Can We Prevent Muscle Loss While Taking GLP-1 Weight-Loss Drugs? With Dr. Richard Pratley

Can We Prevent Muscle Loss While Taking GLP-1 Weight-Loss Drugs?

GLP-1 medications like Zepbound have changed the way we treat obesity. But as more people lose significant amounts of weight, another question has emerged:

What happens to your muscle?

It's normal to lose some lean mass—including muscle—during weight loss. But researchers are now asking whether preserving more muscle could improve long-term health, particularly as we age.

In this episode, Dr. Eeks speaks with Dr. Richard Pratley, lead author of a new randomized, double-blind, placebo-controlled clinical trial investigating whether an investigational antibody called apitegromab can help preserve lean mass in people taking tirzepatide (Zepbound).

Together they discuss:

• Why people lose lean mass during weight loss

• What "lean mass" actually means—and why it matters

• Why muscle preservation has become one of the biggest new questions in obesity medicine

• How apitegromab works by blocking myostatin—a protein that acts like a brake on muscle growth

• The results of the study and how much lean mass participants preserved

• Why preserving lean mass doesn't automatically mean preserving strength

• Whether concerns about muscle loss on GLP-1 medications have become exaggerated

• The importance of resistance training and adequate protein during weight loss

• Whether future obesity treatment will focus less on body weight and more on body composition

• The bigger question: Are we entering an era where one medication leads to another—or is there a better path???

This conversation explores one of the most interesting—and practical—questions in obesity research today: Can we lose fat without sacrificing too much muscle?

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Transcript

SPEAKER_00 0:00

Welcome to the Causes or Cures Podcast, your gateway to understanding health and groundbreaking medical research in a fun and easy to understand way. With Dr. Eeks as your host, join us as we sit down with the world's leading doctors and scientists to unravel the mysteries of health. From practical tips on well-being to the latest breakthroughs in medical research, we cover it all. Don't forget to subscribe. Now let's ignite our curiosity and together dive into today's episode.

SPEAKER_02 0:31

Hello everybody, and welcome to Causes or Cures. I'm Dr. Eeks, your host, and thanks for joining in. So, GLP1s, right? They're always in the news. There's a lot of people taking them, and they're helping lots of people lose weight. But as millions of people lose weight on GLP1 medications, one question keeps coming up. What happens to the muscle? To the muscle. So losing some lean mass is expected, but many people are worrying that they're losing too much. So researchers are now testing new ways to preserve muscle while people lose fat. Which naturally leads to another question. Are we solving one problem or creating a future where every medication comes with another medication? Should we worry about that at all? Today I'm joined with Dr. Richard Prattley. He's lead author of a new clinical trial exploring one possible answer to the muscle loss question. So we'll talk about what lean mass actually is and pay attention to that, why it matters, what his team found, and whether the future of obesity treatment is shifting from simply losing weight to improving body composition. All right. So give me a few seconds here, gang, while we connect to Dr. Prattley. All right, everybody, we are connecting with Dr. Rich Prattly, and we're going to talk about a very popular topic: GLP1s and lean muscle mass loss and all of that. But first, Dr. Pratley, can you tell our listeners a little bit about yourself and what you do?

SPEAKER_01 2:24

Sure. So I direct the Advent Health Translational Research Institute Diabetes Program. I've been a clinical researcher in diabetes for almost 40 years now. And my career has spanned everything from working for the NIH to going to a pharma company and then working at both universities and in the private sector as I'm doing now. But it's always been a focus on diabetes and obesity. Of course, I see patients with diabetes and obesity in my clinic as well. So I'm tuned in to sort of the day-to-day struggles that many patients experience with diabetes and obesity.

SPEAKER_02 3:06

All right. So you're a researcher and see patients and to the best of both worlds, I guess. Oh, good. Well, we need that. Um, so everyone is talking about losing weight on GLP1 drugs. Um, it's always in the news. So, what made you start worrying or thinking about what people like losing lean mass as part of this?

SPEAKER_01 3:33

So that's a really important question because it is so popular both in the uh popular press, but also it's a topic of discussion within the scientific literature at the moment. What we know uh going way back years, uh years ago, is that when people lose weight, they're not just losing fat mass, which is what we want them to lose, but there's also a little bit of loss of lean body mass as well. Now that's measured in different ways. Some of that lean body mass, of course, is muscle mass, but some of it is other things like tissue fluid, organ mass, and so on. And we've kind of accepted that across the different weight loss interventions, this constitutes maybe 25% or so of the total uh weight loss. And this is consistent regardless of the type of weight loss with uh diet, exercise, or even bariatric surgery. So this is something that our field in obesity has uh accepted for years. Now, with more and more people uh using the GLP1 receptor agonist, there's been concern that these might result in more loss of lean body mass.

