Episode 014 - GLP-1 Overview with Dr. Jeffrey Davis
Welcome to Episode 014 of the PHW Podcast. In this episode, Dr. Kristin Marvin and Dr. Jeffrey Davis explore the controversial world of GLP-1 medications. Dr. Davis shares the surprising 20-year history of these medications, from their discovery in Gila monster saliva to their current use for weight loss, and explains the science of insulin resistance and type 2 diabetes.
This wide-ranging discussion covers the alarming truth about muscle loss on GLP-1s, why the 5 Pillars of Health are non-negotiable when using these medications, and the critical role of protein intake and resistance training. Dr. Marvin and Dr. Davis share real clinical examples, discuss who may be a good candidate, and explain PHW's personalized approach to using these powerful tools safely.
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Episode Transcript
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We've kind of gotten used to seeing bigger adults, right? Um I remember I had um a parent bring her son in and say, "I think he's got a problem because he's too skinny." And she said, "Look, you can see his ribs." And uh the grandma h the grandma happened to be uh in there. And I I asked her, I go, "What do you think?" And she goes, "That's what little boys used to look like." I mean, that was a profound statement. There was a mother who thought her son was abnormal cuz all of his friends had excess atyposity to the point where they couldn't see their ribs when they raised their hands.
And grandma noticed I remember kids looking like that. Welcome back listeners to the PHW podcast. I'm the host today, Dr. Christa Marvin, joined by my best friend and colleague. No, I'm teasing.
We're just being cheeky after a long day of clinic. We have had a very long day. But joined by um Dr. Jeffrey Davis, owner of Prairie Health and Wellness and Dr. Extraordininaire.
Everybody loves that. Everybody loves you. Um today, podcast number 14. Number 14. That's a lot. It's a lot.
It's good. I feel like this is a thing now. It's awesome. It's more than just like an experiment.
It's a lot of fun. It's a lot of fun. But we are talking about the maybe somewhat to some people controversial GLP-1 medications. Right. Yeah.
So what we hope to do for you guys as listeners today is to get a good foundation established so that you feel more knowledgeable about the basics of these medications. So we're going to go over like what is a GLP-1 drug and you know where did they originally start? Like what was the purpose? What were they being used for?
Um Dr. Dr. Davis is, I know, going to do an amazing job talking about, you know, what how how they were developed and what they do in the body. Um, how they actually work and we'll talk about like the names of some of these drugs because I'm sure as we'll get into, you can um, you know, get some of them commercially available, but of course in today's world, there's a lot of compounding going on. So, I know we're going to touch on some of those things, too.
And um then we're of course going to share examples with you guys of um where even we've seen very positive you know changes and benefits or clinical benefits with these medications. So let's start at the beginning. Yeah. So what is a GLP1 GLP1? Well um so GLP stands for glucagon like peptide.
Um, and I I think we should back up a little bit and talk about why why was there a push to find uh a glucagon-l like peptide. Um, we we knew about glucagon like peptide because our gut does naturally produce this. It has a very short halflife. So, one to two minutes and it's out of your system. Um, just to give you context, most drugs have halflife measured in hours. Um, some have a halfife measured in seconds. nitric oxide being probably the archetypal example of that.
But what we really needed in the diabetic world was um you know a lot a lot of people when their diabetes got out of control we started using insulin and insulin was an amazing discovery especially for type 1 diabetics because they just don't make any insulin or make make very very little amount of insulin. The difficulty with insulin is it could drop your blood sugar dangerously low. I mean there there's a chance to go into what's called a diabetic coma um where your glucose is is uh so low that your brain isn't operating. And one thing that they noticed with the glucagon like like peptides is it could have an insulin like effect without dropping blood sugar which was kind of a momentous discovery.
Mhm. Now, the downside was is that it it again was metabolized so rapidly you would literally have to give someone an IV infusion of this for it to be therapeutic, which just in in the real world wasn't going to happen. So, and I don't I've never really heard the story of how they discovered that um the there's another naturally occurring GLP-1 and they found it in of all places the Hila Monsters saliva or venom. That's I think the saliva and venom are the same [snorts] or secreted from the same gland. But the hila monster is that you know it's like what a I think a komodo dragon is another name for it's a big lizard.
Yeah. And I don't know what researchers decided to say you know we ought to look at their spit and see like what's what's interesting about that. Let's see if there's anything cool in there. But they did and they found a GLP1 that was similar to human.
I think it shared about half the same amino acid bonds as ours did, but it had a much much longer halflife. So the half-life being longer mean you could you could make it into a drug at that point. So they made this into the drug uh the first drug to hit the market. It's crazy to think about this but it came out 20 years ago. Wow.
And I remember using this in clinical practice 20 years ago. Um and that one was called Biata and I think Bietta was daily when it first came out. And then they figured out a little change to one of the So peptides get broken down like proteins do, enzymes break them down. Um, the way they got the GLP-1 to last longer was to put a terminal peptide on the on the end of it that resisted that breakdown. So there's probably more technical explanation, but that's essentially how how it works.
It it didn't change the ability for that peptide to bind to the receptor where it was going to have its action, but it it made it so it lasted a lot longer. And they got better at doing that until I think Bietta came out with a once weekly. So the second one on the scene I think was Vtosa and but I'd used both Baya and Vtosa and this was back when I wasn't in functional medicine but I was kind of clued into like you know most diabetics what they really need is they need weight loss. Um they don't they certainly don't need more insulin. I mean we've shown that in our clinic. We measure fasting insulin in everybody every year and what we see in people who get closer and closer to being the diabetic is that their insulin just starts going through the roof.
Well, let's maybe let's pause on that note a little bit and you know make sure our listeners really understand you know type two diabetes because there are different types of diabetes but I think what we should at least establish first is like the most common type 2 diabetes what we call and so I want the listeners to understand like what is insulin resistance and how it develops and the role of blood sugar regulation and all of these things because I think then it can really help drive understanding this GLP1 these GLP1 medications more. So when when we think about diabetes um the the term diabetes comes from the Latin to flow through and this was an observation that I think goes way way back to Aristotle maybe where um patients who had diabetes urinated a lot and that's a that's a very late stage feature of an uncontrolled diabetic. They have polyura, polyypipssia, so they have extreme thirst, extreme urination. And they noticed that they would those patients would pee on the ground if they and I think the way I classically remember this, they peed near an antill and the ants were all attracted to the urine, right?
So there's this classic example in med school where where the story is told that this professor is going around and he's teaching these year one medical students, you guys need to be very good observation, very diligent with testing. And so I want you to watch carefully what I do and repeat it. And so he takes a jar of urine and he dips his finger in the jar and he puts his finger in his mouth and licks it and he's like, "Okay, I want everybody else to do that, too." And people are like, you know, your first year in med school, you're not going to say no. Oh, I'm saying no. So all the students are dipping their finger in the urine and putting in their mouth and they're just horrified.
And he was like, "Okay, you all failed." Because he dipped his index finger in the urine and he licked his middle finger. Oh no. So again, the purpose was to to be very absorbent, but that that was an example of that was how people would test for diabetes. They actually test for sweetness of the urine.
Like literally taste test Yeah. urine. So thank goodness we've got lab tests now that we we can do. But but I really think the the hallmark of diabetes really needs to be told around the story of insulin. And I think insulin is one of the most overlooked labs across any in any primary care clinic. If you're not measuring insulin, I think you're really missing out on the driver of a lot of disease and dysfunction.
