Having gone from diabetes treatment to weight-loss miracle, GLP-1s are already blockbuster drugs. Now a new study in The Lancet shows that GLP-1s help with another common lifestyle disease: alcohol-use disorder.
It’s tempting to claim that we finally have an effective treatment for alcoholism. But in fact, we already have one. The decades-old Sinclair Method—which involves regularly taking a prescription drug before drinking to block pleasure-inducing endorphins, thus retraining the brain—is reasonably effective but seldom used.
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Why do GLP-1s seem likelier to catch on? The answer lies not in the scientific differences between them—the two drugs are surprisingly similar—but in the way we think about how to treat drinking problems.
Start with The Lancet’s results. The pre-registered study conducted a randomized controlled trial of the GLP-1 drug semaglutide (Ozempic/Wegovy) over six months. Both treatment and control groups saw substantial declines in alcohol consumption within six weeks and then slow declines thereafter, but the treatment group’s drop was both bigger and more sustained over time.
The results indicate that semaglutide is an effective treatment for alcohol-use disorder. Since the FDA allows off-label prescriptions and semaglutide already has FDA approval, I expect we will see doctors frequently prescribe GLP-1s to treat alcohol-use disorder.
I’m not a physician, let alone a specialist in addiction medicine. But I am a specialist in how behaviors spread, and much of the literature in my field concerns doctors prescribing new drugs. In this light, it’s interesting to consider why the Sinclair Method wasn’t a big hit for alcohol-use disorder, and why I think GLP-1s will be.
One of the main findings from my field is that the success of a new product or behavior is only partially about its merits. Success also depends on “compatibility” with the existing beliefs, practices, and understandings of a community.
To understand why the Sinclair Method hasn’t been more popular, consider how it works. In this protocol, the drinker takes the pill naltrexone, waits an hour, then drinks alcohol. Naltrexone is an opioid antagonist, which means that, when you take it before drinking, alcohol will still impair judgment, slow reaction time, reduce motor control, and make you sleepy—but it will not give you a buzz. If you expect a buzz but only get a bit sloppy, your brain will learn that alcohol isn’t as fun as it remembered.
Importantly, Naltrexone reduces alcohol cravings only if one continues to drink while on it. Moreover, it takes anywhere from three months to a year to experience substantial decrease in alcohol craving.
Now consider how compatible the Sinclair Method was with addiction medicine and the addiction community in the 1980s and 1990s, when researchers developed, tested, and promoted it. While earlier drugs had been tried for alcohol-use disorder, the dominant approach for treating the problem at the time was the self-help group Alcoholics Anonymous and the closely related Minnesota Model for professional rehab.
Both AA and the Minnesota Model stress that recovery begins with the decision to stop drinking, possibly followed by medical detox, during which doctors do not taper the patient off alcohol but remove it entirely and then prevent delirium tremens with benzodiazepines. Then the patient learns to maintain abstinence from alcohol. In this model, recovery from addiction is conceived of as stretches without alcohol, as in “I just got my 30 days.”
From the perspective of Alcoholics Anonymous and the Minnesota Model, giving a medication like naltrexone may be okay, but encouraging the alcoholic to continue drinking sounds positively dangerous. In this sense, the Sinclair Method’s relative unpopularity is less about its efficacy than its incompatibility with the assumption that time spent not taking a drink is the relevant measure of success.
By contrast, the semaglutide protocol does not require drinking, and so does not set off red flags for AA chapters, rehab centers, loved ones, or courts—all of which posit that recovery is about abstinence.
The irony is that animal studies and observational evidence suggest that GLP-1s reduce alcohol consumption by making drinking less rewarding, which is broadly the same mechanism as the Sinclair Method. However, since the semaglutide protocol is silent on the question of continuing use versus abstinence, it doesn’t sound like yet another lie or excuse to keep drinking.
Another advantage for GLP-1s: prior adoption of similar products and behaviors can promote the rapid spread of new products and behaviors. For instance, when seed companies introduced hybrid sorghum, it was perfectly suited for arid western Kansas. But farmers there had no experience with hybrid seeds and so were much slower to switch to hybrid sorghum than were farmers in temperate eastern Kansas—a region where the new sorghum was not especially useful, but also where farmers had more than a decade of happy experiences with hybrid maize.
Similarly, the average general medical practitioner does not have a lot of experience prescribing naltrexone for its original application of opiate-use disorder. But he has almost certainly prescribed GLP-1s for obesity. This familiarity in another context will make off-label prescriptions for alcohol-use disorder more appealing.
It is a blessing for alcoholics, their families, and society as a whole that we have a new effective treatment for alcohol-use disorder. The irony is that we’ve had an effective treatment for decades. The most important difference between naltrexone and GLP-1s may be less about their pharmacological properties than about how we understand them socially.
It’s tempting to think that we do things because they work. This is especially so for treatments that were developed and validated by medical science. But it is also true that medicine is ultimately a social practice like any other.
For instance, pharmaceutical marketing to doctors affects prescriptions. One way we know this is that limiting pharmaceutical company gifts to doctors, whether in medical school or in clinical practice, reduces prescriptions of expensive new drugs that offer no advantage over generics.
Sometimes effective drugs fail even when they have marketing efforts behind them, as naltrexone did, because they simply feel wrong to doctors, patients, and others. Fortunately, the widespread acceptance of GLP-1s suggests that they may gain acceptance as a treatment for alcohol-use disorder in a way that naltrexone failed to do.