Coffee consumption and the risk of endometrial cancer: Evidence from a case-control study of female hormone-related cancers in Japan.

Coffee has become a popular beverage worldwide. Caffeine, a major ingredient of coffee, has been proposed to have a favorable affect on the modulation of circulating estrogen levels and therefore may be of importance in developments on hormone-related cancers. However, epidemiological evidence is limited and inconsistent. We examined the relationship between intake of coffee and hormone-related cancer risk among Japanese women using data from the hospital-based epidemiological research program at Aichi Cancer Center (HERPACC). In total, 2122 breast, 229 endometrial and 166 ovarian cancer cases were included, and 12 425 women, confirmed as free of cancer, were recruited as the control group. Odds ratios (OR) and 95% confidence intervals (95% CI) were determined by multiple logistic regression analysis. A statistically significant inverse association between risk of endometrial cancer and coffee consumption was noted in Japanese women, with no clear association evident for breast and ovarian cancer risk. Compared to non-drinker, the OR of daily drinking of 1-2 cups and 3 or more cups per day for endometrial cancer were 0.64 (95% CI: 0.43-0.94) and 0.41 (95% CI: 0.19-0.87), respectively, and the linear trend was also statistically significant (P < 0.01). However, there was no statistically significant association between caffeine intake and endometrial cancer. In summary, the results of the present study suggest that coffee consumption reduces the risk of endometrial cancer in Japanese subjects. Given the scarcity of studies of coffee intake and endometrial cancer and other hormone-dependent cancer risk, additional investigations are warranted.

Intakes of fish and marine fatty acids and the risks of cancers of the breast and prostate and of other hormone-related cancers: a review of the epidemiologic evidence.

Marine fatty acids, particularly the long-chain eicosapentaenoic and docosahexaenoic acids, have been consistently shown to inhibit the proliferation of breast and prostate cancer cell lines in vitro and to reduce the risk and progression of these tumors in animal experiments. However, whether a high consumption of marine fatty acids can reduce the risk of these cancers or other hormone-dependent cancers in human populations is unclear. Focusing primarily on the results of cohort and case-control studies, we reviewed the current epidemiologic literature on the intake of fish and marine fatty acids in relation to the major hormone-dependent cancers. Despite the many epidemiologic studies that have been published, the evidence from those studies remains unclear. Most of the studies did not show an association between fish consumption or marine fatty acid intake and the risk of hormone-related cancers. Future epidemiologic studies will probably benefit from the assessment of specific fatty acids in the diet, including eicosapentaenoic and docosahexaenoic acids, and of the ratio of these to n-6 fatty acids, dietary constituents that have not been examined individually very often.

Epidemiology of prostate cancer.

Prostate cancer incidence and mortality rates vary worldwide. In the United States, prostate cancer is the most common malignancy affecting men and is the second-leading cause of cancer death. Risk of developing prostate cancer is associated with advancing age, African American ethnicity, and a positive family history, and may be influenced by diet and other factors. The incidence of prostate cancer increased sharply after the introduction of widespread screening for prostate-specific antigen (PSA), although rates have now returned to levels seen before that time. PSA screening has been associated with a shift toward diagnosis of earlier-stage disease, but this has not been accompanied by a shift toward a lower histologic grade. Although overall prostate cancer mortality rates decreased during the 1990s, it was largely because of reductions in deaths among men diagnosed with distant disease. In contrast, mortality rates for men diagnosed with localized or regional disease increased gradually during most of the 1990s before decreasing slightly among white men and reaching plateaus among African Americans.

[Nutrition and cancer]. / Ernährung und Krebs.

