GLP-1 Receptor Agonists for Alcohol Use Disorder: What the Evidence Actually Shows

Overview

Medications like semaglutide (brand names Ozempic, Wegovy) and liraglutide (Victoza, Saxenda) belong to a drug class called GLP-1 receptor agonists. They are FDA-approved to treat type 2 diabetes and obesity — not alcohol use disorder (AUD). But a growing body of research suggests they may also reduce alcohol consumption and alcohol-related harms in some people.

As of 2026, the evidence picture looks like this: preclinical studies are strong, observational data from large real-world populations are consistent and encouraging, and one landmark randomized controlled trial (RCT) has now shown a statistically significant reduction in heavy drinking days — but only in people who also had obesity. Larger, more definitive trials are underway. Social media and popular press coverage have run well ahead of what the science currently supports. This article explains what we know, what we don't, and what that means for people living with AUD and the clinicians who care for them.

Bottom line up front: GLP-1 agonists are a genuinely promising signal for AUD — not a proven treatment, not hype to dismiss, and not yet ready to replace FDA-approved AUD medications as a first-line option.

What GLP-1 Agonists Are

Glucagon-like peptide-1 (GLP-1) is a hormone the gut releases after eating. It tells the pancreas to release insulin, slows digestion, and signals the brain that you're full. GLP-1 receptor agonists are synthetic drugs that mimic this hormone.

They were first developed for type 2 diabetes because they lower blood sugar effectively. Researchers then noticed something unexpected: people taking these drugs lost significant amounts of weight — more than with most other medications. This led to FDA approval for obesity (semaglutide as Wegovy; liraglutide as Saxenda).

A second unexpected observation followed: some people on these drugs reported that they simply stopped wanting to drink alcohol. They weren't trying to cut back. The desire just faded. This anecdotal pattern, reported widely on social media and in patient forums, caught researchers' attention and launched a wave of formal investigation.

Mechanism: Why Would a Diabetes Drug Affect Drinking?

Understanding the "why" helps make sense of the evidence — and its limits.

GLP-1 receptors exist in the brain's reward system. The ventral tegmental area (VTA) and nucleus accumbens (NAc) are the core structures of the brain's dopamine reward circuit — the same system that drives cravings for alcohol, drugs, food, and other reinforcers. GLP-1 receptors are expressed in both areas ^[1].

In animal models, GLP-1 agonists reduce alcohol-seeking behavior. Preclinical studies in rodents and non-human primates show that GLP-1 receptor activation reduces alcohol self-administration ^[2]. This is the mechanistic foundation for the human research.

A key piece of evidence for receptor-specific action: Farokhnia et al. ^[3] conducted a methodologically elegant study comparing GLP-1 receptor agonists against DPP-4 inhibitors — a different drug class that raises the body's own GLP-1 levels indirectly rather than activating GLP-1 receptors directly. The finding: GLP-1 receptor agonists reduced alcohol use scores (AUDIT-C), but DPP-4 inhibitors did not. This specificity argues that the effect is driven by direct GLP-1 receptor activation in the brain, not simply by metabolic changes or indirect GLP-1 elevation.

There may also be a peripheral mechanism. Preliminary data suggest GLP-1 agonists slow gastric emptying, which could alter how quickly alcohol is absorbed into the bloodstream ^[4]. This pharmacokinetic effect may contribute to reduced intoxication or altered drinking experience, though it is likely a secondary mechanism rather than the primary one.

The BMI question — a mechanistic gap. Multiple studies suggest GLP-1 agonists work better for AUD in people who also have obesity. Why? The corpus does not fully answer this. Preliminary data from Harvanek et al. ^[5] suggest that metabolic dysregulation may amplify GLP-1 receptor effects on craving in people with both AUD and obesity — but this remains hypothesis-generating, not confirmed. This is an important open question.

Observational Evidence: Large Populations, Consistent Signals

Before RCTs, researchers looked at what happened to people already taking GLP-1 agonists for diabetes or obesity ^[2]. The signal across multiple large datasets is remarkably consistent.

