Can Wegovy AKA Semaglutide Treat Alcoholism

Dr. Dawn-Elise Snipes reviews early evidence about GLP-1 receptor agonists (exenatide and semaglutide) as possible treatments for alcohol use disorder. She explains biological rationale (GLP-1, leptin, dopamine interactions), then summarizes two published studies: a Danish randomized placebo-controlled trial using exenatide (n=127, 26 weeks) and a small US semaglutide case series (n=6). Key points: the Danish trial showed large within-group reductions in drinking but no significant differences between drug and placebo on alcohol use; exenatide reduced fMRI alcohol-reactivity in ventral striatum/septal area and lowered AUDIT scores post-treatment, with exploratory benefit in obese patients. The US case series reported improvements in all six patients on semaglutide. Dr. Snipes emphasizes limitations (small samples, homogeneous demographics, need for CBT alongside medication, cost ~USD1500/month, unclear long-term effects) and urges cautious optimism and further research.
Questions this video answers
127 participants.
Exenatide (once weekly).
26 weeks (once-weekly dosing).
Mean age 52 years; all patients were white; majority were men.
No — there were no significant between-group differences on alcohol use, though within-group reductions occurred in both arms.
Chapters
Hey there everybody. I've had several questions over the past couple of days about the news that's coming out that says that semaglutide may be useful for treating alcohol use disorder. So I wanted to go over that a little bit and encourage people to not assume it's the next magic bullet, so to speak. So let's go ahead and get into this. Semaglutide is a GLP receptor agonist. And you're going to be like, well what does that mean? Well let's go back up. Leptin is your satiation hormone and we've talked about that in other videos. Leptin has been shown to interact with the glucagon, like peptide 1 or GLP1 to regulate glucose metabolism and food intake partially by interacting with the dopamine system. Now remember, dopamine is our motivation chemical. It's the chemical that rel. Well, one of the chemicals that your brain sends out that tells us to release energy and do that again. So when dopamine is high, we are in an impulse driven state. When dopamine is low, our energy is low, our hunger tends to be low. Now there are. Dopamine, as you well know, is involved in a lot more than energy and hunger. But it is important to understand its involvement in the addiction process as well as in any process that involves involves compulsive behaviors. Okay, so your satiation hormone, leptin, interacts with GLP1 and that interacts with the dopamine system. Semaglutide is a GLP1 receptor agonist which acts to reduce that hunger and increase the metabolism of dopamine in the presence of alcohol. So that's another interesting thing that we're seeing, that the semaglutide not only reduces hunger, but it also increases the re metabolism or elimination of dopamine in the presence of alcohol. Well that sounds great. That means, hey, I'm not going to be motivated to go after more alcohol. Well, that's possibly true. However, a lot of people with addictions actually engage in their addictive behaviors because they have done so much damage to their dopamine system that they're trying to artificially do whatever they can to self medicate and get their dopamines levels up to where it should be. So I'm not sure how well this will work in the long term. So let's go ahead and take a look at some of these studies. The Danish study. Now this is the relatively big one, 127 participants that they've been talking about and in the Danish study, they used something called exenatide. It wasn't semaglutide. That's okay. But I do want to recognize that we are using two slightly different medications. The exenatide was used once weekly for alcohol use disorder in and investigated in a randomized placebo controlled clinical trial. 127 Treatment seeking alcohol use disorder patients were assigned to receive exenatide or placebo, which means nothing or sugar pill, Once weekly for 26 weeks in addition to. In addition to standard cognitive behavioral therapy. Oh, well, there you go. There goes that hope. And the magic bullet that you take a pill or a shot and you don't have to do anything else. You have to have the CBT. All patients were white with a mean age of 52 years, and the majority of the patients were men. Okay, so this throws an entire another hiccup into this study. Now, it's a great first study, don't get me wrong. But we can't generalize the results from this to people of different ethnicities. We can't generalize it to young people or people who are significantly older. And we need to be careful about how much generalization we do between biological genders. So we do need to step back and do some more factor analysis to identify if there were differences between the male and female men and women in the group. For both groups, the treatment group and the placebo group, the number of heavy drinking days and total alcohol intake were strongly reduced. Yay. Remember, this is using the medication and. And cognitive behavioral therapy. There