. Effect of (-)-epigallocatechin gallate, the main constituent of green tea, on lung metastasis with mouse B16 melanoma cell lines. Cancer Lett 1992;65:51-4.
  18. Sazuka M, Murakami S, Isemura M, Satoh K, Nukiwa T. Inhibitory effects of green tea infusion on in vitro invasion and in vivo metastasis of mouse lung carcinoma cells. Cancer Lett 1995;98:27-31.
  19. Okuda T, Mori K, Hayatsu H. Inhibitory effect of tannins on direct-acting mutagens. Chem Pharm Bull (Tokyo) 1984;32(9):3755-8.
  20. Kada T, Kaneko K, Matsuzaki S, Matsuzaki T, Hara Y. Detection and chemical identification of natural bio-antimutagens. A case of the green tea factor. Mutat Res 1985;150:127-32.
  21. Ruch RJ, Cheng SJ, Klaunig JE. Prevention of cytotoxicity and inhibition of intercellular communication by antioxidant catechins isolated from Chinese green tea. Carcinogenesis 1989;10(6):1003-8.
  22. Graham HN. Green tea composition, consumption, and polyphenol chemistry. Prev Med 1992;21:334-50.
  23. Liao S, Umekita Y, Guo J, Kokontis JM, Hiipakka RA. Growth inhibition and regression of human prostate and breast tumors in athymic mice by tea epigallocatechin gallate. Cancer Lett 1995;96:239-43.
  24. Sakagami H, Asano K, Hara Y, Shimamura T. Stimulation of human monocyte and polymorphonuclear cell iodination and interleukin-1 production by epigallocatechin gallate. J Leukoc Biol 1992;51:478-83.
  25. Sakagami H, Takeda M, Sugaya K, Omata T, Takahashi H, Yamamura M, et al. Stimulation by epigallocatechin gallate of interleukin-1 production by human peripheral blood mononuclear cells. Anticancer Res 1995;15:971-4.
  26. Hu ZQ, Toda M, Okubo S, Hara Y, Shimamura T. Mitogenic activity of (-)epigallocatechin gallate on B-cells and investigation of its structure-function relationship. Int J Immunopharmacol 1992;14(8):1399-407.
  27. Isemura M, Suzuki Y, Satoh K, Narumi K, Motomiya M. Effects of catechins on the mouse lung carcinoma cell adhesion to endothelial cells. Cell Biol Int 1993;17(6):559-64.
  28. Nakagami T, Nanaumi-Tamura N, Toyomura K, Nakamura T, Shigehisa T. Dietary flavonoids as potential natural biological response modifiers affecting the autoimmune system. J Food Sci 1995;60(4):653-6.

General reference books and journals

  1. Alternative medicine: expanding medical horizons: a report to the National Institute of Health on Alternative Medical Systems and Practices in the United States. Washington: National Institutes of Health; 1994. Publ no NIH 94-066.
  2. Lerner M. Choices in healing: integrating the best of conventional and complementary approaches to cancer. Cambridge (MA): MIT Press; 1994.
  3. Ontario Breast Cancer Information Exchange Project. A guide to unconventional cancer therapies. Aurora (ON): R&R Bookbar; 1994.
  4. Fugh-Berman A. Alternative medicine, what works. Baltimore: Williams & Wilkins; 1997.
  5. Peer-reviewed journals dealing with unconventional therapies:
       Alternative Therapies in Health and Medicine
       The Journal of Alternative and Complementary Medicine

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