Alcohol consumption has been classified as a Grade 1 carcinogen by the International Agency for Research on Cancer (IARC; part of the World Health Organization), which is the most severe designation. Additionally, ethanol, an ingredient common to alcoholic beverages, and acetaldehyde, which is the product of alcohol metabolism, are Grade 1 carcinogens; thus, the type of alcoholic beverage does not seem to effect its carcinogenicity.¹ According to a study published in Lancet Oncology, in 2020, an estimated 741,300 new cases of cancer worldwide were attributable to alcohol consumption. This estimate did not include stomach and pancreatic cancers; when these cancers were included in a sensitivity analysis, the estimated amount of alcohol-attributable new cancer cases was 808,700.²

How does alcohol contribute to cancer risk?

Alcohol can increase the risk of developing cancer through various mechanisms. This section provides a brief, simplified overview of these processes. 

Enzymes, such as alcohol dehydrogenase (ADH) and cytochrome P-450 2E1 (CYP2E1), metabolize alcohol into acetaldehyde, which is a carcinogenic, genotoxic compound. Acetaldehyde can also bind to deoxyribonucleic acid (DNA) and create DNA adducts, which have the ability to inhibit DNA synthesis and repair, as well as induce DNA alterations, such as point mutations and structural chromosomal changes. Acetaldehyde can also bind to proteins, altering their structures and functions and impacting processes such as DNA repair.³

The body converts acetaldehyde to acetate, which is not harmful; however, individuals with the ALDH2*2 variant allele metabolize acetaldehyde more slowly than those without that variant allele, which leads to greater accumulation of acetaldehyde and greater exposure to its genotoxic effects.³

Ethanol can induce oxidative stress via increasing production of reactive oxygen species (ROS); the presence of ROS can lead to the production of etheno-DNA adducts that can cause mutations in genes that play a role in cell cycle regulation and tumor suppression. Additionally, cell proliferation and metastasis can increase in the presence of ROS. Chronic intake of alcohol can cause macrophages and monocytes to appear in the tumor microenvironment, where they produce pro-inflammatory cytokines that promote ROS formation.³

Further ways through which alcohol consumption may contribute to cancer risk include:³

• Impairing the processes of DNA methylation and synthesis by disrupting one-carbon metabolism and decreasing folate levels. 
• Altering the metabolism of retinoids, which help regulate carcinogenesis; low retinoid levels have been linked to chronic alcohol intake. 
• Altering estrogen pathways and increasing estrogen levels, which may increase breast cancer risk. 
• Impairing the immune system, which can lead to a decreased ability to destroy potentially cancerous cells and maintain antitumor regulation.
• Causing microbial dysbiosis, thereby weakening the intestinal barrier and allowing bacterial products to reach the liver, leading to chronic inflammation.
• Heavy alcohol intake is linked to liver cirrhosis, which can lead to hepatocellular carcinoma.
• Alcohol intake/alcohol-induced activity might aid the activation of other carcinogens.

Alcohol intake and cancer risk

There is a causal relationship between alcohol consumption and cancers of the oral cavity, pharynx, larynx, esophagus, liver, colorectum, and female breast.¹ Research from the World Cancer Research Fund and American Institute for Cancer Research also further suggests that alcohol convincingly increases the risk of esophageal squamous cell carcinoma (SCC) and postmenopausal breast cancer, and that there is a probable increase in the risk of premenopausal breast cancer and stomach cancer.⁴ The aforementioned Lancet Oncology study found that, globally, alcohol-related cancers most commonly developed in the esophagus, liver, and breast.² This study also noted that cancer incidence increased with increasing alcohol consumption, with intake of less than 20g per day contributing to 103,100 cases, intake of 20 to 60g per day contributing to 291,800 cases, and intake of more than 60g per day contributing to 346,400 cases.²

Other studies have also assessed the impact of varying alcohol consumption levels and cancer risk. A 2023 meta-analysis of 106 articles (which included data on cancers of the esophagus, stomach, liver, breast, pancreas, colon and rectum, larynx, lung, thyroid, and prostate) found that overall cancer risk increased significantly with daily alcohol consumption of 12.5 to 24.9g, 25.0 to 49.9g, and 50.0g or more, with cancer risk increasing with greater alcohol intake.⁵ Researchers identified a dose–response relationship between alcohol consumption and all cancer types, except thyroid cancer. Consuming 0.01 to 12.4g of alcohol per day was significantly associated with an increased risk of esophageal, colorectal, prostate, and breast cancers. Daily alcohol consumption of 12.5 to 24.9g was linked to a significantly increased risk of esophageal, colorectal, laryngeal, and breast cancers. Daily intake of 25.0 to 49.9g was associated with a greater risk of cancers of the stomach, liver, prostate, esophagus, colon and rectum, larynx, and breast. Alcohol intake of 50.0g or more per day was associated with an increased risk of all cancers except thyroid and laryngeal cancers (sufficient data were not available to analyze the relationship between laryngeal cancer and alcohol intake ≥50g/day).⁵ 

