Episode Transcript
[00:00:01] Speaker A: Welcome to Obesity a Disease, the official Obesity Medicine association podcast exploring the many facets of the disease of Obesity A Disease podcast is brought to you by the Obesity Medicine Association. A clinical leader in obesity medicine.
[00:00:28] Speaker B: A 69 year old man who was a long term patient had struggled with central adiposity. His BMI was 33 and he had tried several dietary programs with limited success.
He presented to the office for a regular visit and was happy to report that he had lost 15 pounds over the past three months.
On exam, though, his central adiposity had not changed. Unfortunately, his weight loss was due to muscle loss from a progressive neuromuscular condition.
This case was early in my obesity medicine career and it taught me two things. First, that the scale shows only total weight and not body composition. That I need to be more attentive to what weight is being lost, fat versus muscle.
Second, that I need to be mindful that weight loss may be occurring because of an underlying disease process and may not be the result of intentional efforts.
Hi, I'm Dr. Nick Pennings, professor of Family Medicine at the Campbell University School of Osteopathic Medicine and Director Clinical Education for the Obesity Medicine Association. And today I am joined By Renee Rogers, Ph.D.
fellow of the American College of Sports Medicine, to talk about sarcopenic obesity. Dr. Rogers, tell us a little bit more about yourself.
[00:01:43] Speaker C: Hi, Nick. Thank you so much for having me. I'm excited to be here, but. Yeah, I am a senior scientist at the University of Kansas Medical center, and my work is primarily focused on the relationship between physical activity and exercise and obesity care. And I do a lot of work specifically looking at body composition changes, but not just the, you know, the amount of tissue change that we have during obesity treatment, weight loss, exercise, all those things, but the quality in the functional changes in tissue, too. So I'm excited to have this conversation because this really brings all my worlds together, hopefully in what we're going to chat about.
[00:02:22] Speaker B: Yeah, and those are really important components because we see sarcopenic obesity in our patients, particularly our older patients.
And, you know, that is a concern because when you're losing weight and you're losing fat and muscle, that can be concerned. So why is that particularly dangerous for some of our patients?
[00:02:43] Speaker C: Yeah, you know, and it's so interesting because in 1996, we first thought sarcopenic obesity was right, this idea that you're losing lots of fat tissue, but also you're reducing muscle mass. So it was all about the quantity of the tissue. Right.
And now the most recent definition has been updated to involve muscle Function and how tissue's functioning in the equation. So it's not just about having excess adiposity, having too little muscle, but it's really getting down to the functional status of the patient and what's going on with it. I think that extra layer is a really important starting point for us to be thinking about because if our patients aren't functioning well on a regular basis, that sometimes is the sign that sets off the red flag for us to say, hey, wait a minute, hold on, what's going on? I need to dive deeper into this, to the case in point. But what we really see with this sarcopenic obesity is it's very nuanced in the sense that we immediately think, wow, patients losing weight, this is great, this is the right direction. And the literature signals us to say the way that it's, you know, these are large trials are done, that as a person loses weight, they start to function better. But the reality is sarcopenic obesity is tricky because we actually see the decline in function at the end of the
[00:04:13] Speaker B: day and so change in mass. What you're saying is not just the metric that we should be looking at, but our patient's ability to function, to move, to look at muscle strength and mobility, that those are more important factors.
And you know, now we're seeing patients that are losing weight and you know, with that we see some proportionate muscle loss.
But particularly with the GLP1 therapies, are some patients losing more lean mass than others?
[00:04:45] Speaker C: Yeah, this is like the, this is the question, right? This is the question of the day and what's going on. And you know, there's been a lot of conflicting reports. And I think a big part of this comes down to the way that it's been measured. And in a lot of the clinical trials, you know, with our more contemporary GLP1 receptor agonist or semaglutide or tirzepatide. Right. We're seeing a lot of the body composition metrics being done through DEXA originally. So when you do that and you're using dexa, the compartment size and the estimates of the fat free mass versus the lean mass versus the muscle mass, it's really hard to differentiate.
So initially there was thought that specific to GLP1 receptor agonists that we were seeing about 25 to 40% lean tissue loss.
