Alcohol consumption and the etiology of colorectal cancer: A review of the scientific evidence from 1957 to 1991

Abstract

The relationship between alcohol consumption and colorectal cancer in humans has been examined in 52 major studies in the past 35 years. An association was found in five of the seven correlational studies. An elevated risk was found in about half of the 31 case-control studies and, of these, in 9 of the 10 studies using community controls but in only 5 of the 17 studies using hospital controls (p = 0.008), suggesting that the absence of association when hospital controls are used is due to a high prevalence of alcohol consumption/alcohol-related illness in the hospital controls. Of the 14 cohort studies, an association with alcohol was found in 10, while in 3 of the 4 cohort studies in which an association was not found the alcohol data obtained were somewhat restricted. A positive dose-response effect was found in two of three cohort studies and in all four case-control studies with community controls in which this effect was examined. In both case-control and cohort studies, the association was found for females and males and for colon and rectal cancer. When the type of alcohol consumed was examined separately, beer was the principal type of at-risk alcoholic beverage, with much less risk for spirits and least risk for wine. Statistically significant elevations of risk were more often found in males than in females and slightly more frequently for rectal than for colon cancer and were related almost entirely to beer, rather than to wine or spirit, consumption. The alcohol risk was independent of the dietary risk in those studies that controlled for this factor. There was some confirmatory evidence for alcohol augmentation in rodent models of chemically induced carcinogenesis in six of nine studies. The hypotheses of alcohol as a direct and specific colorectal carcinogen include increased mucosal cell proliferation, the activation of intestinal procarcinogens, and the role of unabsorbed carcinogens, particularly in beer. Also, five of six other human studies showed an association between alcohol/beer consumption and adenomatous polyps, consistent with the hypothesis that alcohol stimulates the colorectal mucosa. General or indirect carcinogenic effects of alcohol include immunodepression, activation of liver procarcinogens, and changes in bile composition, as well as nitrosamine content of alcoholic beverages and increased tissue nitrosamine levels. With alcohol/beer consumption, the overall conclusion on present evidence is that alcohol, particularly beer consumption, is an etiologic factor for colon and rectal cancer for females and males.(ABSTRACT TRUNCATED AT 400 WORDS)

Dietary intake and microsatellite instability in colon tumors

“…These results also provide support for the findings reported in some, but not all studies, that alcohol is associated with colon cancer. 20,21 With few exceptions, results from this study suggest that most dietary factors are not associated with MSIϩ tumors. Although high intake of refined grains increased likelihood of having an MSIϩ tumor, high levels of dietary glycemic index were associated with a lower likelihood of having an MSIϩ tumor than an MSIϪ tumor.…”

“…20,21 If alcohol is associated with certain types of mutations in tumors rather than with all colon cancer tumors, one could expect a weaker association when assessing all colon cancer cases together. Our findings suggest a biological pathway whereby alcohol intake influences risk that involves unstable tumors.…”

“…However, it has been hypothesized that alcohol could influence carcinogenesis by influencing mucosal cell proliferation and related histological changes. 20 These changes have been associated with mucosal hyper-regeneration that may make the mucosa more susceptible to the action of other carcinogens such as cigarette smoke. 20 We have previously shown that cigarette smoking increases risk of MSI in tumors.…”

“…20 These changes have been associated with mucosal hyper-regeneration that may make the mucosa more susceptible to the action of other carcinogens such as cigarette smoke. 20 We have previously shown that cigarette smoking increases risk of MSI in tumors. 6 We further explored factors that could modify the risk of cigarette smoking and MSI.…”

No excess risk of colorectal cancer among alcoholics followed for up to 25 years

“…However, epidemiological data, as summarised in two reviews (Kune and Vitetta, 1992;Potter, 1999), are conflicting, both with regard to the existence of such an association and to possible variations by anatomical subsites. The disagreement continues in subsequent studies (Gerhardsson de Verdier et al, 1993;Goldbohm et al, 1994;Glynn et al, 1996b;Le Marchand et al, 1997;Hsing et al, 1998;Munoz et al, 1998;Tavani et al, 1998;Nagata et al, 1999;Sharpe et al, 2002).…”