Beyond Weight: Fat & Arthritis
Being overweight can make arthritis worse — and not just because every extra pound adds four pounds of force on joints. Fat is an active tissue that drives inflammation. In this episode, a scientist discusses her research into the role of fat, how it seems to affect cartilage and how it might be linked to osteoarthritis. She also offers some tips for achieving a healthier weight. Scroll down for a complete transcript of the episode.
About This Episode
Many people want to lose fat — often to make them look and feel better about themselves. But it’s important for health, too, in ways that might surprise you. Fat is an active tissue that releases many different chemicals and compounds, like pro-inflammatory proteins.
Scientists like Kelsey Collins have found through mouse studies that fat affects cartilage in some way, and it likely plays a role in the development of osteoarthritis — beyond simply adding weight onto joints. In this episode, she explains why she is focusing her research on OA, what research shows so far and why she thinks it will lead to the development of one or more disease-modifying drugs to treat OA, as are available now for inflammatory forms of arthritis. She also discusses how body composition may be involved in fat, why that’s important, and she offers some tips for achieving a healthier weight.
About the Guest
Kelsey H. Collins, PhD
Kesley Collins received her PhD in biomedical engineering on diet-induced obesity in a preclinical model of osteoarthritis. As a postdoctoral research scholar in the Guilak Laboratory at Washington University in St. Louis, Dr. Collins focused on systemic contributors and novel therapeutic strategies in osteoarthritis and rheumatoid arthritis. She is currently a research instructor at Washington University in St. Louis in the Department of Orthopaedic Surgery in the Guilak Lab and will become an assistant professor in orthopaedic surgery at University of California San Francisco in 2023. With a grant from NIH NIAMS, she will focus on the role of fat in OA susceptibility and pain, and on generating a new class of OA therapies.
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Released on November 8, 2022
You’re listening to the Live Yes! With Arthritis podcast, created by the Arthritis Foundation to help people with arthritis — and the people who love them — live their best lives. If you’re dealing with chronic pain, this podcast is for you. You may have arthritis, but it doesn’t have you. Here, learn how you can take control. Our host is Rebecca Gillett, an arthritis patient and occupational therapist, who is joined by others to help you live your Yes.
Thanks for joining us on this episode of the Live Yes! With Arthritis Podcast. Today, we are talking about weight loss. I know you get tired of hearing, from maybe your health care providers, that, “Well, if you really want to manage your arthritis, maybe you need to shed a few pounds.” It’s frustrating I know, and the struggle is real. It is very hard to lose weight, especially when you're in pain and it’s hard to just get moving. But today we’re going to talk about the why. Why is it that losing weight might help us with our arthritis management?
If we knew the why, I think it might make it a little bit more palatable (laughs) to go out there and do what we need to do, to try to be healthier and maintain a healthier weight. But it does affect how our arthritis symptoms are flaring maybe. Or how we're feeling on a daily basis, might affect your fatigue levels. I'm excited to be joined by Dr. Kelsey Collins.1
Dr. Collins received her PhD in biomedical engineering on diet-induced obesity, in a preclinical model of osteoarthritis. As a post-doctoral research scholar in the Guilak Laboratory at Washington University in St. Louis, Dr. Collins focused on systemic contributors and novel therapeutic strategies in osteoarthritis and rheumatoid arthritis.
She is currently a research instructor at Washington University in the department of orthopedic surgery in the Guilak Lab. And in 2023, she will become an assistant professor in orthopedic surgery at the University of California, San Francisco. With a grant from the National Institutes of Health, she will focus on the role of fat in osteoarthritis susceptibility and pain, and on generating a new class of osteoarthritis therapies. Dr. Collins, thanks for joining me today.
Dr. Kelsey Collins:
Thank you so much for having me. I'm really excited to chat about one of my favorite topics, which is what's going on with fat in different types of arthritis.
Before we go into that, though, tell us a little bit about why you're so interested in this and why this topic excites you.
I am really fortunate to have had some direct and indirect experience with thinking about body composition and arthritis. I grew up with a parent who was dealing with psoriatic arthritis. This was before the advent of biologic drugs. And so, my mom was dealing with a lot of her disease and pain and was given quite a grim prognosis at some point that she was going to lose her mobility.
