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Kevin Maggs joins us once again on the Run Smarter Podcast! Previously in episode 32 discussing Knee OA Misconceptions, Kevin talks today about the physiological influences on chronic pain. Also known as pain amplifiers, Kevin dives into areas such as diet, stress, sleep, hypoxia, fats, insulin surges, free radicals, immune cells, autoimmune processes and several other influences that heighten your pain levels and delay or prevent full recovery. Listen now to gain this crucial insight into recovery. To learn more about Kevin, check out his websites: https://livelyhealthclinic.com/ https://www.peakperformancecare.com/ Run Smarter YouTube Channel Become a patron! Receive Run Smarter Emails Book a FREE Injury chat with Brodie Run Smarter App IOS or Android Podcast Facebook group
Expand your running knowledge, identify running misconceptions and become a faster, healthier, SMARTER runner. Let Brodie Sharpe become your new running guide as he teaches you powerful injury insights from his many years as a physiotherapist while also interviewing the best running gurus in the world. This is ideal for injured runners & runners looking for injury prevention and elevated performance. So, take full advantage by starting at season 1 where Brodie teaches you THE TOP PRINCIPLES TO OVERCOME ANY RUNNING INJURY and let’s begin your run smarter journey.
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On today's episode, when acute pain turns chronic with Kevin Maggs. Welcome to the Run Smarter podcast. The podcast helping you overcome your current and future running injuries by educating and transforming you into a healthier, stronger, smarter runner. If you're like me, running is life. But more often than not, injuries disrupt this lifestyle. And once you are injured, you're looking for answers. and met with bad advice and conflicting messages circulating the running community. The world shouldn't be like this. You deserve to run injury free and have access to the right information. That's why I've made it my mission, to bring clarity and control to every runner. My name is Brodie Sharp, I am a physiotherapist, a former chronic injury sufferer and your podcast host. I am excited that you have found this podcast and by default, become the Run Smarter Scholar. So let's work together to overcome your injury, restore your confidence, and start spreading the right information back into your running community. So let's begin today's lesson. It's not too often that I record a podcast interview these days and it actually gets me thinking a lot, like fundamentally of how I'm treating clients and how I understand pain and understand injuries. And if you've listened to several episodes or if you listen to, you know, the start of this, um, well now is, you know, 270 odd episodes, you know that I'm quite fond of pain science. and starting to wrap my head around, you know, that particular field. And I do have guests and researchers to help me understand that who I interview on the podcast, but then you come across Kevin Maggs, who's been on the podcast before he has been on episode 32 talking about the misconceptions of NEOA and has been a great resource. He's one of the guys I follow. you know, there's top tier health professionals that I follow, there's a very select few and he is definitely one of them. And he's had a radical shift in his career, more shifting towards this holistic side of pain and trying to understand pain, inflammation, the effects it has on the body, what causes inflammation, what causes pain signals to fire more easily. And It's a topic that he's discussing now is something that I haven't thought about before. And I reached out to him and we're sort of coming up with some ideas about some episode topics. And he's like, how about I've gone through your list Brody. And you know, you talk about pain a lot and you talk mainly about the, when it comes to pain science, the psychological side and not much talk about the physiological side to pain sensitivity. And he sent me a long email about a template of what we can do. And he's just quoting article after article. There was about 20 articles hyperlinked into this email. And I'm like, Jesus, guy, he's, he's going all in and he spares no expense to bring top quality research. And you can you'll just figure it out as soon as you start listening to this episode. He really knows what he's talking about, really focuses on the evidence, quotes, papers, and so forth. And, you know, if there's some, there's an area that's a bit more puzzling, he'll admit that as well. But we just cover pain science in a different light in the physiological side of things like what can actually be measured. And, you know, he talks what like I thought this would be a 45 minute interview turned out to be a lot longer. And that's only cause I sort of hard pressed him at the end to wrap things up. And yeah, you're going to love him. Um, if you're in the U S and you love what he says and want to do a telehealth call with him, um, he talks about some websites that you can go to and I'll link them in the show notes after this. And like I say, very few interviews. I. have a topic or a discussion where, you know, makes me question how I'm approaching my, my own injuries and how I'm treating clients and my fundamental understanding about pain. So you're going to love this one. Let's take it away. Kevin, thanks for joining me once again on the Run Smarter podcast. Yeah. Thanks for having me Brody. It's been, uh, it's been a few years. You've been having all these PhDs on there and, and forgot about little old me. I never forget about you. I love all the work that you're doing. And for those who aren't familiar, you were on episode 32. So way back talking about Neoway misconceptions, which has been a very popular episode. I point people to that episode all the time whenever they show scans or, you know, have questions about osteoarthritis and you knocked that one out of the park and that was, you know, almost three years ago now. So it's crazy how long ago that was. But you've For those who aren't familiar with you, I'd love you to give a run up as to what your career has been like and particularly any changes in direction from when you're on the first time to now. Sure. Yeah. Well, first of all, congratulations on your book. It's a, it's a great, everybody has a chance to get it. It's awesome. Um, yeah. So I've been in practice for, for quite a while now, um, 25 years. Um, I worked not only just in private practice, but, um, I worked for a triathlon series for quite a few years. Traveled around the country with this triathlon series and my job was to treat the professional triathletes and the amateurs. An instructor for active release techniques for about 10 years. I'm not sure if you heard about it, it's like a manual therapy technique for chiropractors and physical therapists. In 2015, I was invited on to be a speaker for the Running Clinic and that's an organization that teaches continuing education courses for healthcare providers. Mostly on running injuries, diagnosing, managing running injuries, footwear, gait analysis, different topics related to running. Um, and as far as the shift, yeah, I mean, in the last couple of years, I've sort of got a different approach to treating pain. I mean, not that I've abandoned my previous approaches to pain, but, um, it's interesting when you treat a lot of people in chronic pain, which obviously over 25 years, I've seen a lot of them, but there's kind of like two. two sort of general ways that most healthcare providers approach chronic pain. And one is like a tissue specific origin, like disc degeneration or arthritis, or they tell people that they have leg length differences or they're looking for subtle partial tears on imaging. But over time, we've seen many studies come out to show that those factors really have little to no effect on chronic pain. And I know you talked about it a little bit in your book and I know you've had lots of guests on your podcast outlining the evidence that Imaging studies don't really have a lot of correlation with chronic pain. Um, and then the