The Joint Health Blueprint: Preventing Arthritis, Frozen Shoulder, and Bone Loss as You Age

Muscle will develop more quickly than the tendon adaptation. Why are tendons important? What are they? How do we think about them in a global sun? By the time your tendons and ligaments start to adapt to the athletic endeavor you're engaging in, you're almost looking at six to nine months. When someone is thinking about osteoporosis prevention, what do we have to do? Many of them are on menopausal women with low bone density. The most effective programs seem to combine some impact and some strength training. This book does something that I've never seen. It brings a history of muscle. Tell me about why. Why this book? Most books about muscle tell you what to do. And this one's different because it's descriptive. It's not prescriptive. While you're not just progressive overloading your muscle, you're progressively overloading your tendon. People have to be, I think, more thoughtful about what they're eating. You could easily fill yourself with things that don't give you the nutrients you need. I'm curious as to what your thoughts on what we're getting right versus what we're getting wrong. There are a number of topics that I'd love to discuss on this podcast, which include and are not limited to the things that limit our ability to progress, like tendon issues, like back pain, hip pain, things that ultimately limit the quality of life. But let's start with one of the things that I think that we both see in clinical practice, are issues with tendons. Why are tendons important? What are they? How do we think about them in a global sense? Muscle is contractile tissue. Muscle is made of actinomaus infillaments. You have this incredible cross-linking phenomenon that's mediated by our energy molecule ATP. And we contract muscle and ultimately to move bone, but muscle doesn't attach directly to bone. It attaches to bone through tendons. And collagen is our most abundant protein in the body. And no surprise, tendons, that tenderness attachment from muscle to bone is predominantly made of collagen. So tendons are, by definition, they are non-contractile tissue. They're almost like if you think about a short bungee. So they exist in a relaxed state called the crimp state. And when the muscle contracts, it pulls on that tendon, takes the slack out, and then it winds up attaching to the bone to move the bone. And tendons have this incredible quality called viscoelasticity, which is a cool word. But everyone is going to be quizzed on this later. There you go. So viscoelasticity, it means that the mechanical behavior of that structure changes the degree of strain that you put on it. So at low strain rates, tendons dissipate energy. At high strain rates, they really put down the force. And so you could think about as you're walking, you might be putting a lot, some tension through your Achilles tendon, by definition, but you're not putting as much tension through it as you are when you're running, and it's like a really tight spring. So the mechanical behavior of it does change. The tendons are sort of an organizational level. Muscles have the contractile elements. You have muscle fascicles. And fascicles, for those who are listening, are bundles of proteins. So you have the structure, you have a larger structure, and then you also have, within that, these composition of these micro structures of fascicles. Fascals are a fascinating thing because they are present in muscle, tendon, and nerve. And the reason for that is because we're not uniplanar individuals. We don't just function in one plane. We function in forward and backwards, left and right, and also we rotate. And so muscles and tendons, as they're trying to move a bone, they need to have specific elements stressed, not the entire system stress simultaneously, but the fascicles actually allow for tendons to be strained specifically. So you could think about like a pitcher. So a pitcher, the job of a rotator cuff, and this is a cool point that I really like, the job of a rotator cuff is actually to stabilize the ball on the socket. We think about rotator cuff strengthening exercise. You'll see a lot of people with bands and cables and strengthening up the rotator cuff, and it does that. It does rotate the arm, hence its name. But the shoulder is an inherently very mobile joint. It's comprised of four different joints, actually. It starts over here at the sternocovicular joint. You have your AC joint, and then you have your true glen or hemorrhoid joint, and you have the scapulae of the shoulder blade that rests on the back of the rib cage. So there's a lot of mobility in it, which is why on average, unless you're a rockette, you can raise your arm higher in the air than you can your leg. So similar ball and socket joint with the hip, but more stability there. Job of the rotator cuff is to stabilize the head of the ball and socket joint. It's almost like thinking about like a golf ball and a tee. So as you raise your arm into a pitching motion, all of your rotator cuff muscles are active, but different fascicles are actually more stress during different phases of that. So that's one of the fascinating elements of this. It's a really cool mechanical adaptive thing that we've evolved to have, and we have it in all of those mobile structures of the musculoskeletal system. We have it in muscle, we have it in tendon, and we also have it in nerves to allow us to be more athletic in multi-planar motion. So it's very cool and in collagen itself, as most of tendon dry weight is type one collagen, and then you have lesser components of type three, type 11, you have other types as well. And when a tendon starts to become diseased or overloaded, that can change. It's actually part of the process of developing tendinopathy. Let's talk about tendons. Would it be fair to say that you couldn't have a healthy muscle without having a healthy tendon? Or vice versa? Yes. So it is fair to say. And it's fair to say because we have general principles, you know, we use this word homeostasis to describe how everything is regulated. Healthy muscle to exhibit its mechanical effect of moving bone effectively needs a healthy tendon. You can develop your muscle. It's actually muscle will develop more quickly than tendon adaptation occurs. Muscle will develop more quickly than the tendon adaptation. And is that why designing a really good training program is essential to avoid injury? Because essentially the people listening are thinking, well, why do we care about tendons? Nothing will take you out of the game faster than a ACL tear, than an Achilles rupture, tendonopathy, which then becomes chronic. Could you have a, I suppose a better question is which goes first? Yeah. So this is something known as the athletic accommodation timeline. So when you start, let's say you're not a runner or I could speak from a position of truth, I'm not a runner. So I, Neither. Yeah. Yeah. So let's say I start running. The first thing that occurs in the first six weeks is I learn how to run better. And basically that's called neurokinetic response. So starting all the way up in your brain at your motor cortex and going all the way through your nerves as they go through your spinal cord and go through your peripheral nerves and into the muscle, you learn how to coordinate your motion. You basically learn how to use your muscles for more efficient motion. So if you were to test my ability to run in the first day, it's not going to be as good. I'm going to be much more gassed. I'm going to go in deep into those energy zones. I'm going to really kind of stress to do the activity, but I get better at it with time. Then in muscle tissue during, after the first couple of weeks, you start to get psychoplasmic hypertrophy. So your, your muscles start to bring in some products to help them function. Now the body perceives, it seems, putting down collagen, putting down protein. From one aspect, we have a substrate driven issue, which I think you've elaborated on, the importance of leucine, the importance of protein intake. Then the other aspect is you need a continuous stimulus to convince your body to say, we need to put down some new framework here. So then you start laying down some muscle. By the time your tendons and ligaments start to adapt to the athletic endeavor you're engaging in, you're almost looking at six to nine months. And that is much more of a significant timeline than it would take for a muscle to adapt. And by the way, tendon turnover is very slow. It is. So as opposed to muscles, which have a very rich blood supply and a rich nerve supply, tendons do not have a rich blood supply. They're relatively avascular compared to muscle. So they're not going to turn over as fast. About 90% of a tendon is more or less static. And then you have maybe five to 10% that's the variable element that changes with time. So this is one of the important principles that I think gets missed. We hear about this concept of progressive overload. Well, you're not just progressive overloading your muscle. You're progressively overloading your tendons. You're progressively overloading your joint capsules, your ligaments, etc. So this is when I sort of hearken back on my personal training principles. I say, well, where is the periodization? Where are we dropping back? Where's the deloading? Where's are we working towards a goal in two to three months? And then are we scaling back and maybe changing and kind of starting back from a point just to where we started before? You can't just progressively overload until you find yourself into injury. And that's something I very commonly find. One of your quotes I'll steal from you is you can't change what you don't track. And it's and it's too true. And some people are very nuanced. They've know their bodies really well. They've been training for 20, 30 years. They may not need to track as much. But if you're a beginner or even an intermediate and you need to think about, I want to train, I have a long term goal. Well, your short term goal should be proceed without pain, without dysfunction, and really just knock down the goals that are in front of me as opposed to training until I get an injury and change the training types, for instance, or give it up altogether. Right. And that's so, so important. I see that in my office all the time. I ask, what is your training program look like? Well, I do, you know, they'll tell me a split. I do back and buys on Mondays. I do shoulders and tries on Tuesdays. Chest on Monday, universal chest day. There you go. I do, sorry. Yeah, probably chest on Monday. Matt, Matt only does chest on Monday. Matt has a good chest. Lots of push ups. Lots of push ups. And they'll tell me a training split per body part. But what about the global period? Like, how are we actually looking at the overload of these tissues over two to three months? And what is the expectation? Is the expectation that you're going to progressively overload until you're the world's strongest person or are you going to have to scale back? You've heard me say before, muscle is the organ of longevity. Now I'm putting the playbook in your hands. My new book, the Forever Strong Playbook, is your roadmap to building real strength, not just in your body, but in your health, your energy, your life. This isn't theory. Inside, you'll find the exact workouts, protein for recipes, recovery strategies, and mindset tools I use with my patients and live by myself. This book is for anyone and everybody who wants to age powerfully, stay vibrant for their family, and show up strong every single day. When you pre-order, you're not just getting a book. You're joining a movement. The links in the show notes, and I cannot wait for you to dive in. So osteoporosis affected 10 million Americans in 2014, and it's projected to increase by 50% by 2025. But what is so fascinating is we have an increased use in GLP ones. Like Osempic. I'm curious as to what your thoughts on what we're getting right versus what we're getting wrong. Yeah. So the GLP one agonist group of medicines is fascinating. They are currently used a lot for weight loss, and people lose a lot of weight. People also lose a lot of lean body mass, and you'll see ranges in different studies as Louis 15. I've seen 40 to 60%. Sometimes this is proportional to the amount of body weight lost. And so is that bad? Are we losing a lot of muscle mass? And is that going to affect our bone density? You would think it would, but so far studies looking at fracture risk in people using these medications are not showing any increased risk of fractures, and some studies are showing slightly less fracture risk. So that is not showing up to be a concern. The other thing we're seeing is these are basically anti-inflammatory medications. They may even end up helping people with rheumatoid arthritis and psoriatic arthritis and things like that. So you're reducing fat, you're reducing probably some of the inflammation associated with metabolic syndrome. And so people with body, with a loss of weight have less stress on their joints. So people are having less joint pain. We're not seeing an increased risk of fractures. I do think because they basically delay gastric emptying and create a sense of fullness and maybe decreased appetite, people have to be, I think, more thoughtful about what they're eating because you could easily fill yourself with things that don't give you the nutrients you need. So I think, yeah, you got to be really thoughtful about your dietary choices if you're eating less. I think that that's fascinating. I've seen the data that it looks like these medications actually can improve certain pathways in skeletal muscle. It seems like there are positive benefits to it as opposed to this narrative that you would expect to be negative. Right. But I'm not seeing that either. And I'm really interested in what you're saying about how the use of these medications, which by the way, we've never had anything work better when it comes to weight loss, a bariatric surgery, but those complications are challenging. And I love hearing that from the bone aspect, you're not seeing increase in fracture risk because you're hearing tick tock, not that I'm watching on tick tock, but all these other places that it's affecting bone density. Yeah, doesn't seem to be. And maybe having the opposite effect. Do you think that there's so far they can't lose unless you get them taken away from you and then people rebound? Oh, yeah. Right. And again, if they're doing the right things like strength training and eating dietary protein. Oh, yeah, I definitely think people need to strength train while they're going through the weight loss process. When someone is thinking about osteoporosis prevention, and I think I text you, message you, what do we have to do? Do we have to do plyometrics? Are there certain movements that we should think as women that we should all be doing to prevent you? I think about my mom. So my mom is in her 70s, she would cringe. She's like, you can tell everybody because I look so young. That's so my mom. I always round up by a year. I always say I'm 46 now. I just say I'm 47. But I watch my parents in the gym and I am concerned about them jumping or doing any kind of a high total. So both themselves are jumping in the gym. Right. So that's been studied, yeah, the high impact activity and in almost every study there aren't injuries reported. Now these are of course supervised programs and there are people who have bad balance or maybe more of a fall risk. And I think all that has to be taken into account. But there's huge heterogeneity in the studies on exercise programs for addressing bone loss. And many of them are on menopausal women with low bone density. Many of them show gains in bone density ranging from like one person. Training or with plyometric training. Combined, generally combined strength training and some impact training. It doesn't have to be a ton of impact training. Like one of the studies showed improvement in bone density and using like 50 jumps per session a few days a week added to the, you know, it made a difference. So, but the most effective programs seem to combine some impact and some strength training. And a few days a week, they're all over the map in terms of numbers of exercises, numbers of reps. The intensity is at 50% of your, you know, one time max or is it 80% with lower numbers? They're really variable. But in general, like I'll just sort of like for a spew, higher intensity strength training does seem to yield more benefit. In one capacity. In terms of bone density, then the more moderate or low intensity, but the other forms are not without benefit. So where you're kind of seeing some gains in bone mineral density with the higher intensity strength training and the impact training, but you're still, there's still benefit from the less intense, you know, lifting regimens. And to be honest, not everyone, people get injuries. Like I don't mean injuries like falling and breaking your hip while doing these exercises, but just like tendonitis or overuse. I mean, it happens to all of us. Like I love to do pull-ups and every time I do more than 10 sets of 10, I get, I said, tendonitis and I have to take a step back. So, or, you know, if I do, for me, I can't do really high overhead pressing weight because every time I do, I flirt with my IC joint. So that is not one I choose to do at the high intensity. I tend to choose to do that one. Lower intensity, but my point is, yeah, these programs strengthening some impact training and balance training combined are things that help with increasing bone density and reducing risk of falls and fractures. But, you know, honestly, they're quite effective. A lot of the studies range from six to eight months and follow-up will show a few, you know, I would say on average a few percentage points and increase in bone mineral density. Now, if you look at what you get from something like a bisphosphonate over a couple years, you're going to get like 6% increase in bone density. For someone who's listening, a bisphosphonate is a medication that would inhibit resorption of bone. Yeah. Is the quality different of the bone that you get on a medication like a bisphosphonate versus the quality? So, the natural loading of your bone, you've got the pulling and the pushing, all the tension of the skeletal muscle on your bones that stimulates the bone, you know, to grow and have more density. Axial loading or impact stimulates new bone formation. Our bones respond, again, we talked about disuse osteopenia. That's the opposite of use. You know, use increases density. So, where was I going with that? Well, I'm curious as to how if we know that... Oh, the quality of the bone. We're looking at 20 million Americans who are going to have osteoporosis this year. I'm scared. Yeah. So, the quality of the bone, I think, is better when you get it from actual loading of the bones. One thing we see, for instance, with bisphosphonates is you can increase the density of the bone, but is it as normally organized and is it actually laid down in the areas where the stress occurs? Probably not as well as we get with our own efforts that lead to that. And, you know, one example of that is it's not a common problem, but there is something that occurs where people get an atypical fracture who've been on, like, a bisphosphonate for many years. It's called a sub-trochanteric fracture of the hip. So, it's like below the level of the hip joint. Is that when the hip breaks and then they fall? Well, yeah, it's like a break below the level of the hip. And so, that's probably, you know, over time, there's probably micro damage to the bone because it's been, you know, normally bone is dynamic. It kind of resorbs and forms in relation to the stress that's applied to it. But if you're on this medication that's, you know, just preventing resorption, it can become maybe abnormal in area. It's not a common problem, but just an example. If you're like me, you love a good meat stick and are always on the go, but still committed to putting high quality fuel into your body, then you want to check out Paleo Valley, one of the sponsors of the show. Their 100 grass fed and finished beef sticks are clean nutrient dense and free from all the garbage found in most convenient snacks. And by the way, this is Buffalo chicken, no preservatives, no added sugar, no artificial anything. 