I watched how biologics really revolutionized her outcomes and her pain. And now, I think you would be hard-pressed to even notice that she struggles with chronic disease, because she's been able to find a cocktail, together with her health care team, that really works for her, and it's been really great to see. But I've also seen the challenges with certain types of biologics not working for her.
This has really inspired me to think about how we can deliver drugs in different ways or come up with different targets — now that technology has advanced so much — that can help do that same transformative work that we've seen in rheumatoid arthritis in other types arthritis, like osteoarthritis. And so, I was fortunate in my early days of research as an undergrad to get exposure to osteoarthritis, because all of my friends were getting hurt.
I was an athlete in university, and I was getting hurt. And there was a lot of energy at that time about how different injuries can lead to osteoarthritis damage down the line. There was this added level of excitement about: What was to blame for that high incidence? Was it that individuals were having altered loading environments? Was it that, at the time of injury, there is this biology that happens that dooms people to have this degenerative fate? Or is it something else that's going on?
I would go to these meetings as a young trainee and see all this excitement, and I thought, “Wow, this must be a really important question because people are getting really energized about it.” I had been working on my PhD to try to better understand the role of body composition, because body composition kind of unites these two things, right?
I'm glad you brought that up because you recently received a National Institutes of Health grant to explore the role of fat in osteoarthritis specifically and generating these new therapies. Can you tell us a little bit about that?
I got really passionate about this idea of understanding body composition and why having a good body composition versus just a healthy weight might be meaningful. And so, I've done a lot of work using four-legged patients, mice and rats, mostly, on trying to understand that relationship between body composition, muscle quality, fat amounts, and then what these tissues are doing and how that might come together to play into a risk for injury, but also a risk for symptoms and how we can think about reversing that.
We developed a model of mice that have no fat. And the reason why we did that is because we had shown there's a lot of studies that have shown that the amount of body fat is associated with cartilage damage and other pain-related outcomes. But no one had shown the converse is true: that if you get rid of fat, do you see positive things?
What we found is that when the mice have no fat, they are protected from cartilage and traumatic knee joint injury. And that if we can give them back fat using some regenerative medicine and tissue engineering strategies, we can recapitulate or reverse their protection from cartilage damage. And what this really showed us is that somehow fat is talking to cartilage.
And what was cool about this model is that these animals had all kinds of other things that we hear about patients. Like they had insulin resistance, for example, like Type 2 diabetes; they have weak muscles; they have a whole slew of other comorbid issues. But just by taking away fat and putting it back, we could see this relationship and communication between fat outside of the joint and the knee joint itself.
This just speaks to why having good weight maintained and having a healthy diet and controlling what that fat is doing is really important for patients in management of their disease.
Talk about cutting-edge and fascinating research to hear about. So, are you in a phase yet where this research is being worked on with people?
No, this is all still pretty preclinical at this point.
In the end, what is it that you're hoping to achieve with the research?
What I'd like to contribute to is a pool of data that really show that it's meaningful to measure these body composition outcomes clinically. And I think there are efforts going forward where people are starting to track body composition in patients and trying to understand on an epidemiological level what that tells us, in RA and OA.
There's evidence now in both of these big patient cohorts that there's all different subtypes potentially of patients that we can parse out. And that intuitively, it makes sense that an individual who tears their ACL at age 15 and goes on to develop osteoarthritis, versus an individual who starts to show osteoarthritis at age 90, versus an individual that has struggled with obesity and metabolic issues for their life and is starting to see the consequences of that manifest in their musculoskeletal system. These are all probably different trajectories.
And so far, we've called it all osteoarthritis because it all ends up in the same place, which is cartilage loss, pain, disability. But we could probably track and intervene earlier if we have a better idea of what these cohorts look like. I think one of the pieces of that puzzle is thinking critically about body composition and thinking about how we can empower patients, because losing weight is a really tough game.