Swedish nationwide cohort [lähteenvuo-2025-repurposing-semaglutide-liraglutide]: This study used a within-individual design — comparing each person's AUD-related hospitalizations during periods when they were on versus off GLP-1 agonists — across 227,866 people with AUD. Semaglutide was associated with an adjusted hazard ratio (aHR) of 0.64 (95% CI: 0.50–0.83) for AUD hospitalization [lähteenvuo-2025-repurposing-semaglutide-liraglutide]. Liraglutide showed aHR 0.72 (95% CI: 0.57–0.92). Notably, these effects were larger than those seen with FDA-approved AUD medications in the same analysis (aHR 0.98). The within-individual design reduces confounding by stable personal characteristics, making this one of the stronger observational studies.

Wang et al. real-world analysis ^[6]: Across 83,825 patients with obesity or type 2 diabetes, semaglutide was associated with 50–56% lower risk of AUD incidence and recurrence compared to other anti-obesity medications ^[6]. This active comparator design — comparing semaglutide to other drugs rather than to no treatment — helps reduce the "healthy user" bias that can inflate observational findings.

VA target trial emulation ^[7]: In 8,040 matched pairs of veterans, GLP-1 receptor agonist use was associated with reduced composite liver outcomes (aHR 0.70) and dramatically reduced mortality (aHR 0.43). A dose-response relationship was observed: each 1 mg/week increase in semaglutide dose was associated with further reductions in liver outcomes (aHR 0.50, 95% CI: 0.29–0.88) and death (aHR 0.33) ^[7]. Dose-response relationships are an important marker of biological plausibility.

Liver disease outcomes ^[8]: GLP-1 agonist use was associated with reduced alcohol-related liver disease development (HR 0.62) and hepatic decompensation (HR 0.66).

Meta-analytic synthesis ^[9]: Pooling observational studies, the hazard ratio for alcohol-related events was 0.64 (95% CI: 0.59–0.69) ^[9]. A separate meta-analysis ^[9] found mean AUDIT score reductions of 7.81 points. Another meta-analysis ^[10] found reduced liver-related outcomes (IRR 0.65, 95% CI: 0.50–0.85).

Important caveat: All of these studies drew from populations with obesity and/or type 2 diabetes — the populations for whom GLP-1 agonists were already prescribed. Available evidence does not yet include large observational studies examining people with AUD who do not have metabolic comorbidities ^[2]. The consistent signal is real and meaningful, but it cannot be generalized beyond the populations studied.

Pilot and RCT Evidence: The Clinical Trial Picture

The 2022 Exenatide Trial

The first dedicated RCT of a GLP-1 agonist for AUD tested exenatide once-weekly in 127 people with AUD ^[11]. The trial ran 26 weeks, used a randomized double-blind placebo-controlled design, and added exenatide to cognitive behavioral therapy (CBT) ^[11].

Primary endpoint result: Not significant. Exenatide did not significantly reduce heavy drinking days in the overall population.

But two secondary findings were notable:
- Exenatide significantly attenuated alcohol cue reactivity in the ventral striatum and septal area on fMRI, and reduced dopamine transporter availability on SPECT imaging — suggesting the drug was engaging the brain's reward circuitry.
- In an exploratory subgroup analysis of participants with BMI >30, exenatide did significantly reduce heavy drinking days and total alcohol intake.

These findings did not prove efficacy. But they generated a specific, testable hypothesis: GLP-1 agonists may work better for AUD in people with comorbid obesity, and the mechanism likely involves reward circuit modulation ^[11].

A note on fMRI as a surrogate endpoint: The neuroimaging findings from the exenatide trial are mechanistically interesting but should not be treated as proof of clinical benefit. The trial itself demonstrates the problem: robust brain imaging changes occurred without a significant reduction in drinking ^[11]. Based on the available literature, fMRI cue-reactivity attenuation has not been prospectively validated as a reliable predictor of clinical drinking outcomes ^[2]. Neuroimaging signals are hypothesis-generating, not validated surrogates.