SPEAKER_02 4:48

All right. That was um so lean mass, and and you started to say this or you kind of um uh alluded to it, it's not just muscle. Because I think people hear lean mass are like, oh, muscle, but it's more than that.

SPEAKER_01 5:01

I think that's a very important point. Um, a portion of lean body mass is muscle mass, so it ranges 45-50 percent or so. Uh, but another portion is everything that's not measured as fat mass. So this is important from a methodologic perspective. Lean body mass is typically measured with DEXA. DEXA is very good at measuring fat mass, it's very good at measuring bone mineral density and bone mass. Everything else is lean body mass. So that includes both muscle mass as well as tissue fluid circulating plasma volume. When you lose weight, you invariably lose some of that tissue fluid and a decrease in plasma volume due to not needing as much. So there's uh inevitably a little loss of lean mass, but that's not the same as a loss of muscle mass. If we really want to dive into whether or not muscle mass is decreasing, we actually have to do different techniques than DEXA. And the technique that's probably uh the gold standard now is using MRI to measure uh volumes of muscle. And you can measure the muscle volumes throughout the body, but typically this is done uh in the uh thigh muscle.

SPEAKER_02 6:18

That's a good clarification for people to understand. So when somebody says, or you know, hey, I lost 50 pounds, and you know, there's cheering, like, all right, good job, you know, that's great. If I mean if you were struggling with your weight, but if you lose that lean mass, why is the story more complicated, or why should we be concerned about that?

SPEAKER_01 6:41

Well, people are concerned about the lean body mass loss for probably three main reasons. The first is that muscle mass is an important driver of your metabolic rate. And so this loss of muscle mass with the weight loss is associated with a lower metabolic rate. And that can predispose you to weight regain. So that's one concern. It's that adaptation to weight loss. The second concern is that muscle is also a metabolically active site, it's the largest sink for insulin-mediated glucose disposal. So there's concern that that might be adversely affected. And the third uh reason is function. People are concerned if you lose muscle mass, you might decrease function. So let me go through the reality of all of those three possibilities. In the first case, where people are concerned about the decrease in metabolic rate, this is a reality. It does happen that metabolic rate goes down, uh, and that's part of the adaptation to a lower body weight. Um, the second concern about whether or not it might be metabolically disadvantaged advantageous is not so much an issue because as you lose weight, you improve your insulin sensitivity. It doesn't get worse, and that's because the quality of the muscle is actually improving. There's less fat in the muscle, it's less insulin resistant. Now, the third concern is about function. I think that's where a lot of people are concerned. Concerned if you lose muscle mass, you're not going to be able to get up out of a chair. We've done studies on literally tens of thousands of patients with GLP1 receptor agonists and other weight loss uh approaches. And by and large, there's not a decrease in function. If anything, people are able to do more. That's because they are losing so much uh body weight, particularly with some of the new uh GLP1 receptor agonists. So I don't think function for most people is a significant concern. Now there's one important warning in there, and that is that the patients in our clinical trials are not the same as patients in our practice. So I've done a study with a good colleague of mine from the University of Chicago, Dr. Albert Wang, and this is not published yet. But what we did was to compare patients in four cardiovascular outcome trials, and NHANES, the National Health and Nutrition Examination Survey, and the Kaiser Permanente database. They were matched for age, so we were looking at older individuals above the age of 65. And what we found is that the people in real life, in the real world, were much older. They had many more diseases, much more frailty, uh, more cancer, more cognitive dysfunction. So the main takeaway message is the patients in clinic are not the same as the patients in clinical trials. And we can't necessarily assume that just because there are no impairments in function in the clinical trials, that this is not a problem in clinic. Indeed, there are some older individuals who may suffer decreases in function. So we I think we have to be very careful uh as we're prescribing these drugs in older, perhaps more at-risk individuals, as an example.

SPEAKER_02 10:10

All right, so let's get into the um research that you did that I emailed you and you kindly accepted the invite to come on the podcast. So I'm just gonna give our listeners a background and then uh go to you. But so you decided you and your team decided to test a potential way to reduce muscle loss or lean mass loss for folks while they take GLP ones, particularly trzepatide, or the medication sold as Zepbound. Some people might recognize it as that. And for our listeners, you did a randomized double-blind placebo-controlled trial involving a little over a hundred people, mostly women with obesity or who were overweight, where one group of people took the trzepatide, the GLP one plus the placebo, and the other group took trzepatide plus a pipromad. Am I saying that right?

