Genetic Study Finds No Overall Link Between Alcohol Consumption and Cancer Risk

A large-scale genetic study has found no overall link between alcohol consumption and cancer risk, challenging some of the broad health warnings that have circulated in recent years. The research, published in BMC Medicine, used Mendelian randomization—a method that relies on genetic markers rather than self-reported drinking habits—to examine whether alcohol intake causes cancer. The study was led by Susanna Larsson and colleagues, who analyzed data from more than 1.5 million people across four major biobanks and several international cancer consortia.

Researchers tested whether genetically predicted alcohol consumption was associated with the risk of developing 20 different types of cancer. According to the results, there was no significant association between alcohol intake and overall cancer incidence. The odds ratio for overall cancer risk per standard deviation increase in alcohol consumption was 0.96, with a p-value of 0.45, indicating no statistical significance.

This finding stands out because alcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer, meaning it is considered a known cause of cancer in humans. However, the genetic data from this study did not support the idea that alcohol consumption increases the risk for all cancers combined.

The study also looked specifically at breast cancer, which is often highlighted in public health campaigns about alcohol risks. In both biobank and consortium analyses, there was no significant association between genetically predicted alcohol consumption and breast cancer risk. The odds ratios were 1.09 and 0.98 respectively, both statistically nonsignificant.

While the study did not find an overall increase in cancer risk, it did identify moderate evidence of increased risk for certain types of cancer. Genetically predicted alcohol consumption was positively associated with head and neck cancers, and there were nominal associations with colorectal and esophageal cancers. At the same time, some cancers showed inverse associations: kidney cancer and endometrial cancer had statistically robust negative estimates, while non-Hodgkin’s lymphoma, myeloma, and some ovarian cancer subtypes also appeared inversely associated with alcohol intake. The authors caution that these inverse findings should be interpreted carefully due to methodological limitations.

One important limitation of the study is that genetic variants used in Mendelian randomization explain only about 0.2% of variation in drinking behavior. This means that much of what determines how much people drink is not captured by genetics alone. The International Scientific Forum on Alcohol Research noted that complex behaviors such as drinking patterns, timing, and social context are not measured by this method, making it difficult to draw firm conclusions about causality—especially at low or moderate levels of drinking.

The forum also pointed out that moderate drinking appears to play a minor role in the development of most cancers and may even be linked to lower risk for some types based on broader scientific literature.

These findings come at a time when global policy debates over alcohol are intensifying. The World Health Organization has recently called for higher taxes on alcoholic beverages, arguing that increased affordability is contributing to a rising burden of disease and injury worldwide. While heavy drinking remains linked to certain cancers—such as those of the head, neck, colon, and esophagus—the lack of an overall association between alcohol intake and total cancer risk suggests that public health messages warning against any level of drinking may not fully reflect current scientific evidence.

The study’s authors emphasize the need for nuanced communication about alcohol’s risks and call for further research using more comprehensive methods to better understand how different patterns of drinking affect cancer risk across populations.