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Nutritional Epidemiology

Consumption of Coffee, but Not Black Tea, Is Associated with Decreased Risk of Premenopausal Breast Cancer

Department of Epidemiology, Roswell Park Cancer Institute, Buffalo, NY and ^* School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY

¹ To whom correspondence should be addressed. E-mail: kirsten.moysich{at}roswellpark.org.

ABSTRACT

Caffeine has been suggested as a possible risk factor for breast cancer, potentially through its effect of facilitating the development of benign breast disease. However, coffee and tea also contain polyphenols, which exhibit anticarcinogenic properties. A hospital-based, case-control study was conducted to evaluate the role of coffee, decaffeinated coffee, and black tea in breast cancer etiology. Study participants included 1932 cases with primary, incident breast cancer and 1895 hospital controls with nonneoplastic conditions. All participants completed a comprehensive epidemiological questionnaire. Among premenopausal women, consumption of regular coffee was associated with linear declines in breast cancer risk (P for trend = 0.03); consumers of 4 cups/d experienced a 40% risk reduction (odds ratio = 0.62, 95% CI 0.39–0.98). No clear associations between intake of black tea or decaffeinated coffee and breast cancer risk were noted among premenopausal women, although black tea was associated with a protective effect unique to a subsample of cases with lobular histology. Among postmenopausal women, breast cancer risk was not associated with consumption of coffee, tea, or decaffeinated coffee. Results among postmenopausal women did not differ by histologic subtype. Our findings support a protective effect of coffee intake on premenopausal, but not postmenopausal breast cancer risk. Further studies are warranted to confirm these findings.

KEY WORDS: • breast neoplasms • coffee • tea • caffeine • case-control studies

Coffee and tea are 2 of the most frequently consumed beverages in the world. Interest in the association between coffee or tea and breast disease remains high, given the array of compounds present in these beverages that could potentially alter disease risk. Coffee, for example, is a leading source of methylxanthines, such as caffeine. Caffeine has been associated with benign breast disease (BBD),² which in turn is a risk factor for breast cancer (1). The biochemical basis of this association may be linked to the inhibitory effect of methylxanthines on cAMP phosphodiesterase, leading to elevated levels of cAMP and cGMP (2). The lowest levels of cAMP and cGMP are found in normal breast tissue, with the highest levels in neoplastic lesions (2), although a direct causal relation between cancer and these second messengers has not been established. Eliminating dietary sources of methylxanthines was shown to resolve BBD in some women (3,4). However, later studies showed that caffeinated beverages also alter sex hormone binding globulin and estradiol, potentially reducing the risk of developing breast cancer (5). In addition, caffeine has been positively associated with tumor differentiation because women with moderately to well-differentiated tumors had higher caffeine intake (6), suggesting the ability of caffeine to hinder tumor growth.

Coffee and black tea are complex mixtures of caffeine and polyphenols, such as phytoestrogens and flavonoids (7–11). For example, a 240-mL serving of coffee contains 95 mg of caffeine and 0.24 mg of flavonols, whereas black tea contains 47 mg of caffeine and 8 mg of flavonol per serving (12,13). Yet flavonols are only one subclass of flavonoids from foods that are currently quantified by the USDA. Although reference quantities of the full range of polyphenols derived from coffee and tea are not available, it was suggested elsewhere that coffee, in particular, may be an important source of lignan phytoestrogens (14). Additionally, >1 serving of coffee and tea may be consumed daily by many Americans (15), increasing the chance that these beverages represent relevant exposures. In general, polyphenols were found to have anticarcinogenic properties in several cell and animal studies. For example, Way et al. (16) found an inhibitory effect of black tea polyphenols on hormone-resistant breast cancer cells, noting a potential role of black tea in chemoprevention. A recent review of the association between tea and a variety of health outcomes suggests that tea may reduce the risk for some chronic diseases, such as certain cancers and heart disease (10). However, the specific role of tea in breast cancer etiology is not definitive.

Although experimental studies suggested the possible mechanisms by which coffee and tea may influence breast cancer risk, epidemiological evidence on the association between the compounds in coffee and tea and cancer risk has been inconclusive. Although several case-control and cohort studies found no association between coffee or tea consumption and breast cancer risk (17–21), others have noted significant associations that vary by both age (22) and body size (23). Therefore, in light of the limited and inconsistent body of evidence, we conducted a hospital-based, case-control study to further investigate the association between breast cancer risk and consumption of regular coffee, decaffeinated coffee, and black tea.

