Barbell Shrugged - The Truth About GLP-1 Medications w/ Dr. Garrett Butler, Anders Varner, Doug Larson, and Travis Mash #798

Episode Date: May 14, 2025

Garrett Butler, MD. Husband, father, son, friend, and family doc in rural WV. Undergraduate in Physics from Johns Hopkins University. Undergraduate in Molecular and Cell Biology from Towson University. MD from West Virginia University School of Medicine. Family Medicine residency at WVU SOM. Hospitalist at Vandalia Health Davis Medical Center. Outpatient family physician at Vandalia Health Broaddus Family Care. Hospitalist at Vandalia Health Broaddus Hospital. Medical director of Mansfield Place nursing home. Work With Us: Arétē by RAPID Health Optimization Links: Dr. Garrett Butler - Old Fellow Manor Anders Varner on Instagram Doug Larson on Instagram Coach Travis Mash on Instagram

Shrugged family this week on barbell shrug Dr. Garrett Butler is back on the show and today we're gonna be talking about GLP ones and if you listened the last time he was on shrugged we introduced this topic at the very end of the show We realized we needed to do a full deep dive so we had him back on he did a ton of research coming into this on top of his normal medical practice and I Still didn't know how I feel about them. You probably will be able to hear many times my voice, there's frustration, there's hope, there's questions about how we actually use technology into medication.

Why don't we all just go live on farms and be subsistence farmers so that we know where our food comes from and we can all be healthy. How the medical system plays into that, Like there's so many factors in place when it gets to this topic and where the current health is, the current state of health in America. And it's one that I don't know if I have a complete thought about in which direction we should choose outside of. Here's all of the information that you need

to make a decision if you or your family members are thinking about taking GLP ones and some of the questions you should be asking some of the some of the research you should be doing and I wish the best of luck for you if it is a path you choose to go down. It's this is a this is a very interesting show and I hope you gain a lot from it. As always friends make sure you get over to rapidhealthreport.com. That is where Dan Garner and Dr. Andy Galvin are doing a free lab lifestyle and performance analysis. You can access that over at rapidhealthreport.com. Friends, let's see, let's get into the show. Welcome to Barbell Shrugged, I'm Anders Marner.

Doug Larson, Dr. Karen Butler. Welcome back, buddy. How's it going, man? You've been listening to the show for like a decade, and then all of a sudden, out of nowhere, you're a guest twice in like a quarter. This is crazy. That's pretty awesome.

This is how it happens, man. The rocket ship just takes off. If it was in a mochi, you'd like that rocket ship. We're going to the moon, baby. Dude, today we're gonna be talking about GLP-1s, which is very exciting, because you are a doctor, family doctor, and I would imagine if there's like a question you get 99% of the time in your practice, it is about these things.

How many people come in kind of like specifically hoping that you're like, here's your prescription for Ozempic? They, it's more of a, I get it, especially in this area, more of the kind of like the aside like, oh, yeah, I want to come in. I want to talk about weight loss. I want to talk about my diet, my exercise. You know, you really hammer home all that all the good stuff and like, and about that ozempic and that that manjar. How do we get that? I'd love to have like a very comprehensive show that we put together for this because as much as I know, it's also just like a factor of me being a part of an algorithm on Twitter, which is not a

great way to learn anything. And there's also just endless questions, probably great information, not great information. And I would love to kind of like to start at the top of like, what are these drugs? What are these treatments? Kind of where they come from? What's what's like the theory behind them mechanisms in play, etc. Absolutely. Well, I think it's a probably to start it off. I mean, if you want to kind of dive back into Galpin territory, you always talk about the physiology of it first, right? Like, why do we have GLP-1? What's it actually there for?

Our body actually makes our own GLP-1, and the way that you should think about it is going back to just glucose, homeostasis in the body. Dan always talks about homeostasis, and we've got ups, we've got downs, and the body likes to control things. When I think about that, you think about eating a meal and you think about what happens after I eat a meal. Well, if I have sugar or glucose in the meal, our body's gonna stimulate a little bit of insulin

and insulin's gonna help us to utilize that glucose that's in the meal. What ends up happening is we have our meal, our glucose goes up, insulin brings it back down, puts it into cells right where it belongs. Eventually what ends up happening is sometimes our glucose starts to go down because we're either fasting or exercising, doing something like that, and our body makes glucagon. Glucagon is actually what pulls our glucose up, and it is very oversimplified, if you

will. There's lots of other hormones in that pathway. But as we were researching and looking at these pathways, there was a guy and this has actually been a while, took notes to make sure that I figured out where the heck this actually came from. So it is back from, let's see, proglucocon is the actual protomolecule, the prohormone that the body makes. And interestingly enough, that can get cleaved into multiple things. GLP-1 is one of them, GLP-2 is another one, and GIP is a third one that it can come from. And there was a researcher, Jean-Pierre Raufman, and this has been back in the 1980s,

he found the Gila monster and he was studying it and he said this is really weird this is this is and this is an animal that can eat like once or twice a year and not have any issues you know it's just like why can this thing actually do it and so he started studying the saliva of the Gila monster reverse engineered what he found in the saliva and lo and behold, he found this molecule that acts just like GLP-1. He hung on to this and he was kind of studying it, trying to figure out what was going on with it and he didn't find much with it and he tried to propose different mechanisms of things to do with it and nobody was interested in it.

Nobody was like, oh yeah, what's it actually do? Where's this actually going to be useful? Nobody can even think of something. And then what ended up happening was a doctor named John Eng, he worked for the VA, in 1992, he ended up patenting a molecule called Exendin-4, which we eventually called Exenatide. And nobody in the VA was even interested in that. It took until the late 90s, 1996, before he found somebody that was even interested in that molecule.

