Alcohol Consumption and Colorectal Cancer: Evidence and Prevention

Colorectal cancer (CRC) ranks as the third most common type of cancer and is the second leading cause of cancer deaths globally. A sedentary lifestyle, obesity, metabolic syndrome, and alcohol consumption can be factors that increase the risk of early-onset CRC (1).

 Alcohol consumption, even in small amounts, has been linked to an increased risk of colorectal cancer (CRC). The relationship between alcohol intake and CRC risk depends on the dose consumed. The risk of CRC is particularly evident in cases of heavy alcohol consumption, although evidence regarding the risk associated with light to moderate consumption is varied (2).

 Several mechanisms link alcohol consumption to the development of cancers in general, with genotoxicity being one of the most scientifically understood factors. In this process, acetaldehyde, a byproduct of alcohol metabolism, causes DNA damage, such as breaks and alterations in its structure. These changes can result in errors during DNA replication, leading to mutations. Over time, the accumulation of these mutations may culminate in the development of cancer (3).

 In addition to alcohol consumption itself, other alcohol-related factors may influence the risk of colorectal cancer (CRC). A family history of the disease is one such factor, with the risk of CRC being significantly higher in individuals with a family history of cancer (4). Gender also appears to have an impact, with men tending to have a higher risk of developing alcohol-associated CRC compared to women. Body mass index (BMI) and body weight may also interact with alcohol, increasing the risk of CRC, especially in obese individuals (5). Although smoking is an established risk factor for CRC, there is no conclusive evidence that it modifies the alcohol-induced CRC risk (6).

 In light of the evidence, it is crucial to raise awareness about the risks of alcohol consumption in relation to colorectal cancer. Although various factors can influence this risk, alcohol consumption alone is a significant modifiable risk factor. Prevention strategies, including moderating alcohol consumption and adopting healthy lifestyle habits, are essential to reduce the incidence of CRC. Continued research is also necessary to better understand the mechanisms by which alcohol contributes to the development of CRC.

References:

1. Sung, H., Ferlay, J., Siegel, R. L., Laversanne, M., Soerjomataram, I., Jemal, A., & Bray, F. (2021). Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA: a cancer journal for clinicians, 71(3), 209–249. https://doi.org/10.3322/caac.21660
2. Cai, S., Li, Y., Ding, Y., Chen, K., & Jin, M. (2014). Alcohol drinking and the risk of colorectal cancer death: a meta-analysis. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP), 23(6), 532–539. https://doi.org/10.1097/CEJ.0000000000000076
3.  International Agency For Research On Cancer. IARC Handbooks of Cancer Prevention: volume 20A - Reduction or cessation of alcoholic beverage consumption. Lyon: IARC, 2024
4. Cho, E., Lee, J. E., Rimm, E. B., Fuchs, C. S., & Giovannucci, E. L. (2012). Alcohol consumption and the risk of colon cancer by family history of colorectal cancer. The American journal of clinical nutrition, 95(2), 413–419. https://doi.org/10.3945/ajcn.111.022145
5. Fedirko, V., Tramacere, I., Bagnardi, V., Rota, M., Scotti, L., Islami, F., Negri, E., Straif, K., Romieu, I., La Vecchia, C., Boffetta, P., & Jenab, M. (2011). Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies. Annals of oncology : official journal of the European Society for Medical Oncology, 22(9), 1958–1972. https://doi.org/10.1093/annonc/mdq653
6. Fagunwa, I. O., Loughrey, M. B., & Coleman, H. G. (2017). Alcohol, smoking and the risk of premalignant and malignant colorectal neoplasms. Best practice & research. Clinical gastroenterology, 31(5), 561–568. https://doi.org/10.1016/j.bpg.2017.09.012