The complex process of carcinogenesis is mainly due to environmental factors and therefore preventable. Diet may account for about 35% of cancer. This review presents the nutritional evidence for the development of the four most common cancers in Switzerland. The clearest risk factors for breast cancer are those associated with hormonal and reproductive factors. In relation to dietary factors, high alcohol intake, weight gain and adipositas (postmenopausal breast cancer) probably increase the risk of breast cancer. The evidence is less clear for the consumption of (animal) fat, meat, fruit and vegetables (inverse association). Hormones may also play an important role in the development of prostate cancer. There is no convincing evidence that any dietary factors modify the risk of prostate cancer. Diets high in vegetables are possibly protective, regular consumption of fat and meat possibly increase the risk. Intervention trials revealed protective effects of supplementation with selen or alpha-tocopherol. The main cause of lung cancer is cigarette smoking, and smokers whose diet is protective nevertheless remain at high risk. The evidence that diets high in vegetables and fruit protect against lung cancer is convincing, but it is not clear what constitutents are responsible for this effect. Intervention trials revealed no protective effect of beta-carotene, and in high risk groups, lung cancer risk was even increased. There is convincing evidence that diets high in vegetables decrease the risk of colorectal cancer. The same is true for regular physical activity. Alcohol and consumption of diets high in (red) meat, probably increase the risk of colorectal cancer. For cancer prevention it is recommended to choose a predominantly plant-based diet, to avoid obesity, to reduce the intake of fat, (red) meat, alcohol and salt, not to smoke and to be physically active. The main aim of nutritional therapy of cancer patients is to improve quality of life, whereas the effect on life expectancy is very limited.

Estrogenic activity of natural and synthetic estrogens in human breast cancer cells in culture.

We investigated the estrogenic activity of various environmental pollutants (xenobiotics), in particular the xenoestrogen o,p-DDT, and compared their effects with those of endogenous estrogens, phytoestrogens, and mycoestrogens on estrogen receptor binding capacity, induction of estrogen end products, and activation of cell proliferation in estrogen-sensitive human breast cancer cells in monolayer culture. We also quantified the levels of phytoestrogens in extracts of some common foods, herbs, and spices and in human saliva following consumption of a high phytoestrogen food source (soy milk) to compare phytoestrogen abundance and bioavailability relative to the reported xenoestrogen burden in humans. Results show that natural endogenous estrogens, phytoestrogens, mycoestrogens, and xenoestrogens bind estrogen receptor (ER) in intact cells, but demonstrate marked differences in their ability to induce end products of estrogen action and to regulate cell proliferation. All of the different classes of estrogens stimulated cell proliferation at concentrations that half-saturated ER, but only some classes were able to induce estrogen-regulated end products. Genistein, a common phytoestrogen found in soy foods, differed from the xenoestrogen DDT in its effects on cell proliferation and ability to induce estrogen-regulated end products. Moreover, we found that many of the foods, herbs, and spices commonly consumed by humans contain significant amounts of phytoestrogens, and consumption of soy milk, a phytoestrogen-rich food, markedly increases the levels of phytoestrogens in saliva. In conclusion, our in vitro results predict that a diet high in phytoestrogens would significantly reduce the binding of weak xenoestrogens to ER in target tissues in vivo.

Phytoestrogens, body composition, and breast cancer.

To the extent that diet is involved in the etiology of breast cancer, its effect may be mediated, in part, through hormonal mechanisms. It has been suggested that the consumption of phytoestrogens is related inversely to breast cancer risk. Phytoestrogens are weak estrogens of plant derivation that may have antiestrogenic effects through competitively binding to estrogen receptors, thus diminishing the binding of stronger endogenous estrogens. This paper advances the hypothesis that, through this mechanism, dietary phytoestrogens may attenuate the adverse consequences of obesity on the development of postmenopausal breast cancer. Such an association might partly explain the low breast cancer rates observed among postmenopausal Hispanic women despite their greater adiposity, an important breast cancer risk factor. This hypothesis would lead us to expect that obesity increases the risk of postmenopausal breast cancer in women consuming small quantities of phytoestrogens but does not increase risk in women consuming larger quantities. If the hypothesis is confirmed, such as association could have important implications for reducing breast cancer risk through diet, using naturally occurring substances, particularly in women for whom postmenopausal obesity is an important health concern.

Nonsteroidal estrogens of dietary origin: possible roles in hormone-dependent disease.

Equol, a nonsteroidal estrogen of dietary origin, was recently identified in human urine, and is excreted in amounts comparable to the classical steroidal estrogens. We confirm here that phytoestrogens which are abundant in dietary soya protein are converted by human gastrointestinal flora to this weak estrogen. After the ingestion of meals containing cooked soya protein the urinary excretion of equol in four of six subjects studied increased by up to 1000-fold and this compound was the major phenolic compound found in the urine. These data also indicate that some subjects are unable to either produce or excrete equol despite the challenge of a diet containing soya. In view of the increasing use of commercial soya products in the diet and the capacity of human bacterial flora to synthesize this weak estrogen from the abundance of phytoestrogens in soya, the potential relevance of these observations to the diseases implicating steroid hormones is discussed.