It's really hard to lose weight. So, we don't want to trivialize it and make it more demoralizing for patients and ourselves by saying you just need to lose weight. I think if we can explain that you can have a more favorable body composition and that will help with your pain, you can have stronger muscles; you can have better ratio of muscle to fat. These are places that I'd like to go with my preclinical data, to give us a better idea of what a healthy profile looks like, to give us a better idea of what the factors are that are really bad.
We see in rheumatoid arthritis — there's evidence from other groups, too — that fat responses can dictate worse damage and worse pain and behavior. We know that fat is involved; we just don't really know how. There's a lot of efforts at trying to parse out these different specific roles so that we can give patients more empowering messages that are easier to act on versus just, “Oh, lose weight.”
The data do support that weight loss is helpful, for especially osteoarthritis. I think 10% weight loss is the magic number that's been published, that shows a huge mitigation in pain. But it's not just about the weight. Because when we lose weight, we're losing fat, we're losing other tissues.
We recently showed in a paper that fat makes certain factors that are necessary for muscle to be normal in function. But sometimes in high doses, these factors are bad, and they can lead to tissue damage. And we don't really know what factors are to blame or what components are involved in this conversation between fat and cartilage.
The purpose of this grant is to try to understand who's to blame and what pathways we can leverage. And that can lead us to new targets for drug development. But the other purpose is that: We're developing a new way to deliver drugs. By using CRISPR-Cas9 genome engineering, we can take stem cells, and we can rewire them.
The benefit of using a cell is: Cells are really smart. They have developed over so many years to do all these things and have redundancies and all of these pathways that we're only beginning to understand. But if we can engineer cells to be little drug-delivery depots, and we know what we want to make, then we can make, for example, little implants that we can put into people, eventually, that are going to sense and respond to their environment.
And maybe this implant can live in someone so that, in the case of rheumatoid arthritis, for example, if you have a flare, then the implant is there. It's ready to respond, and it can manage the flare for you. And we've done some work in models of rheumatoid arthritis to show this proof of concept works. So, that's the idea. This grant will allow me to explore the mechanism of how fat is talking to cartilage. But also develop this system of delivering drugs. And since these are stem cells, they can be anything they want when they grow up.
We can engineer these cells to make something that we want to see more of, for example, like an anti-cytokine therapy. And we can make those cells have a fat type of phenotype. We can make a little fat transplant, and we can put it in these fat-free mice and test it. What's really exciting is that these two processes don't really rely on each other, in that we can try to figure out the factors and we can develop this drug delivery method in the Guilak Lab.
Are these types of therapies going in line with what we saw with the advent of biologics for rheumatoid arthritis and other inflammatory forms of arthritis? Are they designed to hopefully slow progression or stop the progression of osteoarthritis?
Yes. Of course, the best treatment is prevention, all round, right? Because we know cartilage can't heal itself. It's avascular and aneural. That means it doesn't get a blood supply and it doesn't have a nerve supply, at least not in a healthy situation. As disease manifests, these things change. We want to be able to protect things before they become problematic. If we can sense a signal that fat is sending, or change it before the joint receives it, then we can prevent the disease.
But the reality is: The way that our health care system works at this point is that until we get a good idea for risk profiles, and we know who might be at risk for different diseases, people are probably going to present when they're already feeling some kind of symptom. So, we're probably going to be mitigating, at least to start, until we get to this point that I think we're all really excited about getting to a more personalized medicine approach. Where we can put different machine learning approaches to work to understand what people might be at risk for.
Yeah. You know, a lot of us with arthritis maybe have heard from our health care providers that you need to lose weight to reduce some of your pain. Or you need to lose weight before you have a joint surgery. Can you talk about why being overweight is a problem for joints?
There's a longstanding dogma about loading for joints, with the idea that, as you add body mass to a system, that mass is going to make a load that's more than the cartilage can handle. And the cartilage is going to fall. For the purposes of surgeries, having more mass is a little bit challenging as far as managing the bleeding and the tissues and all of this. I don't do surgeries on people, so I can't fully talk about that necessarily. But in the mice, for sure, when we're doing surgeries and there's definitely some considerations to make in that respect.