So, what's happening is as we increase our intake of simple carbohydrates, um our pancreas has to secrete insulin from the beta cells, the eyelet cells, that insulin's job, there's a lot of things that insulin does, but one of its primary roles is to open up the cell so glucose can come inside. Glucose is absolutely necessary for life, but it's a a little bit of a dichotomy because we don't actually have to eat glucose to live, right? So, um that that dichotomy really or paradox I would say comes down to our liver makes a ton of glucose. And I think Peter Tia is famous for doing the math on this. You know, he's total math nerd.
And he figured out that like for the average 180 pound male that if you could reach into the liver and just turn off glucose production in the liver, not affect anything else, that the average 180lb male would live six minutes before they would die from lack of glucose. So glucose is so important to humans that we do not rely on it from an outside source. So that's why if you're a patient in our clinic, you'll hear us constantly say protein is necessary, fat is necessary, carbohydrates are optional. So in the modern diet where we're eating highly refined foods, we're getting a lots of sugar load, glucose load, we're demanding more of our pancreas. And the pancreas is just like any other organ. If you make it work harder and harder and harder, eventually it can burn out.
And one of the problems is the more insulin is going around as a signal, the cells kind of become resistant to the signal. Um, and that can be affected by obesity and weight change. There's there's a complex interplay that comes in there. But the way I describe it to patients is it would be like if your mom is telling you to clean your room every five minutes.
After a while, you just tune her voice out and you don't even hear it anymore. We've all had that experience, those of us who have kids, where they they tune us out. So, the body's being tuned out to the signal of insulin. And then what happens is there's a point where there's a crisis where insulin is so high. Then finally, the beta cells burn out.
You have beta cell dysfunction. And in the background, really what's happened is glucose has stayed pretty stable for years, you know. So glucose hangs in the 90 to low hundreds. And in the background, what's not being measured is insulin's gone from an ideal of six to maybe 50, 60, even 80.
And then there's just a point where the ba the beta cells basically say, "I'm done. I can't do it anymore." Now your insulin drops down to six. But your diet and your insulin resistance out have now made it so you cannot get the insulin or the glucose rather into the cell. So now your glucose is spiking 3400. And then after that happens for months and months and months, suddenly your A1C begins to rise.
And then when the A1C gets to a certain arbitrary level, we go, "Aha, you have diabetes." Well, really, we need to look at the hyperinsulinemia picture first. So, diabetes, type two is hyperinsulinemia that's chronic and then ends with beta cell dysfunction and and insulin resistance. Whereas type 1 diabetes is where they damage those beta cells right out of the gate. Usually an autoimmune attack, usually happens to kids, adolescents. They cannot make insulin and so they're their glucose spikes and they need insulin. and it's life-saving.
Whereas the type two diabetic really needs to reduce the amount of insulin their body is making by diet and lifestyle changes. So that's kind of the overview I think explaining the difference between type one and type two. Type one they they can't make insulin. They have an absolute deficiency. Type two they have far too much insulin. But unfortunately we used to treat type two by just saying well let's just give you more insulin more insulin.
And we drove insulin resistance even higher. So tell our listeners then also why like why is this important? Like why is this a big deal that when we have high amounts of glucose in the blood that often then correlate? Like is it really the insulin that's causing the harm or is it the results?
You know what I'm saying? Yeah. Um I I wouldn't say it's the insulin that's causing the harm. Um I would say it's the I would say it's the cells response to the insulin leading to insulin resistance. And and the other thing the insulin unfortunately is a growth hormone for fat cells.
So if we have excess glucose, the body says well are they you know is this person doing a lot of exercise and and if the answer is no then you know the body says okay well I got to put it somewhere so it packs it into the liver we get fatty liver from that right because the glucose goes to glycerol to triglyceride triglycerides get stored in the liver that's fatty liver disease actually the number one cause of liver failure right now or um it gets put into the adiposite adiposytes are amazing that's our fat cells they can grow, you know, 100 times their normal size. And the the amazing thing about fat is that it doesn't cost us any any energy to ha to store fat to store. It's like having a it's like having the largest closet you can imagine or or a storage unit somewhere that they just keep adding more and more space and you never get a bill. Yeah.
I had somebody explain it to me once where they said, you know, when you like hop on an elevator and there's a little sign on the elevator that says max capacity, you know, and it gives you a number, right? It's like your So your body, it's like your body has these little signs and it's like max capacity for glucose is x. Max capacity for fat infinity. Yeah. Like we can only store so much glucose, two hours of glucose in the muscle.
Um but but when it comes to fat storage and and that's that's again if I think if we go back and we look where we historically were as humans what an amazing adaptive ability right uh carbohydrates weren't readily available but you know you would be an a hunter gatherer you'd come across a blueberry patch and you'd eat the entire I mean you never get the signal to stop eating sugar right the way you do with protein I mean have a steak and then say do you want another steak rarely you're going to be able to say yeah I'd like one more steak I mean our body says that's it, we can't take anymore. But when it comes to the tortilla chips, I mean, we just keep shoveling them in. So what what is helpful from a standpoint of an acute adaptation becomes a disease when we chronically apply that adaptation, which is what we've done with type 2 diabetes. We just overwhelm [clears throat] the system with more and more carbohydrates. The system becomes resistant to it.
We get more and more obesity, which also drives insulin resistance. M so that's that's the real that's the driver of coronary artery disease. It's the cause of hypertension. Um it's the number one risk factor for cancer. Um probably the driver of of um dementia. So you know so so we were talking like some foundational diseases that really have their roots in insulin resistance.
So a combination maybe of we're getting you know infinite amount of fat which is causing inflammation and dysregulation in maybe some of these organ systems that like you said fat can get deposited into the liver and then are we seeing also an inflammatory response from these just arguably higher levels of sugar in the bloodstream? I mean is that causing Yeah. So sugar sugar is um sticky. So it glycosillates proteins.
So, so famous example of glycosidated protein, everybody would if they've had an insurance physical, they they check an A1C. So, hemoglobin A1C is looking at the uh amount of glycosillation of the hemoglobin protein. The reason we check that is hemoglobin lives inside the red blood cell. Red blood cells on average live about 90 days. Um, so we can look at that and say, okay, that protein's been around on average for 90 days.
How much sugar is stuck to it? we can then back up and go, well, this is probably how much sugar you've had in your bloodstream over those 90 days. Because when you come in and check your fasting blood sugar, you're you're getting a snapshot of the glucose that hour, what it is, and it's going to change based on the meals you eat. It's going to change on whether you how much sleep you got the night before. It's going to change on whether you exercised, the piece of birthday cake I ate last night, happy birthday.
Uh very nice birthday cake that I saw on Instagram. Um yeah so that that's that's a very brief brief overview of diabetes and why it's so important to look at glucose. We really our bodies really want to maintain glucose ideally around 85 on the labs that we get from lab core. So okay so let's let's then uh give the listeners a few examples then of like you know break it down for them like because you know a lot of our listeners maybe they're not in the medical field you and I can sit here and use these terms right. So like give the listeners some examples of maybe then like what we see clinically like why this is important.