other way that a lot of healthcare providers approach chronic pain is this sort of biopsychosocial approach. And there's a lot of people that are focused on that now. Where the idea mostly focuses around the psychological aspects of it, where they, you know, they tell people and not, not that it's not true, but a lot of people are catastrophizing about pain where they. sort of make a bigger deal out of the pain. Like they think it's never gonna go away, and you know, woe is me, and there's nothing I can do about this. That's sort of catastrophizing. And then kinesiophobia is when people are afraid, like afraid to lift, afraid to bend over because they've had, you know, recurrent back pain. What not, and the approach is to take more of a psychological approach where they, you know, they work on mindfulness and coping strategies to accept the pain, right? So. What I've been doing lately is sort of zooming out of all that and looking at the entire person in front of me and understanding why the pain is disproportionate to the tissue damage and chronic pain, but not in a psychiatric way, but more in like a physiologic way. So the approach that I've been taken is sort of like vast and overwhelming. And I don't think maybe that's why a lot of people don't take that approach. But there's a physiologic reason why people have amplified pain even after the tissue is healed, right? So for example, people can have sleep apnea. We know that sleep apnea increases pain, like it lowers the threshold to feel pain, poor control of blood glucose, underlying autoimmune conditions, food sensitivities, stress, underlying chronic infections, you know, the list goes on and on, but there's lots of physiologic factors where chronic pain persists. And it's way beyond the psychological factors. And it's way beyond just the tissue damage as far as why people continue to suffer from chronic pain. So when I say physiologic things, I mean basically things that we can measure. you know, in people's blood and urine and saliva and whatnot, like hormones and different things like that. Yeah. Was there a certain reason or moment for the shift? Was there something in your career or was it just a gradual interest of yours? How did that all develop? I think it, I think it honestly came out of frustration, right? I mean, as healthcare providers, we want to help everybody. And there's a lot of people where you know, you do what you can and they're still in pain. They've seen everybody else and I'm sure you hear this as well, like people say to you all the time, like you're my last hope. Right, like as a chiropractor, people think chiropractors are like backcrackers or whatever, but my patients know that I treat a lot more than that. And so I get a lot of people coming in for whatever, knee pain, shoulder pain, foot pain. And they say openly like, why am I in a chiropractor's office for my ankle? Like, this doesn't make any sense. but I've heard a lot and you're my last hope. And you know, sometimes you can't help them. And so it gets frustrating. So I think, I think if you're a clinician who cares about the people that you're taking care of, you're going to always keep reading, you're always going to keep expanding your knowledge base, you're always going to continue to take continuing education courses to try to, you know, help everybody you can. I think, you know, me reflecting back on the, you know, hundreds of runners that I've treated. Um, there seems to be a certain pattern emerging where, you know, in the book, most of it revolves around the load versus capacity model, and most people. Get better because of it. Um, I would say that if it's a running related injury, it seems to be the case. Um, I do see if someone has a history of depression, anxiety, um, those sort of emotional traits, they struggle to recover. They struggle to respond to that load versus capacity model. Their pain is amplified. They have just like a heightened sense to those pain responses. And that's when I guess I've sort of moved to yes, the load versus capacity model still is in place, but then try to layer on some sort of psychological interventions, like you said, mindfulness, meditation, that sort of thing, trying to reframe or just educate them about pain and pain science and piling on that. But I'll admit, that's just the psychological aspect. And why I was excited to have a chat today is because I really don't have much of an idea about this physiological pain amplifiers or something that might be happening in the background that why these very certain select few aren't responding well. Um, before we dive into that particular category of people, is there, like a lot of people have say chronic pain. Um, a lot of people have chronic issues. I guess maybe we'll start off with what defines chronic and what sort of pain behaviors or pain patterns would you expect for someone to potentially fall into this category because I've had people that have just mismanaged their injury for such a long time. Like they've had proximal hamstring tendinopathy for years, but they've mismanaged it. They've mismanaged that load versus capacity model. And so they might have a chronic issue. They might have chronic pain, but they respond well to a load versus capacity model. So when it comes to chronic pain and those who might lead, who might need to start investigating these sort of things. What sort of, I'm not sure if I'm answering a question, or asking a question here. How can we define chronic pain and what sort of pain behaviors are illustrated in this particular population? Sure. Okay. So there was a lot to unpack there. So let me just, I'm going to go back to just a second with the, you know, when people have, you know, depression, anxiety, mood disorders, If you go onto PubMed, where you know a listing of all the journal articles that have been published and you look up anxiety and neuroinflammation or depression and neuroinflammation, that's the general idea as far as how these mood disorders are taking place right now. They've sort of moved away from the idea that it's like serotonin and dopamine and whatnot. It seems like neuroinflammation, meaning inflammation in the brain, is the main cause of that. We can talk about that later, if you want to get into some details of like, you know, microglial activation and glial activity and whatnot. And I'm happy to talk about that. It gets a little bit technical. But when you have systemic inflammation in your body, from some underlying, let's say chronic infection or something like that, that triggers neuroinflammation in the brain, which can lead to the onset of these mood disorders. So even those tend to have a physiologic. you know, underpinning. And then as far as, you know, the load capacity thing, I hope you don't, I hope you don't think like I've abandoned that model. I mean, I love that model. I mean, that video that, you know, it was the British Journal of Sports Medicine put on their website. Like I think that load capacity model is, it's fantastic. But as you said, there are some people where it just doesn't explain why they continue to have pain. Right. So then leading up to your question on, on chronicity, Like what defines chronic? I think that's kind of the issue. Like if we say an injury, quote unquote, that will last as long as the tissue takes to mend, but people like to say chronic injuries are anything that lasts over three months. I mean, that's, that's technically the definition, but that defend, that depends on the tissue, right? Like tendons take longer than bones to heal. Right. Or even if you have a bone injury, there's certain areas like high risk bone. for stress fractures that take longer than other areas of bone because the blood supply is different. But it depends on the age of the patient. Like if you're 65, you're probably not gonna heal as quickly as you were if you were 16. It depends if there's other comorbidities, right? If somebody has diabetes and there's impaired blood flow, they're probably gonna take longer to heal. So I think what we're really trying to say when we say chronic is like, if the pain lasts longer than a time for the, time that it took for the tissue