What Can You Take to Stop Drinking Alcohol?

Three prescription medications carry FDA approval specifically for alcohol use disorder: naltrexone, acamprosate, and disulfiram. Each works through a different mechanism, and a growing list of off-label drugs and experimental treatments is expanding the options further. Still, fewer than 10 percent of people with alcohol use disorder ever receive medication for it, partly because many people don’t realize these drugs exist. The evidence behind them is stronger than most people expect, and understanding how each one works can help you have a more productive conversation with a doctor.

The Three FDA-Approved Medications

Naltrexone blocks opioid receptors in the brain, which dulls the pleasurable “buzz” that alcohol normally produces. When drinking no longer feels as rewarding, the drive to keep going tends to weaken over time. Naltrexone comes in two forms: a daily 50 mg pill and a monthly injection (sold as Vivitrol) that bypasses the need for daily compliance. It does not make you sick if you drink; it simply makes drinking less satisfying.

Acamprosate (brand name Campral) targets a different system. It works on glutamate and GABA signaling in the brain, helping to rebalance the excitatory and inhibitory neurotransmitter activity that gets disrupted by chronic heavy drinking.¹ The practical upshot is that it eases the low-grade anxiety, restlessness, and insomnia that often linger for weeks or months after someone stops drinking. Those withdrawal-related symptoms are a major reason people relapse, so quieting them gives abstinence a better chance. Acamprosate is typically taken as two pills three times a day, which some people find inconvenient.²

Disulfiram (Antabuse) is the oldest of the three and works on pure deterrence. It blocks the enzyme that normally breaks down acetaldehyde, a toxic byproduct of alcohol metabolism. If you drink while taking disulfiram, acetaldehyde builds up rapidly and you feel flushed, nauseated, and headachy within minutes.³ The reaction is unpleasant enough that the threat of it is supposed to keep you from picking up a drink. Disulfiram works best for people who are highly motivated and, ideally, have someone supervising their daily dose. Its effectiveness drops sharply when left to unsupervised self-administration.

How Well Do They Actually Work

These medications are helpful, but they are not miracle cures. A large 2023 meta-analysis in JAMA found that you would need to treat about 11 people with acamprosate to prevent one additional person from returning to any drinking, and about 18 people with oral naltrexone at 50 mg per day to achieve the same result. For preventing return to heavy drinking specifically, naltrexone performed better, with a number needed to treat of about 11.⁴ Those numbers mean the drugs genuinely help, but that many people still relapse despite taking them.

Disulfiram’s trial record is more complicated. In the same JAMA review, data from three randomized trials showed no statistically significant difference between disulfiram and placebo for preventing return to any drinking.⁴ That sounds damning, but disulfiram is notoriously hard to study in blinded trials because the reaction when someone drinks is so obvious that everyone knows who got the real pill. A separate network meta-analysis that pooled a broader set of studies found disulfiram significantly reduced heavy drinking (risk ratio 0.19 compared to placebo) and improved total abstinence (risk ratio 1.71), which were actually better results than naltrexone or acamprosate.⁵ The likely explanation is that supervised disulfiram works quite well, while unsupervised disulfiram barely works at all, and trial designs mix those scenarios together.

An earlier meta-analysis framed the comparison slightly differently: roughly 8 people need to be treated with acamprosate to achieve one additional case of sustained abstinence, and roughly 9 people need treatment with naltrexone to prevent one additional return to heavy drinking.⁶ The numbers vary between reviews depending on which trials are included and how outcomes are defined, but the overall picture is consistent: both drugs outperform placebo, and neither is dramatically better than the other. Acamprosate tends to support abstinence; naltrexone tends to reduce heavy drinking even if the person hasn’t fully stopped.

Targeted Naltrexone and the Extinction Approach

Most doctors prescribe naltrexone as a daily pill taken regardless of whether you plan to drink that day. But a different strategy, sometimes called the Sinclair Method, involves taking naltrexone only before you expect to drink. The idea draws from extinction learning: if the opioid reward from drinking is blocked every time you actually drink, the brain slowly “unlearns” the association between alcohol and pleasure. Clinical research supports this approach, with studies finding that naltrexone paired with ongoing drinking sessions is effective, while naltrexone given only during abstinence shows little benefit.⁷

Animal data back this up. When rats bred for heavy drinking received naltrexone just before their drinking sessions, alcohol intake dropped progressively over days, and the effect persisted even after the drug was stopped. The researchers found that naltrexone had increased the density of opioid receptors in the brain, consistent with what happens during a normal extinction process.⁸ This targeted approach appeals to people who aren’t ready or willing to commit to full abstinence on day one; it allows them to keep drinking while the medication gradually weakens alcohol’s grip.