were no significant between differences between the treatment and the placebo groups regarding use. Okay, so you have one group that is getting the exenatide and cognitive behavioral therapy, and you have another one that's getting the placebo or the sugar pill and cognitive behavioral therapy. There's no difference between the two groups. So what does that say about the exenatide versus the just cognitive behavioral therapy? It did, however. The exenatide did, however, attenuate the functional magnetic resonance imaging alcohol Q reactivity in the ventral striatum and septal area. What does that mean? That means the areas of the brain that light up when it is exposed to in some way alcohol, those weren't lightened up as much. So the rewarding factor, the rewarding aspect of the alcohol was significantly reduced. So then the people were less motivated to go out and get it. It's like, yeah, I drink and whatever. It doesn't do much for me. So that was good. And why the. Well, that was good. And we really can't draw much more in the way of conclusions from that yet. Poopy, do. You. Now? At six months the people came back and there was no notable difference between the treatment and placebo groups except for the audit score, which is the al alcohol use disorder SC screening tool, which was significantly lower post treatment for the exenatide group. So the people who were in the exenatide group weren't drinking any more or less than the placebo group that was the same, but their score on the audit was significantly lower, which indicates to me that they were having fewer cravings. Exploratory analysis also revealed that exenatide significantly reduced heavy drinking days and total alcohol intake in patients, especially in a subgroup of obese patients. So one of the conclusions that they've drawn is that it's possible that this particular treatment may be effective for people who are obese. At the same time, there may be a mechanism that is contributing to binge eating and obesity and alcoholism that may be addressed by this medication. Now let's look at the American study and this one did use semaglutide. The study was a significant decrease in alcohol use disorder symptoms secondary to semaglutide therapy for weight loss. A case series now in statistics, in order to have a statistically significant group or satisfactory number of people to draw conclusions from, the general rule we use is 30. So this is a case study because there were only six people in it and it's really hard to draw any generalizable conclusions from six people. But you got to start somewhere. The case series presents six patients with positive alcohol use disorder screenings who were treated with semaglutide for weight loss. All of the patients, all six of them subsequently exhibited significant improvements in alcohol use disorder symptoms. That's a wonderful thing. I am glad we're seeing that there might be an option for a certain subset of patients just like any other medication. It's not going to work for everybody. Just like any other medication, there are side effects and I've heard some of the side effects of this can be pretty brutal sometimes. However, dying from cirrhosis of the liver is also brutal. So weighing the costs and benefits are are something that each person needs to do with their doctor. It's important to recognize that however, that if there is an imbalance in the neurotransmitters in the dopaminergic system, then, and the person was self medicating with alcohol to try to increase their dopamine, then when alcohol is no longer helping, when alcohol is actually decreasing their dopamine, they may look for something else. I'm speculating. I don't know would make sense to me. And I was doing one thing for a while and it quit working and I started feeling like crap. I might look for something else. I don't know. There is still a lot to understand about how Semaglutid and some of those other drugs work. And we are seeing a lot of trials with this particular medication for pretty much everything under the sun. And it's important to also recognize that this medication is very expensive. I did a search online this morning and it looks like it's about fifteen hundred dollars a month in order to be on this medication. And they're finding that a lot of people, once they stop taking the medication tend to gain the weight back, tend to relapse, and so they're going to have to potentially be on it for the rest of their life. That's another one of those issues that we need to consider when we're looking at this particular treatment for alcohol use disorder over something like Vivitrol. Just my thoughts, My point in this video was not to recommend or dis or you know, anything, but simply to make you aware of the study studies. The Danish study only had one hundred and twenty seven people. The American study only had six people. Those are the only two studies looking at using one of these GLP1 agonists for alcohol use disorder that have been published in PubMed, that have been published in the medical information database. So it is too early to get too excited, but as I said, there is cautious optimism. Have a great day.










