Summary:
Alcohol is widely used, but its true impact on dementia has been difficult to determine. To address gaps and limitations in current evidence, the researchers of this paper used two large biobanks to examine the relationship between alcohol use and dementia across the full range of alcohol consumption. The researchers used two types of analysis which allowed them to look at whether alcohol actually causes dementia and whether the risks change depending on how much someone drinks. More than 559,000 adults aged 56-72 years were included in the observational analyses, with follow-up ranging from four to twelve years. During this period, over 14,000 people developed dementia. Observational data showed a U-shaped pattern: the highest risk appeared in non-drinkers, individuals consuming more than 40 drinks per week, and those with alcohol use disorder. However, when alcohol exposure was estimated genetically, dementia risk increased steadily with greater alcohol consumption, with no evidence of benefit at low or moderate levels. Heavier drinking and alcohol use disorder were both linked to higher dementia risk. Further analysis showed that people who eventually developed dementia tended to reduce their alcohol intake in the years before diagnosis, supporting the idea that early cognitive decline leads to lower drinking rather than light drinking protecting the brain. Overall, the study found no evidence that any level of alcohol consumption improves cognitive health. Instead, the genetic findings indicate that alcohol use increases dementia risk across all levels of intake. Reducing heavy drinking at a population level could potentially decrease dementia incidence.
Abstract:
Objectives To investigate the relationship between alcohol consumption and dementia. Design Prospective cohort and case–control analyses combined with linear and non-linear Mendelian randomisation. Setting Two large-scale population-based cohorts: the US Million Veteran Programme and the UK Biobank. Genetic analyses used summary statistics from genome-wide association studies (GWAS). Participants 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). Main outcome measures Incident all-cause dementia, determined through health record linkage, and genetic proxies. Results 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. Conclusions 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%.
Article Publication Date: 23/09/2025
DOI: 10.1136/bmjebm-2025-113913
