EP 18: How Surgery Triggers Inflammation and Healing | DEEP FOCUS

In this episode, I explore a little-known biological pathway that may have a major impact on surgical recovery: DAMPs, or damage-associated molecular patterns. These molecular signals help the body recognize injury and initiate healing, but they also influence inflammation, nervous system stress, recovery timelines, and overall resilience after surgery.

We dive into how surgical technique, tissue handling, heat-based devices, and anesthesia can affect these signaling pathways, as well as why strategies like exercise, sauna, preoperative conditioning, and metabolic health may improve recovery outcomes. I also share how a deeper understanding of DAMPs has changed aspects of my own surgical practice and discuss the fascinating connection between inflammation, HRV, brain health, healing, and performance. If you're interested in facial surgery, longevity, recovery optimization, or the science of healing, this episode offers a unique perspective on what happens beneath the surface after an operation.

CONNECT WITH HOST 
Website: https://clinic5c.com/ 
Instagram: https://www.instagram.com/chesnut.md/ 
YouTube: https://www.youtube.com/@chesnutMD 
LinkedIn: https://www.linkedin.com/in/cameron-chesnut-a6910baa/ 

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TIMESTAMPS 
00:00 - Intro
03:24 - DAMP’s
06:37 - Minimally Invasive Access Points
09:04 - Tissue Handling
10:49 - Exercise and Inflammation
13:29 - BDNF
15:26 - Protecting Peripheral Nerves
16:32 - Heat Shock Proteins
19:13 - How My Surgical Process Has Changed
24:50 - 4 Takeaways
27:49 - Outro

ABOUT HOST 
Dr. Cameron Chesnut is the host of the Five Codes podcast and the founder of Clinic 5C, where he leads a team dedicated to integrative cosmetic surgery, regenerative medicine, and functional health. An internationally recognized facial plastic surgeon, Dr. Chesnut is known for producing natural, refined results that enhance rather than alter one’s appearance. His approach blends surgical precision with biological optimization and disciplined restraint, drawing patients from around the world who value excellence, longevity, and holistic care. On Five Codes, Dr. Chesnut uncovers the mindsets and evidence-backed strategies he lives by, helping high performers perform better, recover smarter, and feel their best in every area of life. 

DISCLAIMER 
The views shared on this podcast are my own and are not associated with, affiliated with, or representative of my clinical teaching role at the University of Washington School of Medicine. This content is for general educational purposes only and should not be considered individualized medical advice.

Transcript

Intro

SPEAKER_00 0:00

Welcome to the Five Codes Podcast, where we discuss evidence-based methods to elevate yourself to the next level through optimizing the way you look, move, perform, feel, and connect. We are talking about protecting the body during facial surgery. It's very analogous to how I try to protect the brain from the type of anesthesia that we're using with the surgery that we're doing. But now we're talking about signaling to the whole body. And this is unique because I don't know that a lot of surgeons think about this. In fact, I talked to one of my colleagues recently, and I was bringing up that I've been thinking about this and working through it. And how this colleague had never even heard of these pathways, which we're going to call DAMPS, damage-associated molecular patterns, DAMPs. And this is how our body signals that it was injured. And it interprets everything that we do in surgery with some molecular type of signaling. This gets really interesting because as we get into it, it overlaps with things that we do to pre-condition you for surgery, whether it's exercise, whether it's sauna, it gets into how your sauna benefits you. It gets into how exercise benefits your overall healing and your brain, but especially when we're meeting with things that happen in surgery. And there are some tie-ins to the anesthesia part of this as well. But I'm really looking at the little procedures that I'm doing on the face and how they're affecting the entire inflammatory cascade throughout the entire body. That's basically the nuts and bolts of it. It's important because I think surgeons need to know and think about this. It's important for patients to understand a little bit of what's happening, but also it gives you a little bit of why with some of the things that we're doing leading into surgery, whether that's thermal preconditioning with sauna or whether that's the type of exercise that you're doing. These are things that I talk about all the time. It also illustrates a few things about things that I've changed in my practice that would contradict literature that I published, meaning I published a study on this thing. And as I got a better understanding through these damage-associated molecular patterns, these damps, it changed the way that I practice. And that has to do with cautery, the use of heat during surgery and how it affects wounds and wound healing. So there's a lot to this. And if it's powerful enough to have changed the way that I practice, and I'm talking to colleagues who have never heard about it, I think that this is a really important topic to dive into mostly as a patient. This is going to help you understand some whys. It's also going to help you understand how I think about your entire procedure in a very advanced way. As you get to levels of mastery and virtuosity with things, you tend to make things more complicated. Not necessarily than they need to be, but I will just say you tend to dive into the nuances a bit. And this is definitely an example of that, thinking about molecular signaling during surgery, how that affects everything. If we really get rudimentary and go back into it with my patients, for many years, I've been watching their recovery on a physiologic or metabolic level where the rubber meets the oath with something like their aura ring or their whoop band or their Apple Watch, whatever it may be, and we're looking at something very simple like their heart rate variability, their HRV, which is a signal of sort of uh nervous system stress, central nervous system stress to their healing and how long that can take and how intense of a change they see. And so I've actually been sort of unbeknownst to me a little bit following this for many, many years, but now just with a deeper understanding of the little levers that I can pull. And so