You know what are the either you know talk about some medical conditions or symptoms or things like that where people can really tie it then together the knowing if they have high glucose. Yeah. If there's high glucose or just flatout type two diabetes. Yeah. I mean the the hard part is the early signs where we're checking for it in our clinic there.
It really is a silent I mean I hate to say silent killer but it's a silent killer. I mean until you have you know the the late stages of of hyperglycemia would be you're getting blurred vision right because your lens is now so full of sugar that it's soaking up extra fluid. That's more late stage, right? That's more late stage. Um you're getting up and urinating all the time. You're you're thirsty, right? you're tired because your cells aren't able to get the energy they are because of that profound insulin resistance.
Obviously, weight gain is a huge one. Yeah. Um, dysipidemia, right? So, your your cholesterol is going your triglycerides are through the roof.
So, the the the problem is there's so many people in the United States walking around with profound profound metabolic dysfunction that really don't have any overt symptoms. Yeah. I think, you know, one example I feel like we're seeing more and more in the clinic or in women, especially like permenopausal women. I have seen some like arguably really good fasting labs, but these ladies are coming in and they're complaining. They're like, I have this belly fat that's like appearing and it's not like a big belly.
It's just like a little little pooch. And they're noticing, you know, my pants don't fit the same. I can just see it. I don't see any definition in the muscles around, you know, like my ab muscles, stuff like that, right?
So, um I even as a clinician, I've kind of had to take a step back and be like, okay, even though these labs I think maybe we do sometimes see a lag in the labs maybe, um I think we can see some symptoms. It's just that maybe we've like tried to connect it to something else, right? Like we're blaming another hormone or PCOS is a classic example. [clears throat] PCOS is really should just be called insulin resistance. Yeah. Yeah.
Like di I've heard it called diabetes of the ovaries, right? Like so but like skin tags is a sign of insulin resistance. Skin tags is a good example. Aanthosis nigricans which is a dark rash on the back of your neck makes you know we see that sometimes in kids and parents are like I can't I keep scrubbing and it won't get clean. It's like that's insulin resistance and we're seeing a lot of obesity.
Obesity is probably the biggest most overt symptom, you know, sign that we see. But I think we've kind of gotten used to seeing bigger adults, right? Um, I remember I had um a parent bring her son in and say, "I think he's got a problem because he's too skinny." And she said, "Look, you can see his ribs." And the grandma h the grandma happened to be uh in there. And I I asked her, I go, "What do you think?" And she goes, "That's what little boys used to look like." I mean, that was a profound statement. Here was a mother who thought her son was abnormal cuz all of his friends had excess atyposity to the point where they couldn't see their ribs when they raised their hands. And grandma noticed, I remember kids looking like that.
I knew we had a problem when, you know, we have patients that were supporting to lose weight that needed to be lost. And instead of instead of friends and family like being excited and supportive, you've got friends and family that are like concerned. Oh yeah, that are like are something wrong with you worried about it. You're losing too much weight.
And so yeah. Yeah, I think I think you're right. It's a tough one. But yeah, I mean I do think that there are some clinical signs and symptoms that we can see. I mean I sometimes I even wonder about when people have fatigue, especially fatigue after eating or you know um or even you know potentially things like headaches or aches and pains in general.
Yeah, joint inflammation certainly could be that. So the the hardest part about about that weight gain is that once you've gained it, remember there's no metabolic cost for you to carry that extra 10, 15, 20 pounds. It doesn't increase your metabolic demand during the day. I mean there's a point where someone who is if they had the what we call morbid obesity where they're two, 300 lb.
Yeah, there is a there is certainly a metabolic spend that goes on just moving through their day. I mean, if I gave you a 50 pound sack of corn to carry around all day long, you're going to burn more calories as you walk. Right? But for the most part, their body's basil metabolic rate doesn't change the more atapose tissue they have. So if you go through a period of time where you're overeating and then you know because we commonly hear people, they'll say, "Well, I don't overeat." And I say, "Well, you may not be overeating right now, but you definitely did in the past." Yeah.
At some point, you went into a very positive caloric balance and, you know, probably a stressful event. It could have happened during the holidays or, you know, extended travel. Who knows? But you can go back to your baseline, your basil metabolic rate, and your body says, "Well, we're we're burning exactly the amount of calories that we're eating, and it doesn't cost you to keep the fat around." It'll keep the fat around for a rainy day. So, you have to put those people in an energy balance where they are in a calorie deficit.
And I think that's gets us into probably the heart of what you and I have talked about with what are GLP1s really doing. Yeah. Yeah. Right. Okay. Well, let's move on to that then a little bit.
So, how let's let's maybe touch back on or go back a little bit, but how do these medications actually work? Like, I know you talked about how it's this glucagon like peptide, but like how do we think we understand these peptides? Because it feels weird to call it a drug because it's a peptide hormone, right? Yeah.
And it's actually it's a bioidentical hormone. We want to get right down to it, right? So, let's let's get into how these things actually work or how we think they work. Anyways, so the way we think this is working and I think I think this is pretty well shown that we have some well understood mechanisms of actions and I think we have some less understood mechanisms of action. So we understand glucagon like peptide will stimulate the beta cells to produce insulin.
Okay. Um they also at the same time will block glucagon. So glucagon normally when insulin gets stimulated the liver releases more sugar. So this is where I think the magic of a GLP-1 happens is it says let's release the insulin but let's not have the liver release a lot of gluc glucagon or it really it's glucose that comes from splitting glucagon through glucis or converting fat and protein by gluconneogenesis but the end effect is glucose rises when you get glucagon.
Yeah. So we we're going to suppress the glucagon while we raise the insulin. And that's essentially going to take the circulating glucose and drive it down. And there there is a in doing that we actually create a satiety signal that goes back to the brain and says you're full. And that it may be the glucagon like effect, a suppression effect that has that more so than the insulin.
Um but in in doing that we actually slow the emptying of the stomach. So you're going to feel full faster. Honestly, people can get some of that effect if they just slowed down eating, right? So if you if you ate and every bite you took, you put your fork and knife down like we were and you chew chew chew chew chew. You chewed 27 times or you know whatever our parents told us, you would slow the meal down enough that that satiety signal would hit and but you know we some of us were so busy we don't even sit at a table anymore.
I mean, we literally inhale our food. And as residents, we really learn to inhale food because you may have five minutes before you have to be somewhere or before your code pages. How many people are eating in the car or they're not even sitting down to eat. They're like multitasking at home or whatever, you know? Right. Yeah.
So, the satiety signal is really powerful with these GLP1s. Um, it improves the ability to secrete insulin, which that's the one thing for me that feels a little counterintuitive is that if we're saying that diabetes is a hyperinsulinemic response, wh why aren't these GLP1s increasing insulin resistance? And they don't. And I think it's because their effect is spread out over a time rather than in bursts.
So GLP1s have a lot longer halflife and it's in fact now the modern ones you take once a week. So you're doing a small injection subq once a week and um you're getting that satiety effect. Now with that satiety effect comes side effects. So I don't know if you want to go into the side effects now. Um or we can talk about Yeah, let's talk about them a little bit later because I think we'll definitely get into more some of the clinical stuff that you know um patients will or listeners and patients of course will love to hear.