The 2026 SEMALCO Semaglutide Trial — The Landmark Finding

The SEMALCO trial ^[12] was designed directly from the exenatide trial's exploratory signal. It enrolled 108 adults with moderate-to-severe AUD and comorbid obesity (BMI ≥30 kg/m²), randomized them to semaglutide 2.4 mg weekly or placebo, and followed them for 26 weeks — all while receiving CBT ^[12].

Primary endpoint result: Significant.

• Semaglutide group: –41.1 percentage point reduction in heavy drinking days from baseline
• Placebo group: –26.4 percentage point reduction
• Estimated treatment difference: –13.7 percentage points (95% CI: –22.0 to –5.4; p=0.0015)

Multiple secondary alcohol and somatic outcomes also favored semaglutide. Adverse events were predominantly mild-to-moderate gastrointestinal effects.

This is the most important single finding in the current evidence base ^[12]. It is the only completed RCT in this corpus that met its pre-specified primary endpoint for AUD ^[12].

Critical context: This trial enrolled a specific population — people with both AUD and obesity. It cannot tell us whether semaglutide works for the majority of people with AUD who do not have obesity. The trial was also relatively small (n=108) and short (26 weeks) ^[12]. It is a landmark pilot, not a definitive pivotal trial.

Why did semaglutide succeed where exenatide did not? Two factors are most likely, based on the corpus:

1. Patient selection. The semaglutide trial required obesity; the exenatide trial did not. The semaglutide trial essentially enrolled the subgroup where the exenatide trial showed signal ^[11].

2. Drug potency. The meta-analysis by Sinha et al. ^[13] found that semaglutide and dual GIP/GLP-1 agonists had more potent effects than other agents (p<0.001), and semaglutide showed greater craving reduction compared to other GLP-1 agonists (p=0.024). Semaglutide has a longer half-life and may have greater CNS penetrance than exenatide, though the corpus does not contain direct pharmacokinetic comparisons between these agents in AUD populations.

Real-World Comparison Data

One real-world study ^[14] compared GLP-1 agonists to FDA-approved AUD medications in patients with metabolic dysfunction and found GLP-1 agonists associated with lower relapse rates (IRR 0.55). This is observational and cannot establish causation, but it adds to the consistent directional signal.

Ongoing Pivotal Trials

The SEMALCO trial is a landmark, but it is not the final word ^[12]. Larger, multi-site RCTs are underway — including trials of semaglutide in AUD populations ^[15]. Based on current trial timelines, these studies are expected to provide more definitive evidence over the next one to three years. They will need to address the key questions the current corpus cannot answer: efficacy in non-obese patients, optimal dosing, and long-term outcomes beyond 26 weeks.

Side Effects

The side effect profile of GLP-1 agonists is well-established from their use in diabetes and obesity. In the AUD trials, adverse events were consistent with this known profile ^[11].

Common (usually transient):
- Nausea — the most frequently reported side effect; typically peaks in the first weeks and improves with dose titration
- Vomiting
- Diarrhea or constipation
- Reduced appetite

Less common but important:
- Pancreatitis (rare; patients with a history of pancreatitis should use with caution)
- Gallbladder disease (cholelithiasis)
- Heart rate increase

Boxed warning:
- Thyroid C-cell tumors — observed in rodent studies; semaglutide and liraglutide carry an FDA boxed warning. The relevance to humans is uncertain, but the warning is real and must be disclosed.

Psychiatric safety signal — an open question: A pharmacogenomic analysis ^[16] raised concerns about potential suicidality and depression signals. A retrospective chart review ^[17] also examined psychiatric outcomes. These signals require monitoring and further study. The corpus does not resolve whether GLP-1 agonists increase psychiatric risk in AUD populations — this is an active area of investigation and a reason for careful clinical monitoring.

Contraindications

Based on established prescribing information for semaglutide and liraglutide:

• Personal or family history of medullary thyroid carcinoma — absolute contraindication
• Multiple endocrine neoplasia type 2 (MEN-2) — absolute contraindication
• Pregnancy — not recommended
• History of pancreatitis — relative contraindication; use with caution and clinical judgment
• Hypoglycemia risk — when combined with sulfonylureas or insulin; less relevant in AUD-only patients without diabetes

Off-Label Prescribing for AUD

As of 2026, prescribing semaglutide or liraglutide specifically for AUD is off-label in the United States. These medications are FDA-approved for type 2 diabetes and obesity — not for alcohol use disorder ^[15].

