Williams Cancer Institute

Every Drink Counts: The Impact of Alcohol on Cancer

 

Talking about alcohol often evokes images of celebrations, social gatherings, or moments of relaxation. However, in recent years scientific research has shown that drinking is far from harmless and that its impact on health is much more serious than previously thought, especially in relation to cancer. In 2025, the Office of the U.S. Surgeon General recommended updating warning labels on alcoholic beverages to explicitly include their link to cancer. This proposal is based on a solid body of scientific evidence showing that alcohol not only increases the incidence of tumors but also worsens clinical outcomes. In other words: it is no longer enough to warn about accidents or liver diseases; alcohol must be publicly recognized as an avoidable carcinogen.

The evidence indicates that alcohol is associated with at least seven types of cancer: mouth, throat, larynx, esophagus, liver, colon, and breast, and worldwide, in 2020 nearly 740,000 cancer cases were attributed to alcohol consumption, with men being the most affected due to higher consumption rates. In the United States, it ranks third as a modifiable risk factor for cancer, after tobacco and obesity/overweight. What is worrying is that this risk is not limited to heavy drinkers, but is also observed in those who consume even small or moderate amounts. This means that there is no level of consumption that can be considered completely safe.

The biological explanation for this link lies in the way the body processes ethanol (the type of alcohol we consume). Once ingested, ethanol is metabolized in the liver into acetaldehyde, a highly toxic compound. Acetaldehyde can directly damage DNA and, more seriously, it can interfere with the repair systems of that DNA. When these fail, mutations accumulate that increase the likelihood of malignant transformation. Added to this central mechanism are others: alcohol causes oxidative stress (an imbalance between free radicals and antioxidant defenses), promotes chronic inflammation, alters hormone levels such as estrogen (which increases the risk of breast cancer), and enhances the effects of other carcinogens such as tobacco, since it acts as a solvent and facilitates their absorption. It also affects folate (vitamin B9) metabolism, essential for DNA replication and repair, and weakens immune surveillance, reducing the body’s ability to eliminate incipient tumor cells.

There are also genetic factors that increase vulnerability. One example is the ALDH2*2 variant, common in East Asian populations, which reduces the ability to degrade acetaldehyde. As a result, this compound accumulates in the body, producing visible reactions such as facial flushing when drinking. This response is a clear signal: even small amounts of alcohol can considerably increase the risk of cancer in those who carry this genetic variant.

Researchers describe the relationship between alcohol consumption and cancer as dose-dependent: “the more you drink, the higher the risk.” Heavy consumption (more than three or four drinks per day) is strongly associated with disease development, but what is most concerning is that even low or moderate consumption (one or two drinks per day) is linked to an increased risk, especially in the case of breast cancer in women and, in some studies, colorectal cancer. Although the results at low levels are not always consistent (due to methodological limitations, such as misclassifying people who stopped drinking due to illness as “non-drinkers”), the overall evidence points in the same direction: each glass adds risk.

Figure 1. Alcohol is primarily metabolized in the liver, where it is converted into acetaldehyde, a toxic and carcinogenic compound. Acetaldehyde promotes DNA damage through oxidative stress and interference with DNA repair mechanisms, processes that increase the risk of developing cancers in organs such as the mouth, throat, liver, and colon.

 

Research in this field faces methodological challenges. Most studies are observational, meaning they follow people over time without modifying their behavior, which makes it difficult to completely isolate the effect of alcohol from other lifestyle factors such as smoking, diet, or exercise. However, the strength of the evidence lies in the large number of studies, meta-analyses, and systematic reviews that, time and again, confirm the causal role of alcohol in cancer. So much so that the International Agency for Research on Cancer (IARC) has for years classified it as a Group 1 carcinogen, that is, with sufficient evidence in humans.

The implications for public health are profound. Beyond recommending moderation, society must rethink the way it perceives alcohol. Many doctors already suggest not exceeding two drinks per day for men and one for women, although they emphasize that the safest option is to minimize consumption. This recommendation is especially important in people with a family history of alcohol-related cancer, in smokers, in patients with liver disease, and in carriers of the ALDH2*2 genetic variant, all of whom face even greater risk. For this reason, it is recommended that health professionals routinely ask about alcohol consumption, use brief screening questionnaires, and offer interventions or treatments for those who exceed safe limits.

In short, alcohol, which for a long time was considered mainly a socially accepted beverage, should today be understood as an important risk factor for cancer. Any consumption carries some level of danger, and this increases with each drink. It is not just about cirrhosis or addictions, but about a silent carcinogen that promotes the appearance of tumors in multiple organs. The key is to inform, educate, and support changes toward healthier consumption habits. Each glass we leave behind represents a tangible reduction in cancer risk and a step toward better public health.

 

Main Reference:

Morford KL, Tetrault JM, O’Connor PG. Alcohol and Cancer Risk. JAMA. Published online August 06, 2025. https://jamanetwork.com/journals/jama/article-abstract/2837352

 

Other References:

Rumgay, H., Shield, K., Charvat, H., Ferrari, P., Sornpaisarn, B., Obot, I., Islami, F., Lemmens, V. E. P. P., Rehm, J., & Soerjomataram, I. (2021). Global burden of cancer in 2020 attributable to alcohol consumption: a population-based study. The Lancet. Oncology, 22(8), 1071–1080. https://doi.org/10.1016/S1470-2045(21)00279-5

Islami, F., Goding Sauer, A., Miller, K. D., Siegel, R. L., Fedewa, S. A., Jacobs, E. J., McCullough, M. L., Patel, A. V., Ma, J., Soerjomataram, I., Flanders, W. D., Brawley, O. W., Gapstur, S. M., & Jemal, A. (2018). Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States. CA: a cancer journal for clinicians, 68(1), 31–54. https://doi.org/10.3322/caac.21440

Rumgay, H., Murphy, N., Ferrari, P., & Soerjomataram, I. (2021). Alcohol and Cancer: Epidemiology and Biological Mechanisms. Nutrients, 13(9), 3173. https://doi.org/10.3390/nu13093173

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