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Retatrutide vs Alcohol: The Secret Brain Hack to Beat Addiction

2026-03-30 · 28:46 · 4 min read

A new 2025 preclinical study from UNC Chapel Hill looked at how GLP-1 peptides affect alcohol perception in the brain. They tested semaglutide, tirzepatide, and retatrutide in rats. The results are interesting, and they line up with what a lot of people have been reporting anecdotally for a while now.

Let me walk you through what they found and what's actually happening in the brain when GLP-1s blunt the urge to drink.

What the UNC Study Did

Researchers trained male and female rats to distinguish between feeling intoxicated and feeling sober. The rats would press a specific lever after receiving an alcohol dose to signal they felt the effects.

Once the rats were reliably identifying alcohol's internal cue, the researchers gave them GLP-1 drugs to see if their perception of alcohol changed. They tested both single doses and repeated dosing.

Here's what happened. Acute injections of all three drugs (sema, tirz, and reta) significantly reduced alcohol-appropriate responding. In plain English, the rats were less likely to behave as if they were intoxicated. The drugs muted the subjective signal alcohol normally produces.

Repeated semaglutide dosing over 15 days kept the effect going with no tolerance developing. Once treatment stopped, alcohol perception came back to baseline within about three days.

Why This Matters

The brain has a reward circuit. Alcohol hits it and creates a dopamine surge that feels good. You want more of that feeling, so you keep drinking.

GLP-1s appear to dampen that circuit. They make alcohol feel less rewarding. If a drink doesn't hit the same way, you're less motivated to chase the next one.

This is huge if you think about it. We may have a tool that literally rewires the brain away from compulsive behaviors that cause damage over time. And it doesn't numb pleasure across the board. It seems to specifically dial down the reward from things that aren't serving you.

How GLP-1s Actually Work in the Brain

GLP-1, GIP, and glucagon are known mostly as metabolic hormones. But their receptors are also in the brain, including the ventral tegmental area and the nucleus accumbens. These are the same regions hijacked by addictive substances to drive dopamine release.

When you activate GLP-1 receptors in those areas, you reduce alcohol intake and motivation. The brain becomes less responsive to the rewarding effects of alcohol. You're tempering the dopamine surge at the source.

There's also a gut component. GLP-1s slow gastric emptying, which means alcohol moves into your bloodstream more slowly. A recent human pilot study showed people on a GLP-1 had a delayed rise in breath alcohol and a delayed subjective buzz after one drink.

So you drink, and you don't really feel much. Less reward spike, less reason to keep going.

Sema vs Tirz vs Reta

Semaglutide is the most studied for alcohol. A randomized trial of 48 adults with alcohol use disorder found low-dose sema reduced craving and intake by about 50% in a lab drinking setting.

Tirzepatide adds GIP agonism. A 2023 study mined social media and found 71% of alcohol-related posts from people on sema or tirz described reduced craving. Self-reported survey data showed fewer drinks per occasion and fewer binge episodes.

Retatrutide adds glucagon agonism on top of that. In the UNC rat study, reta was equally effective as sema and tirz at blunting alcohol's effects. The GLP-1 receptor seems to be the critical component for the addiction piece. The GIP and glucagon don't take away from that, and they may add metabolic benefits that help the brain function better overall.

Population-Level Data

A Swedish registry study of over 200,000 people with alcohol use disorder found patients on semaglutide had a 36% lower risk of hospitalization for alcohol-related events compared to those not on a GLP-1.

For comparison, naltrexone, an approved anti-craving medication, gives about a 14% reduction. Which makes me wonder, why not stack them? Low-dose naltrexone plus a GLP-1 could have real synergy, and LDN may also help keep you sensitive to the GLP-1 over time.

A US analysis of nearly 84,000 people with obesity found those treated with semaglutide had 50 to 56% lower odds of developing or recurring alcohol use disorder in the following year.

Beyond Alcohol

The same mechanism may apply to other addictions. Observational data has linked semaglutide to fewer opioid overdose events and lower tobacco use in diabetic patients.

Dopamine pathways are the common denominator across most addictions. People aren't really addicted to alcohol or opioids or nicotine. They're addicted to how those things make them feel. If you can modulate the reward circuit, you may be able to address a lot of compulsive behaviors at the root.