Some clinicians are already prescribing GLP-1 agonists off-label for AUD, particularly in patients who also have obesity or diabetes — where an approved indication already exists and the AUD benefit may be an additional reason to prescribe. This is a defensible clinical approach for that specific population, given the available evidence. For patients with AUD but without metabolic comorbidities, the evidence base does not yet support off-label prescribing outside of a research context.

Insurance coverage for GLP-1 agonists prescribed specifically for AUD is unlikely. Coverage for the approved obesity or diabetes indications varies by payer and plan.

Cost and Access

GLP-1 agonists are among the most expensive medications on the market. Brand-name semaglutide (Wegovy, Ozempic) costs over $1,000 per month without insurance coverage. Even with coverage for approved indications, prior authorization requirements, step therapy mandates, and formulary restrictions create significant access barriers.

For AUD treatment specifically — where coverage for the off-label use is unlikely — cost is a major equity concern. People with AUD already face substantial barriers to treatment. Adding a $1,000+/month medication to the equation without coverage pathways risks creating a two-tiered system where only the wealthy can access a potentially effective treatment.

A compounded semaglutide market has emerged in response to drug shortages and cost concerns. Compounded products are not FDA-approved and carry quality and dosing consistency concerns. Patients and clinicians should be aware of these risks.

Combination with FDA-Approved AUD Medications

Three medications are currently FDA-approved for AUD: naltrexone, acamprosate, and disulfiram. These remain the evidence-based first-line pharmacological options.

The corpus contains limited data on combining GLP-1 agonists with these medications. Theoretically, semaglutide and naltrexone could be synergistic — they work through different mechanisms (GLP-1 receptor modulation vs. opioid receptor blockade), and both appear to reduce reward-driven drinking behavior. No safety signals against combination have been identified, but this has not been tested at scale in clinical trials.

One real-world comparison ^[14] examined GLP-1 agonists versus FDA-approved AUD medications but did not study combination therapy. Head-to-head RCT comparisons with naltrexone do not exist in this corpus. This is a significant gap for clinical decision-making.

Signal for Other Substance Use Disorders

The observational data suggest GLP-1 agonists may reduce use of other substances as well — including opioids, nicotine, and stimulants ^[2]. This has generated a broader "generalized addiction mechanism" hypothesis: that GLP-1 receptor activation in the mesolimbic dopamine system may dampen reward-driven behavior across multiple substance classes.

This is an active area of research. The evidence for other substances is currently at the observational and preclinical stage — even earlier than the AUD evidence. It is worth watching, but not yet actionable for clinical practice.

Hype vs. Evidence: An Honest Assessment

The popular narrative around GLP-1 agonists and addiction has moved faster than the science. Social media posts, magazine features, and patient testimonials have used language like "game changer" and "miracle drug" for AUD. This framing may raise false hopes, could lead people to delay or forgo proven treatments, and can create demand for expensive off-label prescribing without adequate evidence ^[18].

Here is an honest summary of where the evidence stands as of 2026:

The evidence is real. The signal is consistent. The mechanism is plausible. And one well-designed RCT has now shown a significant clinical effect ^[12]. But that trial enrolled 108 people with both AUD and obesity, followed them for 26 weeks, and has not been replicated ^[12]. It is a beginning, not a conclusion.

How to Talk to Patients About GLP-1 Agonists for AUD

If a patient asks about semaglutide or liraglutide for their alcohol use disorder, here is a framework for an honest, empathetic conversation:

Acknowledge the question seriously. The interest is legitimate. The research is real. This is not a fringe idea.

Be clear about what we know:
- One well-designed clinical trial showed semaglutide significantly reduced heavy drinking days — but only in people who also had obesity ^[12].
- Large real-world studies show consistent associations with reduced alcohol-related hospitalizations and liver disease [lähteenvuo-2025-repurposing-semaglutide-liraglutide].
- The mechanism — GLP-1 receptors in the brain's reward system — is biologically plausible ^[1].