to heal. Pain and injury are somewhat different, but if we were to say if the pain lasts longer than it took for the tissue to heal, I think that's different. For example, if you break a bone and the x-rays show that it mended but you still have pain, I'd consider that chronic pain. Or on the other hand, like what we talked about earlier, imaging isn't necessarily what we should be relying on all the time because most people have tendon tears throughout their body and they don't know it. Most people have disc herniations or disc bulges and they don't know it. Same with arthritis, like imaging doesn't really correlate that well with pain. So I think the issue that we want to talk about is, you know, let's say, for example, a person with arthritis, you take anybody with arthritis and they don't feel the same amount of pain every day. They're going to have some good days and they're going to have some bad days. Right. So what happens there? Like if on a good day, when they feel like less pain, if we did an image with their arthritis look better? No. Like did they miraculously heal their arthritis that day? Or on a bad day if we did imaging with their degeneration look worse? No. I mean, the imaging looks the same all the time. And the structural pathology in the joint is the same every day, but yet they continue to have good days and bad days. And so what I'm talking about is that there's like measurable physiologic amplifiers to pain. And it should be our job as health care providers to find out what's going on in that person. So let's say somebody has arthritis and they come in and they're like, I had a great week. But then yesterday it just flared up. I have no idea why. Well, do they have an underlying gluten sensitivity and they ate some gluten, which increased systemic inflammation? And then their body like it exacerbated the pain. Do they have a stressful day at work, which increases catecholamine production and so they feel more pain? Did they eat a lot of like hydrogenated? paracetidrogenated fats, which increases prostaglandins, which is a trigger for pain. And then we know that sensitizes the nerves. Like what's going on with that person? That's really the underlying thing that I wanna get to. Yeah, and would people expect to see this non-mechanical behavior to pain? Like if someone's trying to analyze how much of an influence it does have, let's say they've gone beyond their healing timeframes. they now have persistent pain beyond what would be expected. Are we seeing like a consistent pattern of an increased pain when they are stressed or an increased pain when they are eating gluten? Is the response to that pretty well correlated and pretty like, is the timeframe from that pain amplification to that onset pretty consistent? Yeah, that's a great question and it totally depends on the origin of why they're having the chronic pain, right? Like if you have, I don't want to get into too much of the technicalities, but let's say you have like a food allergy, let's say to peanuts or something like that, that's called an IgE response and that's immediate, right? But if you have a gluten sensitivity, that's an IgG response, which is a different type of immune reaction and that could take days to set in. You know, if you're not getting enough sleep. We know that does a couple of things. It hinders the body's ability to recover after each injury. So studies on that show that like, if you look at a group of people on a specific sports team and everybody's doing the same workout, and you look at some people when they get sleep deprivation, they get an increase in injuries like up to two weeks later because their body isn't recovering after every workout. But on the other hand, we know that sleep deprivation. There's lots of studies on this where the pain threshold is lowered following a night of poor sleep. So people will feel amplified pain. So I guess it's a tough question to answer because it depends on the source as far as the time onset between when the insulting factor was, like with a high glucose meal and raise their glucose. We know that hyperglycemia causes more pain. Like it decreases the threshold for pain. But other things take, take a while. So yeah, I'm going to continue throwing tough questions at you. If there's, let's just like, there needs to be a trigger for pain. Like if someone's stressed, they've got a stressful job. And they say to themselves, look, I was stressed before this injury and I didn't have pain. Now I've rolled my ankle and I've had a lot of pain. And this has persisted for three months. I'd expect to get better in a couple of weeks, but now when it comes to a stressful day at work, you know, my ankles hurting more than usual. Um, but does that mean that there is a physiological, uh, like there's a potential for there to be a pain signal discharge, like, cause is there something still physically going wrong? Why can't I get back to. stressful moments pre-injury where I wasn't getting paid. Yeah. Um, so you have to sort of think of these pain amplifiers as, you know, additive, right? If you think about a nerve that sends signals of pain to the brain, which is technically called a nociceptor, because there's technically no nerves that send pain to the brain, they're called nociception. I know that may get technical, but I don't want people who know their stuff to say that there's pain, like that I'm saying that there's nerves that transmit pain. So there's certain like... locks and keys, right? So on the end, if we like sort of zoom in really, really close on the end of a nociceptor, a nerve that transmits that noxious stimulus, there's little receptors like, um, you know, prostaglandin receptors and different types of like locks that will trigger that nerve to fire. And then there's other chemicals that are basically the keys for that, like bradykinin and hydrogen ions and prostaglandins and things like that. And so let's say you have tissue damage from you, like in your example of rolling the ankle, that will create the immune cells of the body in that local area to release these chemicals called cytokines. And cytokines can signal other inflammatory cells to come in and that can trigger the nociceptor to fire. Right? If we continue down that path, as the tissue heals, there's maybe still a little bit of tissue damage, but that tissue damage is below the threshold for that nerve to fire. But if you add on top of that, low cortisol or other stress hormones that are known to lower the threshold for that nerve to fire or cause that nerve to fire, then they will continue to have pain. So... It's all these things that sort of add up on top of one another. Like if, let's say, like you don't even have to have tissue damage to have pain, right? Like if you think about, you go out on a hard night of drinking and you wake up the next day and you feel like crap, then you got a headache and you're in pain. Like your joints kind of ache, which I know has happened to you. Was there tissue damage? There was no tissue damage. It's just these inflammatory reactions in your body trigger these nosiceptors to fire and now you're in pain. Right? So all these things add up, whether it's an underlying infection or a gluten sensitivity or stress or poor sleep or like, there's a lot of these things. And I hope we can get to some of these. That, that sort of add on top of one another that eventually cross the threshold for that nerve to fire. And if we can. do our best as chiropractors and physical therapists and doctors to get the tissue to heal and manage the loading capacity, that's great. Sometimes there's either other underlying things that continue to trigger these nociceptors. Yeah, it's sort of like a lot of what you're saying. I know that I've sort of my reasoning for it in the past has been cycle. psychological origin, like I've mainly said that, you know, stress and sleep and all this sort of stuff doesn't really necessarily increase, like inflammation, like you're saying from a physiological standpoint, but from a psychological standpoint, I was saying, okay, it heightens the brain's sensitivity or like it, you know, sparks that creates like more urgency, it