HMN 2026: How Treatment for alcohol use disorder can reverse harmful brain effects

When we drink alcohol, our liver breaks it down into acetate, which the body can then burn as fuel. A new Neuropsychopharmacology study has discovered that chronic alcohol use can alter how the brain metabolizes acetate—and that these effects are reversible.

Research has shown that our brain adapts to the presence of alcohol. In a 2013 study, a group led by Graeme Mason, Ph.D., professor of radiology and biomedical imaging at Yale School of Medicine, found that the brains of people who regularly binge-drink have about 25% greater capacity to consume acetate.

But now, his team has uncovered a surprising finding—across individuals with alcohol use disorder (AUD), the brain’s ability to consume acetate significantly diminishes. However, after a month of being treated for AUD, this ability was restored to a level comparable to that of mild drinkers.

Understanding how the brain changes in response to chronic alcohol exposure, as well as recovery, can help researchers better understand how to support individuals with AUD and may provide a way to better mitigate withdrawal symptoms, the team says.

“If you seek treatment for your AUD and you stop drinking, your brain can recover a lot,” says Mason, who was the study’s principal investigator.

AUD leads to reduced acetate consumption in brain

The brain primarily relies on glucose for fuel. But in certain conditions, it can turn to other sources. For example, if a person goes into starvation, the body will switch to breaking down fat in the absence of glucose, which leads to the production of chemicals called ketones that the brain can alternatively use as fuel. A ketogenic diet—in which an individual consumes foods that are high in fat and very low in carbohydrates—causes a similar effect. Or, when exercising heavily, the brain can burn the generated lactic acid.

Drinking alcohol elevates the levels of acetate in the blood. In the 2013 study, Mason’s team explored the effects of alcohol on the brains of individuals who engaged in chronic heavy drinking, or at least eight drinks per week. They found that the brains of those individuals consumed significantly more acetate.

“The message that came out in some of the news outlets at the time was, ‘If you feel tired, you should drink because it gives you acetate, which gives you energy,'” Mason recalls. But he clarifies, “Just because this gives you energy doesn’t mean the process of creating that acetate isn’t harmful.”

Next, Mason’s team embarked on a five-year study looking at acetate consumption in the brain in a larger cohort of participants. In addition to mild and heavy drinkers, the researchers studied patients with AUD in long-term recovery and people seeking treatment for AUD.

“This last group of people drink far more than even those who are binge drinking,” Mason says. Heavy drinkers, on average, consumed about 100 drinks per month. Individuals seeking treatment, in comparison, had nearly 400 drinks per month.

The researchers used a technique called magnetic resonance spectroscopy, which measures chemicals in the brain, to study acetate consumption. As in the previous study, they found that the brains of individuals in the heavy-drinking group consumed significantly more acetate. They hypothesized that they would observe even higher acetate consumption in the group of individuals seeking AUD treatment.

But their findings were so surprising that they initially thought their scanner was malfunctioning. “Early in their detox program, their brains were barely consuming any acetate,” Mason says.

After a month of abstinence from alcohol, the researchers looked at the brain activity of this cohort again. They found that the brain restored its acetate consumption activity to levels similar to those seen in the mild-drinking group. “So, there’s a reason to be optimistic that whatever’s happening with acetate in the brain can go back to normal in a few weeks, and we know that other things will improve at least partly,” Mason says.

Mason has two hypotheses for why the brain may be shutting down its acetate consumption. To adapt to chronically elevated acetate levels in the blood, the brain may reduce the amount it takes in. “The brain doesn’t want too much acetate coming in,” Mason explains.

Alternatively, acetate is primarily consumed by cells in the brain known as glia, which provide support for neurons. Decreased acetate consumption could also be a sign that these cells are impaired. “If the glia are damaged, they can’t provide all the support that your nerve cells need,” Mason says.

The study not only highlights the resilience of the brain but may also point to solutions for addressing symptoms of withdrawal.

The lack of acetate in the brain, either due to adaptation or damaged brain cells, may contribute to worsened withdrawal symptoms because now the brain lacks a fuel it has come to rely on, Mason says. Replacing this fuel as the brain readapts may help alleviate these symptoms. Previous research has shown, for example, that a ketogenic diet can reduce withdrawal symptoms by supplying the body with ketones as alternate fuel.

In future research, Mason is interested in exploring whether scientists can deliver other alternatives to acetate in the brain. “If we can make up for the loss of acetate in some way, it may help,” he says.

This content is provided for information purposes only.