A wide variety of compounds in fruits and vegetables, other than those discussed here, have potential anticarcinogenic activity in vitro. Phytoestrogens in soy products have attracted scientific and popular attention, in part because they are highly consumed in Asian countries, such as Japan and China, that have low rates of cancer. These compounds, which include daidzen and genistein, can bind estrogen receptors but are much less potent than estradiol. In principle, these substances may thus act like tamoxifen by blocking the action of endogenous estrogens to reduce breast cancer risk. Dietary supplementation with a large amount of soy protein slightly lengthens menstrual cycle length, an effect that would be predicted to decrease breast cancer risk only minimally.
Also, soy protein consumption is not the primary explanation for low rates of breast cancer in Japan and China, because rates are similarly low in some parts of China, elsewhere in Asia, and in many developing countries in which soy and related foods are not consumed regularly. In a case control study in Singapore, intake of soy products was associated with lower risk of breast cancer. However, in two case control studies in China that were particularly informative because they encompassed a wide range in levels of soy protein consumption, little relation was seen.
Conceivably, phytoestrogens could even increase overall estrogenic activity among postmenopausal women with low levels of endogenous estrogens. Another group of compounds formed from glucosinolates found in cruciferous vegetables is hypothesized to alter the balance of estrogen metabolism toward less potent forms, but relevant human data are minimal. The possibility that phytochemicals that block estrogen function or modulate estrogen metabolism may provide a nontoxic means of altering breast cancer risk deserves further study, but the available evidence is insufficient.
Foods contain an extremely complex mix of essential nutrients and other compounds that could individually or collectively influence breast cancer risk in ways that may not be detected by the study of individual nutrients. Thus, an examination of foods and food groups in relation to risk of breast cancer could be informative. Because the foods examined in most studies are too numerous to be reported individually, however, published results are likely to reflect a bias toward reporting findings that are statistically significant or that fit preexisting hypotheses.
Despite the potential for biases, inverse associations between intakes of fruits and vegetables and breast cancer risk have been reported in a notably large number of case control studies. These associations have been more consistent for vegetables than for fruits, and for green vegetables in particular. In two cohort studies, however, only weak and nonsignificant inverse associations were seen with consumption of fruits and vegetables. In the 14-year follow-up of the Nurses’ Health Study, evidence for a protective effect of vegetable intake was limited to premenopausal women (relative risk of 0.6 for highest versus lowest intakes; 95% confidence interval, 0.4 to 1.0); little relation was seen with fruit consumption.
Associations between red meat consumption and risk of breast cancer have been reported sporadically. In the largest cohort study, however, no relationship was seen, despite a strong association between red meat consumption and risk of colon cancer in the same population. In the few studies that have examined poultry consumption, little relationship with risk of breast cancer was observed. Although a protective effect of fish consumption has been suggested in a few studies, the overall evidence from case control and cohort studies suggests little relationship. Intake of nuts and legumes has received limited attention in reports on diet and breast cancer, but in general no relationship has been seen.
Walter C. Willett, Beverly Rockhill, Susan E. Hankinson, David J. Hunter and Graham A. Colditz
W. C. Willett: Harvard Medical School, Boston, Massachusetts; Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts
B. Rockhill: Harvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts
S. E. Hankinson: Departments of Medicine and Epidemiology, Harvard Medical School and Harvard School of Public Health, Boston Massachusetts
D. J. Hunter: Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachussetts
G. A. Colditz: Department of Medicine, Harvard Medical School, Boston, Massachussetts