creates more of a sensitized state, it's more worried, like stress and anxiety and depression, like just the state of the brain is a bit more heightened, a bit more alert, a bit more like, um, excitable when it comes to firing off these nerve signals. Um, but I know we're going to dive deeper into something that's a lot more physiological. Maybe we go through those now. Um, I have the list of likely culprits that you have here. which I think a lot of these are fascinating. I know, I don't know a lot about the first one was like the inflammation of the immune cells. Do you mind sort of explaining that and going into why it's important and what the process is behind it? So the immune system is like crazy complicated. So if we look at like immune cells, like T cells and other innate immune cells, like monocytes and macrophages, they release chemicals called cytokines. And these cytokines are designed to trigger inflammation and sort of call out for help for other immune cells to come to the area. But they also lower the threshold for these nociceptors to fire. So in other words, they like increase the sensitization of these nociceptors. So more recently, it's been discovered that these cytokines that are released from these immune cells can also directly activate the nociceptors to fire. So that means that these cytokines, again, that are released by immune cells, they can induce pain without an injury at all. So if you have a gut infection or a lung infection, these immune-driven cytokines can create systemic pain or pain in other areas. So the easiest example is when people, let's say you get the flu, you get body aches everywhere. You just increase systemic inflammation everywhere. So those nociceptors are firing from all different body parts. All right, so the ones that I tend to look at are basically three of them, underlying infections that can cause increased immune cells, food protein antibodies, like gluten and dairy and soy and whatnot, and then autoimmune conditions. Okay, so if we think about like underlying infections like Epstein-Barr, hepatitis, COVID-19. Parvovirus, whatever, they can all lead to chronic pain. So there was a great paper, if anybody wants to read it in BMJ, British Medical Journal in March of 2022, and it was called, Chronic Pain and Infection, The Mechanisms, Causes, Conditions, and Treatments and Controversies. And I'm just gonna read a quote, maybe a little bit long, but it says, Although our bodies eradicate most infections, a substantial percentage will persist in sublethal. or lethal form because of failure of detection or treatment. In other individuals, an infection could resolve but trigger an enduring immune response that results in chronic pain, which can occur in 10 to 33% of nociplastic, so that nociplastic means an alteration of the nociceptors, and post-infectious pain syndromes, or serve as a psychological stressor that initiates or exacerbates chronic pain. So this is all in the literature. And it's crazy when you really start looking into it. Underlying infections are a massive cause of people with chronic pain. So is it that hard as a provider, when somebody comes in with chronic pain, to just get a CBC, right? Just to check their white blood cells. Blood black. Yeah, just check their white blood cells. Like a CBC is the most basic blood work you can get. And if you wanna go deeper, you can check, you know, liver enzymes or something like that, if you want to see, you know, if they have chronic hepatitis or something. More recently, there was a study on COVID, on long haul COVID, and it was a study of over 2 million people. They found that chronic pain lasting at least 30 days was present in 5% of people. It's not some obscene, strange type of thing. If we look at food protein antibodies, you know, people think about gluten right away, right? But there's gluten, there's eggs, there's soy, there's milk. There's a lot of different food protein antibodies that people can form. And if you talk about gluten, there's a differentiation in people who have outright celiac disease, and people who have what's called non-celiac gluten sensitivity. And so celiac disease is differentiated because celiac disease is when your body is forming an autoantibody. So it's an autoimmune condition. Your body's fighting your own cells. And it cross reacts with gluten. So in other words, the amino acid sequence of gluten and some cells in your body are very similar. So your body can't differentiate the difference between gluten and let's say your gut lining or the cerebellum, like cerebellar ataxia is a big thing that happens with people with celiac disease. But If it's non-gluten sensitivity, or I'm sorry, non-celiac gluten sensitivity, you know, those antibodies against gluten or eggs or dairy or soy or whatever, they create inflammation outside the gut. And so people may think they eat healthy, but they have an underlying food sensitivity to let's say the protein in eggs, which is albumin. And so their body's producing antibodies against them, against eggs. and it's creating inflammation in their body, and then they have more pain. So like, yeah, they're eating healthy, but maybe not for them specifically, right? So it is important, and we talked about this earlier, it's important to know that we're talking about IgG antibodies, which can occur like flare up days after the injection. So it's difficult to track sometimes because people expect like, they eat something, they're gonna feel pain right away, but it's not always the case. But like, When it goes back to celiac disease, there's studies that show that 80% of people with celiac disease don't even know they have it. Because it may be manifesting in other ways, right? And so then the other aspect of the immune system is autoimmunity. And most providers will check for autoimmunity. Let's say somebody has widespread joint pain and the provider typically gonna check for rheumatoid factor, maybe ANA, which is anti-nuclear antibodies. Or maybe they'll do the genetic test of HLAB27, but there's a lot of other antibodies that affect joints, right? You can check for CCP, which is cyclic citrullated protein or peptide. You can check for fibrillant antibodies. You can check for collagen complex antibodies. There's a lot of antibodies that take place in the body that attack joints directly and you know, it's a big source of pain. Not only just that, like I mean you can have other autoimmune conditions that are just raising systemic inflammation throughout your body. And when the inflammation goes up, as we talked about earlier, that sensitizes these nociceptors. I'm already thinking of like past experiences. I remember when I got my COVID vaccine, all of a sudden, the next day I had proximal hamstring tendinopathy pain, which was pain that I had. Like I had that injury years prior and I hadn't had pain of that injury for years until like the only thing I could think of is what I got that I got that injection. And then my girlfriend's dad has an autoimmune issue and you know, chronic pain in some circumstances. He got an injection and he, he was with the COVID vaccine and he had a flare up of his symptoms for six months and it took a long time. They didn't know what it was. But then one of his specialists said that's probably due to the vaccine. So that would, I guess, make sense based on what you're, you know, it's sort of triggering the immune system when you have that done. And sometimes that can trigger a lot of that cascading effects like you were talking about. We had, I had Rowena Field on the podcast and she was talking about studies that she's done and the potential for low carb diets for people with chronic pain. Um, this seems to be some link between it helping people with chronic pain. If they're on a low carb diet, would that make sense in your eyes? Yeah, for sure. Absolutely. Like if you look at like insulin surges, when you have carbs, you know, your body is depending on what's called the glycemic index, so there's certain carbs that create more insulin response than others. Um, but basically high blood glucose levels. cause insulin surges and insulin is pro-inflammatory. But the interesting