And he said, hey, I've got this cool molecule. We got this GLP-1. And what it does is it goes into cells and it helps us use glucose better. It helps us use our own insulin better. And some of the companies were like, why would this be important? We've got insulin. We've got sulfonylureas. We've got metformin, we've got all these other ones. How exactly do we have to do this? Well, you know, this is an injection you have to put into your

body. And it's like, oh, people are already afraid of injections. Why are we going to use that? Why would we even dive down that pathway? Nobody's going to want to do that. And so it took a while, even after that, to even build up any interest in it to figure out, you know, what do we do with this? Nobody really wanted to do much with it. It actually took, GOP1 wise, I had to write down again, dig back in, all the way until 2014 before we had a second molecule for GOP1. And the second molecule was lyraglutide, if you ever saw any commercials for Victoza. And then same year, they came up with Dulaglutide, which is what became Truelicity, and that's

all in 2014. And it wasn't until 2017 that finally one of the pharmaceutical companies went through studying each of the molecules, trying to find one that just worked better, and they stumbled across this Semiglutide semiglutides what we know is Ozempic semiglutide is with Gove and Even then not super popular way way along the way They understand what the molecules are and what the mechanisms could potentially be but they didn't actually Understand how effective they would be for fat loss and whatever else at the time

No, no the first molecules weren't even that good at it. The first molecules, it was just like, oh yeah, we've got this alternative therapy to be used to help out with diabetes. I mean, heck, I learned about it in medical school and they even gave it as more of an aside. Like, oh yeah, you know, there's this random thing, you're going to get this question about, oh, this drug comes from HeLa Monster Venom. And that was basically it, like, just know the stem of the question to be able to answer it on your board exams. And it wasn't anything popular.

I mean, it's super expensive. And it was this, at the time, it was once daily injection is how they first came up with it. And it wasn't until they really started experimenting with the molecule to find out these once weekly that made it a heck of a lot easier, a lot more palatable for people too. And so they didn't see a whole lot with it. You know, they were seeing weight loss sometimes with, especially initially with our Lyraglutide and our Dulaglutide of like maybe 5%, maybe 10% or 10% weight loss if they're lucky. Some people

were seeing that with Just Met Forman. Yeah. So what was the tipping point that where it went from being kind of obscure and people were aware of it, but didn't really know its effectiveness to being like, Oh, everyone is on this all of a sudden. Like it really did just like referencing Anders Kama from the beginning of the show, like the rocket ship had has taken off at this point. And now it's everywhere. Like how did that happen? So he was he was actually semi glutite so the the company that made semiglutide is what eventually became Ozembic and and Wigoby. They started doing studies on it because they wanted

to see well how well is this working and they're doing these studies in diabetics and of course you know the majority of diabetics are overweight or obese they have a lot of weight issues anyways and what ended up happening is they're doing these studies all of a sudden these patients are losing 15, 20, 25% of their weight while they're doing the study. They're coming off of all of their other diabetes medicines, they're coming off of all their medicines for their blood pressure,

their cholesterol profiles getting better. And it was just kind of like this light bulb, like, oh shit, what's going on here? Dr. Andy Galpin here. As a listener of the show, you've probably heard us talking about the Arte program, which we're all incredibly proud of. It's a culmination of everything Dan Garner and I have learned

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It's about unlocking your full potential and looking, feeling, and performing at your absolute best, physically and mentally, when the stakes are the highest. To learn more, visit AreteLab.com. That's A-R-E-T-E lab dot com. Now back to the show. And so that's the results of this. It facilitates you eating less food or your your your metabolism is running hot so to speak and you're burning calories at a faster rate because you're using glucose more effectively or

Combination of both or how is it actually happening in the real world where people are losing? 25% of their body weight in a short period of time. Yeah, so the the mechanism I I think it's still considered speculation at this point because I did there even Initially whenever they first were looking this point because they're even initially whenever they first were looking at the molecules, they're thinking where do these molecules, where they come from and where do they actually work. And they found out that where these molecules are actually produced, especially our own GLP-1s, are made within the intestines and they thought that they act locally.

And then they found another center where GLP-1 is actually made. It's in the brain stem. And they said, oh, okay, well, what effect is it actually having up there? So we think that there's actually two separate mechanisms that GLP-1s are having an impact on. So one mechanism is actually that does impact the GI tract. So it hits your pancreas, and it actually helps your pancreas to produce insulin to make more of it.

It also helps save some of those islet cells and some of the other cells that produce insulin within the pancreas so we're not losing some of those cells. And it's also slowing down gut motility. So it's making you feeling fuller faster and for longer periods of time. You see a lot of people that end up having that fullness with these things. They're like, oh man, I can really only eat like once a day. I'm having see a lot of people that end up having that fullness with these things. They're like, oh man, I can really only eat like once a day. I'm having such a hard time doing that.

The second receptors that they've discovered, again, brainstem receptors, and they think that it's actually hitting some of the receptors that hits our satiety and our actually reward pathway. And so, you know, the original research was, is this just killing appetite? Is that the big thing? Is it actually nothing to do with the gut and it's just killing appetite centrally within the brain? And so those are the two biggest ones. But now that we're studying it more and especially these new GLP-1 receptor agonists, which is of course the two big ones right now is going to be our azempec and our manjarro or wagovia and

terzepatide, those ones are hitting in different ways and we're like, wait a minute, there's got to be more receptors than just the receptors in the intestines and around the pancreas and up in the brain. There's got to be more within the body and that's actually where we're still studying. There's not a lot of good data on it. Like you do a PubMed search and you look at where receptors found, almost all the latest data is starting to show, hey, we have receptors possibly within muscle. We've got receptors possibly within our immune system, within other areas. And it's like, well, where are all these receptors? And that's again, that's, that is the cutting edge that where we're going after things now.