Risks and Limitations

Semaglutide gives more people side effects than retatrutide does, milligram for milligram, in my experience. Nausea and GI issues can derail treatment. If someone feels sick, they stop taking the drug, and they relapse.

Pushing doses too high causes more harm than good. We also need more long-term human data, especially on retatrutide since it isn't even approved yet.

The rat study showed alcohol cravings returned within a few days of stopping the GLP-1. So does this mean people stay on these drugs for life? Maybe. Or maybe a GLP-1 gives someone a bridge. A 30-day window where they can step back and be a neutral observer of their own drinking. A lot of people realize they were drinking for social pressure or to escape something, and once that craving fog lifts, they don't actually want it anymore.

My take

GLP-1s reducing alcohol craving is real, and the mechanism makes sense. Retatrutide looks like it'll perform as well as sema and tirz on the addiction side while also being the best of the three for fat loss and metabolic health.

I've never struggled with alcohol. I've had a drink maybe ten times in my life. But I've struggled with willpower around food, and I know how it feels when willpower alone isn't enough. The idea that we have a tool that can give people an actual choice, instead of fighting their own neurochemistry, is a big deal.

You don't change the world by banning things. Prohibition proved that. You change the world by giving people access to something that helps them choose what they actually want for their life. That's what makes this exciting to me.

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Full transcript click any paragraph to jump video

Hey everybody, this is Andrew Williams. I hope you're doing amazing wherever you are out in the world. Today's video is going to be about retitrutide versus alcohol. So there was recently a groundbreaking new study from UNC Chapel Hill about the effects of GLP-1 peptides. They looked at semaglutide, trisapatite, and retritrutite in rodents, not humans, but they did look at it in Rodents on the affects of alcohol and how it actually changes the brain around alcohol so This is something, if you are tapped in, you kind of know what's going on here. GLP One's completely rewired neural networks to help you not crave as bad foods or crave alcohol or craved things, even like smoking.

But they actually weren't able to put it on paper this time. So what I'm going to do in this video is walk through this new study, kind what it found, and then also just look at the mechanisms behind what is going here so we can kind understand when we use GLPs. And I am obviously a fan of RetroTide because it's the newest kid on the block. But when we use GLP-1s, what is going on in the brain? And why is that a good thing that it is rewiring our brain to not crave some of these more compulsive, deleterious behaviors that cause us damage over time? So that's what today is gonna be about.

And I will give credit to where credit is due. UNC Chapel Hill did come out with something good, maybe for once in history of the university. I kind of joke. But I played football at Wake Forest University. Obviously, UNC was one of our rivals, so it's hard for me to give credit to UNC and then also to I have two brothers, one that currently does and another that is a former football player at NC State. And obviously, if you are in a family where you have one or more siblings that play football in NC state, you don't really like Carolina.

So for all those people out there who have no idea what I'm talking about, it goes deep when it comes to college sports here, especially in the southeast and we talk about football and basketball. Anyway, not to go down a rabbit hole, but as always, check out the peptide cheat sheet. That'll be the link down in the description. Obviously fully optimized health is the best private community on the planet. There literally is a whole of records there now as it relates to biohacking peptides and hormone data from other people in that community. We have over 600 people there and the conversations are far wide and numerous in breadth and depth.

So I would say check that out. And without further ado, I'm gonna share my screen and today we're gonna learn about this new study with the reticulatide and alcohol. All right, I'm Hunter Williams and today is all about Retro Tide versus alcohol. We're also going to look at some of the other JLP ones too, but you can obviously see my little photo here. The cool thing about the presentation software I use now is they have all of Probably some not so good things that come from AI, but one of the cool things is you can just put in Red Shrewtide versus alcohol, have a vial squaring off against a beer bottle and it comes up with them

in a pretty cool cartoonish format. So I thought that was funny. But let's look at this new study. There was a 2025 preclinical study again from the University of North Carolina at Chapel Hill that has spotlighted how GLP-1 based medications like Sima, Terz, and Retta can blunt the interoceptive or subjective effects of alcohol. So in the study, they basically, this is kind of what they did. They trained male and female rats to perform a task that distinguishes it from the internal cues of our call intoxication versus sobriety.