DAMP’s

SPEAKER_00 3:24

damage-associated molecular patterns, damps, uh, are some things we've heard of, like uh heat shock proteins. Those are really cool. And we talk about those with sauna all the time and how beneficial they are. But at some level, they can also be one of these damage patterns. Um, damage patterns tell our body I was injured, I was damaged, help basically. Um, and that contrasts with things that we get during exercise called myokines, that was like, I was used appropriately, but now we got some work to heal. Or something that you've heard me talk about before, BDNF, brain-derived neurotropic factor, which is people call like fertilizer for the brain, that's just like, let's grow and adapt. And all of these sort of have a Venn diagram where they overlap a little bit, um, and they can all be protective against one another with the injury on one end and the grow and adapt on the other end, and then the used appropriately in the middle. And so I'm always trying to maximize the healing and minimize the damage, if you will, if we go into that analogy. And this is one of the ways that we do it. So you have heat shock proteins that actually fall into a few of these buckets, depending on how much of them and where they're located, inside or outside of the cell. So we'll get into that. There's mitochondrial DNA, when DNA from that's usually inside the mitochondria, inside the cell, gets exposed extracellularly, it changes the way that our body reacts. It says, oh shoot, I was damaged. I have to do something. There's things called alarmins, S100 family alarmins that get into this. And ultimately those go downstream and hit something called toll-like receptors or inflammosomes, and that releases a whole inflammatory cascade of cytokines and white blood cell recruitment and the change of the endothelial cells, which is the lining of our blood vessels, but eventually there's a spillover of that. Too much damage there leads to spillover, and surgery can cause that. And this is backed in the literature. There is literature of surgery looking at these damps after surgery. It there's a clear link to aggressive surgeries, increased levels of damps, and increased inflammation after surgery. Here's a little tie-in to uh the anesthesia part of it is that those can also change the postoperative cognitive dysfunction after surgery. So higher levels of these damps circulating after surgery predict worse cognitive outcomes after surgery, which sort of makes sense. But a lot of times in the anesthesia world, you're hear you will, or I will hear, and I hear from anesthesiologists that say, well, surgery creates the POCD, not the anesthesia itself. Well, there's some truth to that in this, that aggressive surgery can create postoperative cognitive dysfunction, but it's not the only part of that. There's neuroinflammation that happens from anesthesia and the agents and low blood or low oxygen, which is called hypoxia and things like that as well. But there is some truth to this fact that the systemic inflammatory overload of surgery can lead to changes in the brain. And it's through these damage-associated molecular pattern pathways. That is one of the ways they get there. And so we know that improving those damage-associated molecular patterns in surgery can produce better outcomes, not just neurocognitively, but an overall systemic inflammation. And so that led me to this level of like, well, I'm doing very minimally invasive or as minimally invasive as I can when it comes to the types of facial surgeries that I'm doing. So