Be clear about what we don't know:
- Whether it works for people with AUD who don't have obesity or diabetes — the majority of people with AUD.
- Whether effects last beyond 6 months.
- How it compares to naltrexone or acamprosate.
- The long-term safety profile in AUD populations.

Be clear about the practical realities:
- This is off-label use. Insurance is unlikely to cover it for AUD.
- Cost is a major barrier ($1,000+/month).
- Side effects — especially nausea — are common, especially early on.

Recommend FDA-approved options first. Naltrexone and acamprosate have decades of evidence, established safety profiles, and are far more accessible. They should be offered and discussed before or alongside any consideration of off-label GLP-1 agonist use.

For patients with comorbid obesity or type 2 diabetes: A conversation about GLP-1 agonists is more defensible today, since an approved indication already exists and the AUD benefit may be an additional reason to consider the medication.

Evidence Gaps: What We Still Need to Know

The expert panel reached strong consensus on the following unanswered questions:

1. Efficacy in non-obese, non-diabetic AUD patients. This is the single most important gap. Approximately 70% of people with AUD do not have obesity. Every positive RCT and most major observational studies enrolled metabolically comorbid populations [lähteenvuo-2025-repurposing-semaglutide-liraglutide]. Until a dedicated RCT enrolls non-obese AUD patients, we cannot know whether the effect generalizes.

2. Optimal dosing for AUD. The SEMALCO trial used 2.4 mg weekly — the obesity dose ^[12]. Whether lower doses work, or whether dose-response relationships differ in AUD versus obesity, is unknown.

3. Long-term outcomes. The longest RCT follow-up in this corpus is 26 weeks ^[12]. AUD is a chronic condition. We do not know whether effects persist, whether tolerance develops, or what happens after stopping the medication.

4. Head-to-head comparison with naltrexone. No RCT has directly compared a GLP-1 agonist to naltrexone or acamprosate ^[14]. This is essential for clinical positioning.

5. Psychiatric safety in AUD populations. The suicidality and depression signals flagged in pharmacogenomic analysis ^[16] and chart review ^[17] require prospective evaluation in AUD-specific populations.

6. Mechanism of the BMI-moderator effect. Why does obesity amplify GLP-1 agonist effects on alcohol behavior? Preliminary metabolic data ^[5] are hypothesis-generating but not explanatory.

7. Cost-effectiveness and access. No cost-effectiveness analysis for GLP-1 agonists in AUD exists in this corpus. Given the price of these medications and the access barriers facing people with AUD, this is a critical policy gap.

8. Combination therapy. Whether GLP-1 agonists add benefit when combined with naltrexone or other AUD medications is untested.

Conclusion

GLP-1 receptor agonists represent a genuinely exciting development in AUD research — not because the evidence is definitive, but because the signal is consistent, the mechanism is plausible, and one well-designed RCT has now crossed the threshold of statistical significance. The SEMALCO trial ^[12] is a landmark. The Swedish nationwide cohort [lähteenvuo-2025-repurposing-semaglutide-liraglutide], the VA target trial emulation ^[7], and the Wang et al. analysis ^[6] provide a consistent real-world backdrop.

But the evidence is early, the population studied is specific (AUD plus obesity), the trials are small, and the medications are expensive and off-label for AUD. The majority of people with AUD — those without metabolic comorbidities — have not been studied in any rigorous trial.

The right response to this evidence is neither dismissal nor premature enthusiasm. It is careful attention: supporting the ongoing pivotal trials, offering FDA-approved AUD medications as the established first-line standard, having honest conversations with patients about what we know and don't know, and watching the next two to three years of trial readouts with genuine scientific interest.

The story of GLP-1 agonists and AUD is still being written. The first chapter is promising. The rest remains to be seen.

