Coffee Consumption and Prostate Cancer Risk and Progression in the Health Professionals Follow-up Study

Kathryn M. Wilson; Julie L. Kasperzyk; Jennifer R. Rider; Stacey Kenfield; Rob M. van Dam; Meir J. Stampfer; Edward Giovannucci; Lorelei A. Mucci

Disclosures

J Natl Cancer Inst. 2011;103(11):876-884. 

In This Article

Results

During 20 years (816 130 person-years) of follow-up, 5035 of 47 911 men were confirmed to have developed prostate cancer. Of these cancers, 642 were lethal, 896 were advanced (642 lethal plus 254 additional extraprostatic cancers), and 3221 were nonadvanced prostate cancers. Two-thirds of all cohort participants consumed at least one cup of coffee per day in 1986, and 5% reported drinking six or more cups daily (Table 1). Men who consumed the most coffee were more likely to be ever-smokers and were less likely to engage in vigorous physical activity (Table 1). Frequency of PSA testing was similar among high and low coffee drinkers, whereas men in the middle categories reported somewhat more testing. High coffee consumption was associated with higher intakes of energy, alcohol, and processed meat, and slightly lower intake of calcium.

We observed a weak inverse association between total coffee intake and incidence of prostate cancer (Table 2). Men who consumed six or more cups per day had an 18% lower risk of prostate cancer compared with men who did not drink coffee (relative risk [RR] = 0.82, 95% confidence interval [CI] = 0.68 to 0.98, P linear trend = .10). The age-adjusted incidence rates of prostate cancer for the highest (≥6 cups per day) and lowest (no coffee) coffee categories were 425 and 529 cancers per 100 000 person-years, respectively. The data suggested an inverse association between coffee intake and risk of high-grade cancers, although the trends were not statistically significant. Coffee was not associated with low-grade cancer.

The strongest associations were for lethal and advanced prostate cancer (men in the highest intake category vs nondrinkers: RR= 0.40, 95% CI = 0.22 to 0.75, P trend = .03 for lethal cancer; RR = 0.47, 95% CI = 0.28 to 0.77, P trend = .004 for advanced cancer). The age-adjusted incidence rates of lethal prostate cancer for the highest and lowest intake categories were 34 and 79 per 100 000 person-years, respectively. Coffee consumption was not associated with risk of nonadvanced cancers that never progressed beyond the prostate.

For comparison with other studies without repeated measures of diet, we repeated the analyses using baseline rather than cumulative coffee intake. With baseline intake the associations of coffee consumption with lethal and advanced cancers remained statistically significant but were somewhat attenuated (the highest vs lowest coffee consumers in 1986: RR = 0.50, 95% CI = 0.30 to 0.84, P trend = .05 for lethal prostate cancer; RR = 0.54, 95% CI = 0.36 to 0.83, P trend = .03 for advanced disease).

To examine whether urinary symptoms affected coffee intake before diagnosis (reverse causation), we looked cross-sectionally at coffee and lower urinary tract symptoms in 1998. We found that coffee intake did not differ in men with and without urinary symptoms. Men were asked to report the frequency of seven urinary symptoms, and these were combined to create four categories of lower urinary tract symptoms scores that ranged from no or low levels of symptoms to severe levels of symptoms.[34] Mean coffee intake in the lowest symptom group was 1.59 cups per day (SD = 1.53) and mean coffee intake in the severe symptoms group was 1.57 (SD = 1.58, P for difference in means = .73). There was also no statistically significant trend in total coffee intake across the four symptom groups (P linear trend = .20).