Minimally Invasive Access Points

SPEAKER_00 6:37

even my facial surgeries are contributing to these damps and the systemic inflammation and the inflammation overflow. And so I've always been thinking about how I can minimize that. And so I've kind of like my first thought pattern honestly took me to, well, I have little baby teeny invisible access points. So I'm gonna be pretty good compared to like some big open access procedure. Um, and there is interestingly surgical literature looking at this. It's in the abdominal surgery literature, looking at open abdominal surgery versus laparoscopy, which is like, you know, through the little holes in the abdomen. And this is where it's not as simple as we'd like to think. It's not just straight up that the more minimally invasive laparoscopy led to better levels than of these damps or lower levels in this case of dAMPs than open laparoscopy did. That is not the case, actually. There's a lot more to it. There are issues with tissue handling, especially when we're talking about the bowels, interestingly, handling different parts of soft tissue differently release more inflammatory mediators, which sort of makes sense. So it's tissue handling, it's blood loss, it's cautery, it's traction. And it's traction just means how much you're pulling on the tissue. It's the reperfusion time. Like if something is pinched and doesn't have blood flow for a sec, what happens when that comes back? So there's a lot more nuance to it than just the access point, which was good for me to really understand in here because that, again, this is practice changing for me. It's not just that I'm making minimal incisions, it's every single area that I'm working or dissecting. It's is this necessary? How important is this to our outcome? What's this doing to our overall inflammation? Which is essentially how fast is my patient, this friend of mine, how fast are they going to heal from this afterwards? Uh, my patients tend to be very much seeking uh minimal downtime, getting things done as fast as they can, but also we both have the same end goal of like, let's let's achieve these absolutely next level results together. So I'm always weighing these together. And these damage-associated molecular uh patterns help me get another way to think about, okay, here's is it worth creating this extra dissection plane for our end results? So I'm always balancing these things, I'm finding the best, and it's a little bit different for everybody along the way. And so it's important to think about these damage-associated molecular patterns, how they work, what leads to them. And I would encourage all my colleagues, I teach all my fellows this

Tissue Handling

SPEAKER_00 9:04

that there's so much nuance to the procedure that we're doing in the tissue handling, like how aggressive we're being. I'll see a lot of surgeons that are just kind of like, they're fast, they're just moving through things really quickly and they're stretching and they're dissecting quickly, and you know, they're getting it done and they look, you know, they look like they're fast and they know what they're doing, and it's kind of tough. And and I've always had an uneasy feeling about that. I can go back to when I was in my residency and my fellowship training working with different surgeons and seeing that. And it never felt right to me. It felt very um, you know, rushed or kind of showy, or I was like, well, I'm not impressed that you're fast or that you're doing it that aggressively. That doesn't really show me anything. Um, I've always gravitated towards this more sort of like thoughtful, delicate, slow, methodical, kind of like flow state approach for me a little bit. And interestingly now, flash forward, you know, decades later, I have this uh molecular pathway to explain even something that just didn't register with me then. But I still see it to this day. I break that in my fellows very quickly when I'm teaching them, which is we need to be gentle with our tissue handling. And this is why, because all of those things matter. It's not just the minimal access. That definitely helps, you know, having little teeny areas that we're working through is part of it. But we're also thinking about what are we pulling on? How long are we pulling it? Where are we dissecting? What's happening with our blood flow? Uh, how much cautery are we using? Because cautery leads to very directly to something called the heat shock protein getting released. And this is where one of my practice areas changed a little bit. Uh, and we'll get into that in a sec, because that sort of segues us into the next phase of this is that these dams are saying, I was injured, I was damaged, help, send signals out, you know, send help basically. Mitochondrial DNA is exposed. Our body's like, that's not supposed to be there. Let's let's roll.

Exercise and Inflammation

SPEAKER_00 10:49

But there's other elements of this that happen when we exercise and our muscles. These are called myokines. And the most famous of these myokines is exercise-induced IL6. And I only say that to say that this interleukin 6 also, on the flip side, can be pro-inflammatory. But when it's exercise induced, it tends to have this more adaptive response. This is sort of our body saying, I was used appropriately, meaning my muscles were used and broken down, and now it's time to grow and adapt and get stronger. So you have this exercise-induced IL-6 that decreases inflammation in certain pathways, like TNF alpha, tumor necrosis factor alpha. Um and then that's important to mention because on the other end of the spectrum, when IL-6 and TNF alpha exist together, that's very pro-inflammatory, like a whole different animal, right? So exercise and the nuance of creating this exercise-induced interleukin 6 causes this anti-inflammatory cascade. And this is important for us to know because this is when I'm having my patients exercise very specifically before they come in to see me. And again, most of my patients are already pulling that lever, I would say, but we might alter it a little bit. And it might have to do with their lactate threshold, their strength training, their endurance training. Those types of things, increasing this inter exercise-induced interleukin 6, this is where the rubber meets the road, quite literally change our systemic inflammatory profile. So we know that we are going to have better outcomes after surgery. This is a molecular pathway to support this and to sort of give us, you know, the answers to why this is happening. But exercise is going to improve our systemic inflammation via this exercise-induced IL-6 and the cascade that it produces with IL-10 and decreasing tumor necrosis factor alpha to make it so that you are going to respond better to your surgery. And to me, this is wildly fascinating and a really important mechanistic support as to something that we all know is happening anyway. And this is going to be your systemic inflammation afterwards. It's going to be your neuroinflammation afterwards. This is one of those mechanisms as to how that improves. This is in addition to things that I talk about like hypoxic or carbon dioxide hypercapnic tolerance that are going to improve your ability to withstand hypoxia or things like that during your surgery in a completely different mechanism. So this is, I highlight this IL-6 or this exercise-induced IL-6 because this is like the overlap of our Venn diagrams. The two circles overlap here, where if you have happen to have a little bit more of this damp activation with your surgery, we now have a mechanism with exercise that is going to change the systemic profile of it.