SPEAKER_00 10:57

Epidomogram.

SPEAKER_02 10:58

Oh, no, see, I wasn't. A pitogromad over a 24-week period. Okay, so before we get into what you found, can you as simply as possible explain to our listeners what a pitogromad is and why is it called that? Like, I wish it was an easier name.

SPEAKER_01 11:17

Uh this is something that we struggle with with all of the new medications. Uh they come up with these generic names that do not roll off the tongue. Um and um the only thing I could tell you is the mab at the end of the name signifies a monoclonal antibody. Uh so this drug is a monoclonal antibody that targets latent myostatin. Myostatin is a molecule that's produced by muscle that um actually feeds back onto the muscle and prevents uh further growth of the muscle. And so it's a break on muscle development. We know from genetic studies in animals, for example, that if you have a mutation in uh myostatin or in the receptor, these animals develop massive muscles. They're not necessarily uh super animals, though, because there's some downsides associated with uh that uh unrestrained muscle growth. Um, so that was the genesis for selecting this target. The idea is that if we neutralize this myostatin molecule, we might be able to improve muscle mass. And this has actually been tested in patients with rare muscular disorders like spinal muscular atrophy. In those patients, this does improve muscle mass and it also improves function. So in this study, we were testing specifically whether or not epitomag would decrease the loss of lean body mass in patients who were already losing mass through the actions of terzepatide.

SPEAKER_02 13:02

And how did the patients take it?

SPEAKER_01 13:05

So this medication was an intravenous infusion. This wouldn't be useful for the clinic. This was more of a proof-of-concept study. Now, and I the infusion is fine for people with these uh rare genetic diseases, but not for patients who uh might have to take this uh in combination with a weight loss medication. So it was really more of a proof-of-concept study that we did here.

SPEAKER_02 13:33

Okay, so a pitygromab, a pedogromab, I can't say that word very easily for some reason, but it just to recap, it blocks the myostatin, and the myostatin is like a break on muscle growth. Okay, I like that. I can picture a break, and I think people can get that image in their head. All right, so as you mentioned, you use dexascans, essentially a way to measure body composition to um figure out uh estimate changes in fat and lean tissue lost during the study. So, did the group taking the GLP1 plus the antibody, Pitogromab, maintain more muscle than the GLP1 plus placebo?

SPEAKER_01 14:14

We can't tell because we only measured lean body mass. Uh, we assume that that's muscle mass based upon the mechanism of action of this drug. What we saw in the study was, first of all, that there was uh a similar amount of weight loss in the group on placebo and the group on epitomagreb plus trzepatide. And that amounted to about uh 12% or so at 26 weeks. Uh so if we continued the study, we would have seen greater weight loss because that's what's seen in the trzepatite or uh zep bound trials. Um what we saw though at 26 weeks uh was that the lean body mass loss was about half of what it was with uh the trzepatiter, uh Zepp bound plus placebo-treated patients. And I think that's an important finding, particularly going back to my comment that the lean body mass is not just muscle mass. This drug works on the muscle. So I think what we're seeing here is a preservation of muscle mass and then the loss of some of that lean body mass that represents the tissue fluid uh associated with the excess adiposity. Uh we don't know that for sure because we didn't do MRs in this study, uh MRI in this study. This was uh just an initial proof-of-concept study. But for future studies, that's definitely uh the way that we should go to uh analyze both the amount and the quality of muscle mass.

SPEAKER_02 15:49

And just for our listeners, I put it in pounds because we're in the US. So I saw the kilograms, I'm like, gotta change that to pounds. Um so the terzepatide plus placebo, the people lost 7.7 pounds of lean mass. People taking terzepitide plus the antibody lost about 3.5 pounds of lean mass. So that's like 4.2 additional pounds of lean mass, the difference at 24 weeks. Okay.

SPEAKER_01 16:15

Yeah. So the other thing that we found was there actually was a little bit of improvement in function in the patients that received the epidemic grab. Their uh ability to get out of a chair. This is uh one of the functional measures that's included, uh, improves slightly. This group didn't start with any particular dysfunction. They were pretty functional uh for starters. But I think that's uh a sign that uh we're not doing harm. We're actually having potential effects that might be beneficial in the right patient population.