In addition, we conducted several other analyses to assess possible reverse causation. Results for lethal and advanced cancers were similar when men with distant metastases or unknown metastasis status at diagnosis were excluded (data not shown). We also studied the subset of men with advanced cancers that were localized at diagnosis (stage <T3b) and spread only later (n = 294), because these cancers were less likely to be symptomatic before diagnosis than cancers that were diagnosed at an advanced stage. The risk was similar to that seen for all men with advanced cancers (RR = 0.20, 95% CI = 0.06 to 0.65, P trend = .02). We also examined coffee intake with a 4-year lag period between exposure and outcome to avoid using the FFQ data that were collected immediately before diagnosis. The associations with lethal and advanced cancers were somewhat attenuated but remained statistically significant using this exposure measure (RR = 0.58, 95% CI = 0.33 to 1.01, P trend = .02 for lethal cancer; RR = 0.59, 95% CI = 037 to 0.94, P trend = .008 for advanced cancer).

To examine whether confounding by PSA testing might explain our findings, we stratified by time period and evaluated the pre-PSA and PSA eras separately. The association of coffee and advanced disease was similar in both time periods (for 1986–1994, RR of advanced cancer for the highest vs lowest categories of intake = 0.41 [95% CI = 0.20 to 0.85, P trend = .06]; for 1994–2006, RR = 0.53 [95% CI = 0.26 to 1.05, P trend = .03]). We also examined a subcohort of men who reported PSA testing in 1994, with follow-up from 1994 until 2006. We observed inverse associations between coffee intake and risk of lethal and advanced cancers in this subcohort that were of similar magnitude to those in the main analyses, but the estimates were not statistically significant, perhaps due to limited power, given the small numbers of lethal and advanced cancers in this highly screened group (in the screened subcohort, RR for advanced cancer [n = 199] = 0.39 [95% CI = 0.11 to 1.34, P trend = .29] for the highest vs lowest category of intake). Coffee consumption was not associated with nonadvanced cancer in this subcohort.

To investigate the role of caffeine vs other components of coffee, we studied regular and decaffeinated coffee separately and found similar associations for both with lethal and advanced cancers (Table 3 and Table 4). Compared with men who drank no coffee at all (regular or decaf), men who drank six or more cups per day of regular coffee had a lower risk for advanced cancer, adjusting for decaffeinated coffee intake as a continuous variable (RR = 0.69, 95% CI = 0.38 to 1.27, P trend = .01). Compared with nondrinkers, men who drank four or more cups per day of decaffeinated coffee had a lower risk for advanced cancer, adjusting for regular coffee intake as a continuous variable (RR = 0.67, 95% CI = 0.43 to 1.05, P trend = .02). To compare these associations quantitatively, we included caffeinated and decaffeinated coffee as continuous variables in the same model. For advanced cancer, these relative risks were not statistically significantly different from one another (each one cup per day increment: RR = 0.94, 95% CI = 0.89 to 0.99, P = .03 for regular coffee and RR = 0.92, 95% CI = 0.85 to 1.00, P = .04 for decaffeinated coffee; P for difference in coefficients = .68). Similar associations for regular and decaffeinated coffee were seen for lethal cancer (for each one cup per day increment, RR = 0.94 , 95% CI = 0.88 to 1.01, P = .08 for regular coffee and RR = 0.91, 95% CI = 0.83 to 1.00, P = .05 for decaffeinated coffee).

To further explore whether the association with lethal and advanced disease was related to caffeine or to other components of coffee, we studied total caffeine intake from all sources. Caffeine intake was inversely associated with lethal and advanced cancers (the highest vs lowest quintile: RR = 0.77, 95% CI = 0.61 to 0.96, P trend = .01 for advanced). However, when coffee and caffeine were included in the model together, coffee intake continued to be associated with lethal or advanced disease, whereas caffeine no longer had a statistically significant association with lethal or advanced disease (RR = 0.86, 95% CI = 0.65 to 1.13, P trend = .23 for advanced).

We used the repeated measures of coffee intake over time to study the effect of latency time by relating each measure of coffee intake to prostate cancer incidence during specific time intervals after exposure. In this analysis, coffee intake was most strongly inversely associated with risk of advanced prostate cancer for the shorter latency periods, 0–4 and 4–8 years after exposure, and weaker for 8- to 12-year and 12- to 16-year lags (Table 5). Coffee consumption was not associated with nonadvanced cancer for any latency period.

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