thing about that is like hyperglycemia, so in other words, high blood glucose levels, as well as hypoglycemia, which is low blood glucose levels, they both have been shown to increase inflammation throughout the body and pain, right? So there's a term called dysglycemia. which is different than like hyperglycemia is a lot of blood glucose, like high blood glucose levels and hypoglycemia is low blood glucose levels, but dysglycemia is like a roller coaster of up and down, right? And that has been shown to create more inflammation than hyper or hypo. So let's say you have somebody who's trying this, you know, thing that a lot of people are doing now with intermittent fasting. So let's say they eat at like six o'clock at night, and then they fast until noon, so that's like 18 hours. So their blood glucose level has dropped. And then they think, I'm gonna have a fruit smoothie because fruit is healthy, right? But fruit has a very high glycemic index. So now their blood sugar shoots through the roof, which creates this huge insulin response. And it triggers inflammation. And that inflammation has been shown, like if you have insulin resistance, like let's say like pre-diabetes or type 2 diabetes, there's studies on this where the inflammatory process lasts longer if you have insulin resistance than if you don't have insulin resistance, right? And again, You know, as a healthcare provider, how hard is it to check someone's fasting glucose levels? How hard is it to run a hemoglobin A1C or a glucose tolerance test? It's not that hard, right? Or talk to them. Like even before you have to run blood glucose levels and do blood tests, like ask them, how's your diet? Do you eat a lot of sweets? Do you eat a lot of carbs? Do you eat a lot of like high glycemic index foods? Let's track your diet for a few days. Let's see how you're doing. You know, it's not that hard. Or like blood glucose monitors are super cheap. You can check that out. But chronically high blood glucose levels, and this may get a little technical, but chronically high blood glucose levels lead to this thing called advanced glycolytid end products. So I know it's not a familiar term, but. Advanced glycosylated end products are when free radicals or lipids or proteins bind to glucose and then that accumulation like the bonding of those two compounds is called advanced glycosylated end products. And nosiceptors, well other cells in the body have what's called rage receptors. It's a funny name for it because it's interesting. for advanced glycosylated end products. That's what the acronym RAGE stands for. And so these RAGE receptors trigger inflammation and they trigger free radical production, which hopefully we can talk about later. But RAGE receptors is highly implicated in upper extremity and lower extremity osteoarthritis and rheumatoid arthritis. So when your blood glucose is out of control, and this goes back to what you were saying about like, maybe high carbohydrate diets, it may lead to more pain. But I think it depends on the individual. If you wanna take your running wisdom to the next level, then I highly recommend signing up to receive regular Run Smarter emails. Once you sign up, you'll receive my weekly blogs, research paper summaries, and podcast insights. You might be aware that I regularly post information across Facebook and Instagram. but I know not every blog will reach you. There are simply too many posts competing for your eyeballs and I'd rest a lot easier knowing that runners who want this content are receiving it safely into their inbox. Plus the additional links and resources I include within my emails means you will get the upper hand than reading it on social media. So if this interests you, there'll be a sign up link in the show notes. I wanna make this like really, I guess, practical for those who are listening, um, in terms of like action steps they can make or something that they can do. And you've mentioned blood tests, you've mentioned have a look at your diet, inspect your diet, have a look at your carbs. Um, you know, what, what would be the steps that they can take? Yeah. So that's, that's fantastic. And I would love to talk about that because it's like, I think it's important to, to keep your blood glucose levels stable. So rather than doing And not, I hope nobody's gonna get upset with what I'm about to say, but rather than doing intermittent fasting, have like five meals a day, but small meals, small meals that have a low glycemic index, like low carb. Keep your blood glucose levels steady throughout the day. Like I know intermittent fasting is a big thing. The studies on it are a little mixed as far as weight loss goes. Like when you do intermittent fasting, you're actually cutting the total caloric intake through the day. And studies are showing if you cut the caloric intake through intermittent fasting or not intermittent fasting, it's just the cutting the caloric intake that loses the weight. It's not necessarily the intermittent fasting, which is totally different. And we can talk about this later if you want, but totally different if you're in ketosis. If you're on a ketogenic diet, then I think intermittent fasting is a good idea, but you know, we can talk about that some other time. That was going to be my next question because that was one of the, I guess, for someone who isn't trying to lose weight, one of the proposed benefits of fasting is that it raises your ketones and the ketones is meant to, I don't know, reduce inflammation or like clean up, you know, the body give it time to rest and that sort of stuff. So, but again, that would lower. your glucose levels. And again, that's probably we don't want that roller coaster. But I think if you if you want to raise your ketone levels, you have to be what's called keto adapted. You have to have like the idea of a ketogenic diet is to deplete the glycogen in your body. And then when you deplete the glycogen, and we can totally get into this if you want, but on a microscopic level with the mitochondria, you're going to forego glycolysis. to create pyruvate and go to acetyl-CoA and go into the Krebs cycle, which ultimately leads to, you know, production of ATP and whatnot. But you're gonna use fatty acids to go through beta oxidation. And the beta oxidation is gonna use ketones to go into the mitochondria. So if you're just sort of like eating high sugar meals all the time and having lots of glycogen stores, if you fast for like 12 hours, I don't think you're gonna be producing many ketones. But I agree, I like ketones are very anti-inflammatory if you're in ketosis. And the great thing is, is keto, like ketones can cross the blood brain barrier. And so they can really help reduce neuroinflammation and a variety of different conditions. Okay. Yeah. So practical steps, you say like, have a look at your diet. You can measure your glycogen or glucose in your blood. you get some blood tests, if you feel like that's something that, you know, is there something that is there like a type of blood test? Like if someone can go to their doctor and say, I'm looking to have this work done? Are there any common culprits that would be a good first step for people to like, because there's so many blood tests out there and so many things you can look at in a blood test? Is there like a primary, this is our first look? some elements around that blood work? Yeah, if we want to start out like at the very basics, I would just say like a CBC, complete blood count. And what we call in the US, we call it a CMP, which is a complete metabolic panel, which includes like liver enzymes and glucose and electrolytes like sodium and chloride and things like that. If we really want to get into the glucose testing, like when you do a complete metabolic panel, it's typically a fasting test. So you want your blood glucose to certainly be under 110. I mean, if it's under 100, that's technically good. And if it's under 110, that's, but if it's being like, if it's being 100 and 110, then we consider that pre-diabetic. If it's over that, we would consider that diabetic. But it's not the best test, right? Like if you do a hemoglobin A1C, that's technically testing for