Yeah. Um but let's stick on how they work because I think you touched on some really good points, right? that you said stimulating insulin release from the pancreas. Um right when blocking glucagon blocking glucagon um the delayed gastric emptying which certainly can give some signals to people right central signaling back to the brain to say you're satiated and what's interesting so that's one of the less understood effects would be the satiety signals because there's now some evidence to show that that spillover can have an anti-hedanistic uh effect. So, people who have a a gambling problem, right, people who have a problem with alcohol, they're starting to see some benefit that when they're on these medications, they don't have that compulsion that they normally have.
Um, the the way I've heard my patients describe it is is that they're they're that drive they have to seek food for comfort because, you know, we we all eat for various reasons. We eat because there's a social reason to eat. We eat obviously because we're hungry and we need energy. But a lot of times we eat because we're bored. I mean that know that's one of mine is when the kids go to bed.
I sit on the couch and finally get some alone time and I'm like hm let me go see what's in the pantry. It's a terrible time to be eating. Like my body does not need those calories. So for a lot of people they say it turns off that that kind of food noise. Yeah.
Great great term, right? That says where it's the refrigerator saying, "Hey, come come check me out." Yeah. Yeah. Um and so people will literally say like they'll go into their pantry habitually and they'll look and they'll go, I don't feel like eating. Yeah. And so that there may be some retraining of the brain that happens because you know obviously our goal isn't to have people on these medications forever.
I mean especially in our clinic, we're always trying to find like lifestyle changes. But I will say these are these are powerful powerful drugs that can help people who are really struggling with with weight loss. Do we think that this is a hormone in the body that we see like naturally decline for people as we age? I know I've I've heard that question posed before that, you know, that could be, but I don't know if you have any thoughts on that.
Yeah, I don't know. Um I haven't looked into that one. Yeah. whether GLP or or become resistant to GLP as we age. Or maybe it's some of those other things, you know, that change, you know, that may be even somewhat more indirect in a way that can set us up for some of this stuff, too, because obviously there's there's arguably many changes happening metabolically in the body that can make somebody insulin resistant. It's not always just the overeating factor, right?
Well, and we're starting to see some supplements that are claiming to have a natural GLP effect. And so, you know, I'm I'm curious to see how that industry evolves over time. I think the thing they're always going to be bumping up against is if you're stimulating the body's natural production of GLP, you're you're always going to be bumping up with that very short halflife. Yeah.
Yeah. Okay. And then yeah, it seems like you kind of touched on this earlier, but when we can get those types of mechanisms better supported for people, well then you're going to see some of these other areas like you said, like maybe changes in cardiovascular risk or changes in some of these other metabolic issues get better. And this is what I think is comical is that you're you're now hearing people say that, oh, when when people are on GLP1s, their their cancer risk is improving. um their risk of heart attack is going down and and people are saying these drugs are amazing. They're they're keeping people from having heart attacks.
It's not it's a secondary right secondary effect of losing weight, right? It's a it's a secondary effect of the lifestyle changes we're trying to achieve in our clinics. Y um you know, if you're decreasing your insulin resistance, you're losing their excess ataposity, your visceral atapost tissue, right? the fat that's in and around your organs that we measure in our patients every year using the DEXA scan. You're um taking the fat that's out of the liver and congesting some of that liver's effect. You're going to improve so many metabolic pathways from weight loss alone.
So, I think those are all secondary, but they're good. Now, I don't want to downplay them, but they definitely are beneficial. They're beneficial. Yeah. Yeah. Yeah.
Another really interesting area I've seen is fertility. Oh, yeah. like women that are struggling to get pregnant and especially like you mentioned earlier with PCOS and some of [clears throat] this metabolic dysfunction women are getting pregnant with these medications even so far far reaching effects for sure for sure. Okay, tell us some you mentioned some of them earlier but what are some of the common JLP1 medications that people are going to hear? So the first one was Biata, then Vtosa.
Those were approved for diabetes early on for diabetes. Um then it's funny, I started noticing early on that my diabetic patients that were doing the best were the ones losing weight. And so on Biata and Victtosa, I saw them losing a lot of weight. And I was like, why don't I just start using this in people that are overweight? So I started using this off label um years before it was approved.
So So Victtosa was the first one that sought approval. And what's what's interesting is the company sought to make a new drug. So they called it Saxenda, but the label said do not use with Vtosa because it is VTOSA. It's the same thing.
It's the same drug, different name, but they went through a whole different approval process rather than seeking an expanded indication. Yeah. And the reason is the price. So when they released that one that it was mainly a cash drug, $1,000 a month. You would think over what 15 years that price would come down.
Not much. Geez. So, Vtosa went to Saxenda and then I think interestingly we have the the combos now are are the ones that I find to be fascinating. So, we now have GLPGIP. So, that's WGO, Mangaro.
Um there's a there's a new one that probably is going to be approved next year. Um that is a GLP, GIP, and Glucagon. So, that's a fascinating one. that the weight loss on that one. They're saying, you know, it could be 40% weight loss. So, you know, we and you and I've seen these people do kind of get to the point where they plateau on their weight loss and they they kind of get to I think a resistance point. Um so, some of those drugs I don't I'm not sure what the commercial name's going to be, but um those are something to kind of keep an eye out for.
Okay, cool. Cool. There's going to be a ton of these drugs flooding the market because because yes, literally driving the economies of some of the countries where these are produced like in in Norway for instance, I think that it has revolutionized just like their GDP. Wow.
Can be measured by what we're consuming medications that we're consuming in the United States. And frustratingly, you know, if you're in the UK and you wanted to get on one of these GLP ones, I think they're around $80 a month. In the US, it's 800. 800. Yeah. Wow.
Yeah. and sometimes more, right? Yeah. Yeah. Yeah.
Okay. Um I know we mentioned a couple of examples where these medications can show clinical benefit. Is there anything else that comes to mind before we move on? Uh in terms of other drugs that could show clinical benefit, no, these medications, you know, we were just obviously talking about like fertility and how we tied it to Yeah, I think I mean I've heard anecdotally um we've started to hear that this idea of micro doing So, we should we should probably touch on this. So, so the dosing the typical way that dosing works with GLP-1s um is that you keep increasing the dose until you can't stand the the dose anymore.
Yeah. You're essentially in in other words, increase it until you get to a toxic level and then and then back off or stay there in some cases. So, what does toxicity look like with these? Well, it's nausea, it's vomiting. I mean, the heartburn on some of these medications can be severe for patients.
So, there are significant side effects that can happen. um you [clears throat] know there there's a certain kind of meillary thyroid cancer that it's contraindicated in. This was actually seen in rat studies at thousand times normal human dose. So I don't think we've seen any of that uh thyroid cancer in the human trials and certainly hasn't been a safety signal but it is contrindicated. Um, I would say constipation, fatigue, you know, because some people have such a suppression in their drive to eat that they literally go all day long and not eat and they're they're tired because they don't have any energy because they still have some of that insulin resistance that they haven't fully figured out how to unlock their fat cell and start getting into that glucanogenesis from the stored fat. So, but in so some practitioners out there have begun really dialing the dose back and and the hard part with micro doing is you can search for what the dose of micro dose is and there's no definition and so I would say it's just probably a sub therapeutic dose or probably a dose under what the industry would would typically dose. Um [snorts] so one nice thing about using a smaller dose is that you know you're paying for a volume of the drug. you're going to go through the drug slower, so it may lower your monthly cost by using a smaller dose.