Off-Label Medications

Several drugs developed for other conditions have shown promise for alcohol use disorder, though none have FDA approval for that indication. Baclofen, a muscle relaxant that works on GABA-B receptors, has drawn particular interest because it is one of the few options considered safe for people with advanced liver disease. In a pivotal randomized trial of people with alcohol dependence and liver cirrhosis, 71 percent of those taking baclofen achieved and maintained abstinence, compared with 29 percent on placebo.⁹ No liver-related side effects were recorded, which matters because the standard FDA-approved medications carry at least some hepatic concern for this population.¹⁰

Gabapentin, an anticonvulsant, has also shown efficacy in some studies, and it may be especially useful for people whose drinking is driven by anxiety and sleep problems. Topiramate, another anticonvulsant, has positive trial data as well. The evidence for these off-label medications is more mixed than for the approved drugs, with some trials finding solid effects and others less impressive results. In the network meta-analysis mentioned earlier, gabapentin and baclofen both significantly improved abstinence rates compared to placebo.⁵

Emerging Treatments That Are Generating Buzz

Two very different experimental approaches have made headlines recently. Semaglutide, the GLP-1 receptor agonist best known as a diabetes and weight-loss drug (sold as Ozempic and Wegovy), showed intriguing results in a randomized trial of adults with alcohol use disorder. Low-dose semaglutide reduced grams of alcohol consumed in a lab setting and cut drinks per drinking day and weekly cravings, all with medium to large effect sizes.¹¹ Semaglutide did not, however, reduce the total number of drinking days, suggesting it may help people drink less per occasion rather than stop entirely. Preclinical studies in rats have shown that GLP-1 receptor activation reduces both alcohol intake and relapse, adding biological plausibility to the clinical findings.¹² Larger trials are needed before semaglutide could earn an indication for alcohol use disorder, but the early data is more than just hype.

Psilocybin, the psychoactive compound in certain mushrooms, has also shown striking early results when combined with psychotherapy. In a randomized trial, participants who received psilocybin-assisted therapy had significantly fewer heavy drinking days over an eight-month follow-up compared to a control group. Specifically, the psilocybin group averaged about 10 percent heavy drinking days versus roughly 24 percent in the control group.¹³ An earlier proof-of-concept study found that abstinence increased significantly after psilocybin administration and that the intensity of the psychedelic experience itself predicted reductions in drinking and craving.¹⁴ Psilocybin is not a take-home pill; the model involves one or two guided sessions in a clinical setting with trained therapists, which makes it logistically and legally complicated. But the effect sizes are large enough to sustain serious research interest.

Supplements and Nutritional Support

No supplement can replace prescription medication for alcohol use disorder, but a few deserve mention. Thiamine (vitamin B1) is critical for anyone who has been drinking heavily. Chronic alcohol use depletes thiamine, and the deficiency can cause Wernicke’s encephalopathy, a brain emergency marked by confusion, unsteady gait, and eye-movement problems.¹⁵ Left untreated, it can progress to permanent amnesia and cognitive damage known as Wernicke-Korsakoff syndrome.¹⁶ High-dose thiamine replacement, often given by injection initially, is the standard preventive treatment during detox and early recovery.¹⁷ Thiamine does not reduce cravings or help you drink less; it protects your brain while you’re getting there.

Kudzu extract, derived from a plant used in traditional Chinese medicine, has shown modest effects in small lab studies. In one controlled experiment, participants given a single dose of kudzu extract drank about a third fewer beers than those given placebo and drank more slowly.¹⁸ A separate study in heavy drinkers found that kudzu extract reduced weekly drinks consumed by 34 to 57 percent and increased the number of abstinent days, though it did not affect cravings.¹⁹ These studies are small and short-term, so kudzu is nowhere near ready for clinical recommendation, but the consistency of the direction across trials is notable. The proposed mechanism involves increasing blood flow to the brain and slowing alcohol absorption, making people feel the effects of each drink sooner, so they stop sooner.

Why Medication Plus Therapy Beats Either Alone

Medication addresses the biological pull of alcohol, but it does not teach you how to handle triggers, repair relationships, or restructure the routines that revolved around drinking. That’s where therapy comes in. A systematic review and meta-analysis of 30 studies found that combining cognitive behavioral therapy with medication produced better outcomes than medication with standard medical care alone.²⁰ The combination likely works because the two approaches target different parts of the problem: the drug dampens the neurochemical drive, while the therapy builds coping skills and addresses the psychological context of drinking.²¹

In practice, this means that picking up a prescription for naltrexone and doing nothing else is better than doing nothing at all, but pairing it with regular therapy sessions, a support group, or even structured online counseling will likely get you further. Many addiction specialists consider medication and psychosocial support as two halves of a complete treatment rather than alternatives to each other.