A 2014 meta-analysis of 572 studies also evaluated the relationship between alcohol consumption levels and cancer risk.⁶ In this study, light alcohol intake was determined as intervals of daily alcohol consumption with a midpoint of 12.5g or lower, moderate intake was defined as intervals of daily consumption with a midpoint of 50.0g or lower, and heavy intake was defined as intervals of daily consumption with a midpoint greater than 50.0g. The results showed that individuals with light alcohol intake had a significantly increased risk of esophageal SCC, breast cancer, and cancer of the oral cavity and pharynx, compared to nondrinkers and occasional drinkers. Moderate alcohol consumption was linked to increased risk of the aforementioned cancers, plus colorectal and pharyngeal cancers. Heavy alcohol consumption was further associated with elevated risk of liver, stomach, pancreatic, lung, and gallbladder cancers.⁶ 

Limitations of these meta-analyses include potential recall bias/underreporting of alcohol consumption, as consumption is typically self-reported, inability to distinguish between former drinkers and nondrinkers, and heterogeneity among studies.^5,6

Alcohol reduction or cessation and cancer risk

A Working Group associated with the IARC published a review on the current evidence of alcohol reduction or cessation and alcohol-related cancer risk.⁷ Data from epidemiological studies showed that alcohol cessation or reduction decreased the risk of oral cavity and esophageal cancers; longer duration of cessation appeared to be linked to greater risk reduction. The current research on laryngeal cancer suggested an association between alcohol cessation of 20 years or greater and decreased risk. Lesser durations of alcohol cessation and reduction in alcohol intake did not appear to reduce laryngeal cancer risk, and confounding due to smoke and chance could not be fully ruled out; as such, the authors concluded that there was a plausible relationship between alcohol reduction or cessation and risk reduction, but further research is needed. There was also limited evidence on the relationship between alcohol reduction or cessation and decreased colorectal cancer risk due to inconsistent evidence. Research on breast cancer suggested a plausible association between alcohol reduction or cessation and decreased risk of breast cancer, though this might only apply to hormone receptor–positive cases. There was inadequate evidence to determine the impact of alcohol reduction or cessation on reducing the risk of pharyngeal or liver cancers. Data from mechanistic studies, which examined exposure to acetaldehyde in saliva, DNA damage, and intestinal permeability, showed an association between alcohol reduction or cessation and decreased risk of alcohol-related cancers. It should be noted that most of the mechanistic studies included data from individuals with alcohol use disorder attending rehabilitation programs.⁷

Bottom Line

Alcohol is a carcinogen, and there is no safe amount of consumption in terms of cancer risk. In general, greater alcohol intake is linked to increasing cancer risk. Limiting or eliminating alcohol consumption can help mitigate this risk, but more research on the impact of alcohol reduction or cessation on the risk of developing various types of cancer is needed to fully understand this relationship.

Sources

1. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Personal Habits and Indoor Combustions. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol. 100E. Lyon, France: International Agency for Research on Cancer; 2012.
2. Rumgay H, Shield K, Charvat H, et al. Global burden of cancer in 2020 attributable to alcohol consumption: a population-based study. Lancet Oncol. 2021;22(8):1071–1080. 
3. Rumgay H, Murphy N, Ferrari P, Soerjomataram I. Alcohol and cancer: epidemiology and biological mechanisms. Nutrients. 2021;13(9):3173. 
4. World Cancer Research Fund/American Institute for Cancer Research. Diet, Nutrition, Physical Activity and Cancer: A Global Perspective. Continuous Update Project Expert Report 2018.
5. Jun S, Park H, Kim UJ, et al. Cancer risk based on alcohol consumption levels: a comprehensive systematic review and meta-analysis. Epidemiol Health. 2023;45:e2023092. 
6. Bagnardi V, Rota M, Botteri E, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer. 2015;112(3):580–593. 
7. Gapstur SM, Bouvard V, Nethan ST, et al. The IARC perspective on alcohol reduction or cessation and cancer risk. N Engl J Med. 2023;389(26):2486–2494.