Now more recently, as many of us are starting to research this in deeper stance, we're actually seeing that those numbers might not be quite as high as was originally estimated. There was recently a report that came out that said, this might be right around 15%.
[00:05:50] Speaker A: So.
[00:05:50] Speaker C: And that's lean tissue specifically. So when we think about that, it may not be anything specific to GLP1 receptor agonist per se. It has to go back to the general rule of large magnitude weight loss. Right. And whenever we're losing a large amount of weight, we naturally typically, and sarcopenic obesity is a little different. But what we naturally usually see is some amount of lean tissue loss.
[00:06:18] Speaker B: So maybe you could explain like what, what is the difference between lean mass and muscle mass.
[00:06:24] Speaker C: Yeah, absolutely. This is again another thing that is commonly misspoken. Even we see, you know, when we're talking to patients, the first thing we want to say. Right is you might be losing muscle. Right. But the estimates are, we have to remember that muscle is a component of lean tissue. So. Right. We can start really broad. Your, your fat free mass compartment is everything other than your adipose tissue, your fat.
And that includes bone, organs, tissue, cartilage, muscle. Right. Everything is in your fat free compartment. Water also. And then we start to narrow that down in terms, and then we get into the lean tissue compartment, which means we remove the bone out of that equation. So now we're looking at everything, water, organ tissue, connective tissue and muscle, all those things. Right. And then muscle is just a sub component of that lean tissue compartment.
Now it's estimated that that can be somewhere around 50% of that lean tissue compartment. So it makes up a substantial amount. But it would be incorrect for us to, when we are referring to changes in lean tissue that happen with weight gain or weight loss, to call that all as being muscle tissue. And we see that totally in the media. Right. Everywhere.
[00:07:38] Speaker B: So when we're seeing those changes in muscle size or in lean size, as patients are losing weight and they're losing body f, they're also losing fat from within those tissues. Right. And so that is that also measured when they're looking at changes in lean mass and muscle mass, the, the loss of fat within those tissues.
[00:08:01] Speaker C: Yeah, that's again, that's where it's tricky and it really comes down to the method that's being used. So for a lot of the large scale clinical trials, they're using dexa. So it's looking at the compartment size. Right. So as that, that inter mile, you know, intramyl cellular fat or intramuscular fat is what we like to, as, as we start to lose some of that, that whole compartment's going to shrink in size. So those numbers, those estimates can be a little bit off. And unless you're doing something like a CT scan or an MRI or the newer D3 creatine delusion methods to get estimates of skeletal muscle mass, those numbers aren't going to be really, really precise.
However, I will say that some of our more updated bioelectric impedance analysis BIA devices are doing a fairly good job at approximating muscle specific tissue changes.
Some of them are correlated with MRI data.
So there is hope to get better measures in the clinic to get at the muscle measure, which we still want to do. It just may be that we need to be following trends over time very, very carefully, not just taking a one measure and expecting that to be our end all, be all answer.
[00:09:19] Speaker B: And so those changes in muscle size may not necessarily reflect a change in muscle function. Which is brings us back to what we were talking about before, why it's so important to be measuring and looking at muscle function. So what about some of the ways that you look at muscle function?
[00:09:38] Speaker C: Yeah, no, you're right on Nick, with all of this. And the Sarcopenic Obesity Global Leadership Initiative has recently published an algorithm that really can help you to dive into this. But you know what's surprising, I think even to myself when I first read it, but it makes a lot of sense and maybe for many people that are listening, is it actually should be done in two sequential stages. And the first stage is to look at function and then dive deeper into body composition changes. And in a lot of ways that makes sense because in your clinic, if you don't have, you know, that sophisticated BIA device that's highly correlated, you know, with, you know, looking at MRI data, and we all know we're not sending every patient for MRIs and dexas and all those kinds of things you can get at muscle function. And one of the, you know, the really nice ways to do that is to perform a sit to stand test in the clinic. You know, getting up and out of the chair five times, timing it, noticing it, watching what's going on with the patient, seeing their function and what's happening.