SPEAKER_02 16:49

Okay. And your population, if I remember correctly, they weren't older. They were relatively young, right?

SPEAKER_01 16:55

They were relatively young in their 40s, mainly women, uncomplicated uh uh overweight and obesity by and large. Um but the idea then, again, is uh do a proof of concept study, see if we can measure changes in lean mass, uh, and then in future studies, target the patient population uh with potentially sarcopenia or older individuals where the loss of muscle mass might have more consequence.

SPEAKER_02 17:23

Okay, that was actually my next question. Um, was like, what would you say to somebody who would look at the results and be like, okay, but show me improvement in strength, falls, mobility, right? Because you you want to see improvement in function, right?

SPEAKER_01 17:37

Yeah. Yeah. So um what I will say is that patient population, the more impaired patient population, is actually kind of difficult to study because they tend not to be enrolled in clinical trials. And for a proof of concept, uh, it's difficult to uh target that patient population. But that definitely is where you would want to go with future studies because that would be the group that would benefit most from this sort of intervention. Not everybody's gonna need uh this uh muscle-sparing uh piece of the treatment. But uh an older patient population that might already start out with some frailty uh and decrease muscle mass would be perfect. We know that muscle mass declines with uh aging. So there are probably ways to select a patient population that would really uh benefit. Um and I I'm very excited about the possibility of studying this class of medications in those target populations in the future.

SPEAKER_02 18:37

All right. So uh you prescribe, I assume, these medications in your current role. Not the experimental antibody, but yeah. I do. Yes. So what advice do you give to patients, particularly people who are like worried about losing lean muscle?

SPEAKER_01 18:56

Yeah, so there are two pieces of advice. First of all, these medications are particularly powerful uh with uh marked effects on appetite. And many people just cut their intake down a lot. And what I have to advise people is that they need to maintain good nutrition during the weight loss phase, and particularly they need to have protein in their diet. Um, protein is very important, uh, and you don't want that weight loss to be coming from your protein stores. So the second piece of advice is that exercise helps. And there actually are studies of weight loss combined with exercise that shows preservation of muscle mass. So I think that's particularly important, and that has a number of other beneficial effects uh as well. I think that helps to um improve the metabolic effects of the weight loss. Uh, I also think that uh it helps to improve function uh over the long term. So it's not just about preserving muscle mass, as we said earlier. It's really about uh function. And exercise, particularly uh exercise that includes both aerobic and resistive exercise, is really an important uh modality that people should be engaging in. The other part of exercise is I think that's an extremely important uh addition to your lifestyle to help maintain the weight loss over the long term.

SPEAKER_02 20:27

I mean, do you see people though stop taking these medications? And then obviously, I mean the studies show the weight does come on pretty fast. And would you say that a high percentage of people who you start on the medication stop taking them?

SPEAKER_01 20:41

Yeah, so that's the unfortunate part of these medications. Um, it turns out that around 50% or so uh in real-world data uh stop taking medications within about a year or so. And that's probably for different reasons. Uh, it has to do with excess in some cases, so um, they may not get insurance coverage or may not be able to continue paying out of pocket for these medications. Uh, the second might have to do with um side effects. So these medications do have side effects. Some people just don't like uh having those prolonged effects on uh appetite because eating and the pleasure of eating and the social aspects of eating is very important to them. And so they'll stop taking the medications to return to sort of a more normal lifestyle. Now, what we know from clinical trials is that when people stop the medications, they regain the weight pretty quickly. Um, not necessarily all of the weight, not necessarily all people, but it certainly does come back. And that makes perfect sense. These are powerful medications, they have a biological effect. If we think about other disease states like high blood pressure, high cholesterol, we don't expect that if we get people down to go and then stop the medication, they're gonna. Stay the goal. We keep treating them. And that's what we should, in general, be doing with these obesity medications. But it's hard. This is an area where there isn't such good insurance coverage and people are paying out of pocket. So all these reasons do contribute to the lack of people staying on the medications. And then it does result in some weight gain in many people.

SPEAKER_02 22:28

What do you think when you see the headlines? You always see like Ozempic something, right? The other day I saw Ozempic feet. And I was like, what the heck is Ozempic feet? And of course I'm not sure.