glycosylated products. And it tests for, you know, sort of an average of your blood glucose over the past. three months or eight weeks, typically three months. The best test is a glucose tolerance test where it's a pain in the ass, but you gotta go, you go to a lab under a fasting state and they test your blood glucose level and then they give you, I think it's 75 milliliters of a high glucose concentration. And then they test your blood an hour later to see how your insulin levels are, you know, affecting the blood glucose. And then they test it an hour later. And you can even do a three hour glucose tolerance test or three hours later they test it. But you have to be sitting there in the lab, not allowed to exercise because that burns glucose. And it's basically, it's probably the best marker for how your body is handling glucose. If you have the time to go sit in the lab for two hours. Well, they can listen to some episodes of the podcast or, you know, this one will go for over an hour. So, um, you know, we can do that. I've, I've just realized like, we're not going to probably get through all the list of stuff. These, um, physiological processes that you mentioned. So you had, um, the, the histamines, the prostag... Gladden says that way. Yeah, prostaglandins are interesting prostaglandins There's direct receptor sites on nociceptors for prostaglandins Prostaglandins are fats in the body like not fats like hey, you got a fat belly fat. They're like fatty acids And they can go through a couple different processes. There's Some prostaglandins that are anti-inflammatory and there's some prostaglandins that are pro-inflammatory and I don't know if you I know in Australia you guys aren't allowed to have like ads on TV for medications, but in the US every freaking third commercial is for a drug. But there's a lot of like pain relievers that they focus on what's called the COX2 enzyme, which is part of the enzyme that goes through the process of producing prostaglandins to get it down the pathway of like the good anti-inflammatory prostaglandins. But you can change that with your diet because if you have a diet high in partially hydrogenated fats or trans fats, that fat that you eat is going to be going down the pathway of a pro-inflammatory prostaglandin, which directly triggers pain and inflammation. But if you have a diet high in omega-3 fatty acids, which are known to be anti-inflammatory, that's because it goes down the pathway of... anti-inflammatory prostaglandins. So if you're having a lot of fatty fish, certain nuts, flax seed oil, those are high in omega-3 fatty acids. But if you're having a lot of processed foods that you get out of boxes and bags and a lot of fried foods, those are going to be producing fats in your body that are pro-inflammatory through the prostaglandin pathway. And again, You know, it's not a routine blood work, but you can test through specialized labs for prostaglandins. But the reality is just eat healthier, eat less processed foods. Take like two grams of omega-3 fatty acids a day. That has been shown to be significantly anti-inflammatory. There's actually some studies where they measure blood inflammatory markers, which, you know... or like interleukin-6, interleukin-1, tumor necrosis factor alpha, nuclear factor kappa B, all these different inflammatory chemicals. And they give people these partially hydrogenated fats and they see these inflammatory chemicals rise in their body. But if they do the same thing, but then the person also right after ingests omega-3 fatty acids, that inflammatory reaction doesn't happen. So like the omega-3 fatty acids tend to block that I'm glad you say just eat healthy because people are going to listen to this episode if you didn't mention that and just be scared to eat because we've talked about carbs, we've talked about proteins, we've talked about fats and they're just going to be like, what can I eat after that? And so glad it's just, you know, healthy, sensible eating, less saturated fats, processed foods. Yeah. Like I'm a big proponent of the Mediterranean diet. I think that's a big anti-inflammatory diet. Ketogenic diet is good. I don't know if you necessarily have to follow any particular diet, but if you're in chronic pain, I don't think it's, it's not that big of a deal to go get tested to see if you have antibodies against gluten and dairy and eggs and whatnot. Just to make sure, or like, if you don't want to do that, it's totally fine to go through like an elimination diet. You know, go on what's called an anti-inflammatory paleo diet or an AIP diet. Do that for a month. If you feel great. you probably had some auto or not auto immune, some immune condition to some food proteins. And then you just got to reintroduce them slowly and see what you did. If you don't want to spend the money on blood work, just try that method. It's totally fine. I think that that's a good call. Like the level of urgency for you to take these actions are for people with chronic pain. Like if someone doesn't have chronic pain, And their diets horrible. Yes, obviously we want to eat healthier, but you know, someone who does want to indulge and have some carbs or like, you know, fluctuate their, their glucose levels every now and then totally fine. If, but this is mainly on the conversation of chronic pain. If you do have chronic pain, maybe you look at all of these things. And if you do find something, if you're better from it, obviously we'd, um, you know, raise that to on, on the priority list, put that high on the priority list to eliminate certain things or change something about your stress or sleep or nutrition to reduce that proposed inflammation. And everybody's got a certain level of interest on this, right? Like I've, I've brought this up with countless patients and they just say to me, like we can talk about this in a second, but like, um. Fat is technically called adipose tissue, and adipose tissue releases what's called adipokines. And there's an abundance of literature that shows that increases systemic inflammation and pain. And we can talk about that in a second. But I've had lots of different people where they come in chronic pain, and I say, look it. It would be good if you could lose a little bit of weight to lose the fat, because fat creates inflammation in your body. And their adamant that, you know, look at I eat healthy, I'm fine. And I go through their diet and they eat all this processed crap and they're just not ready for it. And so I back off. I don't think you can force this on people who aren't ready for it, to your point. It can become overwhelming. And I think there's a danger in that. Yeah, and I do think it probably requires a bit more of an in-depth analysis because sometimes I ask my clients, I want to diet like, and they say, oh yeah, it's really good. And I say, okay. And then I just move on. But like, to your point, someone could be fasting and then have a smoothie high in fruits and you go through that rollercoaster of glucose and, you know, promotes inflammation and, you know, most people would consider that process to be extremely healthy. And. So it does probably require a bit more of an analysis, a bit more of an understanding of what does, what is pro-inflammatory and anti-inflammatory. Very good points to make there. There's, you know, you've talked about free radicals, hypoxia, insulin surges. We've kind of dabbled into a little bit cortisol. You said the low cortisol dampens or like lowers the pain threshold to amplify or to send that pain signals. I'll let you pick one of these or we'll probably go through two more. Um, we've got the gut microbiome. Let's pick one. What, one of the biggest ones, well, if we can talk about hypoxia and the microbiome, that would be good. So when it comes to hypoxia, basically what, what hypoxia means is low blood oxygen. Right. So tissues experience low blood oxygen through a variety of different things. It could be an injury, infection, a lack of blood flow or, you know, low blood oxygen, secondary to sleep apnea. COPD, you know, if they have asthma or bronchitis, they're gonna have trouble getting the oxygen saturation. High altitude