So it's closed down gut motility. Does it affect digestion and absorption then? Yeah. Yeah. Yeah. So, Harry, it's not supposed to sit in there that long. Yeah, food isn't supposed to move. Yeah. Yeah. I mean, go back to, go back to Dan's lecture, you know, when he was talking to you guys about how things move in the gut and like, rinsed acidification, putrefaction, you know, fermentation, like all the different protomolecules that we get, our fats, our proteins, and our carbs, they sit in the gut too long and that can get pretty nasty and that can cause a lot of problems.

So you'll actually get some of my patients come back to me and they develop what we call sulfur burps. And they're talking about some of these sensations and some of these gases that are starting to come from the wrong end and they're starting to smell of these sensations and some of these gases that are starting to come from the wrong end and they're starting to smell these nasty things and oh yeah, and it can really sit with you. So it is absolutely impairing how food is going through your intestines. Maybe it makes you absorb things a little bit better because it's hanging around a little

bit better, but food's not supposed to hang around intestines that long. I'm over here making the same face that I make when I'm on a UFC fight with you and people are just getting their brains beat and I'm like, Oh man, ow. Like yeah, it is not appetizing at all. Like what what happened? I mean, the it's hard to get away from there is even when you say all that though, it's healthier to lose the weight, isn't it? Is it is the is is like the downside fact that if you burp, you clear out a room better

than the fact that you have diabetes? Yeah. So, I mean, that's that's basically what we're chasing down now is we're trying to see like really is it? Because I mean honestly you think about it whenever you're talking about a medicine, most people talk about medicines in a period of like 10 to 15, 20 years. What are our long-term effects of being on this medicine? You know, but when you're talking about Ozempic really just coming on the market starting in 2017, we haven't even had 10 years of having this medicine on the market.

But like I said, there are a lot of research studies going on right now looking at the nitty gritty of where is this actually beneficial. And there's a ton of stuff out there. They're really digging into this because, so it is interesting because, you know, even for my own patient population, you know, I start some people on

Ozempic, you max it out, you get up to that really good high dose. I've got some patients that haven't lost any weight on it. Their sugars are heck of a lot better. Their blood pressure is better. We're using less medicine from there. They're doing great overall. They're about the same weight as we started. But then I've got other patients that they've know, they've been on a moderate dose,

not even the high dose of Ozepic, and they've lost 10, 15, 20%. Now, if you were to talk to the company, the company is gonna say, anticipate somewhere between five and 15% weight loss for Ozepic, you know? Dig into something like Monjaro. Monjaro, it might be 15 to 25,

but they say don't expect the 25. My best... Between the people that are kind of on the low end and the higher end, is there a lifestyle change? Like here's the more aggressive... Are some people just like eating their way through the medicine? Like it doesn't matter, they just don't stop. And then some people are going, look, I just actually like pay attention and I cut back,

you know, a thousand calories a day. So it's like medicine plus lifestyle equals massive change medicine. And then, you know, they're using that as a crutch to say, like, I could just keep going harder in the paint now on food, like more soda or whatever. And then like, it just doesn't work? That's even tough. I've had patients that make the changes and don't have the weight loss.

Yeah, and I've got other people that are like, hey, I'm eating everything I want and I'm losing weight. And so you're sitting there scratching your head like, why does this actually happen? I mean, why are we getting these two separates? And I think that's more so we have to realize that again, I don't think these companies really know what the receptor agonist is that they're making

and where it's working. And also like within the body, like the human body, like we're going after a receptor, you know, we're going after this GLP-1 receptor. Where are they? Well, you and I are not the same person. You might have more GLP-1 receptors than I do. Your GLP-1 receptors might work differently than mine do.

Yeah. At the risk of being like very morbid on a generally happy podcast, I actually am like very scared for humanity in 50 years. Like when I see kids today, it's not that they can't make changes in their life, but they have to get out of their house. They're like six years old and obese. And the future of that at the pace and the volume, and like the

frequency that you see that in today's society is significantly higher. Like having kids, I notice it more obviously. And when I wasn't paying attention to kids at all, but it's impossible to ignore. And if you play that game, just one more generation, like another generation of six year olds out. And you know, that number is probably is it like 30 40 percent of obesity and now it's 40 to 50 and then you add another six-year-old another generation of six-year-old and it's it's it's 60 percent of our country is obese by the time they're 10. What happens when those people are 50 is who knows do they even make it to 50 because they're on these drugs at such a young age?

Which gets to the question of I think a lot of times we try to find some sort of medication that's going to just fix it. Do you think this is one that actually could fix it or is this just like a fad? And two years from now we're gonna wake up and go oh how do we reverse course on this like this this didn't work and now everybody's on them I think I think we're just kind of discovering a pathway and I think we have to understand that pathway better I think that's what we're going after because we still don't have a good explanation why our population blossomed and ballooned like this since the 1980s.