SPEAKER_01 22:42

So I'm not completely dismissive. People are reporting things that they're experiencing on these medications. They may or may not be directly related to the medications. But I think it's important to pay attention to the things that people report, even if you don't think it's directly related. And I'll give you an example. I had a patient in one of my clinics that was treating for obesity. She was a middle-aged woman, probably in her mid-50s, and I put her on one of these weight loss medications. And she came back for a follow-up visit in about six weeks and had lost 20 pounds. She was delighted. She was excited. She was bubbling over. Not because of the weight loss, but because of her stressed urinary incontinence, which she'd had since her last child, was gone. She was able to get out of the house more. She didn't have to wear pads. She was able to engage in physical activities and sports and things that she'd always done in the past. So this was a real change in her lifestyle and her quality of life. And I thought to myself, that's kind of random. But then I thought, maybe not. Maybe there really is something behind this because if you lose abdominal fat, you might change the abdominal pressures. That might be just enough to change bladder function. And this lady, maybe it did. So I think the the message is that we have to pay attention to what people report because sometimes there are effects that may be beneficial that we don't anticipate. I wouldn't have anticipated that. Now there's a study that's ongoing that's actually testing this.

SPEAKER_02 24:19

Oh, interesting. Yeah. No, I think that's good. Yeah, listen to people, don't be dismissive, take everything into account. It's a good way to be in general.

SPEAKER_01 24:27

You know, some things are kind of predictable, like Ozempic face. Yeah, if you lose weight, some of it's going to come off of your face, and maybe you're going to see more wrinkles. Um, so you pay your money and you take your choices. Wrinkles, less fats, more fat, less wrinkles.

SPEAKER_02 24:47

Wrinkles, wisdom lines. I don't know. Yeah. But that is an issue for people. They'll be like, oh, the face aged so much.

SPEAKER_01 24:55

Yeah. What I try to do though, uh in clinic is redirect the conversation from appearance to health. Because really what we're trying to do with weight loss is to improve people's health and their health span and to a certain extent their lifespan. We know that these medications can help reduce risk for heart disease and kidney disease, things that impact on their life, and they decrease mortality. Um, so those are important outcomes. Uh and um, yeah, people like to look good, but it's not just about that.

SPEAKER_02 25:28

That's such an important point. And I think anybody who's on social media runs runs into that. Anti-aging has been reduced to what your face looks like. Like what are the wrinkles on your face? What are the lines? But to your point, that tells you very little about what's going on inside someone, like how well they really are aging and functioning, essentially. So good is going to change that coverage.

SPEAKER_01 25:50

It doesn't matter what you put on your face, that's not gonna make you live longer. What matters is what's happening to your metabolism, to your heart, to your kidneys, and to your brain.

SPEAKER_02 26:00

Yeah, yeah. Amen to that. But that is a hard I I guess because everybody, you're bombarded with all these like, oh, look 10 years younger. And it's just such a myopic, wrong focus of what a it means to like age well, really. It's it's kind of silly, but we're superficial creatures, I guess. I don't know.

SPEAKER_01 26:19

Well, I I think that's that's a a function a little bit of our society. Um, but to your point, um, it's you know, when people uh are on these medications, I think we talk about health, and health is important, especially to us as providers, but we should also talk a little bit about function, which is where we started this whole conversation. And if you can get out uh because you weigh less and do more, uh, that's an important outcome. And I think people tend to lose sight of that uh fact a little bit, that uh their lives actually can be better with the weight loss. They'll be able to do things without feeling short of breath and you know, and without having pain when they exercise. There's some really interesting studies that are going on uh that show that uh these medications decrease osteoarthritis pain substantially.

SPEAKER_02 27:13

Yeah. Okay. Yeah. No, that that's a good point. I mean, function, getting out more, probably having more confidence. I mean, you know, people feel better. Yeah, absolutely. So do you think we are entering a future where weight loss drugs routinely get paired with muscle preserving drugs, or do you think it's gonna be more of precision medicine, which is, I know, kind of a tagline today, but like we're gonna you're gonna figure out who's gonna benefit the most from them?

SPEAKER_01 27:39

Yeah, I think uh initially it's going to be uh more precision medicine focused on people who have impairments and who nevertheless need the benefits of GLP1s, for example, uh, because they have heart disease or kidney disease. But we don't want to have uh muscle loss that impairs function. Uh, that's the obvious target. One thing I am worried about, though, is there are so many people who are using these medications at an early age. Now, these medications are approved for weight loss in adolescence. So, what are the long-term consequences of that weight loss and potential effects on uh muscle mass over time? So I'm not entirely convinced that uh it's just the older patient population that stands the benefit. So I will probably be sitting on a beach uh and retired before we get the answers to those questions, which is fine with me. But I think people need to think about the future uh in a world where these drugs become more accessible, in part because there's a medical need in the younger patient population. If you have obesity and diabetes as a young person, your outcomes, your consequences are much more severe than if you get it as an older individual. So we need to treat those people. We need to treat them with good medications, but we also have to think about the long-term consequences.