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In ancient Rome, doctors and trainers had a big fight over who would corner the market in what we now call healthcare. And the doctors who won that fight won it in large part by putting down athletes who trained to build mass, to build muscle. There was one Galen of Pergamon, and he said that athletes who trained to build mass were incapable of rational thought. He said that they actually smothered their souls with the slime of this muscle. And that kind of marked muscle as a locus of anxiety and marked it as something, there was something wrong about building muscle that has, in a way that has lasted right up until today. So I had an experience when I turned 40 of starting to train in a more serious way than I ever had before. And it really changed me. And I was fascinated by that. I wondered why I didn't know more about muscle. And I went looking for a big book that could kind of help me understand muscle in all the ways that you just mentioned. I couldn't find it. So I had to write it. And to be fair, you are an acclaimed journalist and author. You have been contributing editor at Vanity Fair. You have contributed to the New York Times, GQ, the list goes on. You've been a very curious person, which is evident in this book. After you had this moment of understanding we had really missed the mark on skeletal muscle, how did you decide about the sections in this book? As you began to formulate, there's three big characters. There is this story that becomes interwoven. How did you begin to break that down and think about it? Most books about muscle tell you what to do. And this one's different because it's descriptive. It's not prescriptive. So I knew from the beginning that my way into talking about muscle was going to be through individuals, really fascinating people. I knew that one of them had to be a doctor. I knew that one of them had to be an ancient, a scholar of ancient Greece in some way because we get so many of our ideas about athletics and medicine from there. And I knew that at least one of them had to be a really high level athlete. And so I found these people. It took a long time hunting for them, but it's just casting. And you find the right balance of characters and then you let them start playing on the page. How long did it take you to write this book? Eight years, full time. Eight years, full time. And for the listener or the viewer to give you a perspective of how in-depth this is on the history of muscle, it is exactly that. There were many things that really struck me about this book. I would love for you to touch a little bit about the history of muscle performance, the idea of the gymnasium. I'm fascinated by the way that the ancient Greeks looked at skeletal muscle. The first thing to know about how ancient Greeks looked at skeletal muscle is to really sit back and take in the fact that they didn't see it. Now, that sounds impossible because you look at an ancient Greek sculpture and to us, it seems that they're obsessed with muscle. But it's really the lines of articulation around muscle that they believe do the work of movement and specifically the tendons. They thought that the fleshy part of muscle, the muscle bellies, the contractile tissue that we now know moves us. They thought that was just dumb stuff that was maybe for padding, maybe for insulation, like Aristotle thought that your glutes were a built-in beanbag chair. He called them useful for resting the body. It's not until just before the classical period of Greece that scientists start to open up the human body that had been proscribed in Greece before and they begin to see how muscles work. They know that somehow muscles are part of movement, but they believe that there is a portion of hot air that gets trapped at the body at birth called numma. Numma is the word for breath or wind from which we get pneumonia. Numma is circulating in the body and numma basically blows up the muscles like a balloon and then they deflate and that is part of the process of muscle. This is crazy. The idea how wrong we got skeletal muscle. I mean, the next big beat in the story of discovering skeletal muscle is under the Roman Empire and the doctor Galen. He understands that muscle has to do with movement, but he still thinks that there is a mysterious substance like a portion of hot air trapped in the body called numma that causes us to move. He says that the brain is completely in charge and muscle is just something it uses. We don't begin to understand that the contractile part of muscle actually moves us until the 17th century and then we don't really begin to understand how it's integrated with the neurological system, how the brain and muscle are partners. It's not a hierarchical relationship until the late 19th, early 20th century, even though I don't think we've accepted that yet. I think we're still pretty intent on thinking the brain's the boss and the muscle is always second fiddle. That's really fascinating. Did they look at muscle as something different? I mean, there was, we can think about words as words like victory. I know that that was something that you had wanted to put in the title before. Have we really changed the way that we have thought about muscle? Was it something to be revered back then and then transition to now it's okay, well, you're a knuckle-dragger or just what do they say, all brains and no brawn are all brawn and no brains. Greeks were fascinated by muscle even before they knew what muscles did. They were running races at the Olympics for hundreds of years before they had any idea that muscles had to do with movement. Okay, but we know that it's muscles that are making the sprinters win the race. They believe that strength is actually, it's not only something that an individual builds through training, it's not only an individual accomplishment, it's a collaboration with the gods. You have to train, but then you also have to be given the gift of strength. That's fascinating, the gift of strength. Yeah, I mean, Greeks were as likely to talk about strength as something you receive as to talk about strength as something that you have. That is an unusual way to frame it. But there is a connection between that and current physiological thinking in that there remains an element of mystery in performance, an element of unpredictability in performance that you see in something like the supercompensation effect after a periodized training regimen. Charles Stocking, who is one of the main characters in this book, he's a classicist who worked his way through graduate school as a strength and conditioning coach for Bruins athletes at UCLA. He's become really the world's greatest expert on the Greek language of strength. And Charles says that he thinks the supercompensation effect is a modern analog for Greeks' description of great performances on the battlefield or in athletics as being a gift from Zeus. It's their way of explaining what we have come to understand as a physiological adaptation. What is the supercompensation effect? Supercompensation effect, just in simplest terms, is the outcome of a certain kind of cyclical training. So you can't push harder and harder all the time. You've got to take a couple steps forward, a couple steps back, periodization. The many forms of it are ways of organizing our training to build up to a moment where we have a high level of performance. Just before we reach that highest level, we take a rest. And in that rest, our bodies repair ourselves so that we can leap ahead of where we were before that rest began. And I have a quote from your book, and it's, ancient Greeks considered strength not mainly as a quote, an individual accomplishment based on individual effort, but as a paradoxical phenomenon that depended partly on what a person did and partly on what help and gifts the person received from the gods. You know, I'm sure the listener, well, you guys better be interested in muscle, but really understanding we talk about it in terms as if we've always known it. This is the bicep, this is the quadricep. But very few of us, myself included, have thought about the history and putting it into context of what was thought of it before we knew it was Acton and Myosin and that these muscle fibers and muscle bellies were attached to various parts of the body. And there's a whole history of what we imagined it was. And let me give you a really concrete example of the gift and of strength in action. As the best as we can tell, the very first Olympic event was called the Stadeon. The Stadeon was the equivalent of the 200 meter sprint now. And the way the Stadeon was set up, it started, the Stadeon was a race between two altars. The first one was an altar to a hero who was a human who lived a long time ago, but was especially blessed by the gods. The other altar was Tzuzus, the greatest of the gods. On the altar to Tzuzus, they had laid out their sacrifice to him, which was the best part of the bull, the fleshy thighs. Now, this is a time when meat is not a part of anybody's regular diet. So the whole community is there and they're looking forward to this feast on meat, which they never get to taste at the end of the day. Everybody's watching this. The priest of Tzuzus is standing right by that altar and he's got in his hand a torch. And what the athletes are looking at as they're getting ready for the race is the torch in that hand because what they want to do is be the first to get there, take the torch, light that meat on fire, and give everybody this just great gift they've been wanting for the whole four years. And you run faster if you're trying to complete the sacrifice that brings your community together than if you're just going for a run. And they all believe that the person who wins, wins because Tzuzus gave them a very particular kind of strength called Kratos, spell it K-R-A-T-O-S. And Kratos is only given by Tzuzus. It is the strength of winning. Wait, $3,000? Wait, is that number right? I spent more money on skincare. 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So for instance, like impact exercise in particular seems- You need to find impact exercises for someone. Like a jump, like it could be jumping rope or a box jump or jumping jacks, running, something there's like some takeoff and landing, there's a little flight basically. That's different. And when we think about that, that's different than doing say a leg press. Because I would think that a leg press would build more muscle, but what I'm hearing you say is that the takeoff and landing actually that targeted activity if I'm not staking, stimulates bone of more robust way or differently. Is that true? Yeah, because you're kind of like, it's more like twice the ground reaction force that you would have with just like standing or walking for instance. So a leg press is a load bearing exercise. Load bearing exercise is good for bone density. Like in the opposite, that would be not load weight, but like being on crutches and getting again- Or being an astronaut or something like that. Being an astronaut is the extreme example of disuse osteoporosis. So yeah, load bearing, muscle pulling on bones, those things do stimulate bone formation, but you get an extra from impact. Even though you can't weight it as much. Yeah, there's a response in the bone that increases bone density. So now not everybody can jump because they've got some people have some near. So I don't want people to think they need to go like jump rope for 30 minutes. You could just do add a little impact to your routine a few days. Yeah, what else could they do? So they could do a small jump. You could just hold on to the back of a chair and jump 30 times. You could do some jumping jacks. There's some evidence that actually pool-based jumping can increase bone density. So like you'd be in a pool and you would jump out of the water, but then still land. And that's probably a combination of the resistance exercise it takes to overcome the water to jump out of the water, but then land into it. So obviously you're in a place where you're not completely submerged to do that, but that may be an option for people who can't do a lot of land-based jumping. And if you were to think about how you would design or what you would tell everyone to do, would you say have them jump? And this might be in your book because I haven't gotten a copy of it yet. Throw that out there. I was thinking about that in my area. But in all fairness, I've looked at multiple research papers that you've put together. So I'm so excited for your book. I think it is going to be tremendous because there's a lot of information out there about building muscle and body composition, but really when it comes to bones and joints. Yeah, not all in one place. I think it's going to be tremendous. I tried to put everything all in one place that all of my patients asked me all the time and I just wanted it so badly to be in one place for people. That was my goal. Well, it's not going to stop me from calling you with these questions that I have. So we're all good. What would you have someone do if they were to prioritize? Because it's tricky, right? You have to prioritize muscle for metabolic health, but you also need strong bones. So I'm curious as to how often someone would need to do some kind of activity. What does the volume look like? Yeah. So first of all, bone health starts very early. So I think we need to backtrack a little bit when you're like a child. So my kid. Yes. One of my very close friends who's a brilliant woman, Tammy Scruppella, who's chief orthopedics and sports medicine at University of Wisconsin, which is very unusual, a female chair of orthopedics. What an underachiever. Yeah, she's total underachiever. But she has this amazing body of literature. It's like a 25-year project where she took kids as young as seven up into their teenage years and followed them for like 25 years. And they were gymnasts. So this is loading of the bones, including upper extremity, lower extremity back, and compared them to kids not participating in organized sports. And she followed them into adulthood with dexa scans and other studies of the geometry of bone. And what she found was that these gymnasts ended up, depending on what part of the body, with 15 to 40 percent more bone density than their comparison group maintained even into adulthood. Now, at around age 30, we typically say that's when bone density starts to decline. So your adolescent and early adulthood years are when you build up your base. And if you don't build up your bone density before the age of 30, that's where you start from. So now we can maintain from there with interventions and try to not fall into the 1% loss per year. Can we build after 30 and 40? So some of these, you know, you're kind of trying to slow the loss, right? Because you typically will lose 1% per year. No matter what? Well, these resistance strength training programs and impact programs do show that we can gain bone mass back. You're probably not ever going to get, you're never going to get above where you were when you were age 30. I mean, because from for muscle mass, you can get above where you were when you were age 30. Do you think that it's possible? I think if we gain muscle mass, I don't, I haven't seen any literature to suggest that you would gain, that you would ever be higher