Essentially the rats reported feeling alcohol's effects by pressing a specific lever after receiving an alcohol dose. I don't know how to train rats in study but apparently they know to basically give the task to where it either will get the alcohol or not get alcohol. So once the animals were reliably discriminating alcohol's interoceptive cue, the investigators administered the GLP-1 related drugs to see if the medications disrupted their perception of alcohol, so basically they train them to get good effects of the the high of drinking alcohol first and then they use the GLP-1.

So this included both acute, which is single dose and repeated dosing phases of GLp- 1. Here's what happened. Acute injections of each estrog which was SEMA, TERS and RETTA all significantly attenuated alcohol-appropriate responding in the rats. In plain terms, that means that the rats were less likely to behave as if they were intoxicated, suggesting the drugs muted the subjective intoxication signal produced by alcohol. So, notably, the repeated semaglutide dosing over a 15-day period maintained this effect, with no apparent tolerance developing.

So once the treatment stopped, the rats alcohol discrimination returned to baseline after about three days indicating the effect was reversible and tied to the drugs presence. It did go away after time, but basically this is what we found. We found that all three, GLP-1, Sima, Terz, and Retta, acutely disrupted the rat's ability to recognize the alcohol stimulus, implying a reduction in alcohol subjective effects. This supports the idea that these drugs make alcohol feel less rewarding or noticeable to brain. Basically what were doing is taking alcohol, which makes you feel this reward circuitry inside of your brain.

And with a GLP-1, we are modulating the pleasure that you get from that. So if there was ever an antidote to addiction, especially in the form of alcohol addiction it would be this because it literally is rewiring the brain to not have pleasure from bad things. What's so cool about it, too, is it also gives you pleasure from good things. So it's not like numbing your pleasure or from anything in general. It's numming it from bad things, which is crazy if you think about this in principle. When they looked at semen glutide, it was given every other day for two weeks. Maybe they have been listening to people talk about the proper administration of GOP1s instead of once weekly to do it every day,

which is the best thing you should do. But basically they gave seman glutides to the rats every single day. And its blunting effect persisted through the treatment period and normal alcohol responses only reemerged a few days after the drug was withdrawn. So it suggests that continuous GOP1 receptor activation can durably alter alcohol's subjective effect without quickly wearing off. So by altering the effects of alcohol, GOp1-based therapies could reduce the craving for alcohol and the risk of relapse. If a drink doesn't feel the same or produces a weaker internal reward inside of our minds, it's obviously Kind of goes without saying that an individual

might be less motivated to seek the next drink. So the authors note their findings align with reports of reduced drinking in patients on the medications. In fact, a recent clinical trial on adults with alcohol use disorder found that semen glutide, obviously because this is more studied now because there's more access to it, pharmaceutically speaking. and clinically speaking, significantly decreased alcohol craving and consumption paralleling the animal results. Now let's look at kind of what mechanisms are at play here. So that's great, I know, right? It's that it blunts the brain.

But if we understand why something is having an effect, we can actually look the root cause of, okay, let us just say GOP1s reduce the craving for alcohol. Why? And if understand, why it actually helps us to be able to use it more in practice. The question is, why would a gut hormone-based therapy for diabetes and obesity affect alcohol in the first place? So it lies in interconnected metabolic signals and brain reward circuits. So when we have GLP-1, GIP, and glucagon, they are traditionally known as hormones for regulating blood sugar, appetite,

energy balance. but their receptors are also found in the brain. Just as there's GLP-1 receptors in their heart, there are GLp1 in your brain, and there is GL1 receptor in you stomach. These GLPs obviously affect reward, motivation and addictive behavior. GLP-1 is produced in the gut and the brain stem, and GLp- 1 sensitive nerve cells project to key reward areas such as the ventral tegmental area, otherwise known as a VTA, in a nucleus accumbens.

So these regions are central to the brains reward circuitry and are hijacked by addictive substances, one of which is alcohol, probably the most common in our society today, to drive dopamine release and reinforcement. So activating GOP1 receptors in these brain areas can reduce alcohol intake and motivation to consume alcohol by dampening the alcohol-induced reward signaling and modulating dopamine neurotransmission. So GLP-1 agonists may decrease craving and consumption by tempering dopamine surges and reward-related firing in the brain,

making the brains less responsive to the rewarding effects of alcohol. is we introduce alcohol that makes us have a dopamine surge and we want more of that because it feels really, really good. When we introduced the GLP-1, it goes to work in these receptors in the brain that basically dampens the dopamine signaling that we are getting from the addictive substance or behavior. So I think you could extrapolate this and this is likely what we'll see in next 10 to 20 years as these medications become more and more mainstream because its going to happen.