But what we've worked on, and what others have really shown, is that the loading due to the body mass is actually insufficient to explain the damage, at least in the context of osteoarthritis. And there's some really beautiful work done by Tim Griffin and Dr. Guilak — I think the Arthritis Foundation sponsored this work — that showed that you can have mice that are like up to three times the body mass of normal mice, they have this certain knockout in one of their genes. And despite that, they still had no evidence of worse cartilage damage.
Systematically, since that paper in, I think, 2007, 2008, we've been trying to create a speed of data to really show that in reality. There's probably an interface between loading and the altered biology. But definitely there is a big role of altered biology. And I think we're starting to see and appreciate that, where historically we would've thought of rheumatoid arthritis as a systemic disease, and we would've thought of osteoarthritis as a local disease, I think there's a lot of data now supporting that osteoarthritis may in fact be a more systemic disease than we originally thought. And one of the big contributors to that is this fat-signaling piece.
You talk about loading. Can you define what loading is for everyone?
Sure. So loading is just the forces that are going through your body. As we stand up on our two feet, we have loads from our body mass that are going through both of our knee joints. And I think this is one of the first sets of data that really illustrated to this role of fat and obesity being so complicated, in the context of osteoarthritis. Because there was some great data that showed us that individuals with obesity also have hand osteoarthritis. If it's just due to loading due to body mass, we're not ... at least most of us are not … standing on our hands.
We can't explain that incidental finding of hand osteoarthritis purely by loading. Of course, there's loads due to muscle and tendons crossing our joints in our hands. Of course, there is loading, but not loading due to body mass. So that was the first kind of big, I think standout piece of, data that said, "OK, how do we think about this, if it's not loading due to body mass?" Because that's what we've always believed was the key source of damage, at least in the knee joint.
Loading, to answer your question, is this: this force that's due to different components. Could be due to muscle, it could be due to our size, that that's getting transmitted through our joints. And cartilage is considered a load-bearing tissue, so it's supposed to be able to manage this up to a certain point.
Right. So, I think the number that I've long heard is that for every pound that you are overweight, it's actually four times the force of loading on the joint. Right? So, we're now finding that may be not necessarily true, but it does have an effect.
Yes. And it's also interesting because, in individuals with obesity, for example, you might actually see that these people would show more muscle and more muscle force in an absolute scale. But when you're thinking about normalizing due to body size or body mass, then that can potentially taper off. And we also know that muscle quality can be affected by obesity, such that you might have, for example, adipose or fat cells living in the muscle tissue or on the side of it, and that can affect the muscle and the loading.
And so, it's a really complicated system. We can't just think of people as boxes of a given mass and that two people of same given masses are going to have the same loading environment and inflammatory environment. And I think we now appreciate that — whether you have good high-quality muscle, how much fat you have, what the fat is doing relative to your size — all are important components to the equation.
Yeah. For our listeners who don't know: Osteoarthritis is the arthritis that your general population and your average person thinks of when you say the word arthritis.
It’s always been thought of, in the past, as a disease that's wear and tear on your joint and the cartilage. But from the research that we've been working on with Dr. Guilak, Farshid Guilak, and his teams of researchers, we know that's not really the case. There is an inflammatory process around osteoarthritis. It might be more systemic than we originally thought. Explain the switch to that thought, and why we need to move away from saying it is just wear and tear, to our listeners?
The big take-home message in osteoarthritis research, especially, is just listening to the story that the data are telling us. I think a lot of investigators from a lot of different groups are showing that there's different components of the system. For example, there's a lot of interest around the bacteria that live in your gut, and the gut bugs, and how modulating the gut bugs might be beneficial for downstream pain and also fat signaling and other components.
We’re also working on in the lab some different diets. There's a group in the lab that's looking at, for example, Omega-3 supplementation, because for those of us that struggle with our weight, you know, it's easier to add things than take them away, so it's always nice when you can tell people to take a supplement. So, omega-3 fatty acids might have some protective capacity, and there's data around this, in protecting cartilage and mitigating inflammation. I think the degenerative process kind of has this implication of: We're kind of doomed.
That our cartilage can't handle it. But there are reports that there are individuals that are well into their 90s that don't have evidence of osteoarthritis damage. And I think now that we're better understanding what can lead to cartilage damage, like knee joint trauma, like fat signaling, there's certain genetic markers that have been shown to be associated. There's a lot of data to show that certain diets can lead to cartilage damage on their own, including work that I did as a PhD student. So, I think we're just getting a more full picture.
