The cravings they did not expect to quiet.

It started, as these things often do, in the comments. Patients on semaglutide for diabetes or weight began posting that they had stopped drinking. They had not meant to. The wine after dinner stopped sounding good. The lunchtime beer began tasting wrong. They felt no special virtue about it. They had simply lost interest, in the same quiet way they had lost interest in the bread basket.

Researchers had been watching this signal in animal models for nearly a decade.¹ By the time it arrived in the patient forums, several small clinical trials were already underway. By 2024, the literature had grown large enough to take seriously. By 2025, the FDA had begun signaling that addiction indications were a plausible new lane for these drugs, not a sideshow.²

The cleanest way to read this story is one substance at a time.

Alcohol

This is the strongest signal and the most-studied use case. A randomized clinical trial published in 2022 found that exenatide, an older GLP-1, did not reduce heavy drinking days overall in patients with alcohol use disorder, but did reduce them substantially in a pre-specified subgroup of patients with obesity.³ A subsequent trial of semaglutide, smaller but better-designed, found that the drug reduced both craving and weekly alcohol intake compared to placebo over twelve weeks.⁴

The most striking evidence is observational. A 2024 analysis of electronic health records covering nearly two million people found that patients with alcohol use disorder who were prescribed semaglutide for diabetes had roughly half the rate of alcohol-related hospitalizations compared to matched patients on other diabetes drugs.⁵ Observational data cannot prove causation. The signal is large enough, and the matching is careful enough, that even cautious investigators have begun describing alcohol as the indication most likely to reach approval next.

What patients describe is not abstinence. It is indifference. The drinking does not stop because it has been forbidden. It stops because the reward signal that made it interesting no longer fires the same way.

Nicotine

The data here are thinner. A few small randomized studies have found that GLP-1s reduce cigarette consumption in smokers, though the effects have been modest and the trials short.⁶ The most interesting pattern is that nicotine craving, like alcohol craving, appears to soften before any structured quit attempt. Patients in some of these studies were not actively trying to stop smoking. They reported smoking less anyway.

Several Phase 2 trials are now testing semaglutide specifically as a smoking-cessation aid, with the first read-outs expected in 2026 and 2027. The mechanism is plausible enough, and the unmet need large enough, that this lane is being run in parallel with alcohol rather than waiting for it.⁷

Opioid use disorder

The signal here is more careful. Opioid use disorder is not, mechanistically, the same as alcohol or nicotine dependence. The reward circuit is involved, but so are receptors that GLP-1 does not act on directly. A handful of small studies have looked at whether GLP-1s reduce craving in patients on medication for opioid use disorder.⁸ The early results are mixed. Some patients report less craving. Others report no difference. The trials are too small to draw a verdict, and the consensus in the addiction-medicine literature is that this is the indication most likely to take years to clarify.

That has not stopped the speculation. Several investigators have begun pointing out, correctly, that even a modest effect on opioid craving, layered on top of existing medication-assisted treatment, would represent a meaningful public-health gain. The trials to test that proposition are now running.

Gambling, compulsive shopping, and the question of reward itself

The most interesting story is not about a substance at all. Case reports have begun to appear of patients whose compulsive gambling stopped after they began a GLP-1 for weight loss.⁹ The same has been reported, anecdotally, for compulsive shopping, binge eating disorder, and even some forms of impulsive sexual behavior. The pattern is consistent enough that addiction researchers have begun to ask whether GLP-1s are acting on something more general than any one substance: the reward circuit itself.

That hypothesis has neurobiological support. GLP-1 receptors are densely expressed in the ventral tegmental area and the nucleus accumbens, the regions most associated with reward processing.¹⁰ Activating those receptors appears to dampen the dopaminergic response to a wide range of rewarding stimuli. Food. Alcohol. Probably more. The clinical trials needed to confirm this for non-substance behaviors are several years away. The mechanism is no longer fringe.

The drinking did not stop because it had been forbidden. It stopped because the reward signal that made it interesting no longer fired the same way.

What clinicians are doing now

Two things are true at once. The evidence for any non-obesity addiction indication is still preliminary, with the partial exception of alcohol. And patients on these drugs are already, in significant numbers, reporting changes in substance use that their prescribers did not predict. This puts the clinical community in an awkward middle position. Off-label prescribing for addiction has not become standard practice, and probably should not until the trials are done. But the question is being asked in every endocrinology and internal-medicine clinic in the country.

The most measured response, in the literature, has been to record the changes patients report, to refer to specialists when those changes are significant, and to resist the temptation to oversell. The drug is not a cure for addiction. Whether it is a useful adjunct, for which substances, and at what dose, is the question the next five years of trials are designed to answer.

Editorial content. Not medical advice. The findings described above come from published trials, observational analyses, and case reports; individual response varies and several indications remain investigational. Talk to your prescriber and, where appropriate, an addiction-medicine specialist before changing how you take any medication.