SPEAKER_02 29:07

Right. Both the good and the potentially not so good. I was talking to someone about childhood obesity rates the other day because uh there was like a Gallup poll that showed, you know, the adult obesity rates, there was a bend like for the first time. Obviously, that's self-report. The CDC does measurements, but it's still a trend that's interesting. And you didn't see it with child obesity. You just mentioned that these drugs were being used in adolescence. I think is it 12 years old that they're okay, but not as much or as much as not very much.

SPEAKER_01 29:38

Uh relative to the number of kids who could be eligible. And I think that's that's probably for a couple of reasons. Uh first of all, there are fewer people that are um competent, skilled uh in prescribing for kids. Second, I think that just like you know, we thought in adults, we thought that, you know, this is uh a lifestyle problem and uh you know it really should be solved with lifestyle changes. Problem with kids is you know they live in an environment where they don't necessarily control the food that they eat or their activity, it's all controlled by their parents. And we know that obesity is familial for both genetic causes as well as social and demographic uh causes. So, you know, we really have to treat the family unit if we're trying to target obesity in kids. And there are just not a lot of ways in clinical practice to be able to effectively do that. There are not a lot of models. So it's uh I think a challenge. And that's probably part of the reason that there's not a huge amount of use of these drugs in kids. But there are kids that are already suffering uh problems like diabetes and worse cardiometabolic profile because of their obesity. Um and those high-risk kids uh are probably pretty good candidates for these medications.

SPEAKER_02 31:02

Right, right. I mean, and kid obesity starts younger than 12 today. Like it so in that group, I don't know. I mean, obviously prevention, everybody's trying to figure out prevention.

unknown 31:15

Yeah.

SPEAKER_02 31:15

But the treatment in that group is, I guess, not as evolved.

SPEAKER_01 31:21

It's not. Um in part because it's uh difficult. There are few people who are working in this area, and uh we just haven't figured out the most effective approaches. But I completely agree uh that this is all about prevention. And to me, it really starts uh with the pregnancy. You know, if you have a mom and a family that's already overweight or potentially has type 2 diabetes, their children are going to be more likely to have uh obesity and diabetes. So we really need to start uh from delivery or even before delivery. We need to have healthy pregnancies uh so that uh we can minimize the risk to kids. So it's really a lifespan intervention that we're talking about. But if you think about our healthcare system, we're not set up to do lifespan interventions. We're not set up to do prevention, we're set up to treat the very serious end organ complications. We do that very well.

SPEAKER_02 32:22

Yeah.

SPEAKER_01 32:22

It's just way too late. We need a different approach.

SPEAKER_02 32:25

I mean, suppose that's what people in public health are supposed to do, focus on the prevention side of things.

SPEAKER_01 32:30

Um Yeah, you better get going. You better get off this public this uh Zoom meeting and uh get on to your public health.

SPEAKER_02 32:37

Save the world. But no, but it's true that there's all this pressure on doctors, like doctors don't provide nutrition. And I'm like, well, my God, like consider it considering managed health care and the pressure on doctors, and to your point, the severity of things that they have to figure out. I'm like, I don't know if they have time to do prevention in the way it needs to be done.

SPEAKER_01 32:58

Yeah. I think it's difficult. I think there are some examples uh where public health has made an impact. One is smoking. We've decreased uh rates of smoking, and that has had uh an impact on cancer and mortality, but that was a huge effort, uh, and it was a public-private partnership, and we need to have at least as intense an effort around uh diet and obesity and exercise. Uh, the problem is people can't stop eating. They can stop smoking, but you can't stop eating.

SPEAKER_02 33:31

Yeah, yeah.

SPEAKER_01 33:32

Um, so it needs to be a slightly different uh approach.

SPEAKER_02 33:36

Yeah. No, that's a good point. You need food to survive, you don't need cigarettes to survive at all. So some listeners might be thinking now, well, wait, I need a drug for weight loss, and now I might need another drug to help preserve muscle. So, how do you respond to concerns that we're solving one problem with more and more medications?

