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Individuals with alcohol use disorder have much higher concentration of glutathione in certain brain areas

by Vladimir Hedrih
July 25, 2025
Reading Time: 3 mins read
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An analysis of neuroimaging data from individuals with alcohol use disorder showed that these individuals tend to have higher concentrations of the antioxidant glutathione in the dorsal anterior cingulate cortex region of their brains. Interestingly, individuals with this disorder who had fewer heavy drinking days in the past two weeks tended to have higher concentrations of glutathione in this brain region. The research was published in Drug and Alcohol Dependence.

Alcohol use disorder is a medical condition characterized by an inability to control or stop drinking alcohol despite negative consequences. It involves both physical dependence and psychological compulsion to consume alcohol. Symptoms include tolerance, withdrawal symptoms when the person stops drinking, and continued use despite harm to health or relationships.

Chronic alcohol use affects the brain’s structure and function. It can shrink brain volume, especially in areas like the prefrontal cortex and hippocampus, which are important for decision-making, memory, and self-control. Chronic heavy drinking also disrupts neurotransmitter systems, including GABA, glutamate, and dopamine, altering mood, behavior, and cognition. Long-term alcohol use can damage white matter in the brain, slowing down communication between brain regions. It may also reduce the brain’s ability to produce and regulate certain antioxidants, increasing vulnerability to oxidative stress.

People with alcohol use disorder tend to have problems with attention, impulse control, and emotional regulation. Some brain changes can improve with abstinence, but others may be long-lasting or permanent, depending on severity and duration.

Study author James J. Prisciandaro and his colleagues wanted to compare concentrations of glutathione in the brains of individuals with alcohol use disorder and those of light drinkers. Glutathione is the brain’s primary antioxidant. When chronic heavy drinking increases oxidative stress in the brain, the brain increases the production of glutathione to try to compensate for this change and reduce it.

Oxidative stress is an imbalance between harmful free radicals and the body’s ability to neutralize them with antioxidants (like glutathione). With continued heavy drinking, the body’s capacity to counter oxidative stress through increased production of antioxidants is eventually overwhelmed, resulting in diminished levels of antioxidants and cell and tissue damage due to oxidative stress.

The researchers analyzed data from a previous study that included 20 individuals with alcohol use disorder who were not previously treated and 20 light drinkers matched with them on demographic characteristics. These individuals completed a Time-Line Followback daily drinking interview for the previous 14 days, allowing researchers to map their alcohol use patterns.

After that, they underwent magnetic resonance imaging of their brains. The researchers used the neuroimaging data to estimate glutathione levels in participants’ brains. Most participants were men of European descent in their twenties who had last consumed alcohol within 7 days before undergoing neuroimaging for this study.

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Results showed that participants with alcohol use disorder drank much more alcohol than light drinkers. Neuroimaging showed that they had significantly higher concentrations of glutathione in the dorsal anterior cingulate cortex region of their brains compared to light drinkers. Interestingly, individuals with alcohol use disorder who had fewer heavy drinking days in the past two weeks tended to have higher concentrations of glutathione in this brain region. This association was not present among light drinkers.

“The findings from this preliminary study are consistent with an interpretation of compensatory GSH [glutathione] upregulation [increase in production] in response to moderate oxidative stress in treatment-naïve individuals with AUD [alcohol use disorder], adding unique support to oxidative stress models of alcohol-related cellular damage and highlighting the potential promise of antioxidant treatments for AUD,” the study authors concluded.

The study sheds light on the biochemical changes in the brain associated with heavy drinking. However, it should be noted that these data come from a small group of mostly young males. Results on other demographic groups might not be identical.

The paper, “Brain glutathione levels and associations with recent drinking in treatment-naïve individuals with alcohol use disorder versus light drinkers,” was authored by James J. Prisciandaro, Joseph P. Schacht, Andrew P. Prescot, and Raymond F. Anton.

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