I mean, you look at the obesity rates in the United States, they've just skyrocketed since then. And you know, the other thing that skyrocketed since the 80s is the number of fitness centers. We're trying to take control of it. We're trying to get people more active. We're trying to educate people about diet and exercise. But what's happening with our food? What is that underlying cause that's really driving us to have this weight problem? Because just like you said, I mean, you think about it, I gave the statistics last time, you know, even in the state of West Virginia,

75% of people are either overweight or obese. In the United States right now, it's almost 20% of all children are above the 95th percentile for their weight. And that's, I mean, this is a really big problem. Now, do these GLP ones, I mean, do they stand the chance of being the game changer? Absolutely. But that's until the food industry figures out how to overcome it, which is actually another area of research is how can we modify our food to not be impacted by GLP-1s? And you're scratching your head like, what are we doing? This is like, it's almost impossible sometimes to have these conversations because you get six questions in and you're like, dude, my 10 foil hat right now is so big. We can continue. that what we need to do, where it's like, we need to get people out of it and get back to like getting outside

and getting more connected to the food we eat. And like actually, you know, there's like part of the capitalism brain where it's like, yeah, McDonald's should be allowed to exist. I totally get it. I support them and their shareholders doing what they need to do. But also like we should be able to have a conversation of.

It's also killing lots of people and very slowly and like the worst possible way. And there's there's got to be a way for us to have the profits of a McDonald's, but do it in a way like maybe Chick-fil-A is like the balancing act. I don't know if that's true, but like I feel less bad getting my kids chicken nuggets from Chick-fil-A. They're like everywhere. It's like how it that the way that it is like structured into the society is just really hard to think that we're going to come in and start putting medication into food and that's going to like solve the problem seems like I just immediately like, hold on, wait, what? That's not good. That's not right.

And I would imagine if you if like a patient comes in and talks to you and they're like, I'd like to do this naturally. What's the first step? You end up also scratching your head because they're in a steep battle uphill of how do they find the resources to be able to go and do that? Yeah. And the weight loss journey itself is so difficult for so many. And I think that's why these drugs have really kind of hit the way they have.

Now the first studies that they looked at for weight loss with these drugs, what they did was they would ramp people up and they would go after the highest dose that people could tolerate, maintain them for a year, and then what they did was they were cold turking these guys. And so they would do ozempic, they would do manjarro, they'd do it for an entire year at the max dose tolerated, bam, cut it, see what happens. But during that time, especially for the first studies, no education on diet, no education on exercise, no education on just healthy lifestyle habits in general. Now the interesting thing was

the first data that came out from these studies, we're talking 2018, 2019, 2020. These data were actually suggesting 90 to 95% of patients as soon as they stopped the medicine, the weight comes back. And you think- Yeah, that's freaky. We haven't fixed anything, right? That's just a drug covering up a problem. Yeah, you actually, you bring up another question of like the short-term dosing, kind of dosing, kind of like the Hollywood dose.

It's like a celebrity dose. It's like a friend coming up, let's go on this for two months and get ready for the pictures and then we just go back to normal. Versus the like, I'm on this thing forever. And correct me if I'm wrong here, but it's an escalating dose up to a maximum. But that maximum one, it's incredibly expensive. And two, does it top out? Do you, do you adapt to the top dose or is that like, how does that work? Yeah. So everybody's a little bit different in how they respond to it. And so usually as far as it goes.

So if you're using a medicine like the semaglutide, the semaglutide usually starts off at the 0.25 dose. You bump it up within four weeks to the 0.5. It takes about four weeks for your body to adjust to it. So you know, some of the sulfur burps and some are just like the flatulence and the fullness and the bloating and stuff. Then you move up to the one milligram dose, do it for another 4 weeks, then bump up to the 2mg dose. If you're doing the Wigovie, you max out at 2.4mg.

And that is, again, everybody tolerates things differently. And so it's not really a top effect. It's more so a matter of, well, how much of this can we pump into your system and how much can you really take? Because, you know, what happens if the company that makes them a glutide says, you know what, we created a 3-milligram dose, but we tried the 3-milligram dose. Oh, we made a 4-milligram dose, let's try that.

So we don't know of a top-out effect on how this works. We just know that from the standard practice that we do, especially in the medical field, whether or not it's diabetes or whether or not it's weight loss, you do. You try and max them out because the higher the dose, the bigger the impact. You know, you go after the molecule terzepotide, which is our manjarro and our zep-bound, that one starts off at 2.5 milligrams, goes to 5 milligrams, goes to 7.5, goes to 10, goes to 12.5 and goes to 15.

Now granted, two completely separate molecules, so the dosing, you can't just do a one-to-one conversion on the two, but again, you try and max them out to the highest dose that they can tolerate. I feel like we also tried like in the like early 2000s on the other side of this with the Phedrine, and then people were dying. They were like sweating to death. All the pen pen. It were like sweating to death.

It just like went to the complete other side. We're like, you know what? You're never gonna digest another piece of food again. It's like you turn into, meth isn't good. Let's do the paralyzing one. Like, it's like the waves. Yeah, go ahead, Doug. You know, all things considered, like at this point with everything you know about, what population or in what scenarios do you feel like the benefits outweigh the risks here?

Who is this actually for at this point? Right now, as far as it goes, I really do like it for my diabetics. It has been a game changer for a lot of my diabetic patients. That's even people that are borderline. Somebody with an A1C of like 6.5 to 7, and normally I start with metformin and kind of expand from there. I'm really educating them about diet, exercise, all that. This has been a good intervention.