Like osteoarthritis: We look at cartilage as our endpoint. But we also know that bone is involved. We know that the synovium, which is the tissue outside the joint, that has roughly 50% inflammatory cells, that can get involved. We know there's a fat pad in the joint that can be involved. And I think what's really exciting about the field right now is that people are encouraging looking at crosstalk. We're really interested in fat cartilage crosstalk, but bone cartilage crosstalk — looking at how all these tissues are talking to each other.
And we can do this in clinical samples and in preclinical work as well, to really get a handle on how this conversation is happening. Because that dynamic nature might be really important to understand the disease. We can't just focus on one tissue, one outcome, and this is facilitated by all this wonderful technology and financial support from groups like the Arthritis Foundation that really makes this possible for us to look at these relationships. And we think that there's going to be some clues for treatment in that as well.
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The biggest thing that we can do, that research supports, is stay physically active and move our bodies. But just from your standpoint, my takeaway in hearing you talk, which is obvious, you're very passionate and excited about this research, and I am, too. Because there hasn't been anything historically for people with osteoarthritis. And I have it in my spine. And so, it's hard to stay physically active when you have so much pain. And you know that losing some weight might be good.
But what I'm hearing from you, too, is it's not just about the weight. It's what, your BMI? What is your body composition? Is there more muscle than fat? We need to pay attention to that, and maybe focus on that versus the number on the scale. But what things can we do to stay physically active or eat healthy if we are having so much pain?
Pain is such a tricky thing. One really exciting movement that's been happening in the preclinical realm is that we are really challenging each other and ourselves to look at pain in the animal models. And I think this will help us better understand these relationships. Because we hear clinical reports all the time: that pain and structure don't always match up. And if you don't have structural damage, there's really limited things that you can get, treatment-wise, from clinicians
But pain and avoidance of pain, and fear of pain, in patients is a really complicated topic. But the one thing about activity, specifically, is that I think, overwhelmingly, the literature supports the notion that going from nothing to something is far and away the biggest opportunity than going from something moderate to something really sophisticated, like high intensity interval training or something that seems less approachable.
But if you can routinely do something, that is better than nothing, that will have more return on investment than the risk of getting hurt or having other additional injuries by pushing yourself to do something that's too hard.
I think when you don't know how to do these things with your body, and you don't feel comfortable going and picking up a tennis racket or going to an exercise class at the gym, because you don't want to look silly, I see how that is super intimidating. But I think there's a lot of evidence that doing something simple, like doing a 30-minute walk five times a week, is something that might be more approachable.
A lot of us have a health tracker and you're monitoring your steps. I know I try to challenge myself each day. I think people are stuck on what we heard for so many years, right? You've got to exercise moderately, three times a week or 150 minutes or whatever it is. And if that sounds way too far-fetched for you, don't even think about that. Think about, OK, yesterday I did a thousand steps; today I'm gonna try to do 1,200; and then tomorrow, if I didn't have more pain, I'll hit 1,500.
But build it up and have a goal. And then just know that you give yourself a little grace: that there's days that you can't do it. But like you said, we've had other episodes where we've talked about this. And one of our guest experts talks about physical activity snacks. Just building more movement into your day as you go along could really help get you there. Right?
I love our conversation. And just really hearing you talk about how: Don't think about it, just as the fact that I don't wanna look at, think about it as a factor that might be contributing to my inflammation, right? In my body, in the breakdown of cartilage or whatever. It might be more; it's more than just that number on the scale. It is more about: What is your body mass? What is your body composition made up of? And maybe thinking about it that way isn't as daunting. It might be a little more motivating to say, “OK, well, I really do need to take a look at my nutrition and how I'm eating.” And is there a magical diet? No, right?
There are other ways that people can monitor their metabolic health. I'm not a fan of standing on a scale; I don't even own a scale. In the past, I've done things like measurements or monitoring how clothes fit. I think for a lot of people, the scale can be pretty overwhelming. And I think that there's other ways to approach healthy goals around fat mass and body composition that don't always have to be so scale-centric.
