Ozempic-Like Drugs Could Have a Surprising Effect on Alcohol Cravings

Imagine ordering a drink you would normally enjoy, then finding you barely want to touch it.

Some people taking Ozempic-like medications have described just such a change.

Could these drugs help people with alcohol use disorder? A review published in Biological Psychiatry brings together the evidence.

It suggests a promising possibility, but also an important distinction: drinking less does not necessarily mean craving alcohol less.

Ozempic's active ingredient, semaglutide, belongs to a class of drugs that mimic GLP-1, a hormone involved in regulating appetite and blood sugar.

Researchers are now testing whether the drugs also change people's relationship with alcohol.

Mette Kruse Klausen and Anders Fink-Jensen, researchers in Denmark, examined randomized trials, health record studies and reports from people taking the medications.

In one, 127 people seeking help for alcohol use disorder received psychotherapy alongside either weekly injections of the GLP-1 drug exenatide or a placebo. Across the entire group, exenatide did not significantly reduce heavy drinking days compared with placebo.

An exploratory analysis suggested that participants with obesity might have benefited.

Brain scans from a subset of participants also showed a weaker response to alcohol-related images in regions involved in reward. But these findings cannot establish that the drug works only for people with obesity, or explain precisely why drinking might change.

A different research team tested semaglutide in 48 people with alcohol use disorder who were not seeking treatment. Those assigned the drug drank less during a laboratory test than those given placebo. They also reported fewer drinks on days when they drank and less weekly alcohol craving.

The drug did not, however, significantly change the number of days they drank or their average drinks per calendar day.

Craving, the amount consumed on a drinking day and the frequency of drinking are distinct outcomes.

The strongest published evidence comes from a 26-week trial in The Lancet, one of two trials in this review that Klausen and Fink-Jensen also co-authored. It enrolled 108 people with obesity who were seeking treatment for moderate-to-severe alcohol use disorder.

All received cognitive behavioral therapy and were assigned either weekly semaglutide injections or placebo.

"Semaglutide produced a significantly greater reduction in heavy drinking days: a 41.1-percentage-point reduction from baseline compared with 26.4 points with placebo, corresponding to a treatment difference of 13.7 percentage points," Fink-Jensen told ScienceAlert.

The 13.7-point figure is the trial's estimated treatment difference, not the result of simply subtracting the two rounded reductions. Participants receiving semaglutide also reduced their overall alcohol intake more than those receiving placebo.

"So the evidence is increasingly consistent that semaglutide can reduce heavy drinking and the amount consumed when people drink," Fink-Jensen said. "Evidence for an effect on craving is promising but less consistent."

A newer randomized trial of oral semaglutide adds to that distinction. It found fewer heavy drinking days, but its primary laboratory measure of craving triggered by alcohol-related cues did not differ significantly from placebo. A separate measure of cravings reported during daily life did improve. The study was published online on July 29, after the review had been accepted.

Health record studies have also linked GLP-1 prescriptions to fewer alcohol-related events. They can follow large groups of people, but cannot establish on their own that the medications caused them to drink less.

How could a diabetes medication change alcohol consumption? The brain's response to reward may be part of the answer. Appetite, signals related to calories and slower stomach emptying could also contribute. The researchers cannot yet say which mechanisms matter most.

Nor is it clear who would benefit. The largest published semaglutide trial included only people with obesity, while the smaller trial found no clear evidence that the effect on drinking depended on body mass index. Researchers also cannot yet say whether any reduction in drinking is independent of weight loss.

"Obesity may influence the response to GLP-1 receptor agonists, but we do not yet know whether BMI is an important treatment modifier," Fink-Jensen said.

The drugs can cause nausea and other digestive problems. Larger, longer trials must establish who benefits, what happens after treatment stops and how GLP-1 drugs compare directly with existing medications for alcohol use disorder, including naltrexone and acamprosate.

Fink-Jensen disclosed a previous unrestricted grant from Novo Nordisk for research on metabolic problems in people with schizophrenia, and an unpaid role on a company trial advisory panel. The Lancet alcohol trial lists the Novo Nordisk Foundation among its five funding sources.

"I would characterize GLP-1 receptor agonists as a promising emerging treatment strategy rather than an established treatment for AUD," Fink-Jensen said.

For now, the clearest signal is that semaglutide may help some people drink less heavily. Whether it reliably quiets the urge to drink, and for whom, remains a question worth pursuing.

The research has been published in Biological Psychiatry.