Alcohol consumption and dementia risk in steatotic liver disease: a nationwide cohort study

A nationwide cohort study of more than 3 million adults found that dementia risk varied substantially by steatotic liver disease phenotype and alcohol consumption pattern, suggesting that liver health and alcohol exposure may have distinct implications for cognitive outcomes.
The analysis included 3,071,829 adults without baseline dementia who underwent health examinations in 2012. Participants were classified as having no steatotic liver disease, metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction-associated alcohol-related liver disease, or alcohol-related liver disease. Outcomes included newly diagnosed all-cause dementia, Alzheimer’s disease, and vascular dementia.
Over a median follow-up of 5.4 years, 72,545 cases of all-cause dementia were recorded, along with 56,999 cases of Alzheimer’s disease and 8,923 cases of vascular dementia.
Across all dementia outcomes, steatotic liver disease was associated with a significantly increased risk. Alcohol-related liver disease showed the highest dementia risk among the steatotic liver disease subtypes, followed by metabolic dysfunction-associated steatotic liver disease. In contrast, metabolic dysfunction-associated alcohol-related liver disease showed largely neutral associations, except for a modest increase in vascular dementia risk.
The findings highlight the importance of distinguishing steatotic liver disease subtypes rather than treating the condition as a single clinical category. Alcohol exposure appeared to modify dementia associations, but not in a uniform way across dementia outcomes.
Further stratification of metabolic dysfunction-associated steatotic liver disease by alcohol consumption revealed an additional pattern. Individuals with metabolic dysfunction-associated steatotic liver disease and no alcohol intake had consistently higher risks of all dementia outcomes. By contrast, those with metabolic dysfunction-associated steatotic liver disease and within-threshold alcohol intake showed more heterogeneous associations.
The observational design means causality cannot be inferred. The authors emphasised that the findings require further validation in studies with longitudinal assessment of steatotic liver disease status and alcohol exposure.
For clinicians, the study reinforces the potential value of considering liver phenotype and alcohol consumption pattern when assessing long-term neurologic risk. It also adds to growing evidence that metabolic and alcohol-related liver disease may intersect with brain health in clinically meaningful ways.
Source: J.W. Han , et al. Alcohol consumption and dementia risk in steatotic liver disease: a nationwide cohort study. Hepatol Int. 2026; https://doi.org/10.1007/s12072-026-11112-5