exposure, lots of things like that. Or it could be not enough oxygen perfusion. So perfusion means the ability of the oxygen to get pushed through the blood vessels into the tissue. So in cases like that of like atrial fibrillation, where it's like in a regular heartbeat, there isn't enough force to push the blood or push the oxygen through. And so if we just take one of those, for example, like obstructive sleep apnea, let's say. Right, so if you have obstructive sleep apnea, so generally, it's not always, but when you snore, you typically have. obstructive sleep apnea. But that lessens, intermittently, it lessens the amount of oxygen being delivered to the brain and the peripheral tissues. So that sensitizes nociceptors. It increases neuroinflammation. It increases the sympathetic pathways, which is like your flight or fright, flight or fight pathways, which increases pain. and it reduces your body's own opioid production. And I would love to talk just very quickly at the end if we can talk about your body's own opioid production, that would be good. But like, there's a great paper by Kashmarsky in just last year in 2022. It's called the role of inflammation, hypoxia, and opioid receptor expression in pain modulation in patients suffering from obstructive sleep apnea. I'm just gonna read a quote. It says, there's more and more evidence at a clinical, both at a clinical and a molecular level that sleep disordered breathing may be responsible for aggravation and or modulation of both chronic and acute pain. This is very well established in the literature. Right, so there's studies where they measure oxygen saturation at night with people with obstructive sleep apnea and it shows a direct correlation to increased pain in the morning. And if they use a CPAP it reverses that process. And that's a direct correlation. So like how hard is it? to ask someone, to ask a patient like, hey, do you snore at night? Does your wife say that or does your husband say that? Whatever, and go through a sleep test, see if they have that. And I can tell you from personal experiences with my own patients, people who have that, who have chronic pain, they get on a CPAP and it's life-changing as far as their pain goes. Because you get rid of that inflammation, you get rid of that sympathetic pathway, and it stops. sensitizing the nociceptors. So it's something simple that you can do. Just ask, if you're in chronic pain and you think you snored at night, go get a sleep test. Yeah. It's, and again, a lot of these things are, you know, people probably don't realize there's a direct correlation to pain and symptoms. They're mainly just focusing on, they're probably focusing on something else that maybe I've told them about, like their footwear or like, you know, running too far or running too fast. Yeah. May not even consider this. Again, again, I hope, you know, what I was saying earlier, like, This isn't to abandon the load and capacity idea. And it's not to abandon other aspects of imaging and whatnot, it's just like, this is another parameter to look at when someone has chronic pain and there's really not a great explanation for it. You know, if someone has low back pain because they started working out and all of a sudden tried to go max deadlift on their first day, like, okay. That's a load capacity issue. We don't have to do a sleep study test. We don't have to check your blood work, you know? But if there's something that you're having trouble explaining, I think doing these basic interview questions with people to find out their history, and if there's a clinical suspicion, run some blood work. It's not that hard, right? So, go ahead. I'll say, yeah, I was gonna say a good example of that. I had a... a client of mine, Maddie, who came onto the podcast to talk about her chronic pain. She had bilateral plantar fasciitis several years and we tried the load capacity stuff with her and after a while she just went out for a long run and it was the best she's ever felt and didn't make mechanical sense. I'm like, well, you know, you're having these like shortish runs and still getting pain. And then you go for this 10 K run and you feel fine. She's like, yeah, but I felt great. I was out in nature. I felt like I was getting a workout. I felt like I was back and she's talking about all these psychological, um, benefits that she's getting from it. And she says on the days where I am worse, it's usually at the end of the day when I'm like dwelling on a lot. I'm like, you know, focusing on the pain and being like, is this ever going to get better and very, very psychologically linked. And once we found that out, she then starts going down. other strategies to help. And we sort of like moved away from the load versus capacity model more towards, you know, I guess, self-talk and visualizations and, you know, meditations, deep breathing, all that sort of stuff. And she improved really quickly. And she had, she had plantar fasciitis for several years. And so to your point, it's, if it makes, if you're noticing change in symptoms due to something that's physically demanding. If there's that correlation, then maybe this isn't, you know, high on your priority list for investigation, but you know, there's, there'll be a lot of circumstances, a lot of people listening to this way, it's probably going to prompt a lot of action to which they probably hadn't thought about before. Yeah. So, yeah, I totally agree. And maybe again, we can talk about it at the end, but I think that there's certainly like an opioid production issue there where she was in nature, enjoying things and your body can produce its own opioids, right? Let's talk about that because you did mention about the opioid reduction. Can you explain more about that? Sure. The evidence is really clear on taking opioids, like in terms of a pill. It helps short term, but the evidence is overwhelming that taking opioids increases pain perception over time. pretty overwhelming in the literature, but what's called endogenous opioid production, in other words, your body's own production of opioids does not have that long-term effect. It has a totally opposite. So how do you increase your body's opioid production? Well, we know physical exercise does it. We know laughter does it. It's not overwhelming to tell someone in chronic pain to get the hell off Twitter. and looking at these social media like political things, and instead watch a comedy. Go watch a movie, go watch a comedy. Laughter increases opioid production. Healthy relationships are really important, and they can go both ways, right? Like an unhealthy relationship is gonna increase inflammation in your body, it's gonna increase stress and catecholamines. But a healthy relationship increases opioid and endorphin production in your body. Sex does the same thing. Sex increases opioid production. Any sort of touch or massage, go get a massage. That increases opioid production. Doing volunteering or like pursuits of passion. Having a pet increases opioid production. Yoga, meditation. Like these are all things that you can do. Like if you imagine like, I don't know what you guys call it in Australia, but like a teeter totter, a seesaw type thing. On one side, we've got like, inflammatory cytokines from immune cells and prostaglandins and insulin surges and fat cells and all that crap. And on the other side, you've got opioid production from physical exercise and massage and healthy relationships and sleep. Good sleep is like really tied in with pain. Exercise can be its own, you know, opioid producer. And you have to like balance out the two and hopefully skew it more towards the good side. Yeah, that's really like you've, you've listed a lot of very practical things there. Because anyone can do that. Anyone can watch a comedy, go for a walk, you know, appreciate nature. You know, call a friend. Those sorts of things is just something so practical and can have really good outcomes in terms of. seeing progress because a lot of times with this chronic pain, people retreat away from a lot of those things. They don't socialize, they don't exercise, they start eating poorly. It pulls them into a bit of a downward spiral where