Genetic study finds no overall cancer link for alcohol intake

A major genetic analysis reports no association between alcohol consumption and overall cancer risk, offering a more nuanced view than some headline health warnings. The findings arrive as global policy debates intensify over alcohol affordability and taxation.

A new paper published in BMC Medicine examines whether alcohol consumption causes cancer using Mendelian randomisation, a method that relies on genetic proxies rather than self-reported drinking. The study by Larsson et al. draws on data from more than 1.5 million participants across four large biobanks and several cancer consortia.

The analysis tested genetically predicted alcohol consumption against the risk of 20 cancers. As per the abstract, no association was observed between alcohol intake and overall cancer incidence, with an odds ratio of 0.96 per standard deviation increase in consumption and a non-significant p-value of 0.45.

Overall cancer risk remains neutral

The absence of an overall cancer signal is one of the paper’s most striking outcomes. Despite alcohol’s classification by the International Agency for Research on Cancer as a Group 1 carcinogen, the genetic data did not support the idea that alcohol consumption is a cause of all cancers, according to the study’s conclusions.

Among cancers often cited in public health messaging, breast cancer showed no association in either biobank or consortium data. The odds ratio was 1.09 in biobank analyses and 0.98 in consortium analyses, both statistically nonsignificant.

Where risks appear and where they do not

The study did find moderate evidence of increased risk for certain sites. Genetically predicted alcohol consumption was positively associated with combined head and neck cancers and showed nominal associations with colorectal and oesophageal cancer.

At the same time, several cancers displayed inverse associations. Kidney cancer and endometrial cancer showed statistically robust negative estimates, while non-Hodgkin’s lymphoma, myeloma and some ovarian cancer subtypes were also inversely associated, according to the results section.

The authors caution that such inverse findings should be interpreted carefully due to methodological limitations. Still, the pattern aligns with parts of classical epidemiology, as outlined in the accompanying commentary.

Limits of genetics in measuring drinking

A key limitation lies in how little drinking behaviour is explained by genetics. The variants used in the analysis account for roughly 0.2% of variation in alcohol consumption, a figure the authors themselves describe as extremely low.

In its assessment, the International Scientific Forum on Alcohol Research points out that complex behaviours such as drinking patterns, timing and context are not captured by Mendelian randomisation. This weakens the case for drawing firm causal conclusions, particularly at low or moderate levels of intake.

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

Policy context and public messaging

The findings arrive amid renewed pressure from the World Health Organisation, which has argued that alcohol is becoming too affordable and has urged governments to raise taxes. As reported by the drinks business, the WHO links affordability to a rising burden of disease and injury.

However, while heavy consumption remains associated with certain cancers, the lack of an overall cancer signal and the null results for breast cancer suggest that blanket statements about any alcohol consumption increasing cancer risk may overreach the available evidence.

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