You know, if you are dealing with older adults, you know, the SPBB is a nice test, the performance battery where you're doing balancing testing, you're doing walking speed and you're also doing that sit to stand test. A lot of places will like to do a six minute walk test to take a look at the function of the person. Although that's a little tough if you don't have a large enough corridor in your clinics to do it. But even just, you know, I always like to say you know, standing in a, if you do have any kind of a hallway and watching your patient walk down the hall, noticing what they're experiencing, looking at the gate, looking at, you know, how they get in and out of the chair, that can be, you know, a really interesting way to learn a lot about your patient without even asking any questions. And then we also always have talked about this and it comes up a lot. But grip strength testing, you know, does tell us a lot. And I know it's a little tricky, right, because it's not looking really at the lower body function, it's really looking at upper body function. But if we are seeing someone like the case that you had, you had initially described at the start of the conversation is you would definitely be seeing some changes in the weakness and function with that much muscle tissue loss in that amount of time.
So these functional measures can make you go, huh, that's interesting.
And the reason why I think this can be so very powerful is in a lot of our clinical trials where we have been doing, you know, some kind of a lifestyle based intervention and maybe we're working with folks that are, you know, they're carrying excess body weight and adiposity, but they're not really in a state of heavy metabolic dysfunction. Right?
They haven't been carrying that adiposity for a while. And they're maybe at less risk for sarcopenia. When they do the tests that I just described to you, we really see a quick ceiling effect, right? We see that they're, they're fairly strong actually and they're able to do sit, to stand, test, test, no problem. They don't have a hard time balancing because they really can navigate their body weight or they've learned how to do it well. While their gait speed may be slower overall, when you watch them walk, they, they function for the most part as best as they can given their body size versus when you start to see someone that may be experiencing some decreases in function or sarcopenic obesity that may be more at risk for it, you'll start to see those chair sit to stands are a little bit harder to navigate. We see maybe they can't get through all five or when we watch them walk, we see, you know, a really slower pace or we start to really notice a lot of compensation side swaying balance issues.
And that sometimes can be a sign of that break between someone living with obesity that actually has a lot of muscle to compensate for my body size versus I'm a person living with obesity that may be in the stage of sarcopenic obesity or moving towards risk of sarcopenic obesity?
[00:13:49] Speaker B: And are there some clinical red flags that we should be looking for, especially if we're going to start a patient on a GLP1 looking for significant weight loss? Maybe, you know, our patients who are more sedentary, our patients who have had obesity for longer periods of time are older patients.
Are those patients that we should be looking at maybe function before starting these and monitoring that?
[00:14:13] Speaker C: Yeah, I mean, I, you know, I'm always a proponent of saying we should assess function right along with that body composition. You know, that's my bias. Right. But definitely I think that it's really, you know, as we get older, right. We have that every decade after 30. Right. 3 to 8%, you know, increase in muscle mass, size, fibers, all those things start to go down after age 30. So as we get older, there is absolutely a higher risk. And I think that there are quite a few people. John Batsis has done some great work in this space. Carla Prado has put out some nice papers looking at this, if anyone's interested in some continuing reading. But we tend to see that the population prevalence in the United States right now is looking at somewhere around, I think it's between 25 and 30% of people have sarcopenic obesity.
It tends to be that more of them are older adults. So there's definitely that aging population is at a higher risk of developing it. And as we age, there's also a natural tendency for an increase in that fat infiltration we were talking about both at the inter myo level and then intra those lipid droplets within the tissues that naturally goes up due to changes in the metabolic status.
There's a lot of work also being done to understand who is it a greater genetic predisposition for sarcopenic obesity.
Interestingly, there's a higher proportion of Mexican Americans that have sarcopenic obesity. So it's something just to consider in this space. But I do feel that while we've studied this, we've not studied this probably as extensively. And this age of GLP1 receptor agonists have really brought, brought a lot, lot of attention, especially for our older adults that are being treated for type 2 diabetes, you know, insulin resistance with these agents.
[00:16:11] Speaker B: And you know, I see patients with lipedema and they too have difficulty with progressive decrease of function and, and loss of muscle strength, really struggle with trying to build muscle even with physical activity and resistance training.