But anecdotally, we've heard of this being helpful for people who have autoimmune disease. is probably the area that you and I have been most interested in sort of whether that's an offtarget um effect of GLP1 that we don't completely understand or whether maybe insulin's being involved in that or is the fact that insulin resistance is going down that we're seeing less inflammation and so there's maybe some cross talk with the immune system that's saying you know because inflammatory pathway is very powerful for modulating the immune system so we're getting less inflammation you know some of the fat loss is going to decrease inflammation so I don't think we completely completely understand and there's just unfortunately not a lot of trials that are looking at this as an autoimmune um treatment. But I think as as it continues to be used like that, we hopefully will get more information. These are the citizen scientists that are reporting back to us. Um and again, I think for the most part it's a very safe drug when used appropriately and we'll kind of talk about what what we define as appropriate use in our clinic.
Well, let's talk a little bit about that now. That's a good segue. Um but let's first kind of set the stage for you know I think when we had patients initially coming to us asking about some of these medications it was because you know they're asking about the skinny shot or you know because a lot of like arguably celebrities and maybe some bigger name people in media were like miraculously dropping weight. So yeah, honestly it was brilliant marketing because again these drugs have been around for 20 years and been used for weight loss for more than 15, but just in the last five you've really started to hear people talk about them and I think it was the celebrities. I mean people started really noticing and then you know Hollywood's starting to use it and suddenly everybody wants to be on it.
Um, so the the biggest fear I have and and probably my biggest critique of the FDA approval process when it comes to these medications is the FDA never required the companies to show where the weight was being lost. Right? So you know we do segmental analysis in the clinic try to do it every year on patients where we do this uh dexa scan body composition scan so we can tell how much of your body is fat how much is lean body mass bone density things like that so if for instance I give you a drug that you lose 50 pounds of weight but you lost 50 pounds of bone density that would be terrible I mean you'd be walking around like a fragile egg. Yeah.
Um, and the reality is as as we've looked at the postmarketing data, those of us who do this kind of measurement, we've seen an alarming trend of people losing both fat and muscle at largely the same rate. And so when you look at the the studies on this, these aren't done by the companies that that have approved the drugs. There are other studies, up to 40 to 50% of your weight loss is in lean body mass. Now, the reason that's devastating is that your lean body mass is your metabolism, right? Your resting metabolic rate is defined by how much muscle mass you have.
Because contrary to fat that doesn't have any energetic cost, muscle has a very high energetic cost. So, the more muscle you have, the more calories you burn at rest. Um, and probably the more calories you burn through activity, right? You can, and you can also soak up more glucose. I mean, there's a lot of benefits to muscle.
We've talked in podcast in the past, but when you're losing weight, my my rule for our clinic is that if you be if you lose more than 10% of your lean body mass, we got to stop that. We got to reassess what's going on. So, I I have had several patients um a handful I should say, who as they've lost weight, they are getting fatter. You might say, "Well, how does that happen?" They're losing muscle faster than they're losing fat. And so their body fat percentage on the DEXA scan is going up as they're getting skinnier. What's happening?
They're losing their metabolism. When those patients try to come off that drug and they have a habit of eating a certain way, they're going to find that they are left with a metabolism that's three, four, five, 600 calories less than what they used to burn and they are going to gain weight back at alarming rates. Not good. Not good.
Well, depends who you are. You're the drug company. You go, great. It's not a bug. That's a feature.
Yeah. Oh, you're going to be a customer for life. [gasps] That's right. I don't see the problem. Yeah.
So, those of us who are in lifestyle medicine, we're like, that's a problem. Huge problem. So do you think part of this part of the problem too is that you know I mean and I certainly don't pose this to try to like push blame on some doctors or providers who are giving these medications but it does seem interesting to me that like you were saying the history of some of these medications. It sounded like well that was something you got from your family med doc because you were struggling to control your diabetes or maybe an endocrinologist because you saw the specialist you know for that system. But now with these medications, so maybe let's go into this a little bit before we get back to some of the clinical side of things.
Back to more of the history of you know these medic the original medications you were talking about they're commercially available through like your commercialies but then entered the compounding situation. So there was a massive shortage that happened partially fueled by co partially fueled by these drugs were just becoming more popular being prescribed more. Mh. There is a clause in the compounding pharmacy rules that says if there's a shortage of a substance, compoundingies can step in and make up the shortfall. So compounding pharmacies did and so suddenly you saw med spas, cosmetic clinics um starting to prescribe this online online.
Um yeah and and and during COVID you you could have a doctor from you know Utah uh taking care of your obesity by literally just having you subscribe to uh a jailite type of situation. Yeah. Um and and I would so I mean I think that's part of it that that's being drawn by that. But I think the other part of it is I think there's a lot of family docs out there that that know patients struggle with weight loss. I mean I myself it's it is difficult right? I mean because we we just have these habits of eating.
I mean I struggle with weight loss. I think as physicians we really desire to help patients achieve and have a better life. And so when you have a drug that you're like, well, the drug companies say it's safe and they haven't they haven't told you about, hey, you know, make sure they don't lose muscle, right? If you're not clued into that, you're thinking, "This is awesome.
Look at their A1C is coming down. They're losing weight. They're gaining so much confidence. They come in here. They're smiling.
They feel great in their skin. Again, that's an amazing feeling for a provider when you're like, I'm going to do this for everybody." So that I think that's driving it, but then you also have the cosmetic clinics that are driving it and then all the online stuff which I think expired a couple months ago. So I don't know how those online clinics are doing now. Yeah.
Yeah. So yeah. Yeah. So I think it I think it's multiffactorial about why it's being used so much became very widely available arguably probably very easy to get and then yeah maybe providers not always having some of the clinical insight the extra resources that like we'll get into kind of later how we manage you know more so in our clinic but I think that the big point is that the accessibility doesn't always equal like the best care when it comes to you know the nuance that some of these things and and we're now seeing when one of the reports I read was actually that and sometimes this muscle loss isn't just skeletal muscle. Yeah.
But there have been some cases of heart failure now with GLP1s, which means you're losing heart muscle. Heart muscle isn't something we make more of. You know, you don't go into the gym and pump iron to make your heart bigger. Yeah. Um so, so I think we will start to see some heart failure that is irreversible and that and that's that's obviously that saddens me.
I don't want to see that. So always I think with medications we have to respect that there's a little bit of poison with every pill. There are side effects that need to be respected that understood deeply and then we need to really understand what's a proper way to use these tools because in the end that's a tool right and as an integrative clinic we're going to use all the tools that we have available to us. Right. So it sounds like these are you know who would really benefit from these medications are type 2 diabetics that are trying to or struggling with glucose control. Right.
But individuals maybe that would, you know, be put into the obesity category, struggling to lose weight, having other metabolic markers of like insulin resistance, things like that, right? Yeah. The the person I would be cautious in using it is the one who's like, I want to get ready for bikini season because, you know, again, because if half the thing that if every bikini season they're losing five pounds of muscle with five pounds of fat, Yeah. and they're gaining it back faster, they're going to be on uh kind of a destructive cycle. I think of sorts.