than your age 30 with bone density. But, and again, these studies, but however, these studies on, now Tammy's work is unusual because there aren't many studies looking at the younger population like that. But if you look at, you know, most of the studies on these interventions were already, we're taking people already osteopenic or osteoporotic and trying to reverse some of that, you know, with the interventions and the, and the gains aren't huge, but they're enough that like if you gain a few percentage points, you might tip yourself from osteoporotic back into osteopenia, you know, take your T score from negative 2.6 to 2.5. But you're, if you're not losing, you're winning because of the natural, yeah, because losing your winning. Yeah, because the natural history would be to lose 1% of your bone mass per year or if you're post, if your men are bald as a woman, 2% per year. You do a lot of surgery. And what are some of the perioperative risks associated with oral contraceptive use? What should we be thinking about? Yeah, well, number one, a lot of your patients or my patients, if I ask them if they're taking any medications and they're a teenager, college age girl, they will say no, because they don't think an oral contraceptive pill is a medication. So you have to specifically ask, and I always ask my patients this when I'm thinking about surgery or scheduling surgery, do you have any personal or family history of blood gluts? Do you smoke? And do you take any contraception? And then I have, they say yes, I ask them what type of contraception. If it's a combined oral contraceptive pill, meaning an oral pill that has estrogen in it, there is some increased risk of blood clots from even an outpatient sports medicine surgery, like an ACL surgery, for instance, it's been shown to double the risk of a blood clot. And if you're also obese or a smoker and using an oral contraceptive, it quadruples the risk. So that's not good. So we need to do some risk assessment. You also do have to pay attention to things like a Nuvo ring, because that's, you know, an estrogen delivery, that's exogenous, we don't know the clotting risk is as high as it is with an oral contraceptive, but that's still a risk. So basically, exogenous estrogen, that's, you know, part of a contraceptive delivery is a risk for a period of blood clots. So sometimes that may affect our post-op plan in terms of blood clot prevention, or just kind of raise our antenna in terms of concern for screening for a blood clot if someone has calf pain or swelling. But there are a lot of contraceptives that don't have a risk, like progesterone only pills don't have that risk, and Moraine IUD doesn't have that risk. One that I hate the most to see young women on is depoprovera. It does increase risk of blood clots by- It's a shot, right? The depoprovera shot. Yeah, it increases risk of blood clots, but it also has a supposedly reversible effect on bone density, it reduces bone density. So I had a patient recently who, you know, had a knee injury, and I was trying to fix a fragment of bone on her tibia, and this is someone who has some nicotine exposure and is on depoprovera, and the bone was just crumbling, just really poor quality. And, you know, while the bone loss may be reversible, when someone goes off of depoprovera, you never know when someone's going to injure themselves and need a surgery. So they have the bone loss while they're injured, that's not good. So you said something there that I wasn't anticipating, and I'm looking at my producer over here smiling. A lot of individuals use nicotine, nicotine gum, nicotine mints. Do we know, is it the nicotine or is it the smoking that- The nicotine. Oh gosh, everyone is crying right now, including my husband. He loves this. Nicotine use is bad for all things, orthopedic surgery, wound healing, infection, your bone, fracture healing, tendon healing, rotator cuff tear healing. You just heard a lot of people's heart right now, because it's a thing. So I did my fellowship in geriatrics, and one of the things, actually, I did it at Wash U. It was really hard. I don't recommend anyone doing it. Just kidding. You know, they're always looking for fellows, please. But one of the things is they were talking about nicotine use and the impact on brain, brain function, positive impacts for Parkinson's and other type of memory challenges. And now we're hearing from you, from your mouth to God's ears, nicotine exposure is not good for bone tendons and anything orthopedic. It's great to know. Yeah, unfortunately. We're all crying now. You said something else. You said oral contraceptive or exogenous estrogen use. What about individuals that are using the patch? Transdermal estrogen used at the level in menopausal hormone therapy has no increased risk of clotting, as opposed to the oral versions, which do, and that's because the transdermal delivery basically bypasses that first pass to the liver that can affect the clotting cascades. So transdermal estrogen is quite safe. Now, one question mark is if you were having a major orthopedic surgery where you have another risk factor, does transdermal estrogen add to that? I mean, in the non-interd population, there's just really almost no risk for transdermal delivery. So transdermal delivery is very safe. I don't want to open up a can of worms here, but we talked about estrogen. When you are discussing menopause hormone replacement therapy, are you thinking about estrogen? Are you thinking also about progesterone and testosterone? Oh, right. So if you have a uterus, you can't use, again, I'm not a women's health doctor, but I do know this, you can't use unopposed estrogen. You have to have some form of progesterone to protect your uterus from uterine cancer. So that could be in the form of a merena IUD combined with a transdermal patch, or you could have oral progestin, something which has other benefits like sleep and things like that. I was just thinking in terms of bone health. Is it something that you are thinking about for bone health? Yeah. Testosterone therapy is, of course, not FDA approved. Approved for women, unless it's for low libido, which it is approved for. And I think probably many of your listeners know that yes, women have testosterone is just at a much lower level than men, about 10%. So there's a lot of research going on in terms of should testosterone be used for bone density and maintenance of muscle mass. And I think currently that's certainly not a common use for it. And I think we're still gathering data on that. But it would make sense that for at least women who have lower testosterone levels than they should, that the testosterone would contribute to certainly muscle mass. And we know muscle mass contributes to bone density. But yeah, right now, that's not sort of a typical part of a regimen in terms of menopausal hormone therapy. Not yet. Not yet. Yeah. If you are young, you suggest you have five kids. Did you have start your kids early? Yeah, they all have participated in sports. And we have a couple that didn't love sports, but sometimes we would go on walks and they would call them forced marches. But you know, like most of our kids enjoy sports. I'm peeing, you know. But yeah, I think sports participation in athletics is really important in adolescence and very important in girls. Because if girls aren't participating in high school sports, they're probably not going to go off into college and then like go do a regular workout. Like I can't imagine exercising every day. But I grew up always being active. And I also think it's really important to model activity for your kids, like workout with them or them seeing your workout. Like my husband and I were very much prioritized exercise and strength training. And our kids know we have to get a workout in every day. And they've over the years been, you know, we always have a workout room in whatever house we live in. And they've always spent time in those rooms or use the equipment or whatever. So I think you need to model for your kids, but also you got to get them involved in activity, you know, edit, you know, so they're active through those years. And that's from bone density, cartilage, tendons, muscles. I think, yeah, now, you don't want to over develop muscle too quickly and pull on tendons too hard before you're done growing. Because that's when you get things like apophysitis, like you've probably heard of Oskar Schlatter disease or of the knee where people get that bump on their shin bone, they're aggravating the attachment of the tendon to bone. Because when you're not done growing, your tendons are a little stronger than the attachments in some ways. Your tendons are stronger than where they attach to bone. So you can get apophysitis, which is just irritation of the attachment of the tendon to the growth center on the bone that it attaches to, because it's an area of growth. So, you know, that's when, and your child won't know if they're doing too much, because it'll hurt and they'll tell you and it's not, it's just a thing that where you kind of rest as needed, there's no intervention other than rest as needed. But, you know, so sometimes too much activity can lead to apophysitis in kids. But physical activity is very good for children. There's a, you know, we have a huge obesity problem in America. In general, yes, being active is good. You know, you don't want them to be sedentary. When girls go through, let's say, the no longer term for the athlete's triad, the women that are over exercising, under eating, and they lose bone. Yes, this is part of a crewing bone before the age of 30. So, that is a huge risk factor. Like, let's say you had what used to be called the female athlete triad, like when you were in high school or college, you had an energy deficiency, whether it was from inadequate energy intake or just not matching your output with your intake. That's actually a lot of, so the reason the term is not relative energy deficiency is not always with disordered eating. They're kind of just actually, but you're not, you're under fueled chronically. And you'll, this will be the kid that presents with the stress fracture, the cross country, when they don't have been. And what she means by that is that, say, for example, an individual is really active and they're just not thinking about eating and they're... They just cannot keep up with the demands. They're eating a lot of food, but they're just... They're still under fueled. Yes, they're under fueled. So, yeah, and so if you tip into a state of, you know, amenorrhea, where you're not having cycles, you're now in like an estrogen deficient state, very low body weight, you're losing bone marrow density when you're supposed to be building up your base. And so people can get to, so they'll arrive at 30 with diminished bone density. And so you don't want that to happen. Now, let's say you're... And what's done about that? Do they give them the pills? Well, they're, yeah, I mean, nutritional consultation, intermittent consultation, you can use contraceptive pill. But they won't catch up. And again, I don't want to be negative will day. You can, but there's some downstream effect that is not probably entirely reversible. And depends on how long it goes on for and how many bouts of this happen to a person. How genetic is osteoporosis? You know, I don't know if we know the exact genetic propensity, but if that is a question when we're assessing risk, like if you have a family history of osteoporosis, you know, that makes me more likely to send someone for a dexa scan. No, so what I was getting at is if you arrive at, let's say arrive at menopause. And so risk, so menopause in and of itself is a risk for osteoporosis, as is being Caucasian, being thin or underweight. But if you also tell me, oh, I have a history of, you know, amenorrhea or needing disorder, or we didn't call it back then when this person was young red center, whatever, like where you had an added risk to not have as much bone density as you should, those are all adding up for you at that point. You know, these are risk factors that might mean you need to have a dexa scan to check for osteopenia, osteoporosis sooner than is typically indicated, which is 65, which is probably too late. Way too late. Well, our piece, so we have a medical practice and we always have for baseline, we have our patients. I mean, they could be 40 and we want to see a dexa. Yeah. Now for patients under 50, of course, you're not necessarily looking at the T score, you look at the Z score, because the T score is comparing older people to younger people. And if you're under 50, you're kind of still younger people. But yeah, there's, there's value in that, especially with any risk factors. And, you know, I think the frustrating thing about the typical recommendation being to get a dexa scan when you're 65 is that if you get a dexa scan, you're 65 and you already have osteoporosis and no one told you when you were 52 that menopausal hormone therapy can help prevent osteoporosis and prevent fractures in many people, you know, now you're 65 and you're kind of, you're kind of out of the window of time where it's recommended to initiate menopausal hormone therapy, which is within 10 years of menopause. So a lot of people are missing the boat. There are a lot of people who are seeing doctors who got their medical training when there was a lot of misinformation about menopausal hormone therapy and don't provide it. And it truly is indicated for prevention of osteoporosis. So, you know, unfortunately, I think some of the most long term consequences of menopause are musculoskeletal and bone density is, you know, osteoporosis is one of the biggest ones. So, you know, there's just, and there's more and more of a shift in this understanding. But again, if you just think back that initially menopausal hormone therapy or formerly called HRT was indicated for vasomotor symptoms. And that's not even the tip of the iceberg, the long term effect, probably the one that's most life changing is the effect on bone density. I mean, joint pain, inflammation, arthritis, frozen shoulder. Yes, those aren't good things. But the very long term consequences, like it's life altering, mobility altering, if you get osteoporosis and you get a hip fracture, it's, you know, there's mortality and morbidity associated with that. And why is that? Do you, what are some of the rates for morbidity and mortality of falls? And, you know, we were talking about impact training. And it seems that because I was asking these questions before that it really is about the joints or the, the location that you're loading. It's not full body, which I think is fascinating. Yeah. Yeah, no. And so if you look at what's in these resistance exercise programs, you'll see, yes, it does include overhead press and I mean, again, they're all different, but a lot of them have like an upper extremity, pressing maneuver, maybe a deadlift, a squat, some impact, you're trying to get like, large muscle groups, but you're also trying to load, you know, the upper extremities, the lower extremities, the spine. And then the impact, yeah, probably why it's more likely to improve, you know, femoral neck bone density and cortical thicknesses, because that's what you're loading. You're loading the lower extremity with that, with that impact, you're not loading so much your spine or your, your arms, unless you're a gymnast and then you have good upper extremity. And it's a side, they call osteoporosis a silent disease. Silent disease. Yeah. Someone isn't going to know that they have osteoporosis until they break something until they break something, which is terrible. Yeah, or have a stress fracture, like you could be like a master's athlete, you know, what about and if they're younger and have a stress fracture, is that an indication that well, sometimes stress factors are part of energy deficiency syndrome. Okay. Sometimes they're just part of, you know, bad alignment, like you got a high arch and your foot rolls over the side, so you're going to get a stress factor in your fifth metatarsal. That's different, you know, that's an alignment issue. What about tendons? Have you thought much about tendons, tendon health, with hormone replacement, loading them or is that still? Yeah, so tendons also have estrogen receptors and yeah, definitely we see a lot more tendonitis, you know, periarticular pain, you know, around the same time that was the increases in joint pain. Do does hormone replacement, menopause replacement therapy help that? I think the data is not specific enough and that's so, you know, again, looking back at these studies, a lot of them are just like, did you have joint pain or how severe was it? Did it get better? It's the data isn't as granular as it could be, which is really why orthopedic surgeons or researchers need to work with women's health doctors to get more specific information. I started a registry with our women's health department at Duke looking at trying to sort of correlate vasomotor symptoms with musculoskeletal symptoms, so you're, you know, this study, this is so far you're looking at 1,000 participants, is that what this is? Well, right now we just opened it, we have a couple hundred people enrolled, we're going to continue to enroll, but we're trying to look very granularly at joint pain, like which joints are painful? How, you know, is it bilateral? How bad is each joint? Did it get worse or better when you started hormone therapy? You know, what, do your vasomotor symptoms mimic the severity of your joint symptoms? That's interesting. Yeah. Well, we don't know that, I don't think, and so we're trying to be more detailed and granular in our information in that way, but so I think like the, you do see this acute exacerbation of joint pain and arthritis and inflammation early on in menopause, that's less silent, your joints are talking to you, as