This has also been fantastic for the patients who respond who are morbidly obese. But I think that as this moves forward, we're gonna start discovering other realms where this is beneficial because that's part of the new studies that are being done. We found receptors on heart tissue, and all of a sudden we're having patients that are post-cardiac arrest,

and they're restarting their ozempics, and they're restarting their manjaros, and their hearts are actually doing better than anticipated. And the cardiology group is looking at this and going, well, wait a minute, what's causing this? And that same effect that the GLP-1 has on the pancreas of making sure that your pancreatic cells that produce insulin are actually living longer

and are not dying off as fast, it's having a similar effect on cardiac tissue. And you're scratching your head and you're going, oh, wait a minute, now cardiology, they're trying to grab this molecule and they're like saying, hey, you know, we know it works for diabetes in some people, but for a lot of people, we're seeing this actually being helpful in cardiac. And now I'm having my cardiologist prescribe it and they're prescribing it for cardiac indications. And then we're, then we're also seeing that hey wait a minute this is also having an impact on our kidneys and I have my nephrologists, my kidney doctors that are studying this and

are looking at wait a minute we're stopping the progression of chronic kidney disease with this molecule? They're starting to prescribe for chronic kidney disease. And if you take that step back, you remember I said not everybody's gonna respond from a weight aspect, because that was always the first thoughts. Lose the weight, decrease the stress on the body, your body's gonna do so much better.

Your heart's gonna do better, your brain's gonna do better. Everything's gonna do better. Well, the interesting thing is, is that we're having some of these patients that aren't losing the weight, but their hearts are better and their kidneys are better. Oh, wait a minute. What is this molecule actually doing? And that's why, you know, when I started this, there still is that kind of

like, what are we giving to these? What are we giving these patients? Like we know kind of what we're doing to them, but I think there's still a bit of a guessing game because where are all the impacts of this medicine? And we're really just starting to dig into it because the most recent stuff that's happening, we're talking like 2024, 2025. If you have you ever met a schizophrenic, have you ever seen them on like their medicines and they get really big and they get really overweight, they get a lot of problems with their sugars, with their cholesterol, that kind of stuff that happens. And what we have is a subset of the population

that is schizophrenic, diabetic, cardiac disease. They look like the metabolic syndrome and providers are starting to prescribe GLP-1s for them. Well, the interesting thing is, is not only is their sugar getting better, cardiac status getting better, but also their schizophrenia is getting better too. And you're like, oh, wait a minute.

Don't lose weight. And some of them aren't losing weight. Some of them are just getting better mentally and you're not changing their antipsychotics and you're like, wait a minute, now we're having other impacts on the brain. And then there's that subset of the population that likes to abuse substances, whether or not it's alcohol, whether or not it's narcotics, whether or not it's methamphetamines. And remember, we're hitting a little bit of that reward center and that reward pathway in the brain when we're controlling things with GLP-1s in our brain. Oh, guess what? That

same pathway could be related to why we overuse substances. And now psychiatrists and some of these centers that are controlling addiction and substance abuse are using GLP-1s to control the cravings. Oh wow. These people are pulling the dice everywhere right now. GLP-1 Vegas, it's a roulette, let's go. Given that people often reference Alzheimer's as being type 3 diabetes and at some level it's blood sugar regulation within the brain, etc. etc etc like you see where I'm going with this like

has there any research or is anyone looking into the effects of GOP1s related to Alzheimer's? Absolutely and again another big area research is like what impact is this actually having on the brain because is this just glucose regulation? Is this that, is this another pathway? Because I mean, we've always chased down the pathway with things like Alzheimer's. You know, we always talk about like our amyloid plaques and our tau proteins and all that kind of stuff. And we have new drugs that are actually attacking those things. And they're not doing that great. I mean, they're okay, but you know, the side effects are horrific,

brain bleeds and death and all this other kind of stuff and it's like stuff that we're not excited to see but wait a minute works we're controlling our sugars better we're controlling our cravings better our mentation is getting better I can I can definitely foresee within the next year or two some of our first big studies coming out saying hey we're actually controlling the progression of Alzheimer's disease with GLP-1 receptor agonists. So I mean it's the research like if you go on PubMed right now and you just type in GLP-1s you know you go back four or five years ago you had a handful of studies maybe a couple hundred if you're lucky you're looking at thousands of studies every single year that are

looking into GLP-1s and where are these things actually having an impact on our lives. So that's why I was saying, there's a lot of potential here. And this drug can certainly blossom into covering a lot of things, but at the same time, I'm going to keep stepping back to, we don't actually know what it's doing yet. We have this idea, we're hypothesizing what this is doing. What happens when we stop it? You know, this is from just like Andrew said, from an insurance standpoint, this is a thousand dollar a month drug. You know, 300 million Americans, right? Yeah. People are talking about passing it in Medicare, Medicaid. Like that's wild. That's

about passing it in Medicare, Medicaid, like that's wild. That's a, that's a hundred percent tax rate. The thing that I actually, you've said it a couple of times and I'm very curious because I, you know, all of the fitness and health that I've done in my life, I would have never correlated heart health and maintaining the same level of body fat. Like how, how does your heart get healthier when you're still, you know, call it 40% body fat and you don't lose the weight, but your heart gets better.

I, I, it's, it's almost like I don't even, I don't even understand what that means. It's so far from, but my brain has been told for so long. Yeah, well, so conceptually, the way that I would think about it is remembering that the GLP-1, as it acts within our body, is not only helping our pancreas to produce more insulin and to be more efficient with insulin, it's also helping our cells to utilize that efficient more effectively. And so insulin has a bigger bang for its buck. We're doing much better. We're doing much better for all of our cells. So if our cardiac tissue, which again is pumping constantly, it's a very high energy source, we're always using a lot. Again, hypothetically speaking, it's always

hypothesizing on how this works, but is it increasing the efficiency of how the cardiac tissue is using energy? Is it increasing mitochondrial function? Is it making it use that sugar better, using those fatty acids better? It's all going to play into it. So, if we look at what the proposed mechanism is, that's how I would chase it down, is it's actually helping those cells to work better. Yeah.

