
According to the
One area of ongoing research is how alcohol can affect the brain. Published in Neurology, a recent study explored the impact of alcohol consumption on various aspects of the brain, specifically dementia-related neuropathologies.
It found that moderate, heavy, and former heavy drinking were all associated with
Former heavy drinking was also linked to having a lower brain mass ratio and poorer cognitive abilities compared to never drinking. While more research is needed, the results indicate the possible damaging effect of alcohol on the brain.
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.
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.”
The research does have some limitations. For one, researchers had to rely on family members for information such as clinical information and data on participants’ drinking habits.
It is possible that these reports from next of kin were inaccurate. They also missed “longitudinal follow-up data” before participants’ deaths, such as on how long participants had been consuming alcohol.
Furthermore, this study focused on people in one country, so data from other countries may also be useful in drawing stronger conclusions.
The study did find that heavy drinkers were more likely to die early but had lower frequency of high blood pressure, neuropathologic lesions, and stroke when researchers did the univariate analysis. The authors think this could be because of survival bias, which is linked to lower life expectancy in this demographic.
Researchers also note that since the study was cross-sectional, it does not show causality. The study’s cross-sectional nature also did not allow them to look at the long-term effects of components like heavy drinking.
Moreover, it is possible that reverse causality is part of the reason for certain results, such as why they observed cognitive problems in former heavy drinkers.
Finally, researchers did not examine participants’ vitamin deficiencies, which could have amplified the observed cognitive decline. Future studies should take vitamin status into account.
Study author Alberto Justo, PhD, a researcher at the University of São Paulo Medical School, told MNT that: “Future research should focus on cohort studies to better understand the causal relationships between alcohol consumption and brain changes over time. This research will help clarify how different levels and durations of alcohol intake affect cognitive health.”
Tony Thrasher, DO, MBA, CPE, DFAPA, who was not involved in this research, also cautioned that:
“While there were limitations (well documented) pertaining to the thoroughness of data collection (from next of kin) and longitudinal knowledge of said alcohol consumption, the overall numbers are fairly striking. Past studies have already demonstrated that heavy drinkers die multiple years earlier when compared to nondrinkers. While still noting survival bias is present, the study gives hope to those health care providers who look for data sets to support them during motivational interviewing.”
So far, the data indicate some very real potential dangers that alcohol consumption can pose to the brain. Justo noted that:
“Our study found that even moderate alcohol consumption may lead to vascular changes in the brain, such as hyaline arteriolosclerosis. We also observed that former heavy drinkers had reduced brain mass and poorer cognitive abilities. This highlights how alcohol, even in moderate amounts, can significantly impact brain health. These findings suggest the need for increased awareness about the risks of alcohol consumption on brain health, even at moderate levels.”
The findings could be highly relevant to clinical practice down the road.
“Potential clinical implications of this study are the finding that heavy alcohol use or a history of heavy alcohol use can lead to accelerated subcortical disease in the brain which would manifest as a cognitive impairment,” Kamal.
“Such people over time may progressively demonstrate paucity/slowness of thought, memory issues, trouble with executive functioning etc,” he explained, adding that “accumulation of such small vessel disease in the brain typically can lead to a condition called vascular dementia.”