I think the place where this makes the most sense is those with with the super obesity, the the morbid obesity, the ones that are destroying their their hips and their knees, their backs are being torn up by excessive weight that they're carrying. It is very very difficult again to get into a steep enough caloric deficit um to be able to start shed some of that weight. So, I think it's effective in those patients, but again, we and and I would say in the in the super obese category, I probably would allow for a little more lean body mass loss because again, that person is carrying a little bit of extra muscle just to carry the extra weight that they're that they have. have. Yeah. So, that I think there's some nuance in in helping that patient out.
So, what I'm hearing you say is this is not a quick fix. This is not a substitution for some of the important lifestyle factors that we still preach, correct? Teach, right? And and I would say it is a amazingly powerful tool when used in combination with what we're trying to do with lifestyle.
Well, let's get into that because I feel like that's definitely more of the approach that we try to take at PHW. Right. So, I just walk you through like a typical patient. We're going to be obviously checking fasting labs. We're going to look at fasting glucose and insulin. identify hyper triglyceridemia.
We're going to correct for essential fatty acid def deficits. We want to get all of those things lined up. Vitamin D deficiency important for insulin resistance. Then we can have the talk about GLP1s. Once we have a DEXA scan and we can say, okay, how much fat do we need to lose?
What's your lean body mass? And and most importantly from that DEXA scan, you need patients need to understand how much protein do I need in a day? Because if the GLP-1 suppresses your appetite so much that you don't get the protein, your muscle mass is going to go down because your body is going to look for energy both from fat and from muscle. It can digest your own muscle to make glucose. It could digest your fat to mean glucose. Go back to the beginning of the conversation.
Glucose absolutely essential for life but not essential for us to eat. So we'll typically with GLP1 patient, we'll actually have a DEXA scan every three months to monitor that. And I often times they don't patients will go, "Oh, I don't I hear you. I'll make sure I work out." We get that first DEXA scan.
What do we see? We see the black line go down. We see the red line go down right behind it. And I And that's my little yellow flag. Hey, you're losing weight, which is great.
You're also losing muscle. Is that a little bit of almost like a litmus test for you because I one thing I probably we need to go back even a little bit even though in our heads because we practice this way in the clinic, but let's make it ultra clear for our listeners. before you even get to that GLP1, you're going through pillars. Yeah, you're doing all your labs. You started naming some of the pillars, but like let's really clarify it for patients so they get it.
So, who I if I want to set patients up for success and then they're going to use a GLP1 as one of the tools. Obviously, we're not going to use it as solo therapy. We want to make sure number one, you're getting seven and a half hours of sleep, right? You're waking up feeling rested. Eight, eight or more, maybe even for some of us.
For some of us need more. Um, we're gonna want to be making sure that the food we're eating is is good food. Uh, you know, I watched a a Instagram reel today where this guy was going through a grocery store saying, "I'm going to just make a meal with uh I'm going to make tacos." And so he goes and picks up some flour tortillas, 37 ingredients. Picks up some taco seasoning, 14 ingredients. He picks up, you know, he's picking up all the ingredients.
He's like, "This is 179 ingredients for a taco." Taco. And so, you know, we're always trying to push our patients towards whole foods. Think about where your meat comes from. You know, we've said it many times on this podcast, but it's more important what your meat was eating than what kind of meat you're eating. Yeah. You grass-fed, pasture-raised, regenerative if you if you can find it and afford it.
Um, you know, we we want to be eating organic vegetables that need to be organic. If they're, you know, part of the dirty dozen, make sure those are always organic. If they're the clean 15, you can get non-organic versions. So, that's our pillar of nutrition.
So we have sleep, nutrition, movement, probably the most important pillar when it comes to weight loss. And that's where I really tell patients. You need to be you need to have a habit of muscle centric exercise. So what do we mean by that? So muscle centric is an exercise that is going to produce an adaptive change in the muscle that leads to muscle protein synthesis.
So muscle protein synthesis the the recipe for that is you need to spend time under tension. uh that tension needs to get close to or reach failure, right? So the the last rep of the last set needs to be so difficult that you almost can't complete it or you complete it and you have no more left in the tank. And then you have to have an adequate amount of protein to fuel the muscle protein synthesis. And I think this is one of the things that's exciting is we know that as you age, there is a resistance to muscle protein synthesis that happens.
So the aging nonweightlifting patient actually needs to eat much more protein than a 21-year-old younger patient. So let's say after age 50, you need a lot more protein. However, the caveat is if that patient is doing a muscle hypertrophy program, right? Time and retention that's approaching failure. Their protein requirements go back down to what a younger persons are.
So they can actually it's easier for them to eat in a deficit because they're not having to get all this extra protein. So we we want to be focusing on the protein intake, right? And so again, goes back to the DEXA scan. The two flanking pillars we have in our clinic are going to be detox and stress management. Why is stress management important?
If you are a stressed out individual where your body feels like it's in flight or fright, um you're fighting lions and tigers and bears, oh my, all day long, your cortisol is going to be through the roof. Cortisol is the body's best way to store fat. M if cortisol is pinged, your body's like, I don't know what's going on, but we're ready for a blizzard. We're ready for a famine. We're going to pack this fat on. We're not going to let this girl lose anything, right?
We've got to get the cortisol down. So, we need stress management. We need We need people to lean into saying no. They [clears throat] need to create margins in their life, create downtime, get away from the phone, go out in nature.
All of those things are going to be helping with stress management. On the toxin side, most of our detox pillar pe people always say, "What detox should I do every year?" Like, first of all, you're detoxing every day. You're sweating, you're pooping, you're peeing. But more worry more about what toxins you're put in your body. And the toxin that we most willingly put in our body as Americans, although this is going down now, is alcohol.
And I I cannot find a benefit for alcohol, especially in the patient that's trying to lose weight. I just tell them, you got to stop drinking. Got to stop drinking. So, we want to reduce toxins from plastics.
I mean, you're drinking out of glass. I'm drinking out of ceramic. Um, we're very insistent. We tell patients, "Don't heat up plastic in the microwave." Um, fellow employees in the in the shot laser beams out of your eyes. I'm like, "What are you doing?" And they're like, especially the new ones, they're like, "Who is this freak that's attached to?" I'm like, "I promise I care about you.
This is why I'm doing this." You know, so we're we're trying to reduce our exposure to microplastics. Um, you know, there there's so many toxins in our environment. I tell patients, you should filter your water in your house, your drinking water. You probably should have a whole house filter because in the shower, even chlorine can be a toxin in high doses. So, that's our detox pillar.
So, we really do we work on those with everybody. This is critical for the person who's trying to lose weight because if the body senses that it's not being toxified, it has adequate nutrition in the form of protein and fat, that you're getting adequate sleep, right? And that you're getting an adequate signal for muscle protein synthesis, that's where the magic begins to happen, and you feel so amazing when you do all those pieces together. I try to tell my patients, I'm like, you're going to get the best result with this if you do these other things. If you just think you can take these medications or supplements, right? Or Yeah.
Because I say, "But what supplement stack should be on?" Like, "Well, tell me about your sleep. I only get about four hours of sleep." Don't even worry about supplements, brother. Like, it's there's not none of them are going to matter at this point. Right.
Right. Yeah. So, I think that's that should probably be one of the biggest takehomes for our listeners is that if we want to use these tools, you know, safely, effectively, we can't just use it alone, like you said, as a monotherapy. Right. Right.
