GLP-1 Medications and Cravings: What Emerging Research Reveals About Alcohol, Nicotine, and Addictive Behaviors

*Compounded semaglutide and tirzepatide are not FDA-approved and are not approved or indicated for the treatment of alcohol use disorder, nicotine dependence, or any substance use condition. This article is for educational and informational purposes only and does not constitute medical advice. Clinical data referenced here reflects published research on FDA-approved pharmaceutical compounds unless otherwise noted. Individual results vary. Consult your licensed healthcare provider before starting, stopping, or adjusting any medication. Care at Prescriva is delivered by independently licensed providers, not by Blue Oak Services LLC dba Prescriva, which is a management services organization.*

---

Something unexpected has been happening in clinical settings and patient communities since GLP-1 medications became widely prescribed for weight management. People who started semaglutide or tirzepatide to lose weight began reporting changes that had nothing to do with the scale. They were drinking less alcohol, sometimes without even trying. Cravings for cigarettes softened. Compulsive snacking patterns eased in ways that felt different from ordinary willpower.

These reports were anecdotal at first. Researchers took notice. Over the past three years, a growing body of clinical and preclinical evidence has started to explain what these patients were experiencing, and why it makes biological sense.

This article reviews what the science currently shows about GLP-1 medications and their effects on craving and reward pathways. It does not argue that GLP-1 medications are treatments for addiction. They are not approved for that purpose. What it does offer is an honest look at an emerging area of research with real implications for people managing weight alongside other health goals.

---

How GLP-1 Receptors Work in the Brain's Reward System

To understand the craving connection, it helps to understand where GLP-1 receptors actually live in the body. Most people think of them as gut receptors involved in insulin secretion and appetite regulation. That is accurate, but incomplete.

GLP-1 receptors are expressed broadly throughout the central nervous system, including in regions that govern reward, motivation, and habit formation: the ventral tegmental area, the nucleus accumbens, the hippocampus, and the prefrontal cortex. These are the same regions that become dysregulated in substance use disorders and compulsive behavioral patterns.

A 2025 review in *Medical Sciences* examined the neurobiological and translational evidence for GLP-1's role in craving and addiction (PMID 40843757). The authors found that GLP-1 receptor activation in these reward-related brain areas modulates dopaminergic signaling, reducing the rewarding properties of both food and substances of abuse. In animal models, GLP-1 receptor agonists consistently decreased self-administration of alcohol, cocaine, nicotine, and opioids. The authors characterized the mechanism as a blunting of reward salience: the brain simply assigns less motivational weight to the substance in question.

A 2024 IUPHAR review published in *Pharmacological Research* explored the translational case for GLP-1 receptor agonists in substance use disorders (PMID 39032839). Bruns and colleagues found converging preclinical evidence that GLP-1 receptor activation in the mesolimbic pathway reduces dopamine-driven reinforcement of addictive behaviors. The reviewers noted that semaglutide, as a long-acting GLP-1 receptor agonist with demonstrated central nervous system penetration, is one of the most pharmacologically relevant compounds for studying these effects in humans.

---

GLP-1 and Alcohol: The Strongest Evidence So Far

Alcohol is where the clinical evidence is most developed. Multiple studies have now examined the relationship directly, including a randomized controlled trial.

The most significant study to date was published in *JAMA Psychiatry* in April 2025. Hendershot and colleagues conducted a randomized, double-blind trial of once-weekly semaglutide versus placebo in adults who met criteria for alcohol use disorder (PMID 39937469). Participants receiving semaglutide showed significantly greater reductions in heavy drinking days compared to those receiving placebo. They also reported lower alcohol craving scores across the treatment period. This was not a study of people using semaglutide for weight loss who happened to drink less. It was a prospectively designed trial testing semaglutide specifically as an intervention for alcohol use disorder. The results were clinically meaningful.

Earlier observational evidence pointed in the same direction. A 2023 analysis published in *Scientific Reports* looked at patients with obesity who were taking either semaglutide or tirzepatide for weight management and examined their alcohol consumption patterns (PMID 38017205). Quddos and colleagues found that both medications were associated with significant reductions in alcohol use across the study population, independent of changes in weight.