SUBJECTS AND METHODS

    Study population. The study population included individuals who received medical services at Roswell Park Cancer Institute (RPCI) between 1982 and 1998, and who agreed to complete a comprehensive epidemiological questionnaire. Individuals with missing data on coffee or tea consumption were excluded from the current analyses. The case group consisted of 1932 individuals with primary, incident breast cancer, identified from the RPCI tumor registry and Diagnostic Index. Patients in the case group were predominantly Caucasian (98%) and ranged in age from 23 to 97 y. Median time from diagnosis to participation was 19 d, with 69% of cases participating within 6 mo. Controls included 1895 women who received medical services at RPCI for nonneoplastic conditions, and who were randomly selected from a pool of 5700 eligible women. These participants came to RPCI with a suspicion of neoplastic disease, but were not diagnosed with either benign or malignant conditions. Controls were most frequently treated for breast diseases (14%), genitourinary diseases (9%), and digestive diseases (7%). No other diagnosis accounted for >2% of the controls with known diagnoses. Like the cases, women in the control group were predominantly Caucasian and ranged in age from 21 to 94 y. Controls were frequency matched to cases on 5-y age intervals and residence inside or outside western New York. The RPCI Institutional Review Board approved the conduct of the study.

    Questionnaire. All participants completed the Patient Epidemiology Data System (PEDS) questionnaire, which was offered to all new patients as part of the admission process. Questionnaires were returned by 50% of patients. The PEDS questionnaire requested detailed information on demographic background, occupational and environmental exposures, tobacco and alcohol consumption, diet, reproductive experiences, medical history, and family history of cancer. More specifically, the instrument captured information regarding the number of daily servings of regular (caffeinated) coffee, decaffeinated coffee, and black (caffeinated) tea. Although participants were also asked about decaffeinated tea consumption, including green tea, very few participants reported consumption of these beverages, precluding meaningful analysis.

    Statistical analyses. All statistical analyses were calculated using SPSS for Windows, version 11.0. Odds ratios (OR) and 95% CI of beverage type and breast cancer risk were computed by unconditional logistic regression in separate models for regular coffee, decaffeinated coffee, and regular tea. The 3 beverage variables were categorized as follows: none, <1 cup/d, 1 cup/d, 2–3 cups/d, 4 cups/d. These categories were based on both the distribution of the control group and categories considered to be logical and meaningful. Participants who consumed none of the specified beverage (i.e., nonconsumers) served as the referent category for all regression analyses.

To assess for possible effect modification, all analyses were stratified by menopausal status based on self-report from the PEDS questionnaire. For the small number of women who were missing self-reported menopausal status (< 2%), age was used as a proxy for menopausal status. Women who were <50 y old at time of survey were considered premenopausal, whereas women 50 y old were classified as postmenopausal (24). Potential confounders were evaluated separately for each beverage type because correlations among regular coffee, black tea, and decaffeinated coffee were weak (r 0.13). The weak associations among beverage types suggested that it was important to consider potential confounders separately because each beverage likely represented a distinct exposure. Known and suspected breast cancer risk factors that had significant relations to beverage types were included in multivariate models if they changed point estimates by at least 10%. All multivariate models were also adjusted for the matching variables, age (continuous) and residence in western New York (no/yes) to control for potential residual confounding. Adjusted models for each beverage were also assessed for confounding by intake of the other 2 beverage types, but no significant changes in point estimates were noted. Trend tests to assess for dose-response relations were computed by treating categorical predictors as continuous variables in logistic regression models. Statistical tests at the P < 0.05 level were considered significant.

RESULTS

Comparisons of characteristics of breast cancer cases and hospital controls were stratified by menopausal status (Table 1). Among premenopausal women, cases were significantly less likely to have had irregular menstrual periods, were older at the time of first birth, and had fewer live-born children compared with controls. For postmenopausal women, cases were significantly more educated, were more likely to have had their first pregnancy after age 30, a family history of breast cancer, or a personal history of BBD. Postmenopausal cases were less likely to have had irregular menstrual periods or have taken HRT. On average, postmenopausal cases had higher BMI, younger ages at menarche, older ages at menopause, and older ages at first birth.

