GLP-1s Like Ozempic May Be a New Treatment for Addiction
Will research trials show GIP + GLP-1 drugs like Mounjaro treat cannabis use?
Updated May 16, 2026 | Reviewed by Lybi Ma
Could Mounjaro or related drugs treat cannabis use disorder and other substance addictions? Maybe so. GLP-1 receptor agonists like Ozempic and Victoza were originally developed to treat type 2 diabetes, but their weight loss effects were quickly discovered. More recently, attention has shifted from the gut to these drugs’ effects in the brain—specifically, systems that regulate motivation , reward, and behavior.
GLP-1 receptor agonists appear to function as neuro-metabolic modulators of reward. New data for alcohol and nicotine use disorders are positive, still emerging, and there is also hope about GLP treatment for cannabis use disorder (CUD), which has accelerated quickly. According to recent surveys from late 2025, approximately 12 percent of American adults have used GLP-1 medications such as Ozempic or Wegovy. The cannabis industry has discussed this widespread use of GLP-1 weight-loss drugs as a disruption. Some dispensaries have noted how these medications reduce classic cannabis-related appetite or the “munchies.”
Recent research revealed that metabolic disease and addiction share overlapping biology. Both involve dysregulation of reward processing. In substance use disorders (SUDs), this issue presents as increased craving, impaired control, and heightened responses to cues. But large observational studies suggest patients prescribed GLP-1 drugs for diabetes or obesity experience lower rates of alcohol use, smoking , and substance-related complications. These data are promising but not as reliable as data from a randomized trial. That’s coming. The National Institute of Drug Abuse (NIDA) announced they are sponsoring a clinical trial testing whether Tirzepatide could effectively treat cannabis use disorder.
GLP-1 receptors are found in key brain regions, such as the ventral tegmental area and the nucleus accumbens, which are central to the mesolimbic dopamine system. Ozempic and other GLP-1 receptor agonists dampen mesolimbic dopamine signaling, reducing reward salience and drug reinforcement across addictions. A new Biological Psychiatry review sharpens the case that GLP-1 drugs may affect addiction through brain reward circuits, not simply by reducing appetite. In animal models, GLP-1 receptor agonists reduce cocaine, methamphetamine/ amphetamine , and nicotine-related behaviors, including drug taking, motivation to use, and relapse -like seeking. Mechanistically, the common thread appears to be dampening drug-evoked dopamine signaling in the nucleus accumbens and engaging GLP-1 “anti-craving” circuits involving the VTA, nucleus accumbens, lateral septum, laterodorsal tegmentum, and nucleus tractus solitarius.
GLP-1 patients regularly report a decreased “pull” toward substances, rather than increased willpower . This distinction is important because it may represent a decrease in craving itself. And it appears to be preconscious; affected people may use fewer (or no) substances and not agonize over it. They reduce pathological drug and alcohol craving by normalizing dysregulated reward circuitry rather than suppressing it globally.
The best data and signals are for GLP-1 receptor agonists, not in psychiatry but in addiction. In April 2026, Nora Volkow and Xu reviewed reports of lower rates of alcohol-related events, reduced opioid overdose risk, and associations extending to nicotine, cocaine, cannabis, and other substances. New VA data from over 600,000 individuals with type 2 diabetes shows GLP-1 receptor agonist use was associated with a lower risk of developing a substance use disorder. GLP use among people with preexisting SUDs was linked to reduced hospitalization, overdose, and mortality. Together, these findings suggest a broad anti-craving or anti-reward effect rather than substance-specific action.
GLP-1 Inhibitors Aren’t Substance-Specific
Currently approved medications for addiction are largely substance-specific. GLP's effects appear agnostic to SUD diagnosis or substance.
Comparing this approach to existing treatments offers clarity. For example, FDA-approved naltrexone reduces the rewarding effects of alcohol. Patients taking naltrexone regularly report that drinking feels less pleasurable. In contrast, patients taking GLP-1 receptor agonists often report that they think about alcohol less or feel less drawn to it. This suggests GLP-1 drugs may act earlier in the addiction cycle, reducing cue reactivity and craving, rather than reducing reward after use. This means the desire to drink alcohol is diminished before the person thinks about it.
A treatment targeting shared reward circuitry may retain broader clinical utility. The most commonly studied agents in this context are semaglutide and liraglutide. Developed for treating metabolic disease, they are now being investigated as AUD, CUD, and general SUD treatments. This is important because many patients with alcohol use disorder (AUD) abuse other substances and suffer from fatty liver and other metabolic abnormalities. If it works, the GLP-1 inhibitor could improve both metabolic issues and substance disorders.
Cannabis Use Disorder and GLP-1 Inhibitors
While data for alcohol and nicotine use disorders are emerging, signals around cannabis use disorder have accelerated. The rapid rise of GLP-1 has disrupted the $40+ billion U.S. cannabis market. GLP-1 users on online forums describe reduced cravings and less interest in cannabis.
NIDA is sponsoring a randomized, placebo -controlled clinical trial evaluating Tirzepatide as treatment for cannabis use disorder. This will be a Phase 2–type study enrolling approximately 100 patients with moderate to severe CUD, who will receive weekly Tirzepatide or placebo over about 24 weeks.
One feature making this trial particularly interesting is the choice of medicine. Tirzepatide is not a traditional GLP-1 agonist like semaglutide or Ozempic; it is instead a “twincretin,” meaning it activates two receptors—GLP-1 and GIP—and is currently marketed as Mounjaro and Zepbound. Clinically, these drugs produce greater metabolic effects than semaglutide.
If metabolism and reward are tightly linked, the rationale for potential use in cannabis use disorder is that a stronger metabolic signal might produce a stronger behavioral effect. GLP-1 signaling reduces appetite and modulates reward, while GIP signaling enhances metabolic regulation and may have central nervous system effects. Together, this double activation may produce more consistent effects on motivation, regulating energy balance and reward simultaneously, and possibly amplifying anti-craving effects. However, it’s a hypothesis. Also, it’s unclear whether dual receptor activation will outperform standard GLP-1 agents in treating addiction. In brief, CUD is emerging as a test case for this entire model.
Another key question is whether psychiatric effects are direct or secondary to metabolic improvements. Weight loss, improved insulin sensitivity, and reduced inflammation could also change mood and behavior. However, the early onset of reduced craving suggests at least some direct central nervous system effects.
Outside of addiction, the psychiatric effects of these drugs appear limited. In schizophrenia, GLP-1 receptor agonists improve metabolic health but not core psychotic symptoms.
Overall, GLP-1 receptor agonists are not replacements for existing treatments such as naltrexone in alcohol use disorder. At least, not yet. Instead, they represent a distinct approach targeting craving, cue salience (what the brain pays attention to), and shared reward circuitry.
If ongoing randomized trials confirm current findings, these medications could shift addiction treatment away from a substance-specific model toward a circuit-based model of reward regulation. More broadly, they challenge the traditional separation between metabolic and psychiatric disease, suggesting peripheral metabolic signals can influence central processes such as motivation and behavior.
While conclusive evidence is pending, the convergence of mechanistic, preclinical, and clinical data makes GLP-1 inhibitors one of the most promising emerging approaches to substance use disorders.
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Mark S. Gold, M.D., is a pioneering researcher, professor, and chairman of psychiatry at Yale, the University of Florida, and Washington University in St Louis.
This article is part of the Bringwise Psychology Journal — daily insights on human behavior, mental health, and personal growth.