So I see that in my practice as well. So I think that is something that we really need to be very Mind, mindful and concerned about.
So when our patients are in that weight loss process, what kind of things can they do to help preserve that muscle mass, particularly if they're really struggling to eat? You know, these medications that we can use to reduce appetite can be so potent that patients put themselves at risk for nutritional deficiencies, particularly protein deficiencies. So what kind of strategies can we use to help for those patients?
[00:17:02] Speaker C: Yeah, you know, this is such a, it's such a, such a big question, Nick, but it's my. One of my favorites.
And I think that, you know, you're talking about something that I think is really important. And again, I feel like it's just been so oversimplified everywhere where we're hearing, you know, eat more protein and start resistance training. And, you know, let's step back for a second and let's really think about good clinical, comprehensive care, what that means and how we really help our patients. And the first step is to. What you just described is these are appetite suppressing agents, and that's exactly what's helping to drive the weight loss in a positive way. Right. We're seeing our patients are more full between meals, they're satiated, they're not hungry. We've got that signaling changes, and that is essentially what's helping to sustain the hypocaloric state. So we can see these really positive adiposity changes. Right. But at the same time, to the point you just mentioned, when someone's not hungry, the last thing that they want to do is have that protein. And when we look at the, the recommendations, 1.6, you know, grams per kilogram of body weight, and you start to do the math on that.
Wow. Right. That's a lot. That's a lot of protein. And that can be really tough. And then we also know we need to be eating fiber. We need to make sure for our digestive health, you know, in these patients, we're continuing to think about those things. So I think, honestly, step one in all of this, what I think is critically important is if we want to talk to our patients about eating more protein, step one has got to be, we need to be making sure that we are managing these medications in a way that we are, you know, managing the appetite, not shutting the appetite completely down and having those conversations about, you know, are you able to take in enough, Are you not hungry at all? Have you been skipping meals? And that's where that registered dietitian, nutritionist, if your patients have access and coverage, man, that connection can be so valuable. Right? Because they're really going to help with those eating behaviors and those tricks for getting in the protein and doing all the positive things.
[00:19:12] Speaker B: And that's one of the things I asked, I just want to mention that's one of the things I always ask my patients about, you know, is what is their appetite like, they struggling to eat or. And if that is the case, then, you know, making sure that they're getting enough calories and that they're eating enough. And that's been a whole paradigm shift in obesity medicine for we were forever trying to get patients to eat less and now we need to make sure that they're eating enough and that they're eating the right foods.
[00:19:41] Speaker C: Yeah, it's a different kind of monitoring. It's self monitoring, it's self regulation, but in a different way.
And it's such a big important part of it. And I think sometimes if that natural dose escalation on the label, which most people that are in obesity medicine know that that's not it. It's based on the patient. Right. And the response. But when that goes up, we often see, even in, in our, in our clinical research studies, patients are coming in and they come into exercise and guess what? They can't do the work because they've been under fueling. So we've got this really interesting relationship between. We know we have these two really positive behav.
But we can't get the patients to do these things if they're not feeling well and if they're under fueling. Right. It becomes really tough. The other nuance that I think is really important in all of this that we don't talk about a lot with protein is that when we're in a hypocaloric state, oftentimes a lot of what we're taking in is being used for our metabolic processes. So in the, in the space and in the media, a lot of times we hear people saying we got to take in the protein because that's what helps with muscle protein synthesis and that's going to build muscle.
And I think from a physiological standpoint, in a hypocaloric state, the game changes. Yeah, the game changes because when we're taking in that protein, we may be, it may be helping us to retain some, or maybe a better word is to slow the loss of tissue. Right. Because we're, we're using it for our metabolic processes. But the idea that we're going to build tissue in this state when we're taking in few calories is really tough. It's really tough. I Mean, you look at even like, let's think about bodybuilders for a second that are eating way more. They're even not isocaloric, but they're hypercaloric in that state to build muscle tissue. So we're going the complete opposite direction with our patients to help drive the adiposity loss. So the idea that we're going to build tissue is a little bit tricky. The stars really do need to align with having enough protein and then being able to stimulate. Stimulate the muscle through resistance training. And, and I, I say this in the best way possible as someone that is a firm believer as an exercise physiologist. Right. In exercise, I would love for everybody to do it, but I always try to think through the patient lens.
