GLP-1s and Substance Use: What the New Research Actually Shows

Two large studies published in 2024 by researchers at Case Western Reserve University, using anonymized health records from millions of patients through the TriNetX research network, found that people with type 2 diabetes who were prescribed semaglutide had a measurably lower risk of developing tobacco use disorder or alcohol use disorder than similar patients prescribed other diabetes medications.

The tobacco study, published in Nature Medicine (Wang et al., 2024), compared semaglutide against other glucose-lowering drugs and found a reduced incidence of new tobacco use disorder diagnoses and related events like smoking-attributable disease in the semaglutide group. The alcohol study, published in Nature Communications (Wang et al., 2024), used a similar design and found both fewer new diagnoses of alcohol use disorder and fewer recurrences among people who already had a history of it.

These findings built on years of anecdotal reports, including patients and prescribers noticing reduced interest in alcohol, cigarettes, and even nail-biting or other compulsive habits after starting a GLP-1, which researchers had previously dismissed as unverified self-report.

The proposed explanation goes beyond appetite suppression. GLP-1 receptors are not limited to the gut and pancreas; they're also present in brain regions involved in reward processing and craving, including areas activated by dopamine. Animal studies going back over a decade have shown that GLP-1 receptor activation can reduce the rewarding effects of alcohol, nicotine, and even cocaine in rodent models, dampening the brain's dopamine response to these substances.

This lines up with a broader pattern seen in GLP-1 users: many report a general quieting of "noise" around food, described in more detail in our piece on [food noise on GLP-1](/blog/food-noise-what-it-is-and-why-glp1s-quiet-it). If the same receptor pathway that quiets food cravings also dampens reward signals for other substances, a reduced pull toward alcohol or nicotine would be a plausible extension rather than a surprising side effect.

It's an important distinction that this is a proposed mechanism supported by animal and observational human data, not something confirmed by human brain-imaging studies at large scale yet.

Real-world database studies like these are valuable because they include large, diverse populations, but they have real limitations. Because patients weren't randomly assigned to take semaglutide or not, it's possible that other differences between the groups, such as underlying health motivation, income, or access to care, contributed to the results, even after statistical adjustment.

This is why researchers describe these as hypothesis-generating findings rather than definitive proof. The next step, already underway, is small randomized controlled trials, including a Danish trial testing semaglutide specifically in patients with co-occurring alcohol use disorder and obesity, that can more directly test cause and effect by comparing semaglutide against a placebo in people who didn't start the drug for diabetes or weight loss reasons.

Until those trials report full results, the honest summary is: the signal is real and consistent across multiple large datasets, but it isn't yet strong enough to call GLP-1s a treatment for addiction.

No. As of today, no GLP-1 medication, including semaglutide (Ozempic, Wegovy), tirzepatide (Mounjaro, Zepbound), or any other agent in this class, is FDA-approved for alcohol use disorder, tobacco use disorder, or any other substance use disorder. Current approvals remain limited to type 2 diabetes, weight management, and in some cases cardiovascular risk reduction or sleep apnea, depending on the specific drug.

A doctor prescribing a GLP-1 specifically to treat addiction, rather than for an approved indication, would be doing so off-label, and that decision should involve a full conversation about the limited evidence base and any interacting treatments, particularly if a person is also taking naltrexone, acamprosate, or other addiction medications.

For anyone already on a GLP-1 for diabetes or weight loss who notices reduced interest in drinking or smoking, this is a documented and real phenomenon worth mentioning to a doctor, especially if it opens the door to further reducing or stopping substance use with additional support.

If you're on a GLP-1 and notice you're drinking less, craving cigarettes less, or feeling less pulled toward a habit you'd been trying to change, that's worth bringing up with your prescriber rather than assuming it's a coincidence. It may open a conversation about additional support to fully address the substance use, since the GLP-1 effect appears to be a reduction in craving intensity rather than a complete solution on its own.

It's equally important not to over-rely on this effect. If you have a diagnosed substance use disorder, stopping or reducing other treatments because a GLP-1 seems to be helping should only happen under medical supervision, since suddenly changing an established treatment plan carries its own risks.

This is a genuinely exciting area of research, but it's still early. Many of the same researchers studying this connection caution that patients should not seek out or continue a GLP-1 medication solely for this purpose outside of a clinical trial or a documented off-label discussion with their doctor.

GLP-1 research is moving fast, and it can be hard to separate a promising early finding from an established treatment. If you want help understanding what the latest research means for your own situation, [ask Lea](https://meetlea.ai/chat?q=What+does+the+research+on+GLP-1s+and+reduced+alcohol+or+nicotine+cravings+mean+for+me%3F) to walk through it with you.