Systematic Review With Meta-analysis

Alcohol Consumption and the Risk of Colorectal Adenoma

J.-Z. Zhu; Y.-M. Wang; Q.-Y. Zhou; K.-F. Zhu; C.-H. Yu; Y.-M. Li


Aliment Pharmacol Ther. 2014;40(4):325-337. 

In This Article

Abstract and Introduction


Background. Studies on the relation between alcohol consumption and risk of colorectal adenoma (CRA), a precursor of colorectal cancer, have been inconsistent.

Aim. A systematic review with meta-analysis was conducted to investigate the association and the dose–response of alcohol with CRA.

Methods. A literature search was performed on PubMed to identify relevant studies published up to January 2014. A fixed or random effects model was used to estimate summarised relative risks (RRs) and 95% confidence intervals (CIs) for the association between alcohol intake and CRA risk. Statistical heterogeneity between studies was assessed with the χ2 statistic and quantified by I 2.

Results. Twenty-three case–control studies and two cohort studies were included in the meta-analysis. All drinkers were associated with 17% increased risk for CRA, compared with nondrinkers or occasional alcohol drinkers. The dose–response analysis demonstrated that for drinkers of 10, 25, 50 and 100 g/day alcohol consumption, the estimated RRs of CRA were 1.02 (95% CI 0.89–1.16), 1.06 (95% CI 0.92–1.20), 1.16 (95% CI 1.02–1.33) and 1.61 (95% CI 1.42–1.84) respectively, in comparison with non-/occasional drinkers. The risks were consistent in the subgroup analyses of gender and site of adenoma, while it was stronger in European studies than the studies in the US and Asia.

Conclusions. This study suggests that alcohol intake is related to a significant increase of risk for colorectal adenoma.


According to GLOBOCAN 2012, colorectal cancer (CRC) is the second most common cancer in female and the third in male worldwide.[1,2] Recognition of genetic and environmental risk factors in the development of CRC might contribute to its prevention by a series of preventative measures, e.g. targeted screening in high-risk individuals. To date, several environmental risk factors for CRC consist of low-fibre diet,[3] obesity,[4] a sedentary lifestyle,[5] smoking[6] and etc.

It had been widely accepted that most of CRCs develop from colorectal adenomas (CRAs) and present morphological and genetic progression via an adenoma–carcinoma sequence.[7] As a precursor lesion of CRC, CRA is an informative endpoint for colorectal carcinogenesis. By now, cigarette smoking,[8] red and processed meat intake,[9] obesity[10] and physical inactivity[11] have been suggested to be risk factors for CRA.

Alcohol intake is one of the primary risk factors for human cancers,[12] and potentially, one of the major avoidable factors. It had been demonstrated that alcohol is associated with cancers of oral cavity, pharynx, larynx, oesophagus, liver, breast and notably colorectum.[13,14] There had been several meta-analyses and systemic reviews,[15,16] which supported a positive association between alcoholic consumption and colorectal cancer risk. However, the role of alcohol in colorectal tumourigenesis has been debated. There were some studies previously suggested that moderate to heavy alcohol consumption has been shown to be a risk factor for the progress from adenomas to carcinomas in male.[17,18] Another research reported that low dose of alcohol intake may present a protective effect against the development of CRA, whereas this effect is lost in high dose.[19]

Numerous studies have been done to investigate the association, however no comprehensive meta-analysis is available. To estimate the summarised relative risk (RR) of CRA associated with alcohol, we thus conducted a meta-analysis for all, light, moderate, heavy and past alcohol consumption, and a dose–response analysis of observational studies. In addition, the risk of CRA was evaluated whether it varies between genders, geographical regions, and adenomatous sites.