But to be totally fair, there is a point at which there is just an unhealthy mass, unhealthy fat. For many people, I think just trying to really focus on the multifactorial: trying to eat as healthy of a diet as possible, working with a nutritionist to arrive at what that looks like, trying to do as much activity through... I think the lens is really sustainability. Like, let's move away from doing things to lose weight for a wedding or whatever.
Or have these acute goals and let's think about: What's going to be something that we can all do over the long period of time that's going to help us maintain and sustain, versus just trying to get an acute success. Which is hard when you're in pain because I think the number one thing you want to do is make the pain stop. But I think sometimes these things have to be a little bit more gradual, and that way it will last longer and be able to benefit you more long term.
Yeah, you need it to be sustainable or you'll constantly... That's why the trendy diets and the fad diets not necessarily the case, but eating more of a whole anti-inflammatory diet, and that can be hard for a lot of people, you know?
But I'm one of them. (laughs) But like trying to make sure you do little things at a time. OK, I'm drinking more water now. That's my focus right now. Or I'm making sure that I am incorporating enough vegetables and fruit in my diet. Just tackling one piece at a time. I'm walking farther than I did yesterday. That’s one thing that I love about the Arthritis Foundation's Walk With Ease program. You can find communities across the country that might have the program you can participate in, but it is self-guided, and there's a book that we have. And it just shows you how to get started one step at a time and how to do the stretching and stuff.
Having a lot of health struggles this year myself, I know how hard it is to move and to get moving. But I also know my fatigue levels are high and I'm off meds right now. And so, I've started almost my own little Walk With Ease program again, because I've done it before, and I used to teach that class as an OT. But I'm just doing a few steps at a time and building up every day, walking a little farther than I did the day before. And I'm noticing a difference.
I love that we're talking about weight loss overall and why it's important systemically for us, but even also the mechanics of it, right? So, strengthening your muscles and your tendons and ligaments that support that joint are important, right?
Yeah. And I think losing fat overwhelmingly has positive outlook on many different chronic diseases. And this is why I love hearing from patient voices. What we learn from our clinical colleagues is that you'd be very hard-pressed to find an individual that just has osteoarthritis or just has rheumatoid arthritis. And we're also not just treating knee joints.
We have to think about the whole person. And we have to think about what else is going on with them. And part of it could be mental health-related stuff. Part of it could be other diseases. And we know that fat plays a role in a lot of these different components. So, the cool thing about treating fat and understanding fat biology and these different interactions in individuals with obesity and arthritis is that we have the opportunity to potentially be effective to a lot of different indications and better understand a lot of different things.
So, as an individual, if you're going out as a patient and doing a walk, you're not just necessarily doing something good for your arthritis; you're doing something good for your metabolic health and your cardiovascular health. And it's so great that something so simple…
And mental health.
Yeah, something so simple can be effective across all these domains. I think that that's really exciting. And hopefully people will feel empowered to do that so that they can really kind of hit all of the birds with one stone, which is a good thing I think.
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In the next segment of the episode, we take some listener questions and tips that we get from social media. One person, it's Meg's Fitness, says, "Gaining strength helps me more than changing my weight." Can you speak to that?
I think that that gets back to this idea about paying attention to body composition. It could be twofold. It could be keeping better congruence within the joint, but it could also be, as our muscles get stronger and bigger... We know muscle is the principal tissue that processes our glucose and other components that are associated with our metabolic health. So, as our muscles are stronger and healthier, not only are they going to help with that loading piece, but they're also going to help with their overall metabolic health. They're potentially going to feed back to the fat and help with that signaling and potentially that could also help with pain.
Yep. A lot of times, I think, when people are trying to lose weight and they are doing resistance training, and then they gain weight, they're like, "Wait a minute, I'm supposed to be losing weight." But that happens, right? Because that's just naturally changing the composition, not necessarily getting the pounds off. Right?
Exactly. You can be doing really wonderful things for your physiology. And by just looking at the scale, you might feel demoralized when you're really doing good stuff. And so that's why I think thinking beyond the scale is something that we need to do when we're thinking about body composition and metabolic health.
