Using data from 3 prospective cohort studies, we observed a consistent inverse association for a combined intake of coffee and tea and risk of glioma. Caffeine intake was inversely related to risk in men, but the association was less apparent in women.
Few observational studies have examined the association between tea, coffee, other caffeinated drinks, caffeine intake and glioma risk (7
); interpretation of the literature is difficult given that these studies report on only one or a combination of these beverages in relation to glioma risk, and most had limited data on intake. For example, in one study, no association was reported for high average weekly consumption of ‘other drinks’ defined as regular non-diet soft drinks, diet soft drinks, caffeinated coffee, decaffeinated coffee, tea, lemon in tea, milk or cream in coffee or tea, and sugar in coffee or tea, compared to low intake (10
). Inverse associations were observed among women in two studies where results were provided for combined caffeinated beverages (defined as cola, coffee, or tea). In one study of women, a decreased glioma risk was observed with increasing intake (p-value for trend = 0.03) (11
). In a second study, an inverse association was observed among women (OR = 0.55; 95% CI: 0.30–1.02, top vs. bottom tertile of caffeinated beverages), but no consistent trend was observed among men (12
Regular intake of tea was not associated with glioma risk (OR = 1.26; 95% CI: 0.70–2.25, for high intake, ≥ 41,000 6-ounce lifetime cups, compared to never used regularly) in the only case-control study to report on tea (9
). In the same study, no association was observed for coffee consumption (RR = 1.40, 95% CI = 0.76–2.58, for ≥38,000 6-ounce lifetime cups vs, never used regularly)(9
) and similarly no association was observed for coffee intake in another case-control study (8
). In a cohort of over 133,000 subscribers to the Kaiser Permanente Medical Care Program, 130 glioma cases were identified over an average of 13 years of follow-up (7
) This study reported a suggestive positive association between coffee consumption and glioma risk (p-value for trend = 0.05; RR 1.7, 95% CI = 0.8–3.6 for ≥ 7 cups of coffee per day in the past year compared to < 1 cup per day).
Results for cola drinks are inconsistent; in one case-control study, intake of cola drinks was inversely associated with glioma risk among men (OR = 0.37; 95% CI: 0.19–0.70) and women (OR = 0.39; 95% CI: 0.17–0.91) (12
), while in a second study, no association between regular intake of soft drinks and glioma risk was observed (9
Polyphenols, including phenolics acids and flavonoids are abundant in coffee and tea, respectively (5
). These dietary constituents are known for their antioxidative activities, modulation of xenobiotic metabolite enzymes, and inhibition of tumor promotion (31
), and have shown to possibly protect against cancer (32
). Coffee and tea are also a dietary source of caffeine; on average the levels of caffeine in tea are lower than those in coffee (34
). Caffeine has been studied extensively, and it has been found to both increase and decrease malignant cell development by altering cell cycle checkpoint function, several mechanisms of DNA repair, apoptosis, and key regulatory proteins, including the tumor suppressor protein, p53, as well as carcinogen metabolism (35
). In addition, caffeine has substantial influence on the central nervous system, including decreasing cerebral blood flow (2
), which could influence brain carcinogenesis; the exact mechanism, however, if a causal association exists, will have to be elucidated.
In the current study, we collected information on tea, caffeinated and decaffeinated coffee, caffeinated soda, total caffeine intake (calculated from all caffeinated beverages and foods), and also on the brewing method typically used for brewing coffee, which may be important as specific methods (e.g. filtered, instant) may affect the concentration of certain compounds found in coffee, including caffeine. We observed a suggestive decrease in glioma risk for high daily consumption of tea; and although flavonoid intake was not associated with glioma risk, we were unable to examine the most abundant flavonoids found in tea. Furthermore, we were unable to distinguish between caffeinated, decaffeinated, or herbal teas.
The strengths of our study include its large number of brain cancer cases (n=355), the prospective design, long follow-up, and detailed and updated information on tea, caffeinated and decaffeinated coffee, and caffeine intake. The prospective design precludes recall bias and selection bias is minimized by the very high rate of follow-up over a long period of time. No proxies were needed as information on diet was obtained before the occurrence of disease. The availability of repeated dietary measures in the cohorts permits a consideration of early (baseline), most recent (simple update), and long-term (cumulative updated and restricted analyses) dietary intake. We cannot exclude measurement error due to self-reported diet as a contributor to the lack of associations in the current study; however, we have previously demonstrated the accuracy of self-reported beverage intake in these cohorts, and the repeated assessment of dietary intake may reduce within-person subject variation and better represent long-term average intake. However, we cannot exclude the possibility that these results are due to chance.
Overall, our findings suggest that a high intake of coffee and tea reduces the risk of glioma in both men and women. The results for total caffeine intake, derived from drinks and food, were less consistent across men and women, and suggest that the association may be more complex in women. Our findings are especially noteworthy considering that there are no modifiable risk factors for brain tumors at this time, but because this is the first study to examine these beverages in detail, they need to be confirmed in other populations.