Right. Yes. Yeah. But again, they can be very powerful for turning off that mind chatter, looking for food, the food noise. noise.
Yeah. Um, so how much protein do we want? Let's get into the nitty-gritty on that. So protein should be one pound of protein per pound of lean body mass. Or you could also say per pound of lean body mass goal.
So let's say you're a female, you're at 70 pounds of lean body mass. We really, most females, we want be north of 90. Unless you're just a very vertically challenged person, you should at least have 90 pounds of muscle on you. So, I would I would shoot for a woman having at least 30 grams of protein with every meal. Why 30 with every meal?
Well, there there's this new fact that we found out about about protein metabolism. The first 20 grams of your protein in your meal actually go to your liver for making glucose, that gluconogenesis. So, the last 10 are available available for muscle protein. Like you got to pay the bank first, right? So, you have to pay the bills before you can go out. Um, so if you're always eating your protein in 20 gram chunks, you're never getting the you're living paycheck to paycheck, right?
You're never you're never getting to put it in the savings account that actually is going to go toward muscle sentence. So, so getting over, you know, getting at least 30 grams if you're male, 45 I would say, is probably minimum. Some males need even more of that, especially if you're wanting to gain more muscle mass. So that that's the important thing.
First priority on all GLP ones is protein is non-negotiable because if you are in a protein deficit, you will lose muscle mass even if you're working out in some cases. So one pound of protein per pound of lean body mass. Um some people use one uh gram of protein per kilogram of ideal body weight. That's another equation that's commonly used. They actually come out to about the same.
Um, and then I I really would encourage if you're getting a GLP1 from your physician right now, go find somewhere where you can do a full body DEXA scan. Um, the unfortunately the the inbody the the scans that you do where you hold on to the handles and step on the scale, they're not accurate enough for being able to sense whether you're losing that muscle mass. And then really really encourage people if you're if you're not in a weightlifting program, you're you're probably going to lose weight. And with that weight, you're going to lose metabolism.
And nobody wants to lose metabolism, lose the muscle, right? Yeah. Right. Yeah. I was going to say I think you're spot on, especially from the nutritional side of things, but I think gosh that that weight resistance type exercise is a dang near close second, right?
Because it's just I mean, yeah, it's like you because you're right. I mean, you can you can arguably add some muscle on if you're just hitting the protein piece, right? But you're also if you're not exercising and doing some of these other things I've seen in the clinic where patients will gain weight, they gained muscle, but fat came with it, right? Because they were right. And probably what's happening is again if they're not doing that muscle synthesis, they have a resistance, which means they have to take in even more protein to make muscle, which means more calories.
And you know, you can't eat you can't eat protein without having some fat, right? So you're getting pretty dense calories in most cases, right? Yeah. As a challenge. I mean, I know it sounds like we're beating a drum here, but it's so important. The muscleentric exercise, that's the biggest lever we have in the clinic to move metabolic health in the right direction.
So important, right? I mean, even the active like I I remember I went into the gym one day and we one of our our um former employees was there. He's now in PT school. Matt, love the guy.
I walked in and he Guy smiles all the time. you you know Matt. Mhm. And he says, "Uh, all right. What are you doing today?" And I was like, "Man, I don't not want to be here." I mean, it was kind of like how we walked in the studio today. We're like, "This has been a long day.
I'm tired." Yeah. And he goes, "You know what? Just do 15 minutes and see how you feel." And I thought I was I can do 15 minutes. I'll do 15 minutes.
I'll go home. 15 minutes into it, I wasn't stopping. I felt great. And you know, some of that that's that hope hormone that gets released when we move our muscles. I mean, there's so many other things that happen with muscular movement. That's right.
That I think are beneficial. That's right. Okay. Well, that sounds like a really good foundation. That's certainly our approach, right?
We're really really driving home the importance of those foundational pieces. And then, okay, let's move on to that next step that let's say our patients are doing that, they still we think can be a good candidate for this medication. So, what does that look like? Do we just put them on anything? Do we put them on like the standard dosing? like talk our listeners through what that might look like. So once they've got the pillars in place, they've got a plan for muscle centric exercise at least three days a week.
Um then we're going to move to dosing the GLPS. I don't want to dose the GLP to the toxic effect. I want to dose the GLP to where the mind where we get that brain benefit where they say I just don't think about food as much, right? I would much rather have like a slower weight loss on these medications because I think a slower weight loss is more sustainable and you know hopefully we won't be losing muscle mass right so that would be the first step and I that's the thing I think this is very individualized some people are highly sensitive to GLP ones some people are highly resistant to GLP1 so some of them we have to use much higher doses and each drug kind of has a different dosing parameters so it really depends on which product we use we might be using a compound um if those are still available in some cases as they are.
There's some tricks that compounders can get around by adding things in that like extra vitamins. Yeah, extra vitamins or nutrients that can keep it in the compounding world and those tend to be less expensive than the commercial ones. Um, and some people's insuranceances are paying for it. I mean, talk to your employer. You know, you're you know, when people complain about their insurance, I tell them you you really it's the employer that decides what the plan covers.
Um, it's not really the insurance company that decides that. That's a per policy decision that's made at the at the company level. So there's a lot of people in the company that are obese. I encourage them to talk to the, you know, HR because I I will tell you if if people lose weight in a proper way and build muscle, the company will spend less money.
That's right. That it's insane how much money we are spending on managing diabetes and the the squella of diabetes, you know, all the other diseases that go along with that. So So this this can be revolutionary for really reducing the cost of health care across the board if they just weren't so expensive. Like if we could get these for the price they are in the UK anyway. anyway. Yeah.
Okay. Good. Yeah. So I think yeah the big take-home point with that is that we try to individualize it but if anything nine times out of 10 we're going to start lower often right more of like what you mentioned earlier kind of more what we call micro doing. But again there's not like a real black and white when it comes to micro doing.
We're just trying to reach what's the lowest therapeutic dose for each individual. Right. Yeah. Well, and and let's say you have someone who wants to try micro dosing for the inflammatory effect. And you might say, "Okay, well, you're at an ideal body weight." So, if you start losing weight, we know we've dialed it too high. We need to dial back a little bit.
You know, one thing I realized that we didn't really clarify when we were talking about, you know, the different medications that are available, that's probably worth mentioning is just the different forms. Like you kind of talked about how the common ones are like a once a week injection. Yeah. But that sometimes with micro doing if we're going to go with the injectable options we might do a very tiny dose maybe two or three times a week sometimes right um and there are some oral right oral capsules or tablet versions available yeah um yeah there are there are oral versions available I will say I have not had much experience with the oral ones so I I can't speak to their efficacy my tendency is to say probably injectable is going to be more effective.
Um, but again, I think this is this is what's great about the type of medicine we practice. It's highly personalized. We want to follow up with that patient. We want to understand Yeah. all the dynamics going into their weight loss journey. Yeah.
And ultimately, we want to set them on a trajectory that's going to help them be successful for the long run. Right. Yeah. I would say in my limited experience, I've seen some patients respond well when it comes to kind of the inflammatory piece. they get a reduction in just overall general inflammation with some of the sublingual compounded oral options at lower doses.
But I from a weight loss perspective, it does seem that the injectable higher doses I tend to see that a little more compared to with Yeah, I would agree with that. Yeah. Yeah. Um but yeah, options available. Of course, you know, not giving medical advice here on the podcast at all, but just kind of sharing our observations and like what we see in the clinic, right?