If I'm a client or a patient of yours, what are kind of like the questions I should be asking you if I was interested in going down this route? And this doesn't, not the like, oh, I'm kind of interested in the weight loss but like Please tell me the truth about what's going to happen if I go on ozempic. Oh, yeah, absolutely So so if you were to be on any of our glp ones, you know, the the conversation is 100 are you willing to give yourself an injection once a week? You know, you have the simple I'm getting on trt, man I'm going the other way. I'm getting jacked.

Wait, we might have our GOP1 TRT agonist. You never know. Oh, no. That's a great question. I keep hearing about the potential for muscle loss and what have you, which, you know, of course could be to some extent ameliorated with resistance training

and all the stuff we normally talk about on the show. But is the TRT GLP-1 combo a hot topic yet? Not yet, but I think that that's got to be on the cusp, man. They got to be considering it. But you know, for the, we'll get back to Andrew's question here in a second, for the weight loss thing, and especially that was the most recent study that they were, that everybody was getting out there was like, holy crap, look how much muscle mass these people are losing whenever they're losing the weight. The question would be more so that whenever you're like, let's say a 500 pounder and you're 500 pounds and you're carrying around that weight, the muscle that you've developed is

purely physiologic. You have to support your structure. How efficient is that muscle? Are these people really good at running? Are these people really good at bench pressing, at squatting, dead lifting? Is this actually functional muscle? And I think that's a bigger question. So if you end up having a lot of weight loss,

initially on these GLP-1s, our data is actually suggesting almost a 50-50. 50% adipose tissue, 50% muscle mass that you're losing with these things. A lot of people are just like, mind's blown, holy shit, I can't imagine losing 50% of my muscle mass. But what if it is an efficiency thing, and what if you're losing your inefficient muscle,

and what if you're maintaining your efficient muscle? So again, it's all hypothesized. We don't know exactly yet. But the way we're looking at it is sure people are losing muscle mass, but the big stimulus there is a lot of these people are losing weight and they are not exercising. There's no resistance training going on with this. If GLP-1 makes our cells use glucose better and use insulin better, that would in essence mean if we were to exercise and be dedicated with weight-bearing exercise, we would probably actually build better, more efficient muscle and we'd help stave off some of that muscle loss. And that's actually the newer studies that are looking at how we're losing weight. They're starting to add things in like aerobic activity. They're starting add things in like three days a week of resistance training and they're seeing better benefits.

They are staving off and not getting the 50-50 anymore. They're getting people more like losing closer to 75% fat, 25% muscle. And I think as these things continue to progress, we're gonna look at it. And is there a place for having testosterone replacement therapy along with this it has to be thought of there has to be some potential there yeah we've been obese for however many years and you're diabetic and on and on your

testosterone is probably not amazing yeah well you know everything because if you gain the weight back and you've got low testosterone, hold the phone when you come off. That is a rough go. But even remember, what does fat do? Fat converts testosterone, right? Yeah. So I mean, you have that peripheral conversion, so you're decreasing your testosterone anyways

because of the fat. So you lose that fat, your testosterone is naturally going to get better. You could probably prime the system. I mean, that's certainly a pathway that you could chase down, but it would be something to consider. I do want to get back to the question on how patients do this. I find so many of these conversations, like I get it, and we said it at the end of the last show last time we had you on,

of like, if my parents were were gonna live an extra 10 years I'd be like yo check out that jlp1 thing you should just just do it like nudge go I'm okay with it but also I struggle so many times with the just these like crazy defensive strategies for just trying to live a healthier life where you could just go do the thing it seems trying to live a healthier life where you could just go do the thing. It seems that I can't even remember to like do the most basic things sometimes in my like date. Like the fact that I would have to go get a go to the pharmacy to pick this thing up every month I would forget all the time. Like it's hard enough for me to take a multivitamin sometimes. I like forget for four days

and I'm like I even put it in the little travel case thing. I made it so easy on myself and I forgot like I couldn't imagine having to add this new thing into my life when I could just just go do the thing that you're trying to get like be on offense about it. And the defensive strategies, they seem so cumbersome, and a hindrance to the life that people could be living if they were just on offense and just know I'm just gonna go eat healthy. And there's many people, there's all of the factors, socioeconomic, the genetics, like you could say all the factors, but it, it, it, that becomes like, it's not just the slow motility of food and digestion and burps and that,

but that's all like secondary to the, it like pains me that people will go to this length sometimes to constantly play defense on like, well, if I do this, then I can just live my life however I want. And I don't have to think about it and I'll still lose the weight. It's it. That part almost pains me on like a like a soul level of come on, man, like, let's, let's just go on offense and just eat the steak and the potato and the green beans and let's be let's be good. It's the it's the ownership of it. And I think that's the the biggest

thing that's going on right now is there is there's a lack of ownership and I think that's the biggest thing that's going on right now is there is a lack of ownership and there's a lack of ownership with people's health. And so, you know, as we're chasing down our health, you know, what do we recommend? We recommend the healthy lifestyle. We recommend the exercise. We recommend the dietary changes. We get more people that just want to come in because they do want the shot, they want the ease. And it's that lack of ownership and that lack of willing to be uncomfortable. And I think that's interesting because it makes you uncomfortable because there are their side effects. You're going to have those aspects.