opposed to the osteoporosis is kind of insidiously happening in the background, and you don't know, you have it until you get a dexa scan or, you know, break a hip or your wrist or, you know, a lot of times people will be out being active in fall, playing pickleball or tennis and, you know, get a dysceleradious fracture. Well, you know, we tend to see some of those when people are active, we might see dysceleradious, proximal humorous, my neighbor just broke her proximal humorous skiing, you know. She loves that she's your neighbor though. He jostled, you know, fixed that second. But then, you know, the more, what we typically think of as fragility fractures that happen as we get old, which is the same level fall, you know, tend to be that the hip fractures and the vertebral fractures too. I'm really intentional about what brands I bring into my home, and I've been using Branch Basics, one of the sponsors of the show, this cleaning product, since I was pregnant with my first child. And listen, I've tried all different kinds, but this one I love and I feel safe around. Branch, basics, whether it's in my kitchen, my bathroom, laundry room, everything feels clean without that harsh chemical smell. And frankly, I think it's really important to have a safer cleaning supplies overall. And it comes in a concentrate. So just dive in a little bit for cleaning, for countertops, floors, it is fragrance free, it is safe for kids and pets. I'm so grateful that they are going to be offering you 15% off and free shipping. With this starter kit, all you have to do is go to branchbasics.com slash Dr. Lion. That's branchbasics.com slash Dr. Lion. The reason we are really focused on tendinopathy is because those seem to injure before a muscular injury happens. That's right. It's the common denominator that limits the quality of life. I think it's a huge limiting factor in training programs and progression. And I think it's one of the first things we see when somebody starts weight training, and we start to see these things arise. So we'll go through a couple treatments. Amazing. All right. So we have this relatively vascular structure. It's in a state of disrepair. Let's think about what that means. So the actual structural components are not as strong as they were. And you could think about this like you have a house that is not perhaps built as well as it could be, you have a leak, whatever else it might be. Well, first thing we're going to do is we're going to bring in a GC. And so that's your general contractor. I was like, what's a GC? Oh yeah. So you have tinocytes. So same thing in muscle, you have your myocytes, and you also have your osteocytes and bone. You have these cells that basically look at the tendinomyostasis, and they help direct traffic. And tinocyte is a standard, it's called a modified fibroblast cell, so it helps to lay down collagen and also helps to direct traffic. The tinocytes will sense that something's wrong and they'll bring in other cellular products, one of which is that you will start to grow little blood vessels in the area. So part of tendinopathy is actually when we put color-powered Doppler on ultrasound and we look at a tendon, we'll see stuff light up. That was previously, that is a good telltale, one side versus the other, do you have hyperemia in a tissue? That's already assigned that things are going the wrong direction. Well, now we say, well, now you've aggregated this scar tissue, you've aggregated these other things that are there that are not that helpful. Well, we might have to bring in an excavator. And the excavator is, we have a couple of different treatments for excavation. One of our treatments is called PNT, so percutaneous needle tenotomy, which is when under an ultrasound will actually pass a needle through the tendon several times. Is that where dry needling came from? It's very similar to dry needling. Yeah. This came first and then dry needling was adopted. Yes, so dry needling, depending on your discipline, dry needling is something that could be performed by a physical therapist. For myself, I do these under ultrasound and visualize the portion of the tendon that's in denopathic. Which I just want to highlight that takes a ton of skill. Ultrasounds are not easy to use. And quite frankly, I believe that that's how it should be done, because then you actually can see where the injury is, what tissue you're putting it in. You're not doing it blinded. You are being able to visualize. It's important to visualize. It's also going to tell you whether or not there's a tear there. You don't want to needle a tear, right? So a tear is a different concept. A tear is a separation, so we don't want to excavate or in that area. It's not helpful. So the thought of passing a needle through a tendon several times will actually help induce, take this state of chronic disrepair and convert it to the acute inflammatory phase again, and basically help to cycle out some of that stuff. So that could be done through PNT. It could also be done through something called a 10x procedure, which helps to remove scar tissue, remove calcium that's built up in tendons. The advent of PRP, and YPRP is so interesting. So PRP is a distillation of blood products. So we spin down your peripheral blood. It's still majority red blood cells, but PRP means platelet-rich plasma. And there are two subtypes of platelet-rich plasma, the exact concentrations of which do differ in the literature based slightly depending on the study you're looking at. So you have leukocyte rich, so white blood cell rich platelet-rich plasma, and leukocyte poor platelet-rich plasma. If I were treating a joint, I would use leukocyte poor. I don't need white blood cells in a joint necessarily. But when I have this chronic state of disrepair, I need a whole construction crew, I need my white blood cells. So I'll use leukocyte rich preparations. And I typically perform it with a tenotomy too, to actually put some areas into the tendon where I can distribute that PRP. Now PRP has several growth factors, one of which is platelet-derived growth factor. And this helps to basically stimulate the tinosites and another type of cell that resides in tendons called TSCs, tendon stem slash progenitor cells. So you do have a repository of stem cells within your tendons. It's just a question of mobilizing them. So conceptually, we thought, well PRP makes a lot of sense. Depending on the tendon and depending on the literature that you're examining, it can be very effective. On a hold, I would say it's probably a 50-50 proposition, depending on the chronicity of your tendon problem, as well as whether or not you have a tear concomitantly, and where that tear is. Not all tears are made equal. The tendon itself, right, so you have the muscle coming towards the tendon. You have a myotendinous junction, which basically looks like a finger where the tendon is interlocking with the muscle. And some tears do occur there, and those can be quite tough to treat. But then you also have something called the emthesis, which is where the tendon attaches to the bone. And so those are the most common ones we are treating. Now you can have a tear at any portion in that tendon. So they all have different prognoses. If you have a tendon on the bottom right by the bone, that's a different prognosis than the one up by the top by the bursa. So we try to extrapolate from the natural history of this, what's the percentage chance it's going to heal? Where is it? How big is it? How impactful is it to the amount of strength you can produce in the relevant muscle? How impaired is it? And then would we consider, is this a large enough tear that it should go to surgery? Is this something that we should try PRP in? Important for people to know, if you do suffer a tendon tear, there are different types from a perspective of if we're just looking at a large tendon, you can get what's called a full thickness tear, which is when it's like, as if somebody punched a hole in a paper, goes straight through, from top to bottom. And you usually know when you do those? Yes. That is, I've had quite a few injuries and you know when that happens. It's not like a tendinopathy. You don't necessarily, you know, it might be a little irritation and then you go back to the thing and then you irritate a little bit more. That's right. But when you get a full thickness tear, that is an acute injury that typically will take you to your knees or whatever. Yeah. So the full thickness is the pothole and then there's something called, so we say full thickness incomplete or full thickness complete. Incomplete would just be have a sheet of paper and a punch a hole, punch a hole with a hole punch. Complete means I literally take a pair of scissors and I cut the paper in half. If you have a complete tear, now the tendon is no longer attached to the muscle. That is a surgical problem. Okay. That is not something that's likely to heal by itself. That would be, for example, like a tricep tendon tear or a bicep rupture. Yeah. So, and depending on how important the bicep, so for instance, the bicep is interesting because the bicep is almost like a fifth rotator cuff muscle. There are people walking around with bicep tendon tears without significant symptoms. But if you have a complete full thickness tear, what will occur in time is because the muscle is not seeing any tension, the body deprioritizes it and it will atrophy. And if it atrophies to date, I'm not aware of any way to stop that or reverse it. So those are the circumstances. Like I brought up that example of the 30 to 50 year old guy who pops his Achilles playing back yard football because that's the most common age population to get acute Achilles tendon ruptures. But if that occurs and that tendon is not reattached or it's not approximated and you're putting a boot and something like that, then foreseeably you'll atrophy your gastro-arch and your soleus and that's going to be really tough functionally to go through. So essentially don't delay. I think a lot of the patients that I have and many people listening, they don't want to stop their activity. They'll injure themselves and they don't want to stop. I don't want to get a bicep repair. I can still be just as strong, but if you're going to do the intervention that requires surgery, one should do it swiftly. Yeah, you should be evaluated swiftly and you don't want to see on MRI or on ultrasound. You don't want to see those atrophic changes occur. That's a sign that your that muscle is not going to be as functional as it originally was and therefore your prognosis isn't as good. Again, you see patients often and it'll be daily either a shoulder, a knee or a hip. Do you believe that it's because of patterning? Why are those the common injuries? Yeah, in the shoulder, I think it's because we have mechanical compression underneath the bones of the shoulder and that's known as a symptom. It's called subacromial impingement. So basically, you're moving your shoulder around and the tendon gets caught underneath the bone and that's, you can sometimes hear a snapping sensation when you do something like a military press. For patella, it's because a lot of times patella retendinopathy is part of a greater clinical concept known as patellofemoral pain syndrome, which by the way is most often associated with weakness of the gluteal muscles. So the knee is overloaded trying to do too much work and the glutes are not adequately supporting the knee and the hip. So the posterior chain is actually affecting the anterior chain. Yes, and posterior lateral specifically. So hallmark of patella retendinopathy, patellofemoral pain syndrome, we commonly will look at strengthening up the gluteus mediae on the side of the hip and then the whole goal there is can you get back to walking and running with stabilization at the hips so there's not so much pain at the knee. Once again, smoke versus fire. Your knee hurts, you do have a tendinopathy, but mechanically speaking, there's an insufficiency of some muscles that are higher up in the kinetic chain. That's it just seems really challenging as we think about long term projection of people's lives to figure out that I have a weak glute meat and you have, I don't know, just pick a different muscle. Sure. Are there things that individuals should all be doing? Should we wake up, we brush our teeth, we brush our hair, should we be getting up and doing glute activation? I don't know, eyes, T's and Y's for our shoulder. Are there things that we could embark upon now to very specifically prevent a mechanical injury from a tendon that we don't even know that we have? It's a great question. And in trying to distill what makes a lot of sense, I will give home exercise programs to patients almost to that exact effect. They come in with a back injury, but I say, well, that was an awful time good to start rehabilitating and prehabbing your hips. Is prehab a real thing? Prehab is absolutely a real thing. It's tough because prevention is difficult to study. So it's more, it's very, very difficult to study. So I'm recommending this because conceptually it makes sense not because I have a study to point to that doing, you know, sideline hip abduction exercises helps stave off the onset of something. So what I see for the shoulder, a lot of times the mechanical dysfunction is at the shoulder blade and how it's moving. Either it's elevating too much, it's not appropriately what's called protracting. And a really good test to see how your shoulder blade is working is to do a push-up with a plus. So at the top of your push-up, you push out the ground a little bit more. If you're trying to achieve that motion by rounding your thoracic spine, you can't appropriately actually work through the back part of your rib cage and your shoulder blade to get that to work well. So push-up with a push-up that I like. For the hips, a single leg stance squat. So would that be a pistol squat? So actually I prefer this like skater, skater variety. So your, your, your trail leg is behind you. So I like to see single leg stability and single leg stability is a great determinant of how you are actually going to progress to your gait cycle. So a lot of people, this is a really good thing and I'll show off my PM and R residency here. So, and is this standard? So do all, I do all physical medicine and rehab physicians need to learn biomechanics? Yeah, it's a huge element of our training. It is a part of your training. And I'll tell you why, because you, unless you understand normal biomechanics through the gait cycle, you can't rehabilitate somebody with a stroke. Once they're hemiparatic, once they have a foot drop, it's really tough. So you have to know the normal mechanic, mechanical determinants of gait to understand the dysfunctional elements of it. So I like to see how, you know, with regards to the gait cycle, 60% of your time is in stance phase, 40% of your time is in swing phase. There's a 20% portion that's called double support where both legs are simultaneously on the ground. So your glute mead is actually active to stabilize your pelvis. So if you see somebody with a lot of hip movement while they're walking, you don't want to have 100% stiffness, but you want to have stability. If you have a lot of hip movement when they're walking, it's oftentimes an indicator, well, it's not as stable as it could be. There's not enough muscular tension to support the core. The center of mass in the body is in the pelvis. So my, I always encourage young athletes, I'm like, if you have to focus on a couple things, it would be be very stable through your pelvis. You can't shoot a cannon from a canoe. Okay. So you need stability in the pelvis to put force down through the legs. All athletes, regardless of what you do, are made in the legs. So all athletes are made in the legs. Yes. And I believe that very strongly. Great pitchers have a good set of legs. They know how to really drive off. Even look at Mike Tyson, right? One of the greatest knockout artists that has ever existed in the heavyweight division. He had monstrous legs, right? It was a huge element why he was able to compete with people six inches taller than him. So I believe it's a good stable core that can rotate under load, good, strong glutes and knowing how to keep your spine stable is really important. So good neutral spine throughout the range of motion. And then when you're walking, yeah, you're, you're going to be, you do swing the thoracic spine and rotation a little bit while you're swinging your arms, but you want your body to be stable. You want, you want to be able to walk slow and you want to be able to sprint fast. And if you could do both of those, you kind of check in with yourself. If you can't walk slowly without feeling like you're off balance, something's a little bit off. Do you think that everybody should continue to sprint or never lose that ability? I would love for everybody to sprint. I think sprinting is fantastic. It's also a great check in to see where you're at. But if you are doing it, you need to be very careful with load management because if you haven't done it in a while and you go back to it, it could be a major risk factor for Achilles tendon. And to be clear, well, actually I evolved my hamstring doing a long stride sprint. Would you recommend, you know, people listening to this or thinking, because we're going to cover zone two cardio and training, because you and I really see eye to eye, excuse me, about how there's a lot of discussion about zone two and how that's going to be so effective in cardiovascular health. There's a lot of other ways to train. But this idea of picking up where you left off may not be the best thing. So if you're at home listening to this, moving fast is important because you lose speed and you lose power. But perhaps not picking back up if you haven't sprinted or you haven't done a lot of these motions