So, good to know that there's different, you know, options for people. Um, okay. Let's then kind of talk through once people maybe get to their goal, like they're reaching goals that they have with using this tool, really working on the pillars, the foundational components from a lifestyle perspective. So, then what becomes like that long-term plan or like maybe an off-ramp, you know, plan for people? What does that look like?
I mean what the way I would the way I do this is I would dial the dose back slowly as they're getting close to goal weight. Like let's say for a male we want them to about you know again there should we shouldn't be talking about this as a weight goal. Sure. We should be talking about this as a fat loss goal right? So we want ideally males to be 18% or lower. Um females you know 22 would be great.
Um, so let's say they get close to that or they're at that point or they're starting to dip below it and they don't I mean there is a point where you start losing fat in your cheeks and you say I don't I'm looking too oyic face, right? So we would start dialing back the dose and um I think the the the great thing about how the body is working especially if they've done the muscle centric approach is they will be be able to hopefully eat more than they've been eating in the past and not gain weight right because we've reset that metabolism back down. they can go back to what they were eating before. Like let's say they're 60 pounds overweight, but they aren't gaining weight anymore. They are in a ukaloric state.
We're going to pull them into a deficit. We're going to lose that 60 pounds. They will be able to go back to that you caloric state they're at before and sometimes a little bit higher, right? So it'll be hopefully be easier to manage their weight going forward. I think some people are going to have relapse, right?
Because again, I think some of those that they're they're eating is driven by that dopamine, right? Where they're just constantly like thinking about food. Um, and I think some of those are going to have to go back on the program. And so there there may be some, you know, let's go off of it for six months and then see how you are.
So again, I think all of that's individualist, too. Obviously, the drug companies would love if you just never went off of it. Sure. Sure. And, you know, I mean, maybe there could be some scenarios where people are doing everything they can.
They're really trying to hammer again those like lifestyle components, but ultimately, you know, I think again it's weighing risk versus benefits. like could they be on a low dose? Yeah. So, I think that's where you're going to see people dialing back to back. Yeah. Low doses or even micro doses for management.
And probably those are going to be the ones that are really managing the the brain chatter, you know, that that food noise, right? The food noise. It's a tough one. It's a tough one, right? Um Okay. Wow.
We've talked about a lot. Yeah. Uh what other thoughts do you have? What else maybe haven't we mentioned?
Or is there anything you want to share that you see clinically? Like any clinical like success stories that you've had with it? I mean, honestly, I've had I've had a lot of success stories. I mean, I really I know I know we're hard on the drug industry. I will say this, this is one of those medications is pretty slick.
Mhm. Um the thing that I just keep harping on is I'm so worried about the people that I I can see that they're losing muscle mass and I'm like this is not going to end well for them. I think there's a lot of people that are going to find that that's they're going to be very frustrated with the fact that they are weaker. Their bone density is going to start going down.
I think we're going to see, you know, manifestations of that later in life. We're going to see a lot more osteoporotic type increased fall risk. Increased fall risk, which means increased fracture risk. And I mean the stats on a hip fracture later in life after age pretty alarming. 50% mortality in the first year after a hip fracture. That's incredibly high.
Flip a coin. So I think yeah when we can sometimes teach patients like okay we keep harping on the importance of muscle muscle muscle muscle. But it's like no if you could see some of the potentials that do happen to people. Right. Well and think about our functional movement score that we do right.
So, we're we're doing what an assessment of 13 different movements where we're assessing like what's, you know, hip flexibility and range of motion. I mean, if you're losing muscle mass and you're not able to exercise, that functional movement score is going to go down over time. So, don't rob Peter to pay Paul, right? Don't don't lose weight and not recognize where the weight is being lost. I think that's the biggest takeaway. Whether you're a patient at our clinic, you know, um if you're listening to this and you know somebody who's struggling with this, please send them this podcast.
I I don't want to vilify the approach that they're taking, but I want to give them the tools so that they clearly understand the path that they should be on to have the success that's going to last. And that that is going to be the one that focuses on not losing muscle. Yeah, that's great. I think that's an important thing to encourage listeners and encourage especially listeners that maybe happen to be our patients like come in have these good honest conversations with us like we are not going to you know like poo poo this or or make people feel ashamed that hey I'm really struggling like we struggle with the food noise like right those types of things I think are very real and I think a lot of people experience them and you know sometimes there's you know people or messages out there that are just saying like it's, you know, it's a willpower issue.
Like you should be able to just like, you know, be strict and like do it. And and I'll admit, I mean, when I I I would never I would never say that to a patient because I don't believe obviously in that type of approach, but I will admit when I first started learning about these medications and you know, our brains, we always love to really understand like why is this working? How is this working? What's the why behind it? you know that my brain initially was kind of like, well, why can't people just not overeat? Yeah.
You know, and it's just willpower. It's simple, right? It's just a willpower thing. If only it were so simple.
Oh gosh. Yeah. For sure. For sure. I'm curious, what are your thoughts about them expanding the use to pediatric patients that are obese?
That's a tough one, you know. I mean, because, you know, they're definitely not looking at muscle mass in younger patients. No. So I think like my initial thought from just the general perspective out there where again I really do truly believe that doctors out there like want to help their patients. They care about their patients.
They want to do good right but because of you know certain types of like you know constraints because of insurance or certain you know metrics that have to be met. You can only see a patient for like seven minutes right and you got to keep going. I just don't think there's that opportunity to then really talk about what we just talked through the importance of those foundational pieces and the pillars. But I do because that equally would apply to a pediatric patient. 100%. 100%. It's like man if we started teaching parents and then children that early and like creating that type of environment potentially you're not going to need those medications I think. Right.
But I do think it I I'm not going to say I'm totally against it because I think if again just like how we said with adults, if we can give them the support, give them the education to work on these foundational pieces, but if we still really just need that extra help, I mean, you could change the life of that kid. Oh yeah. From thereability obesity when they're young. Yeah.
So I'm not I mean I'm not going to say I'm like no, we should never use it in kids. But I think boy tread carefully there. Yeah, just tread carefully. [snorts] Um and if anything just we we need to we just need to obviously prioritize and focus on those pillars. Yeah, for sure. For sure.
But yeah, good question though. Woo. It's a tough one. We're going to start seeing more of that.
We're going to start seeing it. And I think I think you're just going to see providers, they're that's just what they're recommending and they're not doing the other things. Yeah. So I think that's where the key is, right? In fact, I would go so far as to say so far my all my patients who are are on those GLP ones and aren't doing exercise, they are losing both muscle and fat almost universally.
Mhm. And I would say on the positive side, universally, every single one of my patients that's in a muscle centric hypertrophy lifting program is losing fat and maintaining and in some cases gaining muscle muscle. And so it it is again it's powerful tool. I know we're harping on it, but I think that's think that's the takehome, right? If you don't hear anything from this at all, don't lose muscle.
Right. Yeah. Exactly. Exactly. Okay. Anything else you can think of before we start to wrap up here?
I think we wrapped it. Good chat. Yeah, good chat per usual. We got through it.
Thank you. Thank you, Dr. Davis. Thank you to our listeners. And uh don't forget to check out our previous episodes like you mentioned a couple times.
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