Study questions whether alcohol consumption decreases dementia risk

A widely reported study by researchers at the University of Oxford, Yale University, and the University of Cambridge, challenges previous suggestions that light-to-moderate drinking may have a protective effect against dementia. The study is published in BMJ Evidence-Based Medicine.
A prospective cohort and case–control analyses combined with linear and non-linear Mendelian randomisation. Data came from two large-scale population-based cohorts: the US Million Veteran Programme and the UK Biobank. 559 559 adults aged 56–72 years at baseline were included in observational analyses (mean follow-up: 4 years in the US cohort; 12 years in the UK cohort). Genetic analyses used summary data from multiple large GWAS consortia (2.4 million participants). Incident all-cause dementia was determined through health record linkage, and genetic proxies.
During follow-up, 14,540 participants developed dementia and 48,034 died. Observational phenotype-only analyses revealed U-shaped associations between alcohol and dementia risk: higher risk was observed among non-drinkers, heavy drinkers (>40 drinks per week; HR 1.41, 95% CI 1.15 to 1.74), and those with alcohol use disorder (AUD) (HR 1.51, 95% CI 1.42 to 1.60) compared with light drinkers. In contrast, Mendelian randomisation genetic analysis identified a monotonic increase in dementia risk with greater alcohol consumption. A 1 SD increase in log-transformed drinks per week was associated with a 15% dementia increase (inverse-variance weighted (IVW) OR 1.15, 95% CI 1.03 to 1.27). A twofold increase in AUD prevalence was associated with a 16% increase in dementia risk (IVW OR 1.16, 95% CI 1.03 to 1.30). Alcohol intake increased dementia, but individuals who developed dementia also experienced a decline in alcohol intake over time, suggesting reverse causation—where early cognitive decline leads to reduced alcohol consumption—underlies the supposed protective alcohol effects in observational studies.
The researchers say that these findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. While correlational observational data suggested a protective effect of light drinking, this could be in part attributable to reduced drinking seen in early dementia; genetic analyses did not support any protective effect, suggesting that any level of alcohol consumption may contribute to dementia risk. Public health strategies that reduce the prevalence of alcohol use disorder could potentially lower the incidence of dementia by up to 16%.
Prof Sir David Spiegelhalter, Emeritus Professor of Statistics, University of Cambridge, commented: “The reporting of this study is misleading. The authors say that “genetic analysis showed a monotonic increasing dementia risk with increased alcohol intake.”. This is untrue. The relationship is with genetically predicted alcohol intake – the actual alcohol consumption is not part of this analysis. And those genetic predictions rely on many unverifiable assumptions, as the authors acknowledge.”
Prof Tara Spires-Jones, Director of the Centre for Discovery Brain Sciences at the University of Edinburgh, Group Leader in the UK Dementia Research Institute, and Past President of the British Neuroscience Association said: “This study by Topiwala and colleagues at Oxford examining the relationship between alcohol use and risk of developing dementia is well-conducted. The authors looked at data from over 500,000 people who provided self-reports of how much they drank and compared this to their risk of developing dementia over time. Further they examined genetics from over 2 million people and compared genetic markers associated with alcohol use and genetic markers associated with increased risk.
“In both parts of the study, scientists observed that higher reported or predicted alcohol use was associated with increased risk or predicted risk of dementia. In the self-reporting study, people who reported consuming small amounts of alcohol (less than 7 drinks per week) had lower risk than heavy drinkers (more than 40 drinks per week). Interestingly, in this part of the study, non-drinkers and people who reported never drinking actually had similar risk of dementia to people who drank heavily.
“In the genetic study, genes predicting higher alcohol consumption were associated with genes predicting higher dementia risk. Unlike the self-reporting part of the study, genes predicting low alcohol intake were not associated with genes predicting low dementia risk. The authors attribute the difference between the parts of the study to people reducing alcohol intake in the early stages of dementia, but this does not explain the increased risk in people who report never drinking.
“Neither part of the study can conclusively prove that alcohol use directly causes dementia, but this adds to a large amount of similar data showing associations between alcohol intake and increased dementia risk, and fundamental neuroscience work has shown that alcohol is directly toxic to neurons in the brain.”
Source: 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 Evidence-Based Medicine, 2025.