It's kind of right on time too, because you look around 70% of people in society are obese or overweight. And we temper the brain's reward circuitry. So it's literally like we are going into the hardware of our minds and changing it to not have bad things, which most of the matrix itself is predicated upon selling to you. So in a way, it's kind of weird because everyone rags on GOP1s from coming from pharmaceutical companies. But in reality, if you look at the downstream effects on this, If 50% of the population began using a GOp1, how much of alcohol consumption would naturally

go down? And one of things I always like to say to people because I don't personally drink, I've never really drank and probably count on two hands the amount of times I had alcohol in my life. It's just never been something I'd been drawn to or wanted to do light at all. So I guess I'm blessed in that sense. If you remove one variable from your life, you don't have to change anything, You don' have t actually do any extra work. You just remove this variable, which is removing alcohol from our life. Things will naturally get better. There will just be something that naturally happens in our lives because of the law of energy dynamics.

your life will improve. And what's cool about this is that we have these tools to be able to do it. So let's continue to look at GOP-1, GIP, and glucagon. We obviously know GOp- 1, right? That's semen glutide, which is obviously a part of turzapotide and retitrutide. But TURZ and RETTA extend the pharmacology because they have the Gip and Glucogon added on. While less is known about Gips, which is turzapotide, direct role in addiction. Some research suggests central GIP signaling can influence appetite and body weight regulation.

So intriguingly, co-agonism of G.I.P. with G-O-P-1, like in turazapitide might have synergistic effects on the brain's homeostatic and hedonic feeding circuits, further reducing the drive for rewarding substances. This synergy is one hypothesis for turtapetide's greater weight loss effects than just semaglutide alone. And then when we bring in retitrutide, which adds in the glucagon agonism, on the other hand, it acts on a liver and energy expenditure, but its receptors also present in certain brain areas. So we do have glucogon receptors in brain.

And so by adding glucagon receptor aganism as retutide does, there may be additional appetite suppression and metabolic stimulation that indirectly reduces alcohol consumption. What we mean by that is that when the increased metabolic rate and altered fuel availability, this can influence brain energy sensing and reward. And so the exact contribution of GIP and glucagon pathways to alcohol related behaviors is still being unraveled. But this 2025 study from UNC was one of the first to test whether the broader receptor activity via these multi agonist drugs would differently impact

alcohol subjective effects. And the finding that retitrutide was as effective as semaglutide in disrupting alcohol's effects suggest that engaging the GOP1 receptor is likely the critical component. So we can say that with relative certainty, it's the GLP-1 that is stopping the addiction component of these things. But what we notice, the GIP and glucagon activity does not work in the opposite direction. It doesn't diminish the effect of GOp1, and it might even enhance overall outcomes by addressing the metabolic health of the brain.

And so GOP1 is good, but GIP plus Guggenheim is even better because it improves metabolism in the brain, which is going to even amplify the effects of the GOp1 that much more. So although GO p1 appears to be the primary driver, GO P1 agonism appears the GIP and the glucagon, at the very least, are only helping. So another mechanism by which GOP1 treatments alter alcohol's effects is through the gut, as we know. GOPs famously slow gastric emptying, meaning they delay how fast stomach contents, including alcohol, move into the intestine and bloodstream.

And this is something, until this study, I didn't actually really ever think about, because I always associate gastroc empting with food, but it's calories in general, cause the good gut has to break down all the calories we have. So what this means is the pharmacokinetic effect can blunt the peak blood alcohol concentration and delay the onset of intoxication. So a recent pilot study in humans demonstrated what's going on here. People on a GOP1 agonist had a delayed rise in breath alcohol levels and a delay subjective buzz after one drink compared to controls,

even when nausea was controlled for. I don't know how they did that. but by literally slowing the absorption of alcohol, GLP-1s reduce or produce a gentler, slower intoxicating effect, potentially making drinking less gratifying or more self-limited. So, Imagine that I pick up my water bottle right here and I drink and drink, and it doesn't make me thirsty. And I have to keep drinking more. Or if like one sip for my Waterball keeps me from getting thirsty the rest of the day, that would be kind of nice.