Safety Concerns and Side Effects Worth Knowing

Naltrexone’s most common side effects are nausea, headache, and fatigue, usually in the first few days. There has been a longstanding concern about liver toxicity: the drug historically carried an FDA black-box warning for hepatic injury. That warning has since been removed, and a study of 160 patients found that liver enzyme elevations temporally linked to naltrexone were rare, occurring at a rate of roughly 1 to 2 events per 1,000 person-years.²² A pharmacovigilance analysis confirmed that acute liver failure is unlikely to be a true adverse effect of naltrexone and that injectable naltrexone showed fewer gastrointestinal and liver-related reports than the oral form.²³ Naltrexone does block opioid receptors, so you cannot take it if you are currently using opioid painkillers or are on medication-assisted treatment for opioid use disorder. Taking an opioid while on naltrexone can trigger precipitated withdrawal.

Disulfiram carries more serious liver risk. The same pharmacovigilance study found prominent liver adverse effects with disulfiram, and the American Association for the Study of Liver Diseases does not currently recommend it due to its adverse effect profile.²³ Acamprosate, by contrast, is cleared by the kidneys rather than the liver, making it the safer choice for people with liver compromise. Its main downside is the dosing schedule: two 333 mg tablets three times daily, which adds up to six pills a day and can be hard to remember.

Medical Detox Is a Separate Step

None of the medications discussed above are meant for managing acute alcohol withdrawal, which is a distinct and potentially dangerous process for heavy, daily drinkers. Sudden cessation after prolonged heavy use can cause seizures, delirium tremens, and in severe cases death. The standard of care for medically supervised detox involves benzodiazepines, which calm the overexcited nervous system during the withdrawal window.²⁴ Benzodiazepines are used for days to weeks during the acute phase, not as long-term treatment for alcohol use disorder itself. Once withdrawal is stabilized, the patient can transition to naltrexone, acamprosate, or another maintenance medication.

If you have been drinking heavily every day and want to stop, do not just quit cold turkey. Talk to a doctor first. Light or moderate drinkers usually don’t face dangerous withdrawal, but people who consume large amounts daily need medical assessment before they stop.

Pregnancy and Alcohol Use Disorder Medications

This is an area where the evidence is thin and the stakes are high. All three FDA-approved medications carry an FDA pregnancy category of C, meaning animal studies have shown fetal risks but human data is inadequate. A scoping review found that disulfiram poses the most concern, with a high risk of congenital anomalies believed to stem from its mechanism of action. Naltrexone appeared relatively safer, though the human safety data comes mostly from studies in opioid use disorder rather than alcohol use disorder. Acamprosate was not clearly linked to adverse pregnancy effects, and two preclinical studies even suggested possible neuroprotective properties.²⁵ Current thinking holds that the known harms of heavy alcohol use during pregnancy, including fetal alcohol spectrum disorders, may outweigh the uncertain risks of naltrexone or acamprosate, but this is a decision that requires individualized medical advice.²⁶

Why the Same Drug Works for Some People and Not Others

One of the frustrating realities of treating alcohol use disorder is that no single medication works reliably for everyone. Genetics is part of the explanation. A specific variation in the OPRM1 gene, which codes for the mu-opioid receptor, has been studied extensively as a potential predictor of naltrexone response. The theory was that people carrying the G allele (the less common variant) might respond better to naltrexone because their opioid system handles alcohol’s reward differently. But the picture has gotten muddier over time. One well-powered study found no significant link between OPRM1 genotype and naltrexone treatment success.²⁷

More recently, a study of extended-release naltrexone found the opposite of what was originally hypothesized: the A/A genotype (the more common variant) was actually associated with longer abstinence, lower relapse rates, and better treatment completion. Carriers of the G allele had nearly triple the relapse risk.²⁸ These contradictory findings suggest that genetic testing for OPRM1 isn’t ready to guide prescribing decisions in clinical practice, despite early enthusiasm. The best current approach remains trying a medication, monitoring the response, and switching if it doesn’t seem to be helping.

Beyond genetics, co-occurring mental health conditions, drinking patterns, and personal goals all influence which medication fits best. Someone whose main problem is intense cravings during abstinence may do better with acamprosate. Someone who wants to cut back rather than quit entirely may benefit most from naltrexone. Someone who is committed to total abstinence and has a partner willing to supervise daily dosing might be a good candidate for disulfiram. And someone with significant liver disease may have baclofen as their safest option. The honest answer to “what can you take to stop drinking” is that several things can help, but finding the right match usually involves some trial and informed conversation with a clinician who knows your full picture.