SPEAKER_01 34:01

Oh boy, that's been one of the concerns uh since time immemorial um with uh medications. Um and it is true uh to a certain extent. As a prescriber, as a physician, um, I'm not excited about prescribing excess medications for very selfish reasons. That's just something else for me to manage, to be honest with you. And we only do it when you know there's really clear benefits, uh, when there's guidelines, and there's strong evidence. I think we still uh have to develop that evidence uh for these antimyostatin drugs, that they're not just improving muscle mass, but they're really improving outcomes, health outcomes or functional outcomes, things that matter uh to patients. And I think when we do that, then that balance uh between benefit and risk becomes a little bit more obvious. But right now we're just in the exploratory stage. That's how medicine starts.

SPEAKER_02 35:00

Yeah, no, I agree. And it was funny because I um I make these videos online, these kind of quirky videos, because I told you I always wanted to be stand-up comedy. But like one thing I looked up was, you know, when the CDC first called obesity an epidemic, and it was like in the late 1990s, and then you saw it go up and up and up and up and up, and it looks like a total public health failure despite the efforts, right? Like, hey, just own it, right? Like it everyone got bigger. Um Do you think that these drugs are what it's gonna, that's the what's gonna be that gets us over, like ahead of the obesity epidemic, or yeah.

SPEAKER_01 35:36

So what look what it looks like for the future is that um they're just a plethora of drugs being developed, treats obesity uh and its complications. And all sorts of different combinations of medications are being explored. Uh, some of them are very, very effective. Um now our top weight loss drug approaches 30% weight loss on average, which is huge. But uh I think in the future people are going to be targeting the different needs and complications, and one of these ways to target it is by through this particular biologic pathway. So I think that the whole field of uh obesity treatment from a medical perspective is evolving very rapidly. And you know, I'm not sure where it's going to uh completely land, but what I do anticipate is that we're gonna be able to be much more precise about the people that we treat, uh, the medications we treat them, because we'll have more options. It's not one size fits all kind of uh approach. And we'll be able to target people at particular risk for different uh complications. We already try to do that in diabetes. So I think it's that treatment is gonna get better and better. I also think that uh with more and more companies developing products that get licensed, that we'll see more competition in the space so that hopefully that will help drive prices down and help with the economic burden of obesity treatment.

SPEAKER_03 37:14

Right.

SPEAKER_01 37:14

I mean, obesity by itself has an economic burden. Uh days lost at work, uh the health consequences. And um, you know, there's a cost for treatment, but somewhere that cost and of treatment and cost of ignoring the problem balance out.

SPEAKER_02 37:31

Right, right. Now, where's your enthusiasm at in terms of prevention, you know, of obesity? Are you excited about some of these changes we see at the national level regarding food policy? Uh I mean, what do you think needs to happen at the prevention, like primary prevention level, I guess?

SPEAKER_01 37:53

Yeah, I know that policy changes are gonna move the mark, uh, to be honest with you. And part of that is because we are swimming upstream against a very large uh food industry that, you know, makes money, uh, as all industries should, by providing something that people want at a price they can afford. But the problem is what they're providing, uh, although tasty, quick, easy, and economical, isn't necessarily focused on health. I think what we need to do is to change that balance uh so that people are able to choose healthier foods that are easy, quick, and cheap. I think that's ultimately uh in this environment, we're not going to be able to solve this with laws, we're not gonna be able to solve this with positions. We have to empower people. That's where the change is gonna come from. If we can uh help people make better decisions that are consistent with their lifestyle and their economic status that over the long run will uh promote better health, then we'll have the greatest impact. But that's not easy.

SPEAKER_02 39:18

No, it's definitely not easy. And you made me think of there was a recent New York Times article where they talked about shame in in public health and how and and I sometimes struggle with this in public health too. Like you have to empower, you want to empower people, and in some ways, I guess that's personal responsibility. I use those words that a lot of people in public health don't like, but then you also don't want to use shame, like you don't want to shame someone for their circumstances. So where do you find that balance? Do you know what I mean?

SPEAKER_01 39:48

Yeah, I think it's uh providing options uh for people, uh empowering them to make change rather than you know, shaming them for the changes that they make because of the environment they live in and their economic circumstances. If people have choices, uh I think and I hope that they'll make choices that uh empower them for the long run. But right now, they don't have so many choices. You know, there are food deserts, there's just um this disparity between uh prepared foods that are easy, quick, uh, and you know, the things that are healthier. So I think the we have to shift the conversation from shame to empowerment. Uh choose healthy, uh, choose, you know, I don't know. I'm not a public health.

SPEAKER_02 40:37

Choose this one. Yeah.