It's funny because that's what's actually going on here is that because of the slowing of gastric emptying, which everyone loves to say is the worst thing ever. It actually slowing down how fast people get drunk, Which means that they drink it and it's like, huh, I don't feel anything and I really want to keep doing it as opposed to, Oh, this feels really good. Give me more of that. And so over time, This could translate to fewer drinks consumed and less cravings since the rapid reward spike is reduced. The gut-brain axis is basically a two-way street. So, GOP1 drugs send signals through vagal pathways and direct circulation that not only cause fullness, but also inform the brain's reward centers about

nutrient intake. GLP, GIP, and glucagon agonists leverage all these angles, slowing alcohol's entry to the system, promoting satiety and fullness and directly tuning down reward circuits, all of which help break the addiction cycle of alcohol and craving. So let's look at SEMA versus TURS versus RETTA, just to go a little bit deeper. So when we look SEMA, which is just a GLP-1, it's highly potent for glycemic control and weight loss, and also when it comes to alcohol consumption. In a randomized trial of 48 adults with AUD, low-dose Sema significantly reduced alcohol craving and intake, so participants on SemeGlutide consumed about 50%

less alcohol in a lab drinking. setting compared to placebo and showed reduced weekly craving scores. Observational data from patients with obesity also indicate a marked decrease in alcohol desire and consumption without semen glutide. And mechanistically, the effects are attributed obviously to the GLP-1, so we know for a fact that's working. Human studies so far have found meaningful but modest reduction alcohol drinking days, meaning the average amount of days per week that they consume alcohol, but we need longer trials. Now, let's look at Monjaro and see what's going on here because we do have a little bit of data around it.

Ter's appetite is even more potent than SEMA for weight loss and glucose in type two diabetes, obviously, right? And when we look at the research and patient reports around Terz, it also is seeming to curb alcohol use. So a 2023 study combined social media text mining, which is very interesting. Maybe we won't even have studies in the future. We're just going to have text binding of social, media and search behavior from people probably already in The Works. Next trillion dollar company probably, but, 71% of alcohol-related posts from people on SEMA Glutide or TURS Appetide described a reduced craving or decreased

desire to drink. So what they did is they analyzed social media data from SMA and Turs and found that 71 percent of anything they talked about relative to alcohol was about how it reduced their cravings, which is funny. And then in the survey cohort, individuals taking trisapatite or semen glutide self-reported significantly fewer drinks per drinking occasion, fewer binge drinking episodes and lower alcohol use disorder identification test scores compared to before starting the medication, which I guess is just a test that they look at to see how addicted people are to alcohol.

They also reported that alcohol fought less stimulating and less sedating than before, indicating a change in alcohol-subjective effects, again, as proven by the RAT study. And while terzepatide has not been yet tested in an actual alcohol use disorder or clinical trial, it is likely that it will continue to have the same effects and maybe even better because of the metabolic enhancement over semen glutide that trisapatite provides. Now we look at red at trutide, obviously it's the gold standard when it comes to fat loss in phase two trial. We all know that 48 weeks of red led to an average of 24% reduction in body weight and also at the highest dose and had the people on reddit had,

the most muscle retention over time. So they lost, they'll lost the least amount of muscle and reddits triple agonism, not only suppresses appetite, but also increases energy expenditure via the glucagon activation, which obviously helps with metabolism. And so in the 2025 rat study where they did look at redda in relation to alcohol, I found it equally effective in blunting alcohols effects as cementers, So in other words, despite its added receptors retrotide still potently reduce the subjective intoxication in animals.

So we don't have human data on this yet. It's not even human approved, but it looks like RETTA in addition to helping with the fat loss will be as good as SEMA and as Good as TERS at reducing alcohol consumption, which I think is important because I wouldn't want people to feel like, oh, well, I've got to use SEMA now because of this specific alcohol thing. You can definitely use it for that. But I just think the benefits for red are so much more and above. So let's look at some of the clinical evidence. Like I mentioned, we had the phase two trial with Sema Glutide with people, 48 people who used it over eight weeks.