like the guys that you're talking about between 30 and 50, jumping on the basketball court, you probably have to build up to that. Is that fair to say? It's absolutely fair to say. Can we talk a little bit about, well, I mean, let's tie up the rest of tendinopathy because I'm curious about some risk factors, which in my mind would include medication. Common medications that may affect tendon health. Yes. The first one that comes to mind is fluoroquinolones. So that's like siperofloxacin, levofloxacin, that's a whole class of medications. Those are antibiotics. Fluoroquinolones are very strongly linked with tendon problems and tendon rupture. We believe that this impacts tendon metabolism and integrity to some degree. So those are of concern. You know, there's some, I think, very good discussion around statins and tendons specifically. So whether or not they're beneficial. So if you have somebody who has hypercholesterolemia, they can actually deposit, I'm sure I know you know this, but xanthomas in their tendons, so fatty deposits in the tendons. So in that case, a statin might actually decrease the size of their tendon and improve the tendon health. But if they have familial hypercholesterolemia, that's right, but not if they just have high cholesterol. It's tough to say. Okay. It's tough to say because hypercholesterolemia, diabetes, gout, these are, and slash hyperurusemia are all risk factors for tendonopathy and smoking. So if you look at the metabolic syndrome spectrum, obesity is also a risk factor. All of these things impair tissue healing anywhere in the body. So in a structure that does not have a great blood supply that's constantly under load, it's very much magnified. That's an interesting concept I haven't quite thought about. Again, because I'm so fixated on muscle, if someone is obese or struggling with any kind of metabolic dysfunction, that would affect tendons in general. Diabetes patients will rehabilitate more slowly than non-diabetic patients, and partly because tissue healing is slower. So it's an excellent textbook that I came across that actually looks at all the metabolic influences on tendonopathy, and chapter by chapter goes through it. And one of the aspects of it was just think about it like it's another structure in the body. It heals more slowly. Bone fractures heal more slowly, microarchitecture and bone is more slow. It's one of those things where it's reasonable to make a leap from one concept to another. If tissue healing and tissue repair is not as quick as it could be or as comprehensive as it could be in one tissue, there's no reason to suggest that it's going to be better than another. So fluoroquinolones can cause a risk of tendon rupture, which it's really important that physicians educate their patients. Don't go sprinting, don't go running when you're on these statins. Statins may have a positive effect, depending on the person. Anything else that is known to affect tendon? Corticosteroids. So corticosteroids, I had a great attending while I was in residency, he said, if you just draw a body diagram, you can find a place that corticosteroids impact every part of it. And it's the truth. You can get hair loss, they can get your skin changes color and texture, and no surprise, it does impair tissue healing. Now the question becomes a very good question because it is part of my practice to provide corticosteroids. And also it's important to point out it's standard of care. It is. It is. And so the question becomes, why are we doing what we're doing? And so in the circumstances of somebody has a tendinopathy and they're getting a corticosteroid injection, that injection should be guided. It should be into the adjacent bursa. You don't want to put corticosteroids into a tendon. That's not going to help anybody. But if you're putting in the adjacent bursa, there's theory that perhaps you're going to anesthetize and kind of decrease the pain signals coming from those little nerve inlets that have actually grown into the tendon themselves. And if I get you some short-term pain relief for three months, which is on average what we counsel people for corticosteroids, if I get you some short-term pain relief and you can do the PT and your mechanics are improved, are you in a better landing spot than if I didn't do it? And that's a conversation I have with everybody around a corticosteroid. Now oral corticosteroids are prescribed for a variety of conditions, rheumatoid logic conditions. And we're talking about a prednisone, a metrol dos pack. That's exactly right. I even use them to some extent when we're treating low back pain patients who have a really bad low back pain bout and they have a flare and we can't get them in for like an injection or epidural. And we can't get them through PT because they're in such a bad spot. We'll use a metrol dos pack. Now, metrol itself is going to be absorbed by the body. Your body does not know exactly where to disperse this medication. It's going to be absorbed, it's going to impact hormone production, it's going to suppress natural production of things like testosterone and sex hormones, it's going to feedback on the pituitary and the hypothalamus and the whole chain and the adrenals. But at the tendon level, it can actually impact your ability to repair. And so if you're susceptible and you have a predating injury and you go through a metrol dos pack and you go exert yourself, there is a potential that you can injure yourself. Now, once again, risk-benefit ratio in everything we do. I've used this phrase with you once before and I'll use it again. There is no free lunch in biology. And it's too true. It's too true. So everything we do has side effects. Everything we do has a potential downside. Everything needs to be weighed for the person in front of you. So in the risk-benefit analysis that you're saying somebody has a tendonopathy, it's been recalcitrant to PT. You've tried to do some stuff, they have nighttime pain. Well, now the nighttime pain is impacting the rest of their body because they can't sleep well. Is pain worse at night? Depending on the tissue. So let's say, so if you have a shoulder bursitis as a consequence of a tendon problem in your shoulder, nighttime pain is a hallmark of it. And is it because cortisol is lower? Why is that happened? Mechanical compression. So when you stop moving tissues that are relatively inflamed, they will touch other structures around them and sensitize them. And then specifically, if you're like a stomach sleeper and you put your arm up to the side around your pillow, you might feel like your your belt wakes up really sore. And that's because you're compressing a tendon. Tendons like load, they don't like compression. Tendons like load, they don't like compression. That's right. So same thing. We're learning a lot of really good one-liners over here. Really, really great. There's a same thing somebody has a gluteal tendinopathy on the side of the hip. Lying on that side will be very painful at nighttime. Extended compression on a tissue that's irritated, you're going to know about it. Somebody has an Achilles tendon problem, shoe fits not correct, or they tried to say they were in the first time in cleats for a while, that they weren't in cleats before, you might inflame that area. Any other medications that can be harmful? There's perhaps more as well. But these are the big ones. Those are the big ones. I think more about the, in some circumstances, some of the hormone replacement that's helpful. I was going to ask you, I was going to ask you on the flip side of this, are there potentially oral agents or injectable agents that could be beneficial for tendon health? Broadly speaking, from a nutrition aspect or like a nutraceutical aspect, what we can take, hydrolyzed collagen has been proven to be a little bit helpful in studies. Lucine, no surprise there has been, I'm sure Lucine's been on this podcast before. No, never heard of it. Yeah, right. So, Lucine is actually a component of a proteoglycan around tendons called decorin, and it can help lubricate tendons. It's also, once again, a concept that makes sense. If it's good for muscle, it's probably good for tendon. So, in these circumstances, good for muscle, it's probably good for tendon. I love this because we have really left tendon out of the conversation. We're back to your neck of the woods and muscle. But the interesting thing is we know that to some degree, it's a substrate-driven issue. You do need adequate protein intake. It is a collagenous structure. Whether you absolutely need collagen, because your collagen is going to be broken down your stomach and brought back, is I think a better question to ask. So, it has been proven to be somewhat helpful. Omega-3 intake has been associated with decreased end tendonopathies. And is that because of its impact? I always think, okay, well, what would the mechanism of action? Would that be an inflammatory perspective? I think it's the low-grade anti-inflammatory aspect of the Resolven pathway. So, I think that that's it. Now, for that reason, it's important to point out a hallmark of tendinopathy is expression of prostaglandin E2. And so, if people don't know E2 is something that is present in acute inflammatory processes, it's why a lot of anti-inflammatory medications work. So, MEGA's act on the same aspect without a lot of the potential downsides. So, I will counsel patients to take omega-3 supplementation. DHA and EPA are superior. So, I will counsel them to do that as well. Now, with other aspects, protein intake, loosened intake, vitamin C is a cofactor and collagen synthesis. So, vitamin C makes a lot of sense. And are there doses that we know of? You know, I'd have to get back to you with exact dosing. I just know that it's a dietary intake of vitamin C is associated with improved tendon healing. And have you heard of, I don't know if you ever use these in clinic, but SPMs, the specialized pro-resolven mediators orally? I've not used them. What is... Yeah, I am not so sure on the data, but we've used them, some of my colleagues have used them a lot with operators. But you and I will have to look at some of the actual data, but I am curious. Yeah. And vitamin D can be helpful as well. So, vitamin D has been proven to be helpful in tendinopathies as well, can help decrease some of the pain. Vitamin D, vitamin C and vitamin D deficient rats have decreased rotator cuff healing after injury. So, it's interesting to think about leucine, glycine, and lysine are the amino acids that are most helpful. But having a good amino acid rich diet with good amino acid profile is probably best. From a hormonal aspect, hormones are really interesting here because I think when we were speaking about this, you had mentioned that when you were back in training, you came across some patients and one of the first signs of some of their hypothyroidism was actually the acute development of tendinopathies, which is fascinating. Yes. Thyroid hormones, basically, T3 and T4 play a role of stopping apoptosis or programmed cell death in tendons, in tino sites, so in your general contractors that are overseeing work on your tendon. So, if you have insufficient thyroid hormones, thyroid hormone circulating, that's perhaps a major risk factor. Another thing that's a potential major risk factor is T4 actually mediates collagen metabolism, so you need enough circulating. The sex hormones are often interesting too. So, estrogen is the interplay of female sex hormones and these deeply collagenous structures like tendon and ligaments is the subject of fascination for a whole body of literature. So, I don't want to do them a disservice by speaking about it very quickly. But there's been a good degree of insight into phases of the ovulatory cycle and risk of injury and in adolescent females who are in the developing stage there and are engaging in sport that perhaps you could have a two to six times increased risk of ACL injury during specific phases. And then we know in the post-menopausal population that tendonopathy tend to develop. So, the absence of estrogen appears to be a problem. Same thing goes for testosterone. Now, testosterone, there's a clear in that same post-menopausal population, the testosterone is going to decrease as well. So, testosterone appears to be beneficial for tendon where the conversation gets very interesting is are the testosterone analogs, are the synthetic analogs detrimental? It's a really good question. So, basically what he's saying is the use of certain anabolic steroids going to injure tendons. I think it's a really good question. And the answer is they appear to be clearly due to the use of them. The skeletal muscle is enormously sensitive to them. But does it need to be testosterone specifically to help tendons? And that's one of the great questions. So, I'd say somebody starts on an anabolic steroid regimen and they're drastically increasing their muscle size. Well, the athletic adaptation curve does not change. You might retain more muscle, have less catabolic effect, you might get more week over week training benefits, but you still need time for the soft tissues to accommodate. So, it's one of those unfortunate things that plagues people is bicep tendon ruptures, pectin and ruptures. That's what we see a lot of time in the gym. And so, it's something important to think about. Does it need to be testosterone specifically? Or is it or can it be something else? From the literature that I was reading, it seems like it needs to be testosterone specifically. So, both estrogen and testosterone play some protective element. And therefore, another question is, in individuals who are taking synthetics, who are on a robotase inhibitors, are they doing themselves some degree of disservice? Thanks to PEEK for sponsoring this episode. If your morning coffee leaves you jittery enough to reorganize your entire house, I feel you. But somehow, still, you're unfocused. You're not imagining it. Most people are running on chaotic energy that crashes midday. Sun goddess matcha has been my solution. It's amazing. It's PEEK's ceremonial, grade organic matcha. It's clean, calm, smooth and steady energy. I drink it mid-morning when I want to focus without feeling like I'm on a caffeine roller coaster and it doesn't stop there. It also has antioxidants that support skin health too. I mean, listen, sign me up. So, bring that heart rate down, no more jitters, and save some money. Get 20% off for life and a complimentary gift at PEEKlife.com slash Dr. Lyon. Try it and let's see if you glow from the inside out. So, there's a great paper here. So, this is titled, Is Hormone Replacing Therapy Association with Reduced Risk of Adhesive Capsulitis in Menopausal Women, a single center analysis. This came out 2023 and I just think it's so fascinating that there's this domain of sports injury and then there's this domain of life injury. What happens to women? What happens to women? Life injury and you talk here about frozen shoulder and that typically hits women between 40 and 60. Yeah. So, I love the topic of frozen shoulder. It is definitely not sexy in the world of orthopedics. People have a woman come in with frozen shoulder like, I'm going to see this person forever. They're going to be in pain. They're not going to need surgery. But I love helping people with this problem. You really can help people a lot and actually just validating what's going on with them is helpful. So, yeah, typically occurs in women age 40 to 60. It was labeled as idiopathic forever and you know what idiopathic means. It means we just don't know what causes it. Yeah, we don't know. We're idiots. But how can it be idiopathic if this happens mostly in women and not in men? In fact, if it happens in men, it's almost always in someone with really poorly controlled diabetes. So, that's a different situation. And of course, diabetes is associated with high levels of inflammation. But so, a low estrogen state is associated with high levels of inflammation and there are some really interesting animal studies that show that the presence of these estrogen receptors in the synovium say of the shoulder and that applying estrogen to the tissue of the lining of the shoulder can reduce levels of inflammation and reduce the fibrosis. And there's an actual pathway in a recent study looking at mice showing how basically fibroblasts are activated without estrogen. And this is kind of probably what contributes to the thickening and the scarring of the tissue around the shoulder joint. But I said the shoulder, right, as opposed to say the hand for the wrist. Yeah, I have wondered about that. I don't know if the shoulder joint perhaps has like an increased density of estrogen receptors or something. And it's not always bilateral, but I will tell you I have many patients that it hits one side and you're later. They're back with the other. But the good thing is when it comes on the second side, they know right away. And if you're developing a frozen shoulder, what happens is, first it's really painful and not stiff. And then it gets stiff and painful and then it just gets stiff. And a lot of times what happens is people wait to come see you until it's just super stiff and they've kind of suffered through the painful phase. And at that point, it's a little bit hard to get rid of, you know, kind of thaws out over a year. But if we catch you when you're still painful and not stiff or painful and stiffening, it'll respond really well to a steroid injection and kind of try to, you know, reverse or shorten the process. And usually when women have it on one side, they know right away when it's happening on the other side. How so someone listening to this and they just hit 40 and they're thinking, Oh my gosh, I do not want to get frozen shoulder. What are they? What are the signs? It starts with usually no trauma. Sometimes people will call this is I would say one