A 2025 commentary in the *Journal of General Internal Medicine* reviewed the accumulating evidence and described the GLP-1 signals for alcohol use disorder as encouraging, while also cautioning that most data remains early-stage and that rigorous trials are still needed before any clinical recommendations can be made (PMID 40272681). The authors noted that the JAMA Psychiatry trial by Hendershot provides the strongest foundation so far, but replication across populations is essential.

For people currently in a GLP-1 program for weight management who drink regularly, this research suggests there may be a secondary benefit, though the magnitude of effect will vary from person to person and is not guaranteed.

---

GLP-1 and Nicotine: Early Signals

The evidence for GLP-1 and nicotine is less mature than for alcohol, but the preclinical signal is consistent and a clinical picture is beginning to form.

A 2024 review in *Physiology and Behavior* examined preclinical and clinical evidence on GLP-1 receptor targeting for nicotine use disorder (PMID 38663460). Herman and colleagues found that GLP-1 receptor activation reliably reduced nicotine self-administration in rodent models and attenuated the dopaminergic response to nicotine in reward-sensitive brain regions. Human data at the time of the review was limited, but the authors noted that several clinical trials were underway.

One of those trials is now beginning to yield results. A 2026 review in *Biological Psychiatry* by Hendershot and colleagues assessed the therapeutic potential of GLP-1 receptor agonists for smoking cessation (PMID 41967661). The authors found preliminary support for the hypothesis that GLP-1 agonists can reduce nicotine craving and withdrawal-related symptoms, with the strongest signals coming from observational data and early-phase studies. They called for adequately powered randomized trials before clinical adoption.

The neurobiology is plausible. Nicotine produces its reinforcing effects through dopaminergic activation in the same mesolimbic circuits where GLP-1 receptors are expressed. If GLP-1 receptor activation dampens dopamine-driven reward signaling broadly, tobacco cravings could be affected alongside food and alcohol cravings.

People who smoke and are enrolled in a GLP-1 program may notice this effect anecdotally. The evidence does not yet support using GLP-1 medications as a stand-alone smoking cessation strategy, and people seeking to quit should work with their provider on evidence-based cessation approaches. But the research direction is meaningful.

---

What About Other Compulsive Behaviors?

Patients and providers have reported reductions in compulsive food-seeking, gambling urges, compulsive shopping, and other reward-driven behaviors in people taking GLP-1 medications. The research on these areas is even earlier than the alcohol and nicotine literature, and most of it is case report or survey-based rather than controlled.

The biological mechanism is the same: GLP-1 receptor agonists modulate the dopaminergic reward circuitry that underlies compulsive behaviors across categories. If the drug reduces the reward salience of alcohol and nicotine, it may similarly reduce the reward salience of other behaviorally reinforcing activities. This does not mean that GLP-1 medications should be considered treatments for behavioral addictions. It means the neurobiological case for such effects is theoretically coherent, and researchers are beginning to study it systematically.

For the purposes of weight management, the most practically relevant observation is that GLP-1 medications appear to reduce hedonic eating, the kind driven by pleasure and emotional reward rather than physical hunger. Research in *Science* identified that dopamine neurons governing hedonic food intake directly oppose GLP-1 satiety signaling. That opposition means semaglutide and tirzepatide are not just making you less physically hungry. They are also reducing the motivational pull of eating for reward. This is one reason people on these medications often describe their relationship with food as fundamentally changed, not just their appetite.

---

Important Limitations to Understand

The craving research is promising, but it comes with real limitations that matter for anyone interpreting these findings.

Most studies on GLP-1 and substance use have been conducted in people with obesity, diabetes, or weight-related conditions. How these effects translate to populations with different characteristics is not well established.

The JAMA Psychiatry trial on alcohol use disorder is the most rigorous evidence we have, but it is a single trial. Replication in larger, more diverse populations is essential before GLP-1 medications can be formally considered for substance use treatment.

Individual variation is large. Some people on GLP-1 medications report dramatic reductions in cravings for alcohol or nicotine. Others report no change at all. The research identifies a statistical signal, not a predictable individual outcome.

