Long-Term Effects of Alcohol: Reduced Brain Mass and Increased Risk of Dementia After Years of Abstinence

Drinking too much alcohol, even in the past, can cause lasting damage to the brain. One study analyzed the brains of nearly 1,800 people and found that those who drank moderately or heavily had more problems with the blood vessels in the brain and more signs of Alzheimer's. This damage was linked to loss of brain mass and worsening memory and reasoning. In other words, excessive alcohol consumption can leave deep scars on the brain, even years after you stop drinking.

Excessive alcohol consumption is a serious public health problem worldwide. Drinking in large quantities is associated with several diseases and an increased risk of death.

Although we know that alcohol can harm the brain, there are still many questions about exactly how prolonged alcohol use affects cognitive functions (such as memory and reasoning) and the changes it causes in the brain in the long term, especially those linked to dementia.

Therefore, a group of researchers from the University of Sao Paulo, Brazil, decided to investigate how different levels of alcohol consumption, from those who never drank to those who drank heavily, relate to the changes observed in the brain after death, analyzing typical signs of neurodegenerative diseases.

To do this, they used data from the Biobank for Aging Studies, a large bank of brains collected from volunteer donors. The participants were divided into four groups:

1. Never-drinkers

   
   

2. Moderate drinkers

   
   

3. Heavy drinkers

   
   

4. Those who were heavy drinkers in the past but had stopped.

The researchers then examined the brains of these people using special staining techniques and laboratory tests.

They looked for signs of Alzheimer's disease, such as the buildup of protein plaques and tangles inside neurons, as well as other changes, such as the presence of Lewy bodies (associated with Parkinson's disease), damage to blood vessels (hyaline arteriolosclerosis), small strokes (lacunar infarcts), and abnormal protein deposition in blood vessels (cerebral amyloid angiopathy).

Participants' cognitive abilities before death were also assessed using a clinical dementia scale, and the ratio of brain weight to participants' height was calculated to measure brain loss.

In total, data from 1,781 people were analyzed, with an average age of almost 75 years. Most had low levels of education (on average, less than five years of schooling), and the distribution by sex and race was balanced.

The results showed that moderate or heavy drinking, or having drunk heavily in the past, was associated with a significant increase in the occurrence of hyaline arteriolosclerosis, that is, a hardening of the small blood vessels in the brain.

In addition, current or past heavy alcohol consumption was also associated with an increase in the formation of neurofibrillary tangles, one of the main signs of Alzheimer's disease.

Those who had a history of excessive alcohol consumption in the past also had a greater reduction in brain mass and worse cognitive performance.

An important point noted in the study was that the worsening of cognitive abilities associated with alcohol appeared to be explained entirely by damage to the brain’s blood vessels.

In other words, hyaline arteriolosclerosis was the main mechanism linking alcohol consumption to the decline in brain function.

Despite the important findings, the authors warn that the study has limitations. Because the data on alcohol consumption were collected at a single point in the participants’ lives, it was not possible to assess how long or at what stage of life people drank, which can significantly influence the results.

Still, the study reinforces the negative impact of high alcohol consumption on brain health, showing that even after stopping the habit, lasting damage can persist.

A, Brain of a normal individual. B, Brain of an individual with Alzheimer's disease. C, Brain of an alcoholic

READ MORE:

Association Between Alcohol Consumption, Cognitive Abilities, and Neuropathologic Changes A Population-Based Autopsy Study

Alberto Fernando Oliveira Justo, Regina Paradela, Natalia Gomes Goncalves, Vitor Ribeiro Paes, Renata Elaine Paraizo Leite, Ricardo Nitrini, 

Carlos Augusto Pasqualucci,  Eduardo Ferriolli, Lea T. Grinberg, and Claudia Kimie Suemoto

Neurology, Volume 104, 2025 May 13;104 (9) : e213555.

doi: 10.1212/WNL.0000000000213555.

Abstract:

Heavy alcohol consumption is a major global health concern linked to increased morbidity and mortality. However, the long-term impact of excessive alcohol consumption on cognitive abilities and dementia-related neuropathology is unclear. The aim of this study was to analyze the association between alcohol consumption and age-related neuropathologic outcomes in a population-based autopsy study. This cross-sectional study used data from the Biobank for Aging Studies, classifying participants as never, moderate, heavy, or former drinkers. Alzheimer disease pathology (neuritic plaques, amyloid deposition, and neurofibrillary tangles), Lewy body pathology, transactive DNA-binding protein 43, lacunar infarcts, hyaline arteriolosclerosis, and cerebral amyloid angiopathy were evaluated following international criteria using immunohistochemistry and hematoxylin and eosin staining. Cognitive abilities were evaluated using the Clinical Dementia Rating Scale Sum of Boxes, and the brain mass ratio was calculated by dividing the brain weight by the participant's height. Logistic and linear regression models were used to investigate the associations between alcohol consumption and neuropathology while we used mediation analysis to evaluate the direct and indirect effects of alcohol on cognition through neuropathologic lesions. We included 1,781 participants (mean age 74.9 ± 12.5 years, mean education 4.8 ± 4.0 years, 49.6% women, and 64.1% White). Compared with participants who never consumed alcohol, moderate (odds ratio [OR] 1.60, 95% CI 1.19–2.15, p = 0.001), heavy (OR 2.33, 95% CI 1.50–3.63, p < 0.001), and former heavy (OR 1.89, 95% CI 1.41–2.54, p < 0.001) alcohol consumptions were associated with hyaline arteriolosclerosis while only heavy (OR 1.41, 95% CI 1.10–2.30, p = 0.012) and former heavy (OR 1.31, 95% CI 1.02–1.68, p = 0.029) alcohol consumptions were associated with neurofibrillary tangles. Former heavy drinking was associated with a lower brain mass ratio (β −4.45, 95% CI −8.55 to −0.35, p = 0.033) and worse cognitive abilities (β 1.31, 95% CI 0.54–2.09, p < 0.001). The association between impaired cognitive abilities and alcohol consumption was fully mediated by hyaline arteriolosclerosis (β 0.13, 95% CI 0.02–0.22, p = 0.012). Moderate, heavy, and former heavy alcohol consumptions were associated with hyaline arteriolosclerosis and neurofibrillary tangles. Former heavy alcohol consumption was associated with reduced brain mass and cognitive abilities. The association between alcohol and cognitive abilities was fully mediated by hyaline arteriolosclerosis. The lack of longitudinal data on alcohol consumption duration restricts the interpretation of our findings.