of the more common things I was walking my dog and my dog really pulls on my arm. But it's not anything you would think would like, you know, cause a trauma. And they often wake up just with pain. The pain is usually okay when you're sitting, but it's painful at the end range of motion. Everyone's sitting in your chair. Go ahead. Yeah. And you know, look down, move side to side, you have the same motion on each side. So the pain isn't usually mid arc, but it's kind of at the end of the arc. And like a classic sign of adhesive capsulitis or frozen shoulder is pain and range of external rotation at the side. There's really almost nothing else that causes that specific pain with that very minor motion. So then the other motion people will start to lose is they'll say, well, it's hard to reach across my body, like shaving under your opposite armpit or fastening a bra or tucking in a shirt. Those are the functional things people start to notice. But I'm always amazed that people don't notice. I would lose notice if I lost like five degrees of motion. But let's be fair. What people don't know is your division one, former division one athlete and married to an orthopedic surgeon with five children. And I'm an orthopedic surgeon. Yeah. So, so they don't, they don't notice. But by the time they come in, they've usually lost the motion and they're painful. The other weird symptom people will say is, oh, my fingers feel tingly, not like cervical radiculopathy, pinched nerve down into my hand, but they'll just have the vague sense that some there's this tingling sensation in their hand. And then some people have like also like lateral opacomalitis because they're basically what's what they're doing is now they're just using their arm like, like T of X arms, using everything from the arm down. So there's probably some positioning, there's probably some inflammation of the capsule around the shoulder. And maybe that spills over a little bit to the plexus of nerves that go down your arm. Wow. But if you inject their shoulder usually within three months of symptoms, the things reverse really nicely. I can't take credit for it, but the tingling feeling in the hand will go away. Usually their range of motion goes back and occasionally you have to like inject them one other time. But it is a full resolution. Yeah, pretty much if you catch it early. It is, I would say, in all things orthopedic for use of a steroid injection, a glenohemal joint injection with steroid is the best indication for a steroid injection. I know people are afraid of steroids, but it can really save you. Not this crowd. Yeah, it can save you a couple of years of, you know, thawing out. So I have a question. You said that one of the reasons is because there's a decrease in estrogen and you treat it not with injectable estrogen, right? Well, yeah, I would love to do a study of, oh, let me have the study I would love to do is apply an estrogen patch right here. But that is very off-label use of transvermal estrogen. So estrogen, you know, menopausal hormone therapy, including transvermal estrogen, is FDA approved for symptoms, you know, vasomotor symptoms, menopause, and for prevention of osteoporosis. You will hear a lot in this episode about good nutrition and things that support muscle health. And at this point, you should be taking clean, high quality, transparent supplements. And Peori is that I love Peori for a number of reasons and a number of different products. My favorite is Peori's 03 Ultra Pure Fish Oil because it's third party tested and certified by the Clean Label Project and IFOS. 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You'll get almost a third off the price, but to get this offer, you need to go to my exclusive URL peori.com slash drlion and use my promo code DrLion. That's P-U-O-R-I dot com slash drlion. In this episode, you are going to hear all about collagen as well. I strongly suggest that you check out Peori's collagen because this is going to be an amazing way to support your body as UH. Luckily, I'm so glad it's approved for that because it's very helpful with that, but it's not approved for myalgias, joint inflammation, polyarthralgia, even though there's mounting evidence that there's so much inflammation associated with menopause, joint pain. Do you know anyone that's doing it? Interarticular? Well, not interarticular, but I will tell you, I have a very close working relationship with my colleague, Dr. Anford, at Duke Women's Health. We are literally across the hall from each other. Did you inject her shoulder with estrogen? No, I didn't inject her. We've definitely helped each other. She's had an early round of frozen shoulder, and she came right over and I injected her shoulder. And I, this is unbelievable, as someone who studies adhesive capsulitis, I mean, I'm an almost 47-year-old female orthopedic surgeon, but a few weeks ago, I had adhesive capsulitis. Of course, I diagnosed myself, but it was classic pain and range of motion, then I couldn't reach across my back. It was front to back, deep in my joint, and I called her right away, and I was like, well, number one, I had my glenohemal joint injected. Number two, it's time for me to go on transtermolestrogen because I'm perimenopausal, and I don't want to bottom out. So I'm, yeah, so we joke around. It's definitely an off-label use, and I'm not saying that every single person that gets frozen shoulder should go ask for an estrogen patch, but we know the basic science of estrogen receptors in synovium. We know even... It's a fascinating conversation. Yeah, I mean, even the Women's Health Initiative studies, they showed that estrogen... So they had a study where 77% of menopausal women in their study had joint pain, and when treated with menopausal hormone therapy with estrogen, there was significant decrease in joint pain, number of joints that were painful, and severity of joint pain, and when the therapy was stopped, there was some increase in the pain. So there are studies that are not new that show this ameliorating effect of estrogen on joint pain, and we know that women are disproportionately, again, affected by arthritis. It's kind of like a geometric proof. It's a matter of putting all these things together, but it's definitely not an FDA approved indication, but there's a lot of menopausal women will present with joint pain. So yeah, I'm... Now I have my transdermal estrogen patch, and I'm hoping to stay on that. I'm on the moderate dose, and then you go into menopause, and then you go up on your dose, but I just don't want to get osteoporosis, and I don't want to get frozen shoulder pain. Come on, you've got to operate. So sometimes I'll have a patient, let me tell you. Sometimes I have a patient who's recalcitrant to things, like they've had a steroid injection, and it's still hurting, and they're also telling me I have night sweats, and I'm depressed, and I can't sleep, and so they need to go see a women's health doctor anyway, but one of their other symptoms is they have a frozen shoulder, and I send them to Anne, and then she treats them. But so yeah, I'm not... And I... Kavya, I'm not a women's health doctor. I'm an orthopedic surgeon. Yes, yes, but you're a very progressive forward-thinking orthopedic surgeon. The estrogen and arthritis, we talked about adhesive capitalitis, which is kind of this inflammation, this shoulder, right? It doesn't seem to happen to men if nearly at all. Unless they have poorly controlled diabetes, typically. Unless it's a good portion of the population, right? It does, huh? Right. We have to say that. But is there a level... Someone comes in and they don't know that there are menopause, maybe they're not up to date with their blood work, or they're not tracking their periods, or maybe they are on an oral contraceptive or have a moraine or some things that they're not aware. They present with frozen shoulder. The individual figures out that they need hormone replacement. Is there a particular... Okay, so I understand that you're a surgeon, but I'm just curious if someone were like, okay, well, what would be the number that we shoot for in the blood? Or is it just blood estrogen? Yeah, blood work is, again, for my work with my women's health partners, as I understand it, is not a great tool because it's so... The issue with hormone levels and period menopause is that they're actually kind of changing in a regular and they're chaotic. And so really, they rely heavily on symptoms, not blood levels. Yeah. Yeah. Which is interesting because for men, there's a total testosterone or free testosterone. Right. And every guy I know is like... Yeah, every guy I know is... My husband's like, where's my testosterone? Is it 900? What's my free testosterone? And the range is so broad. Yeah, I know. As we try to draw correlations to set up a paradigm of thinking, this framework of thinking about musculoskeletal issues with menopause, metabolic issues with menopause, and really begs the question. What I find fascinating is that I worked on some of the early studies of postmenopausal women and body composition changes. And we corrected for diet and exercise and we saw amazing resolution of body fat. And when I say resolution, they lost weight, they were able to maintain lean muscle mass. And I think within the traditional nutritional science world, people, when diet and exercise are corrected for, we see that body composition can be managed. However, when we really begin to think outside the box, the influence of these hormones, because women are saying over and over again that they go through menopause and their body composition changes, and that they're having joint pain, and they're having all of these other symptoms. Right. Increase visceral fat. Exactly. And so it just begs the question, what is it that we know and how can we redefine our treatment for the girls, for people? Mm-hmm. Obviously, we're not there yet. Yeah. It's really fascinating. And we're learning more and more about fat. Body fat is being inflammatory. Fat has lipokines, which are basically something that stimulates inflammation and elevates inflammatory markers. And in obese patients, we know that they're more likely to have arthritis, but not just in weight-burning joints. So patients who have obesity, you would think, oh, this is just mechanical overload of the cartilage. That's why they're getting more arthritis. And we know that's true. Yeah, that is definitely what we would think. Yeah. But they also have more arthritis and non-weight-burning joints. Tell us what arthritis is. And the number one question we get is not that we get, but one of the questions that we get is, does running really cause arthritis? Oh, yes. Which we talked about, or is that a myth? Yeah. So what is arthritis? And I actually explained this in my book because I think people just don't understand what arthritis is. What's the name of your book? Will you share it for us? Yeah. The Complete Bone and Joint Health Plan. And when does that book come out? May 6th. And where's my copy? Oh, yeah. They should send you one. I want to get you signed copy, please. Okay. All right. So, and also I want to add co-authored with my lifelong friend and colleague, Sinin Nyskorsky, who is a dietician. So we got to have her on? Yeah, I know. We're going to have to come back with her. You would love her. But, yeah. So what arthritis is, is basically gradual loss of the cartilage, which is the smooth gliding surface of joints. And over time, the cartilage gets thinner. The body forms bone spurs called osteophytes along, you know, the edges of the joint, you get inflammation and thickening of the lining of the joint called the synovium, then you get like some stiffness, loss of range of motion. Do the cartilage changes because it doesn't glide as well? Well, no, it's probably so this is very confusing. It's multifactorial. So, and also there's different types of arthritis. So osteoarthritis, we think of as wear and tear arthritis, that you just develop over time as you age. And that even has multiple components. Some of it is loading like biomechanical. And some people are just built badly, like if you're really bowlegged or knock kneeed or whatever, you're going to overload parts of your joint and they're going to wear out sooner. Or if you have hip dysplasia. Or you could have a badly shaped joint. Yeah. But, and there's a little bit of a biochemical factor. So even in osteoarthritis, which is, you know, considered wear and tear, we see these elevated inflammatory cytokines and joints, like interleukin one six, tumor necrosis factor alpha. Within the joints? Yeah, like, well, systemically and in the joints. And there are different cell types that are activated. And there's like a kind of a cascade of reactions that leads to breakdown of the cartilage and also cell death of the condor sites, which are the cells in cartilage. But so in osteoarthritis, there's probably a combination of biomechanical and a little bit inflammatory. But then on the other extreme, you have entirely inflammatory arthritis, like rheumatoid arthritis or psoriatic arthritis, where these, these people have very high levels of inflammation, it's autoimmune. The same bad acting cytokines are in their joints and affecting their cartilage, but they're at much higher levels, like the same IL-1 and 6 and TNF alpha. And then somewhere in between, you've got probably like what menopause arthritis is, where you have, is that a thing? Well, I think it's a thing, but maybe not everybody thinks it's a thing, but it's basically where you have now you have a combination of yes, you're over 50. But there's an acceleration of the inflammation, higher inflammatory markers and, and more signaling of that pathway that leads to cartilage breakdown, you know, faster loss of the thickness of the cartilage over time, you know, differences between men and women. So there's probably an interplay between inflammation and then, you know, the biomechanics of aging in women that's different than in men. So men get arthritis, what percent less than women? Women are 30% more likely than men to have arthritis. And that doesn't even up again until we reach age 80. Women are more likely to need a knee replacement than men. Also, women are more likely, this may not surprise you, to present farther into the disease process than men. So we're probably actually underestimating the sex-based difference. So women don't come in for their knee arthritis until it's like much worse, you know, the x-ray looks worse, they have more symptoms. So they've been like, kind of delaying treatment. So there we're probably underestimating the different. If you listen every week and feel like we are in this together, which I believe that we are, learning, growing and building strength, then I've created a way for us to get connected even more closely. It's called Forever Strong Insider, a premium community for listeners who want to go deeper. You'll get ad-free episodes, which I know you'll love, bonus Q&As, where your questions shape the conversation, behind the scene moments because let's face it, I'm hilarious from my daily life and written takeaways to keep at your fingertips. But more than that, you'll be supporting the show so that we can keep creating content that matters. If you've ever wanted to feel part of the inner circle, this is your invitation. Join us at ForeverStrong.SuperCasque.com or through the link in the show notes. So as the listeners thinking, well, how do I know if I have a tendonopathy? Should I go get an x-ray? You would not go get an x-ray. I would get an x-ray only to look at the other elements of it, but MRI and ultrasound are superior for tendon imaging. So MRI has a very good degree of resolution and a very high degree of penetrance. So the benefit of MRI is we can see to the level of the bone and beyond. Ultrasonic will stop at the bone. So very high resolution in some instances higher than MRI. And so I will find commonly on someone's, in a shoulder, I'll find little, what are called interstitial tears in the middle of the tendon that we're not visualized on the MRI because the MRI takes certain cuts. The other benefit of ultrasound is dynamic. So I can actually put the probe on somebody, have them move their shoulder around. And if I'm going to make the clinical diagnosis of you have shoulder impingement, I can prove it. And I can see, is this something where you're acutely catching your shoulder under a structure? That's going to help me formulate a therapeutic exercise routine for this person. On the topic of, you know, not if it's when, it's a tough pill to swallow. I know. And I hate to say it. And I hate to say it as well, because I do believe on one of those people is like, in the ideal circumstance, could we avoid it? Yes, if you didn't do anything, absolutely could avoid. But in that case, you're going to be unafraid trained towards a bad state of health. So you have to make a trade off at some point. Now, with restoration of normal mechanics and loading and periodically deloading, I think we can do a lot for injury prevention. And we know what normal mechanics are, despite the fact that everyone has different arm lengths and different leg lengths. There are standards of mechanics. If you look at like an orthopedics textbook, you know, look at joint ranges of motion, it'll look at specifically what's a norm. Like, and these are all, these are all Gaussian distributions, bell curves. So you're going to wind up with, here you go, you have a majority of people should have 180 degrees of shoulder flexion. They should have 90 degrees of shoulder external rotation when the arm is abducted. You can find these things. Now, if you restore a range of motion, a very important principle in muscle skeletal health is mobility and stability. Okay. When I evaluate somebody, I'm looking at them on a two by two table. Are you weak? Are you strong? And we're talking