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Types Of Bone Cancer

Clinical trials of the use of antioxidant supplements, especially in the prevention of cancer, have yielded controversial and often confusing results. In contrast there is strong evidence emerging that plants, either in the diet or as supplements, can play a significant role in reducing the risk of contracting cancer. Interestingly, two key candidates in this regard, namely green tea (Camellia sinensis) and turmeric (Curcuma longa), are noted for their significant antioxidant activity. This brief review will mainly focus on the human studies that have investigated the potential benefit of green tea and turmeric in the prevention of a range of malignant tumors.

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Green Tea

Green tea is the unprocessed, dried, young leaves of Camellia sinensis. The main active constituents are polyphenols including epigallocatechin gallate (EGCG).

A review of 26 epidemiological and 2 substantial human studies (1974-1997) found conflicting results, but an overall positive association between consumption of green tea and protection against cancer. (1) The studies were mainly case-control studies, relying largely on interview and subject responses. The studies were conducted mostly in Japan and China, with a few in Hong Kong (2), USA (2: one study of Hawaiians of Japanese ancestry), Taiwan (1), Singapore (1), Iran (1) and Korea (1). The effect of tea consumption on cancer may depend on the causative factors of the specific cancer. Two studies each investigated two cancer types (hence 30 studies are listed). Positive association means consumption of green tea was associated with increased risk of cancer. Inverse association means consumption was associated with decreased risk. The results and association for consumption of green tea were:

* colon cancer: 3 studies found inverse association, 1 positive association

* rectal cancer: only 1 of 4 studies reported an inverse association; increased risk was seen in 2 studies

* bladder cancer: 2 studies found inverse association

* stomach cancer: 6 of 10 studies suggest an inverse association and 3 a positive association

* pancreatic cancer: possible inverse association in 2 of 3 studies

* oesophageal cancer: strong inverse effect shown (6 studies), although increased risk with increasing temperature of tea (not specifically green tea)

* lung cancer: 1 study (Okinawan (partially-fermented) tea) found inverse association, slight increased risk in another study

* pharmacological studies (2): chemopreventive effect demonstrated in smokers and volunteers at high-risk of gastric cancer

The results of epidemiological studies published after or not included in this review are listed below:

* cancer (all forms): inverse association (>10 cups/day green tea) (2);

* prostate cancer: decrease in risk observed with (black and green) tea intake of [greater than or equal to] 2 cups/day or [greater than or equal to]500 g/day (3);

* breast cancer (Asian-American women): inverse association (4);

* breast cancer: long-term consumption of green tea ([greater than or equal to]5 cups/day) associated with lower recurrence in stage I and II breast cancer; no improvement in prognosis was observed in stage III breast cancer; increased consumption was closely associated with decreased numbers of axillary lymph node metastases among premenopausal patients (with stage I and II), and with increased expression of progesterone receptor and oestrogen receptor among postmenopausal patients (5);

* breast cancer: decrease-risk for recurrence in women with invasive breast cancer for green tea intake of >[dagger]3 cups/day (for stages I and II, but not stage III) (6);

* ovarian cancer: inverse association with further decreased risk with increasing duration of ingestion (7);

* digestive tract and urinary tract (American postmenopausal women): inverse association ([greater than or equal to]2 cups/day green tea; 1 cup = 237 mL); no association found for melanoma, non-Hodgkin's lymphoma, cancers of the pancreas, lung, breast, uterine corpus or ovary (8);

* gastric cancer: no association. (9)

A recently published epidemiological study which was also not included in the review followed people in Japan over 13 years and found that daily green tea use resulted in delay in cancer onset, reduced deaths from cancer and lower deaths from all causes The authors entitled their study: "Can teatime increase one's lifetime?" and concluded that: "These results indicate that daily consumption of green tea in sufficient amounts will help to prolong life by avoiding premature death, particularly death caused by cancer." (10) All the more significant was that this was a prospective study.

The preventative and treatment potential of green tea has also been assessed in clinical trials. Decreased levels of prostaglandin E2 (PGE2) in rectal mucosa were demonstrated at 4 and 8 hours after consumption of green tea by healthy volunteers. (Inhibition of PGE2 in other settings is related to a lower risk of certain cancers.) (11) Decaffeinated green tea did not confer a preventive effect in alleviating oesophageal precancerous lesions and abnormal cell proliferation in a high-risk population given treatment for 11 months. (12)

Limited antineoplastic activity was demonstrated for green tea (6 g/day) in a phase II (unblinded) trial of asymptomatic patients with androgen independent metastatic prostate carcinoma. Only one of the 42 patients experienced a decline in serum prostate specific antigen, no patients showed tumour response and 7 patients experienced substantial side effects. (13)

Ingestion of and topical application of a green and black tea mixture decreased lesion size in patients with oral mucosa leucoplakia (a precancerous condition) compared to that experienced by the control group. (14)

