This study was a cross-sectional population-based autopsy study conducted in Brazil. Researchers were able to examine the brains of 1,781 participants.
These brains were ultimately from the Sao Paulo Autopsy Service and part of the Biobank for Aging Studies. It specifically excludes brain samples where someone died due to trauma.
The average age of participants was around seventy-five years old, and the sample was ethnically diverse. Participants were at least fifty and had a next of kin who had been contacting them at least weekly in the 6 months before their death.
Researchers did exclude some potential participants, including those with major acute brain lesions or those who did not have any data on alcohol consumption.
Researchers were able to gather data from next of kin regarding factors like participants’ medical histories, alcohol consumption, and the presence of dementia.
They divided participants into groups based on the level of alcohol they consumed. There were never drinkers, moderate drinkers, heavy drinkers, and formerly heavy drinkers.
For this research, 1 dose of alcohol was 14 grams (g). Moderate drinkers had up to 7 doses of alcohol in a week, while heavy drinkers had 8 or more doses in a week.
Former heavy drinkers were heavy drinkers who had ceased drinking up to 3 months before their deaths occurred. Of all participants, 965 never consumed alcohol.
Researchers then sought to examine the brains for several changes, including those that indicated Alzheimer’s disease. They were also able to determine brain weight.
Heavy drinkers face 133% higher risk of brain damage
Overall, the results showed worse outcomes related to alcohol consumption.
Researchers adjusted for clinical variables and sociodemographic data, and found that moderate, heavy drinkers, and former heavy drinkers were at a greater risk for having hyaline arteriolosclerosis compared to participants who never had drunk alcohol.
Heavy drinkers were specifically at 133% increased risk for hyaline arteriolosclerosis. Heavy and former heavy drinkers were also at an increased risk for neurofibrillary tangles, which are related to Alzheimer’s disease pathology.
Former heavy drinkers also had lower brain weights. They had slightly higher average clinical dementia rating scores compared to never-drinkers. In this case, higher scores indicate worse cognitive function. There was no association between heavy and moderate drinking and cognitive function.
The findings also indicated that drinking alcohol did not have an overall or direct effect on people’s cognitive abilities. Instead, researchers found that hyaline arteriolosclerosis mediated the association between alcohol consumption and cognitive abilities.
This could indicate that alcohol affects hyaline arteriolosclerosis, which then may affect aspects of brain function.
Haris Kamal, MD, a neurologist at Memorial Hermann, who was not involved in this research, noted the following about the study findings to Medical News Today:
“The effect of alcohol on the human brain is dependent on multiple factors such as age, number of years of heavy alcohol use, overall health, nutritional intake etc. This study demonstrates that moderate to heavy alcohol use or even a history of prior heavy alcohol use is associated with more arteriosclerosis in the smallest arteries in the brain; such a progressive thickening of the arterial walls and increased deposition of neurofibrillary tangles of tau protein can lead to cognitive impairment including dementia.”