about a specific element of the mechanics, not generalized. For example, raise your arm. Yeah. Like, is this strong? Can you push it against? Exactly. And what I like to look at is say I'm examining somebody's hip and I'm going to isolate one of their gluteal muscles with a specific range. Are you weak in that muscle? So I like to look at weak versus strong and mobile versus stiff. Weak versus strong, mobile versus stiff. Yeah. So to give you an instance, for instance, of who kind of fits in each category. So for our elderly patients who have unfortunately accommodated a lot of, a lot of time and where they are most often stiff and weak. So joint ranges of motion decrease with time. You get calcification of soft tissues. Your joint capsules harden a little bit. You stop moving them as much. So it's natural to see a normal decreased range of motion as we age. So now if you pair that with inactivity, if you pair that with somebody who's not engaging in a lot of resistance training, it'll be paired with weakness. So stiff and weak. Because you hear a lot about that people are very hyper mobile. Yes. And it's interesting to hear, but as they age that they would stiffen. Yeah. Just about everybody stiffens to some degree as you age and just about everybody's more mobile when they're younger. Now there's obviously variations within that depending on what modifiable behaviors you engage in. Now let's take for instance the hyper mobile patients. So hyper mobility does come. It's not always a dedicated Ehlers-Danlos diagnosis. We have something called the Byton score. You should mention Ehlers-Danlos because I do have a few patients with it. People are very curious about that just as we're talking about mobility because there's probably a spectrum of it that's much more common than individuals recognize and it could predispose people to injury and other things. So there is a good evidence based score. It's called the Byton score that can actually be performed in the office to test for hyper mobility. What we look at is can you bend down to the floor, touch your palms on the floor. Can you bend your pinky back getting greater than 90 degrees? Everyone's going to be trying it. Yeah. Go ahead Mia. Yeah. So there's other tests within it, but there is a spectrum of hyper mobility and it's likely due to genetic determinants of collagen. And so when we think about the- It's not treatable, correct? To the degree. Yeah. So it can be treatable with modifiable with exercises and I'll explain that in a moment. Wonderful. But you know these are things that these are relative, not absolutes. So your mobile and weak patients are most commonly hyper mobile. The mobile and weak. Yeah. So on the two by two, stiff and weak is elderly, your mobile and weak are hyper mobile. Now stiff and strong or stiffer and strong is like an offensive lineman. If you examine an offensive lineman's hips, they're not going to rotate a whole bunch, but they're as strong as heck and they could put the power down. So that's stiff and strong. Stiff and strong is not a bad place to be. Then your mobile and strong, those are your Michael Jordan's. Those are the people- Mobile and strong. That's the grail. So if you can, for every bit of mobility that you gain, you have to be stable. So range of motion, if I just stretch myself into a range of motion, but I don't know how to actively activate muscles to protect my body in that range of motion, it's just range of motion for range of motion's sake. Not all mobility is uniformly beneficial, in my opinion. I believe that if you're going to have mobility, you need to have accompanying stability. And if you're a more mobile person, you have a larger responsibility to be stable through a larger range of motion. Now, what are the determinants of mobility? It's a really complicated topic, but you have your bony determinants. So not everyone's hips are shaped the same. Not everyone's shoulders are shaped the same. And those are your more mobile joints. Then you have your soft tissue determinants, things like collagen play much more role there. So whether you're hyper mobile in a joint capsule, women are more mobile in their joint capsules than men. Women have more type three collagen in their tendons than men. So that's going to influence. I didn't know that. Just broadly speaking. Okay. Broadly speaking. So these are some determinants that are going to predict some of the soft tissue extensibility. And then the mobility aspect in really how stable you are, a huge element of that is that that same neurokinetic element we spoke about before and the athletic accommodation timeline. So if you can be stable and you know what muscle to contract in what position, mobility is fine. But I, for instance, I would prefer for a lot of patients to be in a narrower range of motion, but much more stable through it than as opposed to having just a very large range of motion. If you think about the range of motion that we need to accomplish your day to day life, you need to be able to do a good hip hinge. You need to be able to do a good squat. You need to be able to rotate. And you need to make sure that you're producing enough body tension that's centralized in your core to mitigate injury in those circumstances. You don't have to be an elite contortionist to achieve everyday life. And that's why the concept of stretching is a very interesting conversation to have. What we're achieving with stretching is a very interesting conversation to have. Should we do it? This is going to bring me to the yes or no section. Oh dear. Okay. So you're not going to like this because you're very academic, but I'm going, you can only answer yes or no. Okay. Pilates. Yes. Steroid injections. Yes. Zone two. Sure. We've never had a guest answer sure ever. I think it's beneficial. I think at the question, the question is the dose, the type. But see, this is very difficult for people. I always, this is why I'm not on the hill. Okay. If I wanted to, if I wanted yes or no, it would be a politician. Fair. Yoga. Whoa. I love this section of the podcast. Yeah. Is that a yes or no? I'm not, I'm not no, and I'm not yes. I'm going to bow out of that one. I'm going to use my fifth amendment on that one. This then leads me to stretching. Stretching can be beneficial. Okay. So it's not uniformly beneficial. The question is what you're trying to achieve with it. Stretching. Tell us about, should we be stretching before activity? Should we be stretching after? Because I ran out of the gym yesterday because my sister said we trained with Carlos, he's my coach, and my sister said, you know, we are done working out, but we should stretch. I'm like, for what are, what are we stretching? Why are we doing this? And then I said, I'm going to talk to Dr. Gerard because I think you're wrong. We probably don't need to stretch after we work out. Okay. And now I'm about to be schooled. Oh, well, let's see. So there is, this is one of those topics that I have some relevance in, but I don't feel 100% at expert level with. I have a lot more to learn on it, but I'm going to, I'm going to give it a shot for you. So stretching preactivity, decreased neuromuscular firing, decreased stability, not beneficial for power athletes. And can we define power athletes? So pitcher, pitcher, shot putter, elite power lifter. You could even throw fighters in there. That's a powerful sport. So you're producing, power is forced over time. So you're going to produce a force over a very short period of time. So static stretching, probably not beneficial. For anything? Or just, we're talking about power. Pre-exercise for power generation. Now, stretching, there are different categories. There's static stretching. So I'm going to hold a pose for a while, typically 20 seconds or more, and hopes to elongate the tissue. Now you're not just stretching the tendons. You're not just stretching the muscles. You're also providing neural feedback that can actually turn off some sensors that help to protect you under load. Are these the Golgi spindle fibers? Yeah. So Golgi, I'm curious. I wonder if I remembered anything. Hey, so Golgi's interesting. The other apparatus are also interesting, but the static stretching component perhaps has some benefit post-exercise with relation to tendon health specifically. And it may actually help just elongate the tendon. And actually, if you're holding a pose, maybe like with an isometric or let's say you're going to do a heel drop and just hold it there. That could have some benefit. Now, for power or for? For recovery. Recovery. For recovery. Yeah. Now, I say a lot of, I'm going to heavily wait the May here. Okay. I'll take it. Because I think it may help. But I'm also going to tell you from a personal aspect, I don't do it. So I think it's important to know that I don't. Neither does my husband. I've never seen that guy stretch. He is a smart man. So now, if you're going to stretch with the hope to teach your muscles how to engage at a larger range of motion, then you do PNF. So, Properisceptive Neuromuscular Facilitation. And the answer for that is? PNF. PNF. Proprioception. Neuromuscular Facilitation. Okay. So, PNF is a process by which, okay, so I'm going to stretch, say, my hamstring. And somebody's going to push against my leg and I'm going to actually try to contract my hamstring at a larger length than I did pre-stretch. And then I'm going to stretch from there. And so there's typically these on off cycles, like a 10 second isometric at one length, 10 second stretch at another. And you can do that. Now. And the benefit of that is? The benefit of that is you are, you're teaching somewhat that the muscle can relax at a larger length. Okay. So, whether pre-exercise or post-exercise, I'm not clear on. And this seems to work with, a lot of people do it with pain. Yes. So, is PNF used for mitigation of pain? Muscle or? Yeah, it's used in rehab. So, it's used by physical therapists and ATCs and other people who will rehabilitate patients. So, it's definitely part of it. When I design physical therapy protocols for patients, I like eccentrics for lengthening. So, once again, eccentrics, your muscle is contracting periodically or mitigating that the elongation process. I think that could be very beneficial. The stretching component is interesting because once again, we're not just stretching the muscle, we're not just stretching the tendon. We are also gliding the fascial layers. So, here's another. You brought this up. So, here's fascia. Another, that's it. Would you consider that an organ system? It's interesting. It's part of the musculoskeletal system, but it's so richly innervated and so large. It could be. It's on category. What is fascia? Fascia is interconnected, connective tissue that can run the entire length of the body. Incredible. Here's why we don't get taught about fascia as much as we could, we should be. A lot of it is almost as if we, during the process of medical school, well, we, because it's a second average. It's gross. It's necessary. And it's absolutely disgusting. It's also important. It's important. And thank you to everybody who donates their bodies to science. Absolutely incredible that people are willing to do that. When we dissect cadavers, most fascia dries out so much so that it adheres to adjacent structures and becomes incapable of dissecting it off of. Now, I've spoken to some scientists in Italy about this specifically. You did? You were just. I wasn't in Italy. It just happened to me. But you were just thinking, why? I spoke to somebody basically because ultrasound is one of the main ways to evaluate fascia in the living specimen. So there are specific cadaver preservation techniques for preserving fascia. But one of the reasons we don't really understand it or appreciate it to the level that we do is we just don't see enough of it. So fascia can adapt. Fascia is, if not the most richly innervated structure in the body, one of the most richly innervated structure in the body, that means the most nerves. Does it have pain? So does it feel, you feel pain? People feel mild fascial pain. I believe it is a con, it's part of the diagnostic spectrum of pain. So you can have a muscle that hurts, you can have a tendon that hurts, you can have a joint that hurts, you can have a ligament that hurts. And fascia also can hurt, in my opinion. So can you feel it if someone were to say, would that have anything to do with fibromyalgia? It's interesting. Yeah. So the concept around fibro is, I think it's part of it, that fascia is part of the issue. But we also see mild fascial pain in people who don't have fibro. And so we see mild fascial pain in overuse syndromes, a very common mild fascial pain that perhaps some people will experience is if they have pretty large asymmetry in their hips, how their hips move and function, they feel a lot of mild fascial pain in the top of their glute low back area. Now it's tough to discern, and I spend my job doing this every day, discerning what the main pain generator is and then describing how we can appropriately rehabilitate it and treat that pain. Now fascia specifically do adapt to exercise. And one of the best books I've read about this by a guy by the name Bill Parisi, so, and he, the forward was written by Stu McGill. So it talks about fascial adaptation to training. And that basically this fascia system that extends in some circumstances, the length of the body, connects your glute on one side to your lat on the other is a lot of the reason that we don't move like rigid robots. So allows us to move much more coherently. Now the question in this circumstance is how much of a role is that in pain? How much of, how much can we do about it? Now we know that it adapts in some circumstances because there are some athletes that when you take them and train them a certain way, they get athletically worse at what they're doing. Now there's changes at the neurokinetic level there. There's changes at the muscle level there. Presumably there are some changes at the fascial level as well. One of the accounts that Bill talks about in his book is about an elite quarterback who was training like an offensive lineman. So basically they were putting the quarterback through the lifting protocols on offensive linemen and the quarterback, all the numbers around throwing got worse. Spiral got worse, velocity got worse, arms started to hurt. So maybe everybody needs to train towards a specific goal because on some level or another your entire body is adapting to that stressor. So you always have to keep that in mind of when you're training an athlete, they can't all be treated the same. Not any exercises uniformly the perfect one for everybody. For their specific needs, you have to do an individual needs assessment for that patient. So fascia is very interesting. We do visualize it on and specifically where fascia are where the small nerves like say for instance the nerves that talk to the muscles of the back, the fascial layers are where they travel. So the thought is behind myofascial pain is could you have these layers that are not appropriately gliding on each other and patients who have chronic pain, there's some evidence that suggests that they don't glide that well. Rounding this back up to the initial question around stretching, stretching also glides fascia. And so does that have its own therapeutic benefit? Could that actually be helping produce these proteoglycans, these lubricants that are present in the body the same way that they're in tendons? So is it a lubrication problem and can we facilitate that with stretching? So then there's also the question of myofascial release and what we do for individual people. I'm less concerned about the modality we use to get people mobility so much as I am more concerned with us restoring stability through that mobility. Really well said. I'm learning just so much. Can we talk a little bit about training? Yes. I've learned quite a bit and you really have helped me reframe. In fact, we're working on a second book proposal and I'm hoping you will be so gracious as to impart some of your wisdom in part of that process. And I've learned a lot about thinking about how we train the current paradigm, the current narrative is all about zone two. It is that zone two is where we need to focus and then we have other groups that we talk about resistance training, do it three to four days a week. And understandably so. There's only so many ways that we can make global recommendations. That being said, I would love your take about, you and I have spoken about minimal amount of movements, exercise, kettlebells, more effective ways to utilize our body. I'm just going to leave that for you to take it or whatever that you'd like to. Sure. So the concept of zone two is an interesting one. I think that a lot of the excitement around it is that it's helping to promote mitochondrial function and that mitochondrial function appears to be absolutely essential as we age. And can we improve mitochondrial function to decrease things like insulin resistance, improve metabolic health, improve our athletic performance? And the concept there, it's interesting to see how depending on what you look at, these different terms that describe similar phenomena. So sub max VO2 training, zone two, moderate intensity, continuous training. I did a presentation a while back specifically as it regarded patients who were recently diagnosed with cancer, undergoing cancer treatment or finished cancer treatment and what exercise recommendations we could make for them because their VO2 max and muscle mass help predict how they do. And we know that quality of life, mortality, morbidity, the more fit you are from a cardio respiratory and muscular aspect, the better you will do with treatments. So how can we help people? And so the question was in the presentation, should we be engaging in high intensity interval training or