Can Ozempic Help Curb Alcohol Cravings?

Glucagon-like peptide-1 (GLP-1) receptor agonists, such as semaglutide, are a class of medications initially developed to manage type 2 diabetes. Although the mechanism of action has not been fully characterized, it is thought that they act by mimicking the peptide hormone GLP-1, which is released from the intestines in response to food intake (QH). These agonists activate the GLP-1 receptor, helping regulate blood sugar levels by promoting insulin secretion, suppressing glucagon secretion, slowing stomach emptying, and reducing appetite. The immense popularity of these drugs, including Ozempic and Wegovy, stems from their significant impact on weight, which has also sparked interest in their potential effects on other behaviors.

Past studies have suggested that GLP-1 agonists could have a broader application in treating addictive behaviors beyond overeating. Anecdotal reports from patients using these medications for weight loss have frequently included a reduced desire for alcohol. This has led researchers to investigate whether these drugs could be repurposed to treat substance use disorders. Preclinical studies in rodents and non-human primates have shown that GLP-1 receptor agonists can decrease the intake of alcohol and other drugs of abuse.

Several medications are currently approved by the U.S. Food and Drug Administration (FDA) to treat alcohol use disorder (AUD), including naltrexone, acamprosate, and disulfiram (link). These drugs work by reducing the rewarding effects of alcohol, managing cravings, or causing unpleasant symptoms when alcohol is consumed. However, these medications are not widely used, with less than 4% of people with AUD in the past year being prescribed an FDA-approved medication for multi-faceted reasons relating to both patient and provider. This highlights the significant need for new and more effective treatment options.

A recent study has provided compelling evidence that semaglutide, the active ingredient in popular weight-loss drugs Ozempic and Wegovy, may also be effective in reducing alcohol consumption and cravings in individuals with alcohol use disorder. In the phase 2, double-blind, randomized, placebo-controlled trial, 48 participants with alcohol use disorder were randomly assigned to receive either weekly low-dose (0.25 mg/week for 4 weeks, 0.5 mg/week for 4 weeks, and 1.0 mg for 1 week) injections of semaglutide or a placebo for nine weeks total. The primary goal was to evaluate the effects of the medication on alcohol consumption and cravings based on weekly assessments.

Participants who received semaglutide showed a significant reduction in the amount of alcohol consumed on drinking days (Figure 1), and a decrease in weekly alcohol cravings compared to the placebo group. The large error bars are the consequence of the small sample size. The study also found that semaglutide predicted greater reductions in heavy drinking over time. Interestingly, in a small subgroup of participants who also smoked cigarettes, semaglutide treatment was associated with a greater relative reduction in the number of cigarettes smoked per day.

While the precise mechanisms are still being investigated, a leading theory is that semaglutide influences the brain's reward system. GLP-1 receptors are found in areas of the brain that are critical for reward processing, and by activating these receptors, semaglutide may reduce the rewarding effects of alcohol. Animal studies suggest that GLP-1 agonists may decrease the release of dopamine, a neurotransmitter central to the experience of pleasure and reward, in response to alcohol. This modulation of dopamine signaling is thought to lessen the motivation to drink. Further research is needed to explore these speculative hypotheses.

Despite the promising results, researchers emphasize that this was a small, short-term study, and more extensive research is needed. Key unanswered questions include the long-term efficacy and safety of semaglutide for AUD, as well as what happens to drinking behaviors after the medication is discontinued. In other words, these results need to be reproduced in a much larger, longer-term trial. Regardless, the findings from this research are an important step forward in the search for more effective treatments for alcohol use disorder.

Figure 1. Bar graph depicts the mean change from baseline in the number of drinks per drinking day for the treatment group (blue bars) compared to placebo control (orange bars). The treatment period was divided into the first 4 weeks (1-4) followed by the next 4 weeks (5-8). The mean and standard error are shown for each group. The Cohen d statistic describes the normalized effect size with d = 0.20 for a small effect, d = 0.5 for a medium effect, and d = 0.8 for a large effect (Hendershot et al. JAMA Psychiatry, 2025).