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Alcohol, smoking and the risk of premalignant and malignant colorectal neoplasms

https://doi.org/10.1016/j.bpg.2017.09.012Get rights and content

Abstract

Colorectal cancer (CRC) is the third most common cancer worldwide and has a complex aetiology consisting of environmental and genetic factors. In this review, we evaluate the roles of alcohol and tobacco smoking in colorectal neoplasia. Alcohol intake and tobacco smoking are associated with modest, but significantly, increased risks of CRC, adenomatous and serrated polyps. There is consistent evidence of dose-response relationships for both alcohol and smoking, and risk of these neoplasms. Alcohol and smoking appear to be more strongly associated with colorectal polyp than CRC development, suggesting roles in the initiation of neoplastic growths. These lifestyle factors also seem more strongly related to adenomas and sessile serrated lesions than hyperplastic polyps, but further confirmation is required. The gastroenterology community has an important, yet currently underexploited, role to play addressing the modifiable factors associated with CRC and polyps. These behaviours include, but are not limited to, alcohol and smoking.

Section snippets

Pathogenesis of colorectal neoplasms (A)

CRC is initiated when mutations result in the malignant transformation of preneoplastic polyps [1], [4]. In the past, adenomas and hyperplastic polyps were considered to be the two main subgroups of epithelial colorectal polyps [2], [5]. Adenomas were regarded as the sole precursor lesions of CRC whilst hyperplastic polyps were believed to possess no malignant potential [5], [6]. This hypothesis has since been partially negated, and the umbrella term ‘serrated polyp’ is now used to encompass

Epidemiology of colorectal cancer (A)

Colorectal cancer is the third most common cancer worldwide [16], accounting for more than 9.7% of all cancer incidence in 2012 [17]. Each year, almost 1.4 million new cases are diagnosed, making CRC a major cause of morbidity and mortality globally [18] and the fourth most common cause of cancer death [16]. The highest age-standardised incidence rates have been recorded in Australia, New Zealand, Canada, the United States (US) and parts of Europe [18] (Fig. 2).

However, CRC incidence rates

Alcohol and colorectal cancer risk (A)

The association between alcohol and colorectal neoplasia risk is summarised in Table 1. In 2007, a working group for the International Agency for Research on Cancer (IARC) reviewed epidemiological evidence from over 50 studies that reported on the association of alcohol consumption and 27 anatomical sites including the colon/rectum [35]. IARC concluded that there was sufficient evidence to support the addition of CRC to the list of malignancies causally related to alcohol [36], [37]. As

Alcohol and colorectal polyp risk (A)

When evaluating evidence for polyp risk, it is crucial to consider study designs. Due to the asymptomatic nature of many colorectal polyps, it is important that controls (i.e. individuals without polyps) in such studies have had the opportunity for a polyp to be diagnosed i.e. that all underwent an endoscopy. For a number of studies reporting on alcohol, smoking and polyp risk, the sole method of assessment for the colon was sigmoidoscopy, as opposed to a full colonoscopy. Therefore, risk of

Smoking and colorectal cancer risk (A)

The association between smoking and colorectal neoplasia risk is summarised in Table 2. Tobacco smoke is a well established carcinogen, and research confirms that there is a significant association between smoking and CRC risk. Large, multicentre cohort studies and meta-analyses have demonstrated that this association is present for both past and current smokers [55], [56]. Results indicate a significant 38% increased CRC risk in current smokers (RR, 1.38; 95% CI, 1.22–1.56), while former

Smoking and colorectal adenoma risk (B)

Studies consistently report that there is a significantly greater proportion of colorectal adenomas detected amongst smokers compared with non-smokers [69], [70]. A meta-analysis of 42 observational studies demonstrated pooled risk estimates for colorectal adenoma in current, former and ever smokers of 2.14 (95% CI, 1.86–2.46), 1.47 (95% CI, 1.29–1.67), and 1.82 (95% CI, 1.65–2.00), respectively [69]. Again, clear dose-response associations between smoking and adenoma risk have been noted [70].

Interventional studies addressing alcohol, smoking and colorectal neoplasia (A)

For numerous health reasons beyond the association with CRC and colorectal polyps, individuals should be advised not to smoke tobacco. Advice regarding alcohol consumption is less straightforward but, generally, individuals should be advised to limit their intake if they consume alcohol. Although there are some nuances that deserve further study in observational settings, such as accurately quantifying the association between lifestyle factors and serrated polyp subtypes, or age at CRC onset,

Summary (A)

There is a large body of evidence to support the role of both alcohol and smoking in colorectal neoplasia. Alcohol intake is associated with significantly increased risks of CRC, adenomatous and serrated polyps, and there is evidence of a dose-response relationship. These trends appear to be consistent across both genders and different anatomical sites within the colorectum. With regards to smoking, there is a modest but significant increased risk of CRC and colorectal polyps, and again a

Role of the funding source

Ifewumi Fagunwa was funded by a Summer Studentship at the Centre for Public Health, Queen's University Belfast. Helen Coleman is a co-investigator of the Centre of Excellence for Public Health, Northern Ireland. These funding sources did not have any role in the collection, analysis and interpretation of data and in the writing of the manuscript.

Conflicts of interest

None.

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