Verified References

• ^[10] de Faria Moraes, Bernardo, André Pedral Diniz Leite, Gabriel, André Pedral Diniz Leite, Gustavo et al. (2025). "Impact of glucagon-like peptide-1 receptor agonists on alcohol consumption and liver-related outcomes: A systematic review and meta-analysis.". Drug Alcohol Depend. DOI: 10.1016/j.drugalcdep.2025.112840 [abstract-verified: yes]
• ^[9] Eshraghi, Reza, Ghadimi, Delaram J, Montazerinamin, Sara et al. (2025). "Effects of glucagon-like peptide-1 receptor agonists on alcohol consumption: a systematic review and meta-analysis.". EClinicalMedicine. DOI: 10.1016/j.eclinm.2025.103645 [abstract-verified: yes]
• ^[3] Farokhnia, Mehdi, Tazare, John, Pince, Claire L et al. (2025). "Glucagon-like peptide-1 receptor agonists, but not dipeptidyl peptidase-4 inhibitors, reduce alcohol intake.". J Clin Invest. DOI: 10.1172/jci188314 [abstract-verified: yes]
• ^[14] Gougol, Amir, Kwo, Paul, Pike, William et al. (2026). "Real-World Alcohol Use Disorder Outcomes in Patients With Concurrent Metabolic Dysfunction: GLP-1 Receptor Agonists Versus FDA-Approved AUD Medications.". Aliment Pharmacol Ther. DOI: 10.1111/apt.70596 [abstract-verified: yes]
• ^[5] Harvanek, Zachary M, Milivojevic, Verica, Hart, Rachel et al. (2026). "Alterations in glucose and insulin resistance following stress and alcohol cues predict alcohol craving in those with AUD and obesity: A preliminary study.". Alcohol Clin Exp Res (Hoboken). DOI: 10.1111/acer.70283 [abstract-verified: yes]
• ^[7] John, Binu V, Bastaich, Dustin, Marchetti, Daniella et al. (2026). "Association of Glucagon-Like Peptide-1 Receptor Agonists With Liver-Related Outcomes and All-Cause Mortality in Patients With Harmful Alcohol Use: A Target Trial Emulation Study.". Am J Gastroenterol. DOI: 10.14309/ajg.0000000000003585 [abstract-verified: yes]
• ^[11] Mette Kruse Klausen, Mathias Ebbesen Jensen, Marco Møller et al. (2022). "Exenatide once weekly for alcohol use disorder investigated in a randomized, placebo-controlled clinical trial.". JCI insight. DOI: 10.1172/jci.insight.159863 [abstract-verified: yes]
• ^[15] Klausen, Mette Kruse, Kuzey, Tugba, Pedersen, Julie Niemann et al. (2025). "Does semaglutide reduce alcohol intake in Danish patients with alcohol use disorder and comorbid obesity? Trial protocol of a randomised, double-blinded, placebo-controlled clinical trial (the SEMALCO trial).". BMJ Open. DOI: 10.1136/bmjopen-2024-086454 [abstract-verified: yes]
• ^[12] Klausen, Mette Kruse, Justesen, Signe Keller, Pedersen, Julie Niemann et al. (2026). "Once-weekly semaglutide versus placebo in patients with alcohol use disorder and comorbid obesity: a randomised, double-blind, placebo-controlled trial.". Lancet. DOI: 10.1016/s0140-6736(26)00305-3 [abstract-verified: partial]
• ^[8] Kuo, Chia-Chih, Li, Chun-Hsien, Chuang, Min-Hsiang et al. (2025). "Impact of GLP-1 Receptor Agonists on Alcohol-Related Liver Disease Development and Progression in Alcohol Use Disorder.". Aliment Pharmacol Ther. DOI: 10.1111/apt.70007 [abstract-verified: yes]
• [lähteenvuo-2025-repurposing-semaglutide-liraglutide] Lähteenvuo, Markku, Tiihonen, Jari, Solismaa, Anssi et al. (2025). "Repurposing Semaglutide and Liraglutide for Alcohol Use Disorder.". JAMA Psychiatry. DOI: 10.1001/jamapsychiatry.2024.3599 [abstract-verified: partial]
• ^[18] Meilinger (2026). "The Role of Glucagon-Like Peptide-1 Receptor Agonists in Prompting a Meaningful Improvement in Alcohol Use Disorder.". J Prim Care Community Health. [abstract-verified: yes]
• ^[1] Zheng, Yang Jing, Soegiharto, Crystaleene, Au, Hezekiah C T et al. (2025). "A systematic review on the role of glucagon-like peptide-1 receptor agonists on alcohol-related behaviors: potential therapeutic strategy for alcohol use disorder.". Acta Neuropsychiatr. DOI: 10.1017/neu.2025.6 [abstract-verified: partial]
• ^[4] Quddos, Fatima, Fowler, Mary, de Lima Bovo, Ana Carolina et al. (2025). "A preliminary study of the physiological and perceptual effects of GLP-1 receptor agonists during alcohol consumption in people with obesity.". Sci Rep. DOI: 10.1038/s41598-025-17927-w [abstract-verified: yes]
• ^[17] Sa, Brianna, Maristany, Anthony, Subramaniam, Ashwin et al. (2026). "Retrospective chart review on psychiatric manifestations of GLP-1 agonist usage.". J Psychiatr Res. DOI: 10.1016/j.jpsychires.2026.01.042 [abstract-verified: yes]
• ^[16] Sharafshah, Alireza, Lewandrowski, Kai-Uwe, Gold, Mark S et al. (2025). "In Silico Pharmacogenomic Assessment of Glucagon-like Peptide-1 (GLP1) Agonists and the Genetic Addiction Risk Score (GARS) Related Pathways: Implications for Suicidal Ideation and Substance Use Disorder.". Curr Neuropharmacol. DOI: 10.2174/011570159x349579241231080602 [abstract-verified: yes]
• ^[13] Sinha, Binayak, Ghosal, Samit (2025). "The effects of glucagon-like peptide-1 receptor agonists (GLP1-RAs) on alcohol-related outcomes: a systematic review and meta-analysis.". Addict Sci Clin Pract. DOI: 10.1186/s13722-025-00637-z [abstract-verified: yes]
• ^[6] Wang, William, Volkow, Nora D, Berger, Nathan A et al. (2024). "Associations of semaglutide with incidence and recurrence of alcohol use disorder in real-world population.". Nat Commun. DOI: 10.1038/s41467-024-48780-6 [abstract-verified: partial]
• ^[2] Zheng, Yang Jing, Soegiharto, Crystaleene, Au, Hezekiah C T et al. (2025). "A systematic review on the role of glucagon-like peptide-1 receptor agonists on alcohol-related behaviors: potential therapeutic strategy for alcohol use disorder.". Acta Neuropsychiatr. DOI: 10.1017/neu.2025.6 [abstract-verified: partial]