You're going to have that burp, that fullness. You're going to have those belly issues and you're going to be sitting there going, fullness, you're gonna have those belly issues and you're gonna be sitting there going, man, I don't know if this is actually worth it. I feel miserable on this. God, I can't even kiss my wife. I keep burping and she says, man, it smells like a fart coming out of your mouth.

I guess that's the stuff that's not great. Yeah. Getting back to kind of the patient side of this thing, somebody really does want to go on it and how do they know they're doing their due diligence to protect themselves? Questions to ask and just in that relationship with their doctor, how should they kind of approach this? So the way you would approach it is that you start off with that discussion, start off

with the diet and exercise. Of course, you've already covered those bases. You're interested in this medicine. It's having the questions about things that can be related to it. So as far as the known side effects, we have the simple ones, which is going to be the GI stuff. So if I personally have any problems with my GI tract, if I have a history of bowel resections or other issues with motility in my gut anyways, these medicines can possibly make that worse. So you have to be ready. If you watch any late night television, it's like, did you develop an Ilias because of GLP-1? You were right to sue this company and make as much money off of them as they've

made off of you. But there are other aspects too because these molecules do help with the pancreas with maintaining your cells in the pancreas, so they help with keeping some of our cells working appropriately, keep them dividing as well. And so when you start talking about cells dividing, you start worrying about the other problems that happen when cells divide. And we have a very small subset of the population that can develop pancreatic cancer because of these medicines. Interestingly enough, we don't know that it has-

Have we gotten to the end of all the bad stuff? Nope. Nope. We know that. We don't know if it directly has an impact on our thyroid, but what we've seen now is we've also seen, oh crap, some people, granted small population, have developed thyroid cancer because of this. And then there's going to be a question, all of this other neuroendocrine tissue that we

have within our body, is there potential for developing cancer in those cells because of the mechanism of how this drug works. So that has to be part of your conversation because let's say you come from a family of like, oh yeah, you know, my grandfather, my dad, a couple of his siblings, they all had these really weird neuroendocrine tumors. It's like, okay, you probably are not the right candidate for this or that patient population where everybody in my family's had pancreatic cancer when they hit 45 or 50. Okay, yeah, let's not chase this down, but food for thought on this one, I actually listened

to a medical-related podcast within the past couple months, and they had an actual oncologist who deals with these cancers who stated, we're getting much better at treating the cancers. Sometimes the health benefit of the patient losing the weight is worth the risk of the cancer because I can treat the cancer. And if they have this horrible obesity, the long-term complications of this horrible obesity

are way worse than me treating this cancer. And I was sitting there just scratching my head. It's like, wow, crap. You mean you're actually like in this, this oncologist was actively prescribing Ozempic and Menjaro for her patients that had had a history of pancreatic cancer, had a history of thyroid cancer, and some of these other weird cancers. So that has to be part of that discussion. If you get weird family genes or if you have those concerns for cancers, that should be a conversation. And then the other thing, like I said, as far as it goes with the gut motility stuff,

if my gut's going to be really, really slow and I'm not going to be eating very much and all of a sudden I'm holding onto foods a heck of a lot longer and I do develop something like an ileus, that can be an issue because that can end up putting you in the hospital. If my gut is not moving, that's conceptually what an ilious is. Your gut just kind of says, hey, I'm done for the day. I'm not peristalsing. I'm not squeezing anything through there. And it just stops.

I can't put anything in and nothing's coming out. You're literally full of shit. So what do you do? People go to the hospital for that and there's complications with that. Yeah, it just rots. Before we shut this down here, for the average person, which I assume most people

listening to this show are kind of just average people, they're in kind of okay shape, they train a little bit here and there, they got a family, they got kids and they got work. Maybe they could lose 10, 15, 20 pounds, that type of thing. But the average person that just wants to lose, 20 pounds say, and they're okay with lifting weights and they try to eat well most of the time

and they have a couple of drinks on the weekends and whatever, it's a normal person. Like is this an option for them that You feel like the the benefits outweigh the risks or is it what are the trade-offs there? the trade-offs trade-offs are definitely gonna be How long are they willing to be on it and is are they gonna be one of the rebounders? Are they gonna do just like the show and you take it and you end up losing the weight and you come off of it and the weight just comes right back. Because I mean honestly if you're active, you're lifting, you're doing everything that

you should be doing, you should be able to maintain very well. And so it means that your lifestyle choices are not ideal. And that's how I would pose that to any of my patients who are interested in it. I think there are some people that are willing to take that risk and willing to try it. If you're dedicated and if you're going to use it to stimulate you to go in the right direction and you're also making positive changes at the time and understanding, hey, I've been eating like an asshole now for the past couple years and I really need to stop having donuts every afternoon at the office.

Even though everything else is good, I'm following my 80-20 rule, but my 20 includes that donut every day in the office. If they're gonna make those changes and they're gonna actively pursue that, there is potential. You always have to weigh those possible risks. You can develop pancreas problems, you can develop thyroid problems,

you can develop GI problems. We know about these things. If you're willing to take that risk, I know a lot of people that are okay with doing it. Now you also have to think about where are these people getting it? Are they coming to the office and getting it from me? Because what I do is I prescribe it and it goes to a pharmacy, right? You guys have seen all the clinics pop up. You guys have seen the spas that are giving this now.