DISCUSSION

Results from this hospital-based, case-control study provide additional evidence for a potential protective effect of regular coffee consumption, particularly at higher doses (4 cups/d), on premenopausal breast cancer risk. This protective effect in premenopausal women was not seen for black tea or decaffeinated coffee consumption. We also did not find an association between beverage type and postmenopausal breast cancer risk.

Although caffeine was originally suggested to be an important risk factor for BBD (2,3), subsequent research suggests a less clear role for caffeine in both BBD and breast cancer development. A review of clinical trials in which women with BBD excluded caffeine from their diet found inconsistent results regarding the association between caffeine and BBD progression (25). Additionally, the authors pointed out that "benign breast disease" is really an umbrella term used to broadly classify a set of closely related nonneoplastic breast syndromes (25), further complicating the interpretation of studies that do not discern among subtypes. An investigation of the histological composition of >10,000 benign breast lesions reported identifying 3 main subtypes: 70% were nonproliferative, 28% were proliferative without atypia, and the remaining 2% of lesions were atypical hyperplasia (26). In the most recent prospective study of dietary influences on BBD, caffeine was not significantly associated with the incidence of nonproliferative BBD or proliferative BBD without atypia (27). However, the highest quartile of coffee consumption was associated with an increased incidence of atypical hyperplasia for a small subsample of women (27). Thus, the potential association of caffeine and BBD may be limited to this specific histological type. In terms of breast cancer risk associated with BBD, nonproliferative types were shown to confer no additional risk for later development of breast cancer (26), with only the atypical hyperplasia type showing significantly increased risk (28).

In the current study, a personal history of BBD was associated with case-control status only among postmenopausal women (Table 1). However, BBD history was not associated with beverage type in either premenopausal or postmenopausal women in our sample, suggesting that it was not a relevant confounder. When analyses of beverage type and breast cancer risk were additionally stratified by BBD history to assess possible effect modification, results were unchanged among both premenopausal and postmenopausal women (data not shown). Nonetheless, our self-reported measure of BBD history is crude in that we do not have important information on histological types.

Given the complex picture of the association between caffeine and BBD and the role of BBD and breast cancer development, the hypothesis that coffee consumption would therefore be a risk factor for breast cancer development is, perhaps, intuitive but potentially misleading. Because coffee is a complex mixture of biochemically active substances, including caffeine and phytochemicals, it is difficult to know the net effect of this complex array on breast cancer risk. Our results point to the potentially beneficial effects of coffee consumption among premenopausal women, although the mechanisms by which this benefit is conferred are tentative. For example, caffeine was shown to significantly reduce the size of benign mammary gland tumors in rat models (29) and to enhance neoplastic tumor differentiation in women (6), thereby slowing carcinogenesis. Coffee was found to be a major source of antioxidant phytochemicals, such as lignans, which are the precursor to enterolactone (30); high levels of enterolactone may be associated with decreased cancer risk (31,32). Daily coffee consumption was also shown to be positively correlated with the ratio of the serum estrogen 2-hydroxyestrone to 16--hydroxyestrone, a predictor of lower breast cancer risk (33). Ultimately, it appears that the evidence for caffeine via coffee as a breast tissue carcinogen is limited (34), with further evidence to suggest potential anticarcinogenic activity of coffee constituents.

Previous epidemiologic investigations of the association between coffee or tea and breast cancer have produced conflicting results. As the largest single source of caffeine, the role of coffee as a possible breast cancer risk factor has received the most attention. Several earlier case-control studies did not find an association between coffee consumption and breast cancer risk (17–19,35,36). The most recent of these investigations reported an inverse relation between coffee consumption and breast cancer risk (35,36), although the trends for decreased risk were not significant (P < 0.14 and P < 0.39, respectively). However, these 2 studies included menopausal status as a covariate rather than an effect modifier, potentially masking differences between pre- and postmenopausal women. Only 3 previous studies were identified in our review that showed coffee to have a significant relation with breast cancer risk. One investigation (37) found a significant increase in risk for women who consumed <2 cups of coffee/d (OR = 1.6, 95% CI 1.1–2.4), although there was no trend of increasing risk associated with additional increasing coffee consumption. In contrast, a second study found a decrease in breast cancer risk associated with total caffeine consumption from coffee, tea, chocolate, and cocoa (22). This effect was modified by age, with only women 50 y old, and presumably postmenopausal, showing a decrease in risk. This finding stands in contrast to the current study results suggesting a reduction in risk associated with coffee consumption in premenopausal women. The third study found a significant interaction between coffee consumption and body size, with lean women (BMI < 24 kg/m²) showing a decrease in risk and heavier women (BMI 24 kg/m²) showing an increase in risk (23). However, it is difficult to draw firm conclusions about the role of body size in coffee consumption and breast cancer risk from the results of that study because the authors presented only age-adjusted risk estimates and were not able to consider other possible confounders.