So the trial was small, it provided perspective evidence that GLP-1 activation can change drinking behavior in humans in a controlled setting. And hopefully this justifies larger clinical trials, but this is the one that it reduced drinking by 50%. So I thought this was interesting too, and just scoping out some data. So there was a massive Swedish registry published late 2024, that examined over 200,000 people diagnosed with alcohol use disorder and compared those who happened to be prescribed GLp-one drugs versus those were not. so basically they have 200000 of people.

that are in this database of people that were addicted to alcohol, or I guess self-proclaimed addiction alcohol. And they looked at people on GOP1s versus not. The analysis found that patients on semaglutide had a 36% lower risk of hospitalization for alcohol-related events compared to patients not on a GOp1 agonist. They also found, because they did look at lower glutide, which is a weaker form, in my opinion, of semoglutaride and they had 28% higher risk. So for comparison, individuals on naltrexone which is an approved anti-craving medication had about a 14% reduced risk of alcohol related hospitalization.

Now you know where my brain goes. Why not mix them together? If alcohol consumption is issue because if you mix a GOP one with low dose naltrexone, man, you could probably do some wonders. This was probably mega dose, or not mega-dose, but just regular dose naltrexol, which is like 50 milligrams. But even low dose Naltrectol tends to have a similar effect in terms of reducing craving and rewards like GLP-1s. So there could be some synergies there. Also could some be synergies of keeping you more sensitive to the semaglutide over time and not building up so much of a tolerance so you can stay on a lower dose for the longest amount of time.

So all this is observational. It is a large sample size that we do have. So there was another population study in the US examined electronic health records of nearly 84,000 people that had obesity and found that those treated with semen glutide had about 50 to 56% lower odds of developing or recurring alcohol use disorder in the following year compared to those on other weight loss medications. So this reduction was consistently seen in a secondary analysis of around 600,000 patients with type 2 diabetes as well.

Such data involving hundreds of thousands of individuals strengthens the case that GOP1 agonists have a protective effect against problem drinking at the population level. Now, you're probably wondering, well, this sounds great if it works for drinking. Well, what about other things? We don't really have any data yet, but I think when we look at the pathways and the mechanisms we can extrapolate to how beneficial it would be. So interestingly, the influence of GLP-1s may extend to other addictive substances like opioids or smoking. So reports have linked semi-glutide treatment with improved outcomes in opioid use disorder and nicotine addiction as well.

There was one observational study that found that diabetic patients on semi glutide had fewer opioid overdose events compared to match patients not on the drug. Another analysis noted lower rates of tobacco use and reduced need for smoking cessation and healthcare resources in diabetic smokers who were on semiglutides. So obviously there is some sort of modulation from the GOP1 on the brain's reward system and stress systems could be broad spectrum, not limited alcohol. And from a neuroscience perspective, this makes sense. Dopamine pathways and subjective signals are common denominators in many forms of addiction.

People get addicted to the dopamine crash. They don't really care about alcohol, they care how alcohol makes them feel. I think you could say the same for any drug that we have, right? We don' care what drug is in what bottle, what container or what injection we care about what it does for us how it makes us feel and so although alcohol has been the most studied date we can potentially look at these things and I would just encourage anybody that has feedback definitely leave those in the comments or just in communities doesn't have to be my community or ones I'm involved with just help share that because I think this is something that is

possible if we look just any of the risk and side effects of this Obviously, so my thing with semen glutide is a lot of people have bad side effects because it's just not as good as red trutide. People with red true tide have less side-effects, milligram for milligram, than they do with semaglutides. But you could get nausea and other GI issues. So obviously, maybe it stops the alcohol consumption, but if a person feels sick, they're not going to want to keep taking the drug, to which they would probably relapse to drinking alcohol. And so obviously too, there's more serious risk as you go super high in dosages of GOP1s which I do not recommend doing.

You can cause more harm than good, and we just need more long-term data. Hopefully this is something that as we get more of these clinical studies, more metadata around alcohol use and people on GOP1s, it's something helps us really understand. At the end of the day, GOP1s can reduce craving that is undebatable for alcohol, representing a new approach. And there is another way that we can kind of think about this, because again, if we extrapolate the pathways, can we potentially use it to hack reward pathways?

