Kune G A, Vitetta L
University of Melbourne, Victoria, Australia.
Nutr Cancer. 1992;18(2):97-111. doi: 10.1080/01635589209514210.
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)
在过去35年里,52项主要研究对人类饮酒与结直肠癌之间的关系进行了调查。在7项相关性研究中,有5项发现了关联。在31项病例对照研究中,约一半发现风险升高,其中,在10项使用社区对照的研究中有9项,而在17项使用医院对照的研究中只有5项(p = 0.008),这表明使用医院对照时未发现关联是由于医院对照中饮酒/与酒精相关疾病的高患病率。在14项队列研究中,10项发现与酒精有关联,而在4项未发现关联的队列研究中,有3项所获得的酒精数据受到一定限制。在三项队列研究中的两项以及所有四项使用社区对照且研究了这种效应的病例对照研究中,发现了阳性剂量反应效应。在病例对照研究和队列研究中,均发现女性和男性以及结肠癌和直肠癌与饮酒有关联。当分别检查所饮用酒精的类型时,啤酒是主要的有风险的酒精饮料类型,烈酒的风险要小得多,葡萄酒的风险最小。在男性中比在女性中更常发现具有统计学意义的风险升高,直肠癌比结肠癌略为频繁,并且几乎完全与啤酒消费有关,而不是与葡萄酒或烈酒消费有关。在那些对此因素进行控制的研究中,酒精风险独立于饮食风险。在9项化学诱导致癌的啮齿动物模型研究中,有6项有一些证据证实酒精有增强作用。酒精作为直接和特异性结直肠癌致癌物的假说包括黏膜细胞增殖增加、肠道前致癌物的激活以及未吸收致癌物的作用,特别是在啤酒中。此外,其他六项人体研究中有五项表明酒精/啤酒消费与腺瘤性息肉之间存在关联,这与酒精刺激结直肠黏膜的假说一致。酒精的一般或间接致癌作用包括免疫抑制、肝脏前致癌物的激活、胆汁成分的变化以及酒精饮料中的亚硝胺含量和组织亚硝胺水平的增加。就目前的证据而言,关于饮酒/饮用啤酒的总体结论是,酒精,特别是啤酒消费,是女性和男性患结肠癌和直肠癌的一个病因。(摘要截选至400字)