Tea has long been regarded as an aid to good health, and many believe it can help reduce the risk of cancer. Most studies of tea and cancer prevention have focused on green tea. Although tea and/or tea polyphenols have been found in animal studies to inhibit tumorigenesis at different organ sites, including the skin, lung, oral cavity, esophagus, stomach, small intestine, colon, liver, pancreas, and mammary gland, the results of human studies—both epidemiologic and clinical studies—have been inconclusive.
Epidemiologic Studies
More than 50 epidemiologic studies of the association between tea consumption and cancer risk have been published since 2006. The results of these studies have often been inconsistent, but some have linked tea consumption to reduced risks of cancers of the colon, breast, ovary, prostate, and lung. The inconsistent results may be due to variables such as differences in tea preparation and consumption, the types of tea studied (green, black, or both), the methods of tea production, the bioavailability of tea compounds, genetic variation in how people respond to tea consumption, the concomitant use of tobacco and alcohol, and other lifestyle factors that may influence a person’s risk of developing cancer, such as physical activity or weight status.
Clinical Trials
Several clinical trials have investigated the role of tea and tea polyphenols in cancer prevention. However, few trials have examined the effects of tea or tea polyphenols on cancer incidence or mortality.
Two randomized trials evaluated the effects of tea extracts on premalignant oral lesions. One of the trials was a double-blind interventional trial involving 59 people with leukoplakia, which is a putative precursor lesion for oral cancer. The trial’s participants were randomly assigned to receive either 3 grams of a mixed tea product, given both orally and topically, or a placebo. After 6 months, 38 percent of the participants in the treatment group had partial regression of their oral lesions compared with 10 percent of the participants in the placebo group. In addition, fewer participants in the treatment group than in the placebo group had an increase in lesion size (3 percent in the treatment group versus 7 percent in the placebo group). Furthermore, mucosal cell proliferation decreased in the treatment group, suggesting a possible protective effect of tea on the development of oral cancer. In contrast, in the second trial, 39 people with high-risk premalignant oral lesions were randomly assigned to receive one of three doses of a green tea extract—500 mg per square meter of body surface area (mg/m2), 750 mg/m2, or 1000 mg/m2—or a placebo three times daily for 12 weeks. At the end of the trial, no differences in lesion responses or histology were found between the groups.
Two other randomized trials examined the effects of tea on urine levels of 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of oxidative DNA damage that may be a predictor of increased cancer risk. Urinary 8-OHdG levels are higher in individuals with lung cancer than in control subjects, and human breast, lung, liver, kidney, brain, stomach, and ovarian tumor tissue has a higher content of 8-OHdG than adjacent nontumor tissue. In one trial, 133 adult heavy smokers were randomly assigned to drink 4 cups of one of the following beverages each day for 4 months: decaffeinated green tea, decaffeinated black tea, or water. Among those who drank green tea, there was a statistically significant 31 percent decrease in urinary levels of 8-OHdG; in the black tea group, there was no change in urinary 8-OHdG levels. In the second trial, 124 individuals at increased risk of liver cancer due to hepatitis B virus infection and aflatoxin exposure took a placebo or 500 mg or 1000 mg of a green tea polyphenol supplement daily. The two supplement doses were reported to be equivalent to 2 or 4 cups, respectively, of green tea infusions. No other tea or tea products were consumed. Compared with those in the placebo group, individuals who took the green tea supplement at either dose for 3 months had substantially lower urinary 8-OHdG levels). Although these trials indicate that green tea polyphenols from tea or supplements can reduce urinary 8-OHdG levels, it is unclear if reduced 8-OHdG levels are associated with reduced cancer risk.
Additional trials have investigated whether green tea catechins or green tea extracts alter prostate cancer risk. In a double-blind, placebo-controlled study, 60 men took 200 mg of green tea catechin or a placebo three times daily for 1 year. These men had high-grade prostatic intraepithelial neoplasia, which is thought to be a precursor of prostate cancer. After 1 year, fewer prostate cancers were detected in the green tea catechin group (1 cancer in 30 men) compared with the placebo group (9 cancers in 30 men). Two other clinical trials, both uncontrolled studies, investigated the use of green tea extracts to reduce prostate-specific antigen levels in men with prostate cancer and found no evidence of such a reduction.
Another trial examined the effect of tea polyphenols on serum pepsinogen levels in 163 individuals with high serum pepsinogen levels. Serum pepsinogen is a biomarker of gastric atrophy and an indicator of increased risk for stomach cancer. The participants in this trial were given either one or six 100-mg capsules of tea polyphenols daily for 1 year. Each capsule was the equivalent of about 1.7 cups of tea. After 1 year, no decrease in serum pepsinogen levels was observed in either treatment group.
In yet another trial, a possible role for green tea supplements in treating precancerous lesions of the esophagus was investigated. In the trial, 200 Chinese participants with such lesions were treated with 5 mg of a decaffeinated green tea extract daily or a placebo. After 12 months, lesion histopathology was scored as improved, unchanged, or deteriorated. The trial found no difference between the treatment and placebo groups with regard to changes in the esophageal lesions or in abnormal cell proliferation.