GLP-1 medications have their own side effect profile, including nausea, gastrointestinal symptoms, and rare but serious risks. These considerations do not disappear because of potential secondary benefits on craving. Anyone considering a GLP-1 program should discuss the full risk-benefit picture with a licensed provider.

And critically: people who are struggling with alcohol use disorder, nicotine dependence, or other substance use conditions should seek care from providers who specialize in those areas. Evidence-based treatments for these conditions exist and should not be delayed in favor of an unapproved application of a weight management medication.

---

What This Means For Your Weight Loss Journey

For people who are enrolled in or considering a medically supervised GLP-1 program primarily for weight management, the craving research offers a few practical takeaways.

If you drink alcohol regularly, you may notice that your interest in drinking decreases while on semaglutide or tirzepatide. This appears to be a real pharmacological effect, not just willpower or caloric discipline. You do not need to force yourself to drink less: the medication may do some of that work. Some people find this makes it easier to meet dietary goals and maintain the caloric adjustments their program requires.

If you smoke, the evidence is early, but some people do notice reduced desire for nicotine while on GLP-1 therapy. This is worth discussing with your provider, particularly if smoking cessation is a goal alongside weight management.

If you notice that compulsive eating patterns feel different, including less urgency around highly palatable foods or less emotional eating, that is consistent with what the research predicts. The change in your relationship with food-as-reward is part of how these medications work, and understanding it can help you sustain the behavioral shifts your program asks of you.

GLP-1 medications are not a cure for addiction, and the cravings research is not a reason to start a weight management program for any purpose other than weight management. But the neuroscience is real, the early clinical evidence is meaningful, and the research is moving fast.

To learn more about how GLP-1 medications affect the brain's appetite and satiety systems, see our guide on [how semaglutide suppresses appetite](/resources/how-semaglutide-suppresses-appetite). For a broader look at GLP-1 and neurological research, read about [GLP-1 medications and brain health](/resources/glp1-medications-brain-health-cognitive-function). If you are ready to find out whether a medically supervised GLP-1 program is right for you, [check your eligibility here](/start).

---

*This article is for informational purposes only and does not constitute medical advice. Compounded semaglutide and tirzepatide are not FDA-approved and are not approved treatments for alcohol use disorder, nicotine dependence, or any substance use condition. If you are managing a substance use disorder, please seek care from a qualified healthcare provider who specializes in that area. Individual results on GLP-1 medications vary. Care at Prescriva is delivered by independently licensed providers, not by Blue Oak Services LLC dba Prescriva, which is a management services organization.*

---

Sources

1. Hendershot CS, et al. Once-Weekly Semaglutide in Adults With Alcohol Use Disorder: A Randomized Clinical Trial. *JAMA Psychiatry.* 2025 Apr. PMID 39937469.
2. Quddos F, et al. Semaglutide and Tirzepatide reduce alcohol consumption in individuals with obesity. *Scientific Reports.* 2023 Nov. PMID 38017205.
3. Lira MC, et al. GLP-1 Receptor Agonists: Encouraging Signals for Treating Alcohol Use Disorder. *Journal of General Internal Medicine.* 2025 Sep. PMID 40272681.
4. Amorim Moreira Alves G, et al. Mechanisms of GLP-1 in Modulating Craving and Addiction: Neurobiological and Translational Insights. *Medical Sciences.* 2025 Aug. PMID 40843757.
5. Bruns Vi N, et al. IUPHAR review - Glucagon-like peptide-1 (GLP-1) and substance use disorders: An emerging pharmacotherapeutic target. *Pharmacological Research.* 2024 Sep. PMID 39032839.
6. Herman RJ, et al. Targeting GLP-1 receptors to reduce nicotine use disorder: Preclinical and clinical evidence. *Physiology and Behavior.* 2024 Jul. PMID 38663460.
7. Hendershot CS, et al. Therapeutic Potential of GLP-1 Receptor Agonists for Smoking Cessation. *Biological Psychiatry.* 2026 Apr. PMID 41967661.