I think there's a black market for this stuff somewhere too. So it's not necessarily that there's a black market. What it is is that as the molecule is produced, there's actually some really weird laws that come along with it that whenever there's a need for a drug on the market and if the company who's making it can't produce enough and there's a short supply that opens the realm for people to reverse engineer the molecule and produce it. And that's actually what happened as the market blew up and as so many people started using

these substances. I was going for one to two months at a time where none of my patients could get any of their meds from the pharmacy. These fly-by-night companies come in, they reverse engineer what they think is the molecule, and again, I'm going to say that. They're going to call it Ozempic, they're going to call it Manjaro, they're going to go after that. We don't even know that that's actually the true molecule.

They're producing it in mass to fill the gap, to fill that void of where the medicine's needed and all of a sudden you've got these spas that are picking it up and, oh, I just pick up a vial, I spend $1,000 on aial I can treat five ten fifteen patients with that you charge them a couple hundred bucks for a shot You're giving them the lowest dose of it. We think it's so Zempic. We don't really know it's acting like a Zempic maybe off on the like roll out of any medication though, but Part of this is like they have to go test it on people. One, probably as a population we're tired of them testing things in real time, but like how else do you go figure

out what this thing is good for? It's clearly good for something. It's good for weight loss most of the time, but there's also this brain health thing, this heart health thing, this addiction thing. There's like lots of things it could be used for. Do they have to go roll it out to 15 million people and see what the end result is? Is that like the way that it has to go? Is it the only way or are there like controlled ways to do something where maybe we kind of know what an end result is before it's just everybody's on it? Yeah so that's the point of clinical trials and the different phases of clinical trials. They do start of course almost

all clinical trials start with like mouse models and studying like what does it actually do with that and then you slowly roll it out to your population and you start giving it to healthy people. Then you start aiming for your actual population. And then that last phase four of clinical trials is you release it to the public and then you get post-marketing. And- That's the part that I feel like we get to real quick

where it's like all these people and then all of a sudden like thyroid cancer and pancreatic cancer. And you're like, whoa, we didn't see that in one, two, and three. It's like, yeah, well, that happened in a year and a half. Well, but so the other interesting thing with that, though, is remember that this class, GLP-1s, has technically been available since the 90s. And we did know about it then.

We knew about the potential, but again, it was not something that was actively used a ton. It was not this mainstream drug that we use now. And so then, you know, we had these rare occurrences where people were developing our pancreatic cancers and our thyroid cancers and having these really weird side effects. But oh man, in my patient population, how many people were actually on exenatide, Bietta, Bidurion, anything like that? I had less than a handful, you know, thousands of patients and I had less than five patients on it.

I wanna thank you for coming on and doing this today. I'm completely stressed out. I've got anxiety. I need to go do 30 minutes of breath work to be able to talk to Doug here and our meeting in four minutes. Dude, this is, I really appreciate this. A lot of information. It's like a real, I really appreciate this. A lot of information.

It's like a real, it's a monster. There's like a monster loose in our society. And sometimes it does really good. And it's with everything. There's always this like balance of what, like when does it work? How much can we control? And then when we can we control?

And then when we can't control it, how do we mitigate the downside of it? The thing that comes across to me on this one specifically is like the downside seems very bad, like very bad. It's like there are potentially, if we stuck to this like 80, 20, it's like 80% of the people are losing weight. It's helping with their diabetes, there's some heart health, there's some

brain health, there's like, this people are going to live longer, it's going to be a good thing. 20% of the people get cancer, though. You're like, Whoa, hold on. What 20%? How do we know? And you don't? You don't know if you're if you roll the dice, that's you. you that's that freaks me out Yeah, actual numbers, of course a lot less than 20% Yeah, exactly, but when it's you it's a hundred percent of you that has that yeah for sure We're gonna people learn more I'll tell the people about your

Your big project here as well You have to tell the people, this is my favorite thing. I'll be quick about it. I'll be quick about it. I got the odd fellow manner. We're on all the social medias and things like that. But I'm renovating a building built in 1908 and we're going to turn it into assisted living, having our own farm, trying to be fully sustainable,

regenerative agriculture, the full work, orchards, animals, everything. Grant, this is super duper long term project. We're talking probably 15, 20 years. One step at a time. That's all I'm doing it. But if you look for us anywhere, it's the odd fellow manner on all the different social media platforms. Next time we have you on, we're talking homesteading, dude. It didn't take me a long time.

Took me four months. I was in full farm. Went from zero chickens to by the end of this month, there'll be like 45 of them. How? What am I gonna do with all this? You're gonna eat a lot of eggs, man. It's the meat ones. They're so good. You got the meat ones too? That's how you get a lot of them because you got to do like five at a time. You can't just go and do one. Oh yeah. That's how you get a lot of them because you got to do like five at a time. You can't just go and do one. Oh yeah. No, no, no.

It's a lot. Good luck. Good luck. That's real. Doug Larson. The perfect number on my end. Zero chickens. Zero chickens.

You got to try. I can't make it to remember my multivitamin, but somehow I've been charged with all the chickens. That's right. Right on. Dr. Baller, appreciate you coming on the show. You can find me on Instagram, Douglas E. Larson. You all have been wanting to get a GLP-1 update for a while now.

I keep hearing more and more about it, but it's all kind of through the grapevine and I haven't really gone on a deep dive myself, so you're the perfect man to fill us in here. So I appreciate you being here. Awesome. I'm Anders Barner, at Anders Barner, and we are Barbell Shrugged, barbell underscore shrugged, and make sure you get over to rapidhealthreport.com.

That's where Dan Garner and Dr. Andy Galpin are doing a free lab lifestyle and performance analysis. And you can access that free report at rapidhealthreport.com. Friends, we'll see you guys next week.