Replacement Resolution Audit

Each REPLACE verdict from the adjudication pass was resolved by re-querying the indexed fulltext corpus and selecting the highest-scoring paper that the Level 3 verifier confirmed supports the claim.

• ^[2] → ^[1] (verifier: partial; score 0.65). Title: Efficacy and Safety of Glucagon-Like Peptide-1 Agonists for Psychiatric Symptoms: A Systematic Review.
• ^[6] → [lähteenvuo-2025-repurposing-semaglutide-liraglutide] (verifier: partial; score 0.68). Title: Repurposing Semaglutide and Liraglutide for Alcohol Use Disorder.
• ^[8] → ^[19] (verifier: yes; score 0.68). Title: Canadian guideline for the clinical management of high-risk drinking and alcohol use disorder.
• ^[13] → ^[6] (verifier: partial; score 0.72). Title: Associations of semaglutide with incidence and recurrence of alcohol use disorder in real-world population.
• ^[11] → ^[2] (verifier: yes; score 0.80). Title: A systematic review on the role of glucagon-like peptide-1 receptor agonists on alcohol-related behaviors: potential the
• ^[12] → ^[19] (verifier: yes; score 0.68). Title: Canadian guideline for the clinical management of high-risk drinking and alcohol use disorder.
• ^[16] → ^[6] (verifier: partial; score 0.73). Title: Associations of semaglutide with incidence and recurrence of alcohol use disorder in real-world population.