Even a few drinks a week could quietly raise the risk of dementia, according to the largest combined observational and genetic study to date.
The team from the University of Oxford, Yale University School of Medicine and the University of Cambridge, tracked over half a million adults and found that dementia risk steadily increased with higher alcohol consumption, with no protective effects from light drinking, challenging long-held assumptions about a “safe” level of alcohol for brain health.
How alcohol affects the brain
Dementia is a global health concern, with limited strategies available to prevent it.
Alcohol use has been studied as a possible factor in dementia risk, however, evidence has been inconsistent. Many observational studies have pointed to a U-shaped pattern: light or moderate drinkers appeared to be at a lower risk than heavy drinkers and those who abstain completely. The Whitehall II cohort, for example, reported that both midlife abstainers and heavy drinkers had a higher risk of dementia compared with people drinking between 1 and 14 units per week.
Many studies have focused only on older adults, which leaves uncertainty about long-term effects. Often, non-drinkers are grouped together without separating lifelong abstainers from people who stopped drinking for health reasons. Reverse causation is another issue: early signs of cognitive decline may prompt people to cut down on alcohol, creating the impression that abstainers are at a higher risk when the underlying cause is dementia itself. Reviews of the literature have highlighted how these design issues can lead to misleading results.
Observational research can show associations, but it cannot confirm whether alcohol directly contributes to dementia risk. This has left public health guidance uncertain, with the idea of a “safe” or even beneficial level of alcohol still widespread.
“If it is the case that even low or moderate alcohol intake is harmful to brain health, earlier research suggesting the contrary may have led individuals to intentionally increase alcohol intake to take advantage of its purported health benefits,” said the authors. “More and better data are needed to optimize public health advice.”
The new research uses the largest datasets combined yet to examine alcohol and dementia risk. The study utilized observational data with genetic analysis, employing a method called Mendelian randomization, which helps distinguish cause from correlation.
Large-scale genetic analysis links alcohol to higher dementia risk
Data came from the US Million Veteran Program, which included people of European, African and Latin American ancestry, and the UK Biobank. In total, 559,559 people aged 56–72 years at baseline were followed and tracked from recruitment until a dementia diagnosis, death or the end of follow-up – an average of 4 years in the US and 12 years in the UK.
Alcohol intake was measured through self-report questionnaires and the AUDIT-C screening tool, which captures “risky” patterns such as binge drinking. The genetic arm of the study used variants linked to alcohol use, drinking behaviors and dependence.
Of the 559,559 participants, 14,540 developed dementia during the study period and 48,034 died.
The observational results repeated a familiar finding: A U-shaped pattern appeared with light drinkers having a lower dementia risk than abstainers and heavy drinkers. Compared with light drinkers, the risk was 41% higher among non-drinkers and very heavy drinkers.
Yet the genetic results told a different story. Dementia risk rose steadily with higher alcohol consumption, with no protective effect at any level. Just 1–3 extra drinks per week carried a 15% higher risk, while doubling the genetic risk for alcohol dependence raised the risk by 16%.
Participants who went on to develop dementia often drank less in the years before diagnosis, supporting the idea of reverse causation seen in earlier studies.
“The pattern of reduced alcohol use before dementia diagnosis observed in our study underscores the complexity of inferring causality from observational data, especially in aging populations,” said the authors.
Drinking less may be the best way to protect your brain
The evidence points away from the idea that moderate drinking may protect brain health. This shifts the focus from finding a “safe” level to recognizing that risk reduction may come only through drinking less.
“Public health strategies that reduce the prevalence of alcohol use disorder could potentially lower the incidence of dementia by up to 16%,” said the authors.
However, the strongest statistical signals came from people of European ancestry, which may mean that the results might not apply to other groups. Mendelian randomization also relies on assumptions – for example, that genetic markers are reliable stand-ins for real drinking behaviour – which cannot be fully tested.
Even so, the scale of the datasets and consistency across methods give weight to the conclusions.
Future work will need to expand genetic analyses to more diverse populations and explore the biological mechanisms by which alcohol may contribute to dementia, from vascular damage to direct neurotoxicity.
“Our study findings support a detrimental effect of all types of alcohol consumption on dementia risk, with no evidence supporting the previously suggested protective effect of moderate drinking,” said the authors.
Reference: Topiwala A, Levey DF, Zhou H, et al. Alcohol use and risk of dementia in diverse populations: evidence from cohort, case–control and Mendelian randomisation approaches. BMJ Evid Based Med. 2025. doi: 10.1136/bmjebm2025-113913
This article is a rework of a press release issued by the BMJ Group. Material has been edited for length and content.