SPEAKER_01 40:39

You know, yeah, you know, it but it's not just about a food choice uh or an activity choice, it's about uh a lifestyle and a lifespan choice. Like, how do you want to be? Choose your lifestyle, your lifespan for your children. You know, we did a little bit of this around COVID, for example. Uh, and I remember all the billboards uh that uh featured not just the um person that were being target, but their whole family, because you know, the notion was that vaccination would protect the the family. And uh I think things that appeal to people's sense of belonging, their family, uh their generations, um, perhaps are more motivating than you know, your 10-year cardiovascular risk is 10.1%.

unknown 41:30

Yeah.

SPEAKER_01 41:31

Like what the hell does that mean to somebody? They don't know that. What they want to know is, you know, am I gonna make it to my daughter's wedding? Or am I gonna see my grandchildren graduate from high school? Those are important things to people. It's that family connection. We also know that family connection and social connections are extremely important for general health as well as for you know cognitive health over the long term.

SPEAKER_02 41:53

Yeah, yeah, that's so true. Of course, COVID campaign completely bombed, but that's another story for another podcast. Um, what is next for a pedagogram app? Did I say it right? It's been a lot. Okay, early on dimensions.

SPEAKER_01 42:11

It's it's been good. No. Um I think it stops here, actually, for epidemic. Uh, there are other products in the pipeline for uh uh development, newer molecules that can be administered subcutaneously, like uh terzepitide. Uh and people are exploring other pathways as well. Uh again, uh we did this as a proof of concept study, and I think we uh showed that it can work. And now the next step is to how to make it tractable for this indication as opposed to a rare um muscle disease.

SPEAKER_02 42:47

Oh, okay. So you're doing more research in this in the larger area. Okay.

SPEAKER_01 42:51

Not just me. There's a large number of companies and people that are involved in this research. Uh so it's uh it's really gaining some steam. And uh we'll just have to see where it shakes out.

SPEAKER_02 43:03

Well, there's also the public kind of demand for it, like or the fear of losing muscle when they take these drugs. You hear that everywhere you go. So and that tell if and someone else will tell that to someone else, be like, Don't take that drug because you're gonna lose muscle. So that happens too. And then they go to your office and you have to explain things.

SPEAKER_01 43:21

I yeah, and one of the things that uh I use in my clinic to explain people with this kind of concern is if I took you, person without you know, weight problems, and I put a 50-pound vest on you and made you wear that for 24-7 for a year, you would gain muscle mass because your body can adapt. If I took that vest off you after a year, you'd lose muscle mass. But you'd probably feel a whole lot better without having to carry around that 50 pounds, and you'd probably be able to do more. So it's all relative.

SPEAKER_02 43:58

Yeah, it is all relative. I can relate to that because I had to carry a rucksack at what's at West Point, and that was awful. But thank you so much for your time. This was great. I appreciate it. I don't know what the podcast you do, but you did good for the podcast.

SPEAKER_01 44:11

Not too many.

SPEAKER_02 44:11

In fact, you should do you probably should do more. Okay, well, that's just my opinion, just as in science communication. Because well, some I mean, God bless everybody who comes on my podcast, but sometimes people are just they talk like scientists that's just w over everybody's head and nobody gets it, but like you did really good in terms of communicating. So kudos.

SPEAKER_01 44:32

Oh, good. Well, I'm glad to hear that. Thank you for my that sometimes I think I do talk a little bit over people's head, and in my wife's words, like, why would anybody want to listen to you anyway?

unknown 44:43

Well, okay.

SPEAKER_02 44:44

Nice meeting you, e-meeting you.

SPEAKER_00 44:47

Nice meeting you as well.

SPEAKER_02 44:48

Take care, bye-bye.

SPEAKER_00 44:50

Bye-bye.

SPEAKER_02 44:52

All right, everyone. Thanks so much for joining in for today's episode. Let me know what you thought of it. Leave a comment on the episode, or join one of the conversations on my social media pages, respond to my newsletter, send a pigeon, whatever. But pigeons do uh sit outside my window, so they'll come. They'll come. And share it with people taking GLP ones who are worried about muscle loss and see what they think. Yeah. It's interesting stuff. Uh, perhaps a glimpse into the future of what could happen. We'll see. We'll see. Um, all right, and now it's time for the closing quote. This one's from John Dewey. A problem well put is half solved. That's a good one. A problem well put is half solved. All right, everybody. Thanks for joining in, and hopefully I'll see you here next time. Check out some of the other episodes while you're at it. Yeah, there's some new stuff, there's some new categories. All right, that's it. Have a great day wherever you are, be positive, smile, yada yada, and goodbye for now.