moderate intensity continuous training? And the answer is, of course, both can be helpful per unit time. High intensity training might be more beneficial to Jack, your VO2 max upwards. But what are we really thinking about with VO2 max? One is if we're going to test VO2 max in somebody, they should be familiar with the movement of which we are testing them. It's not fair to say somebody has a suboptimal VO2 max, but it's their first time doing a certain athletic activity. They're never going to be, you're going to be gassed if, even if I'm an marathon runner, if you throw me into a box hearing, I'm going to be gassed in two rounds. You might be amazing, but not a normal person. But the truth is I would be gassed and the, it's because I'm not familiar with the movements is the way that I should be. So it's important. That's important caveat. Don't get down on yourself. If your VO2 max is not where you think it should be, because you did some modified Bruce Kropp protocol in a gym, it might not be where it should be because you don't have a familiar with the movement. If you're on a bike, there are so many determinants of how your performance on a bike. Absolutely. You're positioning, you're familiarity with it. What muscles you're activating, your shoe angle with the actual pedal, and I'm out of my league there. I know that that's the very, very surface layer of it. So we're looking at substrate utilization, fats versus carbohydrates versus creatine phosphate. And we're looking at what can be done to maximize fat oxidation. So this concept around zone two, as I understand it, is fat max. Like we're trying to maximally use fat for fuel while we exercise to teach our mitochondria to metabolize fat more readily to decrease insulin resistance. That's what makes sense to me at least. Now, with high intensity interval training, there's no, I think the downside of zone two is time. I think that's it. I think you have two children and a beautiful wife and a full practice. Yes, and time is tough. So I don't engage in a ton of zone two myself. If I had more time in the week, perhaps I would. But then high intensity interval training appears to be as beneficial for VO2 max as the zone two, but you're training it two different ways. From high intensity interval training, you're raising the ceiling of your house higher. You're getting better at pushing it higher. But the zone two training appears to be like you're solidifying the foundation. You're getting better in the lower levels that predict success at the higher levels. So we might be describing it this way, but athletes have intuitively known this for decades. When they run, they're not gassing themselves every workout. They leave a little bit on the table and the body goes through a period of compensation to basically mount a response to that stressor. And then when they do peak one or two times a year, they're in really good shape. So same principle applies to weight training. So should we or could we be going to neuromuscular failure? If our goal is muscle hypertrophy, should we be focusing on just muscle hypertrophy in specific muscle segments or generalized strength and instability? I think these are good questions. But the way I train with kettlebells is I want to be number one thing for me is don't lose stability in all three planes of motion, sagittal, transverse, and frontal like we spoke about before. When you work a kettlebell, most of the time it's in one hand and that by nature destabilizes you. And you're not going to get destabilization if you're working only with barbells. So if you're not going to get destabilization working with barbells. Only, you know, as it relates, right, as it relates to the frontal and the transverse plane. So you'll be stable as all heck in the sagittal plane if you work with a barbell. I was the sagittal plane hero. I went to the gym and I did well done bench, lats. I did squats. I did dead lifts and I became very proficient in those areas. But then I would go play golf and like things would hurt. And I'd be like, well, that's interesting. You know, I'm not the world's best golfer, but it shouldn't hurt as much as it did. And I thought it was basically because I wasn't as proficient in translating force and rotation. So I like to use a kettlebell. I think you can get a lot out of it. I think the work from the strong first organization and Dan John online in his own endeavors have done a great job elucidating the cardiorespiratory benefits of kettlebells that you can get strength and conditioning. And so I try to follow that. I also do something, and we spoke about this term exercise snacks, which I don't particularly love. I don't either. But I can't think of anything. We'll find a way to rebrand it. Yeah, definitely. Yeah. I call it farm hand strength. So if you're working on, and now, let's say you're not a farm hand, let's say you're just somebody mulching your yard, you're not going to basically go to the point where you're falling down every single time. You're going to leave a little bit on the table. You're going to come back to it. You're going to go do a different activity for a short period of time, and you're going to come back to it. And so what I'll do is I'll intermix some sets of kettlebell swings throughout the day. I might do a set at 9 a.m. and do a set at 10.30. I'm not looking to build a sweat. I'm just looking to get better at the movement. So I'm really stressing that neurokinetic element. Am I getting better at the movement? Am I doing a little bit of stimulation of muscle? But by no means am I getting a skin ripping pump out of it. But potentially you could build a workout like that. Yeah. There are, when we look at some of the really good people who are training and what they do in a lot of rehabilitation from injury, sometimes it's three, five, 10 minute rests. And so the question I think in there is, do you want to be really, do you want to be super proficient with a movement? Or do you want to get as much training in in a short period of time as possible? So there's different strategies there. But we move throughout the course of the day. It's not like we only move for 30 minutes and then we're immobilized for 23 and a half hours. So the concept of going to the gym, I think is something that needs some work. Where we think about going to the gym, we dedicate time, but should we be interspersing movement throughout the day? I think some people, fortunately in their jobs, can do that. And some people unfortunately can't do that. But I like, like, you know, I saw you both do a set of push-ups before as its own little stimulant part of the podcast. That's our pre-game push-up. There you go. We do a pre-podcast ritual. Now, is that not helpful because you only did one set? No, of course it's helpful. You didn't know that we're doing some after this? Well, I'm happy to do it. But you did one set in isolation and you benefited from not overloading your tissues, you benefited from a short-term increase in your heart rate, you learned how to become a better push-upper. And that has something to do with it too. So I think coming back to the concept around zone two, it's, if you were to train, I think that probably what makes sense from a metabolic corollary with weight training is like, if you're going to neuromuscular failure, your muscles are on fire, you're not in zone two. Right? I think we can comfortably say that, right? Yes. So you're probably in zone five or four or five. So you're really getting there. Now, if you train and you say you do 10 repetitions of something explosively and then you wait a couple minutes and do it again, could you still be in zone two? And that's the, this concept that has come up called anti-glycolytic training, which is a way to build endurance and strength, which has been subject to my own personal fascination. I'm not in a position where I could speak from an educated perspective on it. A lot of the literature behind it is in Russian. So I can't read it. But I've read Pavel's work and Pavel does a great job with that. And I've recently read a couple of his books and I think it's something I've experimented with the same way that we might all experiment with zone two or a hit training or powerlifting or whatever it might be. I, a lot, I think one of the benefits to my patients is that I've gone through the process of experimenting a lot with this. I played baseball and football. I was a personal trainer. I did a good bit of just, you know, casual powerlifting. I tried to be, you know, a crappy bodybuilder for a period of time and it wasn't great at it. But, and then on top of that, you know, I might not have, I might not be running a marathon like Shane in a couple of weeks, but I did run a half and you learn so much going through those individual experiences. So I try to maintain a radical open-mindedness about what could be helpful and try it myself and if I can. And that's really valuable. A physician that sees patients and also walks the walk and experiences it. And I, I do think that you bring a very unique perspective. In your practice, how do you incorporate some of these things? So you practice in, where are you in practice right now? I'm in Florham Park, New Jersey. I work for Summit Health. Okay. And people could make an appointment with you if they would like to. So let me just tell you guys something. Every guest is incredibly vetted before they come on the podcast. I have so much respect for Dr. Girard. I send patients to him. If you are in the area, if you are not, he is definitely worth the trip. I would love to hear a little bit about what makes your practice different, unique. We've heard a lot about your philosophy and how you think about things from both a biomechanical aspect. I know where you sit from an nutritional aspect, but also your fellowship trained. Yes. I'd love for you to expand upon your training and just your individual practice. So my, my practice is a sports and spine practice. I did a sports and spine fellowship at the hospital for special surgery, which by the way is one of the best in the country, if not one of the best places in the world. Yeah. It's a great place to train, great place to be. I have been, I think the very important take home for anybody who's listening outside of me kind of speaking about myself for a moment is if you can find mentors that are really good for you, really pursue their mentorship. Yes. That's how you and I have developed this relationship. I have a mentor almost at every different phase of the career. So I kind of have mentors that are closer to me in age. I have mid-career people. I have a later stage career people. And I also have mentors who are non-clinical or not even doctors, you know, who are people in different fields. Getting their perspective has been so important. And anything that I do is, is the great fortune of having a great family and a great upbringing and great wife and kids at home and parents and brother and friends. So I'm fortunate that every day I go to work, I feel like I bring the best version of myself because I have a great backing. Amazing. Now from my perspective, from my practice, my practice focuses heavily on the biomechanical determinants of pain. And when we, a patient comes in, let's say I see a back pain patient, it's less difficult to make the diagnosis of a pinched nerve in the back from a herniated disc and more difficult to discern why the disc herniated and to unravel in a relatively short timeframe what determinants in that person's life or in their training predispose them to that injury. And how are those things going to be in conferences to them getting better in the future? So that takes some refining and I've gotten better at it with time, but every day we try to build a little bit. And I try to find what is motivating this person, what are your goals? And I ask every patient, what are your goals for this visit? Some people just want clarity of diagnosis. Well, the first thing we need to do beyond anything else is clarity of diagnosis from a biomechanical element and from a tissue layer element. Do you have a herniated disc? Yes. Why? Repetitive flexion movements without appropriate lumbar stabilization, insufficient hip mobility, and then they didn't have the appropriate brace from the obliques. That's a good starting point. Now let's use this inflection point of injury and let's build you back to a point of antifragility. So the concept of antifragility is one that I borrowed from Nasim Talb's book, which is one of four books in the Encherto, which are very difficult and fun to read. I love, I love... Very thick book. Yes, very thick. There are books about everything. If you ask me what they're about, they're about everything. But this concept of antifragility is actually a concept that is exhibited in muscle and tendon and bone, which is you provide a stressor to a structure. It doesn't break, but in time, if the stressor is adequate, the structure can actually get stronger. So I branded myself antifragile MD because I love that concept. I love, that's the essence of my practice. Can we use stressors rather than hurting you and disabling you to make you stronger? Yes, sir. Well said. And I know that's you too. So I look at is, can we get people from a point of injury to back to a state of athleticism? And what are the goals? Do you want to be on the ground playing with your grandkids? Are you somebody who's going to run a marathon in a couple of weeks? And we kind of look at all these things and the variety of treatments that I can offer. And when there is an evidence-based withdrawal from, we will draw from that evidence-based. If there's no evidence-based withdrawal from, an area will extrapolate based upon the knowledge of my biological foundations. So, but my practice is a sports and spine practice. So I see a lot of hip pain, back pain, shoulder pain, neck pain, to a limit, to an extent elbow and then of course, knee and some ankle foot as well. And the two main, three or four main conditions I treat are back, specifically low back pain, tendinopathy is around the body and then a lot of neck pain. And you'll find that patients who have low back pain have tendinopathic problems as well. And you'll find- in the, in shoulder, it's a whole sling. So the whole, whole sling can have problems, but I think it's, you'll find specifically that there are, there are insufficiencies in the, in the pelvis, in the peripelvic muscles, like the glutes. And so it's not uncommon to find a tendon problem there. So I like to uncover what the root cause is. And that's really what gets me out of bed every morning is root cause diagnosis. And then if your diagnosis is accurate and you can correlate it with the diagnostic testing we have x-rays, MRIs, ultrasounds, etc. And it matches up with a good physical exam. Well, now we have a clarity of diagnosis, then the treatment, everything we provide from a treatment aspect there out is much more beneficial. And what I love about what you're saying is it's not about the end pain or the end symptom. It's a root cause approach, which traditionally medicine is not about a root cause approach. And that's what I think what makes you and your practice so exceptional is that what is at the foundation so that you can get people better. Where do you see the field going? So I think that there's a good interest around regenerative medicine. And there are a variety of regenerative therapies that we have now. PRP, you know, we spoke about the athletic accommodation curve. There's also the, you know, the innovation curve of companies and products. And I'm, instead of like being on the absolute first phase of stuff, I'm probably one phase delayed. I feel the same way. We have to make sure that things are safe, effective, worthwhile for patients to spend their money. Yes. Agreed. And first rule of medicine is do no harm. That's right. So do no harm. Anything we do, we want to understand what we're doing, why we want to put it in the right place. So I think there's some very interesting work that's going on from a stem cell aspect, fat concentrate procedures, further subcategorization of PRP, when to use it, when not to use it. And I think the field will continue to develop that. I think as we evolve as a field going forward, we'll begin to understand a little bit more about things like fascia. We'll begin to understand a little bit more about mechanics other than just isolated joint range of motion and whole body movement. I think that the, it takes a lot of interest in that and study to do it, but I think we're getting there. And I think the last frontier is in a lot of ways the first and most important, which is prevention. An ounce of prevention is worth a pound of cure. And how can we prevent these injuries? Or you see this word circulate online, bulletproofing. Like, are we going to bulletproof your shoulders, bulletproof your knees? And so that's where a lot of my own self experimentation comes in and trying to learn that as well as watch people do it and experiment with that. But as a field, I hope we study more of that. And then of course, predictive analytics around who's going to wear a joint in a specific pattern based upon their bony development. We have some evidence to understand that now, particularly in the hips, but we're starting, I think, to an a greater degree to look at that in the shoulders. Surgeon specifically are doing a great job of looking at that. And then from a tendon aspect, you know, like we said, are the exercises we can engage in, I'm certainly going to do my best to find out. And I think, and to, and to figure out what is the most effective ones, I think that the question becomes minimally effective dose. Of everything, yes. Training, medication. Yes. How much is too much? And are we over training tissues? And that's why we're seeing so many musculoskeletal problems. Or are we just inefficiently training?