A lot of our patients aren't doing it, though. And that really comes back to us stepping back and thinking about that functional state. Again, it sounds like a really good idea to recommend that patients start resistance training, but sometimes we have to step back even further when we're watching them walk down the hallway or we're seeing them struggle to get in and out of the chair and pause and ask ourselves, does this patient need some sort of rehabilitation, transition support before we even start talking about exercise? And I think with our patients with sarcopenic obesity definitely could benefit from this standpoint. They are the ones that really could benefit from someone starting with that basic physical function metrics from occupational therapy or physical therapy to really get them moving in the right direction. And another question that I always recommend that we do is ask about pain.
So many of our patients are living, you know, in larger bodies, are living in a lot of pain. And if they have sarcopeni, sarcopenia, sarcopenic obesity, their muscles are smaller, they're not functioning well. They could be experiencing so much more pain inside of their body than they're even talking to you about. And they also may have just accepted the idea that this is their body and this is how their body is, when the reality is they could really benefit right. From seeing someone that specializes in their mobility, their function, their disability. And if we can work on some of that, we have a better chance of getting them transitioned to a consistent pattern of resistance training. But we often miss that step.
[00:23:44] Speaker B: And certainly if our patients are starting to show signs of frailty, they're also at risk for injury if they start an exercise program and start doing things that they're just not ready to be able to do.
[00:23:57] Speaker C: Yeah, absolutely. I mean, fall risk is something we should always be thinking about, right. And going in Space and place and, and a lot of times our simple recommendation of it's really easy, you just can grab some free weights and start doing this and you know, without assessing someone's space safety at home, having what they need, their balance, their kinesthetic awareness, their understanding of where their body is in space, which can often be limited for not just patients living with obesity, but even more right.
You know, exacerbated when you have sarcopenic obesity because your neuromuscular junctions are less responsive, our body is in general is weaker. So we want to make sure that the person will say their foundation is strong enough to support movement because it may seem like, oh, it's just lifting some weights. But from a physical standpoint, we need to make sure their body's ready for it. From an environmental standpoint, that they're in a safe place to do it, but also from a mental standpoint that they feel like they have the self efficacy or confidence to do it.
And you know, a lot of times one of the best things we can do is talk about the importance of muscle health and protecting it, but help to refer them to that, you know, qualified exercise professional if they have access and, or rehabilitation services, if that's what they need.
[00:25:21] Speaker B: And so as our patients do increase their activity and they're being mindful of the protein intake, is there any recommendations on timing of protein intake with respect to physical activity and types of protein?
Is a creatine supplement appropriate for, for patients when they're exercising? What are your thoughts on that?
[00:25:42] Speaker C: Yeah, you know, there's, there's a lot going on out around it and you know, I'm not a registered dietitian nutritionist, so I don't like to cross my scope too much. I'm always careful. But I do recommend Dr. Stu Phillips is, is some person, you know, that I, I consider to be one of the, the protein resistance training gurus that's out there, but just really knows the evidence and the idea that intake, you know, and timing of protein in the relationship of a hypocaloric state is probably less important than in general. The concept of getting enough protein right, making sure patients are eating enough of it. I think just in weight loss in general, whatever treatment pathway a patient's on, the focus really is about individually driving them towards getting enough and working with them on the right strategies that work for them as an individual and within their, their life and culture that that will match them in terms of doing it. I think when we're getting into that, that performance aspects of, you know, that performance athlete that's training for events, that's when that timing may be more beneficial. What the, you know, based upon what the literature is really saying, I think there's also been some interesting data out there. I had mentioned one point grams per kilogram of body weight. I think for a long time you were hearing about even more than that. And a newer systematic review has just come out that's basically said, nope, beyond that level, you're not really getting much. And you know, between men, between women, between menopausal, you know, status, all those things, it just still seems that 1.6 grams per kilogram of body weight is the number. So. Yeah.