In addition to case-control studies, the association of coffee consumption and breast cancer risk was studied in 3 cohorts, with 2 of these studies reporting nonsignificant findings (20,21,38). However, our study results are relatively consistent with a report from the Nurses' Health Study cohort, which also suggested a trend for decreased risk associated with increasing coffee consumption, (P for trend = 0.02), although their point estimates by category of coffee consumption were not significant (38).

Although both black tea and decaffeinated coffee have been studied considerably less than regular coffee, previous studies have been consistent in failing to find a significant association between these 2 beverages and breast cancer risk (19,22,35,39). The current study found a significant reduction in risk for lobular type breast cancer among consumers of black tea, suggesting the importance of further consideration of histological type in future research. Although our results are based on small numbers, to our knowledge, no previous study of coffee or tea and breast cancer has examined risk by histological type.

Several methodological issues should be noted when interpreting these results. The large sample size was a strength of the current study. Most previous studies of coffee, tea, and breast cancer have not included large numbers of both premenopausal and postmenopausal cases, which allowed for the consideration of a wide range of covariates as well as an investigation of the role of histological types. However, because we employed a case-control study design, several potential sources of bias should be considered. First, selection bias may have occurred because participation was restricted to individuals who were treated at RPCI, a large regional cancer treatment center; they are not likely to represent the general population of breast cancer patients or individuals without cancer. At the same time, there is no reason to believe that self-reported beverage consumption is likely to be different for RPCI patients compared with patients treated in other hospitals. Although the use of hospital controls can decrease recall bias, it also has the potential to introduce selection bias because some controls may have presented with conditions that affected their consumption of coffee or tea. However, selection bias is unlikely to have influenced our findings, given that our control group represented a wide range of noncancer disease categories, limiting the affect of selecting controls from a single disease type (such as BBD) with characteristics associated with the exposures. In addition, results did not differ meaningfully when subsets of controls with various disorders (breast, digestive, or genitourinary diseases in premenopausal women; breast and musculoskeletal diseases in postmenopausal women) were examined separately or excluded from analyses (data not shown).

Second, selection bias may be an important limitation because only 50% of eligible cases and controls agreed to complete the PEDS questionnaire. It is difficult to know whether those individuals who refused to complete the questionnaire differed from participants studied here with respect to beverage consumption. Third, the influence of recall bias may have been less of an issue, because of our use of hospital controls. Furthermore, data on our exposures of interest were embedded with a modified FFQ that requested information a range of dietary exposures, with no clear emphasis on any specific exposure type. Although our assessment of beverage consumption was based ultimately on self-report, it seems unlikely that cases and controls would show systematic differences in their motivation to recall the magnitude of their beverage consumption. In fact, validity of recall of coffee intake is high (r = 0.90) because it is a food that is either regularly consumed or rarely consumed (40). Finally, although it is important to consider this range of possible limitations, previously published studies from the PEDS data base have consistently replicated established epidemiological associations for a variety of cancer sites, including ovary (41), colon (42), breast (43), prostate (44), and lung (45,46).

In summary, our findings suggest that coffee consumption may decrease premenopausal, but not postmenopausal breast cancer risk. Additional research is warranted to better understand the potentially anticarcinogenic roles of compounds in coffee and tea, and how these compounds influence cancer risk in response to beverage consumption.

FOOTNOTES

² Abbreviations used: BBD, benign breast disease; OR, odds ratio; PEDS, Patient Epidemiology Data System; RPCI, Roswell Park Cancer Institute.

Manuscript received 20 July 2005. Initial review completed 24 August 2005. Revision accepted 28 September 2005.

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