Yeah. One listener says: “MAJOR (in all caps) improvement in pain relief with weight loss.” Not surprising?
No. And I'm glad to hear that. And I think getting that message out will help motivate people. Because, I mean, it is really hard. It's hard to lose weight, it's hard to get it dialed in and figure out what's going to work for you.
Who's the best person to help us figure out what our body composition is?
You know, it's such an interesting question. I think for my own experience, I've had really good luck with working with nutritionists. I think nutritionists are really underutilized resources. There are people that can do body composition measurements with skin-fold calipers.
I learned the other day about a service where you can order a glucose monitor, and you can monitor your own glucose and see how it responds to certain types of foods. And I think people are sending away for their own microbiome sequencing and paying for it.
There's one listener who said that weight loss doesn't help. The pain is there 24/7.
I think pain, as I mentioned before, is really a complex thing. And I am not, in any sense of the way, qualified to talk about chronic pain in this sense. But I did see a talk recently that illustrated that there can be some remodeling in the brain and the way that the brain processes pain.
What's so interesting about pain, and about obesity as well, is that these are really survival instincts that have gotten kind of... It almost feels like there's a game of evolutionary telephone, where there's been the best of intention, right? Like we need to have enough energy so that we can live. We need to have enough fat so that we can live. We need to get proper pain signals so that we don't get hurt and that we keep all our limbs when we're running from predators or whatever.
We can see how these things are good in one sense, but we have a lifestyle now. And things have changed so much that we have seen the negative sides of these things, where people have to deal with chronic pain, and people have to deal with obesity and other components that maybe weren't happening before, just because of all of this change that has happened. I think we just have to learn about what these changes mean and try to get a better understanding of the basic mechanisms of them.
Yeah. And we just did an episode on really understanding your pain, the different types of pain. Is it mechanical pain? Is it centralized processing pain? Or is it muscular pain or neuropathic pain, nerve pain? So, make sure you tune into that episode.
Well, there's a lot of energy around — in the animal models — to look at mechanical pain, because it helps unite some of the sensory neurons with the damage. But it's a huge open question and an area that I plan to go into, to try to resolve what the additive effect of putting obesity models onto that are.
Does it continue to be a mechanical type of pain? Or does it become a central pain? Because there's a lot of evidence in obesity literature that there's central pain processing changes. So, yeah, that's great that you guys have that as a resource for your listeners, because that's an area that is hugely of active interest in the research community.
Thank you so much, Dr. Collins, for diving into the why behind body composition and weight loss and how it affects our arthritis. I really appreciate your expertise and your passion for what you're doing. Please keep doing what you're doing. Before we go, could you share with us what you think your top three takeaways are for our listeners?
Well, I think my top three takeaways are definitely that there's more to osteoarthritis than what's going on in the knee. That there's different components of specifically fat outside the joint organ system that we're working really hard to better understand so that we can come up with some new therapeutic targets. I think that there's more to weight loss than just thinking about mass, not just about loading. Thinking about body composition is important and trying to have a little bit of empathy for yourself as you're going through that journey of trying to manage your weight.
And finally, of course: Exercise is medicine, it is really critical. Keep trying to do movement as much as you can tolerate and trying to be as consistent as you can with all of these elements of healthy living. We're working really hard trying to come up with a first-in-class drug for osteoarthritis.
Well, we look forward to that. Thank you so much for all of your helpful tips and explanations of why it matters. I just want to remind our listeners: For any additional resources, just check out our show notes for this episode on our website. Also, we do have that pain management app tool, Vim, which is sponsored by our partner, Tylenol, in helping you tackle pain on a daily basis. You can get tips and strategies for managing your nutrition, managing your physical activity and setting some goals to manage your pain, but also to connect with other people.
Thanks so much, Dr. Collins. It was a pleasure to have you.
Thank you so much.
The Live Yes! With Arthritis podcast is independently produced by the Arthritis Foundation, to help people living with arthritis and chronic pain live their best life. People like you. For a transcript and show notes, go to https://www.arthritis.org/liveyes/podcast. Subscribe and rate us wherever you get your podcasts. And stay in touch!
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