So can't we use GOPs to incentivize good behavior and de-centrify bad behavior? And could this be a new addiction treatment that all the other ones that have seemed to not work on the population because we have higher instances of obesity and overweightness? I don't know about alcoholism if it's on-the-rise or not. But we potentially have something here that could modulate people's brain pathways to keep them from craving hedonic behaviors and encourage good behavior.

And I think if you look at changing the world, what could be more powerful than that? You're not going to change the world by shutting down alcohol consumption. Look at what happened with prohibition. You are not gonna change a world banning things. But you can change world giving people an opportunity to changed their life for the better and have access to something that helps their brain choose what they want to do anyway but they have a hard time because we have this reward circuitry that's inbuilt in our brain. And I've always wondered, do some people have more discipline? than others, do they just have more willpower or do other people not?

I don't know at the end of the day. We're all neurochemically unique. My brain's not anyone else's brain. Your brain is not any else else brain and so when we look at alcohol consumption, I've never had a problem with alcohol at all. I actually think it's disgusting, but that's just my brain, and there's other who literally if they see a drink, it is like they can't keep their hands off of it. and the potential to be able to modulate some of those behaviors or give someone an opportunity to choose, hey, I don't want this in my life. Now I have access to this.

Let me empower myself to take control over my health and change that for the better. It's pretty cool. Now, I think what is yet to be seen is do people return back to their old ways when not using medication? I don't know. In the study, it seemed like that, for most part, they went back craving the alcohol within a few days of being off the GLP-1. So does that mean that people have to stand up for life? Maybe, maybe not. But maybe it also gives people the ability to get off of something and actually have clarity for first time. Because I always say, I think if someone can stop drinking for 30 days, they can be more of a neutral observer around the act of drinking,

and they realize they don't need it. And they realized a lot of it was for social reasons or social pressure or escaping from something or just chasing the high. Maybe GOP1s can give people a bridge to be able to see that in their life, to where like, oh, i don' need that now. Even if you crave it, just like I crave a jelly donut, you know, and I might have it from time to time. I have my jelly donut once a month or twice a months or whatever, but I don't eat it every day. And I want to eat every because I know it's not good and it doesn't serve me.

So long winded rant, that is it for the slides. That is my take at least as it stands in May of 2025 on Retatrutide, GLP-1s, and alcohol consumption. So hopefully you enjoyed that. I think whether or not you struggle with alcohol addiction, it is pretty cool, like I was saying, to examine these medications in so much of a different light than they are traditionally painted. And I Think when we look at these, the use case is very, very multifaceted. and if used properly can do amazing things to help people heal.

At the end of the day, that's my mission in life is to Help people become healthier and more prosperous. And someone that uses alcohol as a crutch or has an addiction to alcohol or uses it in a way that prohibits them from living their healthiest life. A lot of times willpower isn't enough. And I say that because there's been times in my life where will power wasn't. Enough, whether it was like eating tons of junk food or something like that. I never struggled with my weight, but there are times where I've just, I would say if, if you put alcohol in front of me versus I said a jelly donut,

I'm like a dough boy, so I love pastries. So maybe even a cinnamon roll. I would choose a similar role every time. But if I can rewire my brain to understand that the similar roles, okay, if a one at once at a time, but I don't have to have it, I know I have that function and socially function, and physically function. gives me an out and gives you a way to change my life. So I think at the end of the day, this is what that's about. Maybe that is a little too poetic, but hey, that what I want to put out into the world. Hopefully you enjoyed this.

I'd love to hear your comments, especially in the comments section on this one, guys. If this was something you experienced, I would love, not even for me, for the video, just so other people can see it. What's cool about the comment section is it's kind of a wave, even if you never comment, to kind of look and see other people's experience and See what they share with it So if you do have an experience with this, maybe it didn't help you that leave that too But I think the more data we can get out there about this it can help more people to do those things So obviously leave your comment like comment subscribe and to wrap it up. Thank you guys so much again For me to be able to make videos like this.

It is literally a dream come true. So the fact that There's people out. There that support me now support the products from biological labs and all those is a dream come true. And the fact that I can bring these to you now on a day or on weekly basis is amazing. So thank you guys so much really from the bottom of my heart. I have absolutely the ton best amount of gratitude out there for you, guys. Thank you so, much and to everyone who supports channel likes work and all that stuff.