[00:27:19] Speaker B: And, you know, the edge of proteins means more nitrogen waste means, you know, and more. Yeah, hydration becomes more important to protect the kidneys and it gets converted to glucose. So it doesn't, it doesn't always serve the purpose that we want.
[00:27:37] Speaker C: Creatine's another animal. Yeah. Oh, I'm sorry, I was just gonna say creatine. We're learning. We, we, there's, there's benefits out there. There's different pieces. I don't think we've really examined it well within a hypocaloric active weight loss state. So I'd say before we start recommending it, we should probably wait for a little bit more research to come out.
[00:27:59] Speaker B: One other topic I wanted to touch upon was there's been, you know, medications that have been investigated for its potential to build muscle to work on activin and myostatin receptors and inhibit those to promote muscle strengthening growth.
Any thoughts on those? Any thoughts about the prospects for those medications being used in addition to some of the medications we currently use for treating obesity?
[00:28:32] Speaker C: Yeah, I think there's interesting potential, Right. And I think for certain clinical subsets, I would see these as potentially being important agents. However, I will say, as the exercise physiologist, right. We know that even with weight loss, while we see some improvement in mitochondrial function, right. Initially, when we get rid of some of that intramuscular lipid droplet and stuff starts to go away and the intramylcellular fat, all those different things, we do see some function. But David Kelly years ago was one of the first people to talk about this and say that we don't see, though crazy increases in mitochondrial function, we don't actually see the tissue working really as well as it could. Even in terms of insulin resistance, we see an improvement, of course, but if we really want to get the change in the tissue, the muscle tissue, it requires it to be Stimulated. And the same thing goes with protein, right? We can take in a lot of protein, but we're not going to build tissue just with protein alone. We got to stimulate the tissue too. And that comes in the form of contracting it through, you know, exercise or some way. So I think that. So when we go back to these agents preserving or the ability to build tissue, the question becomes, do we really want to preserve that tissue if it's not the most metabolically healthy tissue, you know, in our bodies?
Or is it better to, you know, as we, you know, shed as the body, through its natural physiological process, wants to take and remove some of that lean tissue as we start to lose adipose tissue? Is that okay?
And can we take the tissue that we have and prioritize? I love this word, but thinking about optimizing it, right? How can we do the positive things, take in enough protein, take in the right fuel, engage in physical activity in a way that stimulates it. My guess is that we may be preserving tissue or building tissue with some of these, but I don't know that it's necessarily going to be the best functioning tissue unless we're taking it to the next layer and stimulating it. Now, I'd love to see a study come back where we take one of these, you know, myostatin inhibitors and we look at the tissue and then we exercise the tissue also and see if there's a difference. Maybe that would be great. I also worry because it's increasing lean tissue, but we talked about it already. That's not just muscle, right? There's lean tissue in other places, the heart, other, you know, smooth vessels. What does that mean? And can we actually target the tissue that we want to? Is an interesting question.
[00:31:08] Speaker B: Well, that brings us back to where we started, the importance of function and not just of mass. Right? And so I think that is a great message, a great take home message, and something we'll need to keep in mind as we assess our patients.
Well, this was a very interesting conversation, Renee. I really enjoyed talking with you about this very interesting topic and it's really a very hot topic in the world of obesity medicine. And I'd like to thank everyone for being with us today. If you like this podcast, please share it with a friend and help the OMA as we strive to advance clinician understanding of the disease of obesity. Thank you for being here, Renee.
[00:31:48] Speaker C: Thank you so much.
[00:31:51] Speaker A: Thank you for listening to this episode of Obesity a Disease. For more information about obesity medicine, podcasts and other valuable resources from the clinical leaders in obesity medicine, please visit www. Obesitymedia medicine.org podcasts. If you enjoyed this episode and want to listen regularly, head over to itunes where you can subscribe, rate and leave us a much appreciated review. The views expressed in this episode are those of the host and guest and do not necessarily represent the opinions, beliefs or policies of the Obesity Medicine association or its members. Please join us again for our next episode of Obesity, A Disease.