they're taking away a lot of, not only are they in pain, so they're miserable, but they're also taking away a lot of joy out of their life and pulling those things away. So yes, to say... someone with proximal hamstring tendinopathy that can't sit for very long. So then they stop socializing or going to movies or, you know, driving and those sorts of things. But you can walk out in nature, you can spend time with your pets, you can enhance the recovery process that way, which can be really powerful, which again, people probably don't realize. No, and it becomes a downward spiral, right? Like you see that especially in like, myalgic encephalitis or chronic fatigue syndrome, or fibromyalgia patients where they have just chronic pain. Um... We didn't talk much about it, but like free radical production, technically it's called reactive oxygen species, that triggers nociceptors as well. Right? So if you have a lot of free radicals, which are developed because the mitochondria are making ATP, that creates free radicals. And if you don't have enough antioxidants in your system to quench those, your free radical production goes up. So your oxidative stress is what we call it. So if people are unfamiliar with oxidative stress, it's like what happens when like iron rusts or you leave an apple out too long after you've been into it and it browns, like that's oxidation, but oxidation takes place in your body too. And it's fought by antioxidants. And so that whole process on like a, on a microscopic level is driven by mitochondria. And if, if someone with chronic fatigue syndrome or fibromyalgia. Like we know that pain creates free radicals, like it creates oxidative stress. And then we know that oxidative stress creates pain. So it's a bit of a snowball effect. It's cyclical, right? And if you're in chronic pain, then your body's always producing free radicals, which means it's depleting your antioxidant reserves. And so you end up with less antioxidants, which makes you have more pain. And the irony is that exercise, like an acute bout of exercise, creates more free radicals. So then people who are healthy can do physical training and over time, your body's production of antioxidants and the enzymes that create antioxidants increases. So you end up with this massive reserve of antioxidants if you exercise regularly. But if you have chronic fatigue or fibromyalgia, or in the case that you just said, where you become antisocial, you stop exercising, your body is now producing less antioxidants because you're not exercising, and then it's less able to fight the pain, and then you get more pain which creates more free radicals, but you don't have the antioxidants to fight it and it just becomes this downward spiral. So you take people with fibromyalgia or like it's called myelodic encephalitis or chronic fatigue syndrome, and that you tell them to exercise and they exercise and they have more pain and they get pissed off at you. And it's like, okay, we just have to start with something. Like you'll tell someone, just go for a 20 minute walk and they'll come back and they'll say like, I was in so much pain. Okay, fine. Let's start out with a five minute walk. You know, let's start with a two minute, like, I don't care what it is, but you have to start exercising to start producing your body's own antioxidants to, to reverse this whole process. Yeah. It is like this topic just in nature is just going to, there's so much to unpack. There's so many topics to go through. There's a lot that we didn't cover, which You know, I think if we got through all the stuff that you said, I will get to that at the end. If we got through all of those, there'd be another episode in here. So, um, I don't know, maybe we'd go on. Let's do a bit of a summary. Go on. No, just since, since we're talking about, like, um, since we're talking about like things that people can do. If you want to improve your antioxidant production, you eat a lot of flavonoids. So like foods that have a lot of colors in them. Tea and coffee have a lot of antioxidants. Sulfur containing foods like eggs and onions and garlics. They have a lot of sulfurous amino acids like cysteine and methionine. And their role is to produce glutathione, which glutathione is like the main antioxidant of your body. So again, it comes back to like what we said earlier, if you eat healthier and eat colorful foods and some tea and coffee and... You can take, you can take glutathione supplements for antioxidants, but gradually increase your exercise and that produces more and more antioxidants as you go. If someone wants to learn more about this, are they like, are you active on social media producing this stuff? Or do you have like a website or do you have any resources you can direct people to? Yeah. So, um, I w I just moved from the East coast of the United States to the West coast. So. I'm still doing a lot of telehealth with my patients back home. So people can reach me through that. Like there's a couple of different websites. You can do live or peak Those are my old clinic and my new clinic. And we can do telehealth through that. I'm not as active on social media as I once was, simply because of what we talked about earlier. Like it's pretty toxic. And so I sort of got off a little bit of social media in the last few years. But yeah, telehealth is always available for anybody. Anything else? Any other resources or things that we can point the listeners towards? Um, no, as far as I go, like, no, just telehealth. I'm not really active on social media anymore. Um, okay. Yeah. All right. Well, um, they can read your book. They definitely can. I don't know if it was amazing. This stuff, dude, I was really impressed with that book. Congrats. Thank you. Yeah. Um, it was a tough project. Probably the toughest thing I've ever done, but, um, I mean, I think it probably, it serves you well to do these podcasts, right? Cause it's like, You get exposed to all these, I mean, not me, but all these world leaders and PhDs and all these different topics. And I'm sure you, like you glean a lot of it, like it's a continuing education course for you all the time. Oh yeah, absolutely. There's so much that I hadn't even, like this episode is a perfect example of just, it's reframing the way I think about things or adding an extra layer into so much of my understanding, which, um, you know, putting into a book, it kind of like, once it was published, I kind of fear how much my ideas change over the years. And, you know, once it's in print, it's there. And if my ideas change, it's still there. But, you know, I was very, very proud of like the overall outcome. Anyway, we're gonna wrap this up because we're still recording, but thanks for coming on. Like obviously your depth and knowledge on this particular topic is like outstanding, world-class. And I think, yeah, it can open a lot of people's eyes. And I can see in the, in the future, if like a lot of my audience, if they have any questions and that sort of stuff, maybe we get you back on in a couple of months with a Q and a type of thing around this topic, because like you say, there was tons of stuff we hadn't covered and your knowledge on the research and all this stuff is just outstanding. So I appreciate you coming on, spending your time diving into all of this. And yeah, thanks for sharing. Yeah. Thanks for inviting me. So it's great to be on great. It's great to see you again. And that concludes another Run Smarter lesson. I hope you walk away from this episode feeling empowered and proud to be a Run Smarter scholar. Because when I think of runners like you who are listening, I think of runners who recognize the power of knowledge, who don't just learn but implement these lessons, who are done with repeating the same injury cycle over and over again, who want to take an educated, active role in their rehab. who are looking for evidence-based long-term solutions and will not accept problematic quick fixes. And last but not least, who serve a cause bigger than themselves and pass on the right information to other runners who need it. I look forward to bringing you another episode and helping you on your Run Smarter path.