In a pilot intervention study with heavy smokers, green tea (5 cups/day) for 4 weeks decreased the numbers of damaged cells in the oral cavity, similar to the results observed in laboratory studies. (15) Increasing the consumption of green tea post-diagnosis enhanced survival in patients with epithelial ovarian cancer. (16)

The beneficial polyphenols in green tea also appear to be bioavailable in supplement form. In fact, absorption of polyphenols was actually enhanced when green tea was taken as a supplement in capsule form (compared to consuming black or green tea). (17) The antimutagenic activity of green and black tea is not modulated by the presence of milk. (18) However, adding milk may inhibit the absorption of polyphenols. (19)

Turmeric

In India, turmeric has been used for centuries as a spice and a food preservative, as well as for its medicinal properties. (20) Active constituents of Curcuma longa include yellow pigments (3-5%) known as curcuminoids consisting of curcumin and methoxylated curcumins. (21)

Numerous in vitro and oral in vivo studies show that turmeric and curcumin possess antimutagenic and antipromotion (of tumors) activities, which is probably related to the known antioxidant and anti-inflammatory effects. (22) Oral administration of curcumin significantly inhibited tumor incidence and tumor burden in numerous experimental models of cancer. This anticarcinogenic activity is probably in part related to the capacity of curcumin to induce phase II enzymes.

Epidemiological data suggest that curcumin may be responsible for the lower rate of colorectal cancer in Asian countries. (23) The low incidence of large bowel cancers in Indians observed to 1999 has been partially attributed to the presence of curcumin in Indian cooking. (24) An early 1980s estimate indicates communities in the Indian subcontinent consume up to 1.5 g/day/person of dietary turmeric. (25) In 1993 the turmeric consumption in India was measured at 0.16-0.44 kg/year per capita. An intake of 0.6 g/day per capita is reported in rural areas. (26)

An extract of turmeric containing turmeric essential oil and curcuminoids did not have an effect on leucocytic M1G levels (antioxidant biomarker) in 15 patients with advanced colorectal cancer refractory to standard chemotherapies. Turmeric extract was prescribed for up to 4 months, the daily dose peaked at and corresponded to 180 mg of curcumin (2.2g of turmeric extract). Ingestion of 440 mg/day of turmeric extract for 29 days was accompanied by a 59% decrease in lymphocytic GST activity. Five patients experienced stable disease for 3 months or longer, and in one additional patient abatement of tumour progression may have resulted from turmeric treatment. (27)

In patients with oral submucous fibrosis (a precancerous condition), treatment with alcohol extract of turmeric, turmeric oil or turmeric oleoresin normalised the number of micronucleated cells both in exfoliated oral mucosal cells and in circulating lymphocytes. (28)

Very high doses of curcumin (starting at 500 mg/day) showed demonstrable chemoprevention in 28% of 25 patients with high-risk or premalignant lesions. This phase I trial found that curcumin is not toxic in humans up to 8 g/day when taken by mouth for 3 months. (29) However, curcumin has low oral bioavailability in humans. (27) Nonetheless its metabolites could be the true active form.

Turmeric (1.5 g/day) administered for 30 days to 16 chronic smokers significantly reduced the urinary excretion of mutagens. (30) Studies on humans at high risk of palatal cancer due to reverse smoking demonstrated that turmeric (1 g/day) for 9 months had a significant impact on the regression of precancerous lesions. The treatment also decreased micronuclei and DNA adducts in oral epithelial cells. (31) (Reverse smoking is a practice where the burning end of the cigarette is kept in the mouth and causes a high incidence of oropharyngeal carcinoma.)

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21. Bisset NG (ed). Herbal Drugs and Phytopharmaceuticals: A Handbook for Practice on a Scientific Basis. Medpharm Scientific Publishers, Stuttgart, 1994

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24. Mohandas KM, Desai DC. Indian J Gastroenterol 1999; 18(3): 118-121

25. Sambaiah K, Ratankumar S, Kamanna VS et al. J Food Sci Technol 1982; 19(5): 187-190

26. Krishnaswamy K. Nutr Rev 1996; 54(11): S127-S131

27. Sharma RA, McLelland HR, Hill KA et al. Clin Cancer Res 2001; 7: 1894-1900

28. Hastak K, Lubri N, Jakhi SD et al. Cancer Lett 1997; 116(2): 265-269

29. Cheng AL, Hsu CH, Lin JK et al. Anticancer Res 2001; 21(4B): 2895-2900

30. Polasa K, Raghuram TC, Krishna TP et al. Mutagenesis 1992; 7(2): 107-109

31. Krishnaswarmy K, Raghuramulu N. Indian J Med Res 1998; 108: 167-181

by Kerry Bone, FNIMH, FNHAA and Michelle Morgan

P.O. Box 713 * Warwick QLD 4370, Australia

+61 7 4661 0700 * Fax +61 7 46610788 * www.mediherb.com

FNIMH = Fellow, National Institute of Medical Herbalists (UK)

FNHAA = Fellow, National Herbalists Association of Australia

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