In this pooled analysis of 13 cohort studies, coffee drinking was not associated with risk of colon cancer. The relative risk was null even for comparison of consumption of more than 1400 g/d (about six 8-oz cups or 1.4 L) of coffee vs none. Drinking sugar-sweetened carbonated soft drinks was not associated with risk of colon cancer. In contrast, a modest positive association was observed for relatively high tea intake. The association for each beverage did not vary by tumor site, various colon cancer risk factors, or follow-up period.
As observed in our study, several case–control studies have also reported null associations between coffee consumption and colon cancer risk (44
). However, other case–control studies (50
) have reported statistically significant modest reductions in colon cancer risk (20%–40%), whereas one study (58
) found a statistically significant 120% increased risk among men, but a non-statistically significant 10% decreased risk in women, comparing high vs low coffee consumption. Furthermore, most (59
) of the cohort studies (59
) not included in our analyses also found no association between coffee consumption and colon cancer risk. Six (60
) of these cohort studies were excluded from our analyses because they did not assess long-term dietary intake or did not conduct a validation study of the dietary assessment method used in their study, failing to satisfy our inclusion criteria. Another two cohort studies (59
) were excluded because they did not meet the inclusion criteria at the time the dataset for the colon cancer analyses was finalized but have since joined the Pooling Project. Only two cohort studies in Japan (65
) have reported statistically significant inverse associations with high vs infrequent coffee consumption. However, these results were only observed in women and were based on relatively small numbers (<15 colon cancer case patients in the highest category of coffee consumption). Last, the null association between coffee consumption and colon cancer risk observed in our study is consistent with the finding from one recent meta-analysis synthesizing the publications on cohort studies up to June 2008 (67
Although null associations for coffee consumption have been observed frequently, coffee drinking has been hypothesized to decrease the risk of colon cancer (6
). Coffee consumption may increase colonic motility, thereby decreasing the exposure of epithelial cells to potential carcinogens in the colon (6
). In addition, coffee consumption may reduce the synthesis and secretion of bile acids, potential promoters of colon carcinogenesis (7
). Furthermore, coffee contains some phenolic compounds such as chlorogenic acid and caffeic acid, which have antioxidant properties (6
). However, coffee also contains chemical compounds such as caffeine, which could increase the risk of colon cancer. Caffeine has genotoxic and mutagenic properties at high concentrations (6
). In addition, caffeine has been shown to lower insulin sensitivity (68
), which could increase colon cancer risk (69
). Thus, the complex compounds in coffee with opposing effects may explain the null results observed.
Tea drinking has been hypothesized to decrease the risk of colon cancer. Antioxidants present in tea, such as polyphenols, can protect colonic epithelial cells against oxidative damage to DNA by free radicals (70
). Tea also lowers the formation of nitrosamine compounds and heterocyclic aromatic amines, potential carcinogens for colon cancer (71
). On the other hand, tea also contains compounds with mutagenic and genotoxic properties such as tannins and caffeine (9
), which could increase the risk of colon cancer.
Animal studies have consistently demonstrated a protective effect of tea on the development of colon cancer (5
); however, results from human observational studies have been inconsistent. Tea is the second most commonly consumed beverage worldwide following water (5
). About 78% of the tea produced is black tea, 20% is green tea, and 2% is oolong tea (5
). Most case–control studies have found no association between black tea consumption and colon cancer risk (47
), although a few case–control studies have reported statistically significantly higher (48
) risks of colon cancer of at least 40% when comparing the highest vs lowest level of intake. Among the three cohort studies (74
) that did not meet our inclusion criteria (as described above), one reported a statistically significant (about 40%) reduced risk (75
), whereas the other two studies found no association with black tea consumption (74
). For green tea, a statistically significant 30%–40% reduced risk of colon cancer has been observed in two case–control studies (50
) and in one cohort study (78
); the remaining studies have reported null associations (48
). The studies that have found the statistically significant inverse associations for green tea consumption were all conducted in Japanese and Chinese populations in which green tea was commonly consumed with a wide range of intake, unlike the other populations in which green tea consumption was low.
The observed increased risk with tea consumption in our analysis was unexpected. One possibility is that the positive association we observed was because of chance. However, a cohort study conducted in Singapore observed a stronger positive association between green tea intake and risk of advanced colon cancer compared with localized colon cancer, suggesting that tea may have a promoting effect on tumor progression and metastasis, but this difference by tumor stage was not observed for black tea consumption (74
). As noted previously, although we did not have data on the type of tea consumed in most studies included in our study, black tea is the major type of tea consumed in Western populations. Furthermore, we were not able to examine whether the association that we observed differed by stage.
Consumption of soft drinks containing caloric sweeteners has been positively associated with colon cancer risk factors, including excess body weight (11
); however, this relationship has rarely been examined (2
). We found null associations with consumption of sugar-sweetened carbonated soft drinks, sugar-sweetened colas, sugar-sweetened noncolas, and diet carbonated soft drinks; all of the relative risks were close to 1.0 for an increment of 375 g/d (approximately 12 oz). However, we cannot exclude the possibility that a weak association was missed in our study because about 2% of the study population consumed more than 550 g/d of soft drinks.
Our pooled analyses have several strengths. The large sample size of the study allowed us to conduct subgroup analyses by colon site and to examine whether the associations for each beverage varied by other colon cancer risk factors. The prospective design with high follow-up rate for each study minimized the potential for selection bias and recall bias.
There are also several limitations in this pooled analysis. The null association observed for coffee consumption on colon cancer risk may not be generalized to different ethnic groups because our study population is primarily of European origin. Some degree of measurement error inevitably exists for our estimates of the intake of each beverage, and we were unable to conduct measurement error correction analyses because few studies in our analyses evaluated the validity of coffee, tea, and carbonated soft drink intake. Although high correlations (ie, r
> .5) between the intake estimates from the food-frequency questionnaires and from multiple dietary records or 24-hour recalls were observed for these beverages (23
), we cannot rule out the possibility that the high correlation may result from the correlated errors in the food-frequency questionnaires and in the referent methods. Moreover, for tea and sugar-sweetened carbonated soft drink consumption, we were limited by relatively low consumption levels and a narrow intake range with only 2% of the study population consuming more than 550 g/d of soft drinks. Furthermore, none of the studies measured the type of tea consumed, and few studies measured the consumption of diet soft drinks. Last, personal history of colorectal screening and the addition of milk and sugar to coffee and tea was not directly assessed in several studies, which may have resulted in unmeasured confounding.
In summary, we did not observe an association between coffee drinking and colon cancer risk across a wide range of coffee consumption. In contrast, we observed a modest increase in risk with higher tea consumption, despite a limited range of tea consumption. To further evaluate this unexpected finding, future studies should be conducted in populations with a wider range of intake, and information should be collected on the types of tea consumed and preparation methods. Data on stage of disease should also be collected to confirm or refute previous data suggesting that green tea may promote tumor progression and metastasis. For sugar-sweetened carbonated soft drinks, although we observed no association with colon cancer risk, future studies with a wider intake range and with detailed information on sugar composition would be desirable.