BDNF

SPEAKER_00 13:30

One circle over, if we have this three overlapping Venn diagram, is something like BDNF. And I've talked about this before. I talked about it in the anesthesia episode. I've done a little bit on this just specifically on BDNF, brain-derived neurotropic factor, which people call like miracle growth of the brain, which is probably a little dramatic. But this gets into like the neuroplastic parts of our brain. And inducing that, well, interestingly, BDNF gets released directly by our muscles contracting, specifically like type one fibers. And there's some inter, but there's just some interesting release of brain-derived neurotropic factor when we exercise as well. So now you have this other end of the Venn diagram. BDNF is not saying necessarily I was damaged or I was used appropriately, but we need to heal. It's just all about growth and go. It is, it wants to repair, regenerate, grow. And you're releasing this with exercise as well. And so this seems to really tie into the brain part and the anesthesia, and it does in that way. And I've talked about BDNF levels being elevated. This is very predictive. We know this, that elevating circular elevated circulating BDNF levels, if you look at those interoperatively, those patients are more likely to be neuroprotected after surgery or lower levels of them circulating is more predictive of postoperative delirium and things like that. So this makes sense. If there's study showing that elevated damps systemically in your in your serum are going to be predictive of poor postoperative cognitive situations, like more delirium with more inflammation. Well, that makes sense. On the same side of this, lower BDNF levels circulating predict the same thing. So now if you can increase your BDNF and decrease your damps, now we've got a nice balance going on here. And this is what I'm working so hard to do with you during your surgery, which is me doing it. So when I say that I'm intricate and thinking about it, I'm like thinking about this on a molecular inflammatory level. And on the other end is the things that you get to do before you come in. But there is a bit of a body tie into this as well when we talk about BDNF.

Protecting Peripheral Nerves

SPEAKER_00 15:26

And that has to do with protecting peripheral nerves, which is really important because as any of my patients know when I talk about this, inflammation around your nerves is something worth mentioning because it can change the way that nerves feel. And I think a lot of people have had this in many fashions, which is like, oh, you know, I was kind of numb and my nerves are waking up and I'm getting a sensation, a tingling, or uh, you know, I feel shooting through there or something like that. Well, that's nerves, I'm gonna say, quote unquote, waking up, right? Well, BDNF is supporting the regeneration of these nerves. It's supporting the healing and it's supporting the protection against inflammation that our nerves are having. So it's more than just happening in our brain. And BDNF is really overlapping again on that Venn diagram to be mostly on the protective end, but it is a lever that we can pull around surgery with exercise to again pre-condition us into that. Now, there are a few unique nuances in here of things that have changed my practice, right? Um, there's also the aspect of how some of these different damps can also be protective depending on where they're at. So

Heat Shock Proteins

SPEAKER_00 16:32

I'm a sauna lover. I know many of you are sauna lovers, and so let's talk about heat shock proteins because this is a very confusing topic because heat shock proteins on one end is a damage-associated molecular pattern. Help, I was injured. Inflammation, bad. That sounds bad. It is bad. We don't want that, right? I don't like to label things as bad. Um, but that's that is a pathway we are trying to minimize, at least. On the other end, we all hear about sauna and inducing heat shock proteins and how helpful they are to us from a cardiometabolic standpoint, which is also true. So, how do these both exist at the same time? Well, there's nuance here, and it also explains why saunas are good leading into surgery. So, intracellular inside of the cell, heat shock protein is a protective thing. That is what we're talking about when we get induction with heat preconditioning, like thermal preconditioning. That's a good thing. When it gets outside of the cell, when it gets released into the serum, that's not good. That falls into the damp category then. And there's surgical studies showing that heat shock protein 70, HSP 70, is predictive of poor outcomes after surgery if it's in high circulating levels. But intracellular HSP is predictive of good wound healing, of faster wound healing. And you can actually use that therapeutically a bit too with these heat shock proteins, but we can easily pull this lever with thermal preconditioning with sauna use. So preconditioning, heating with the sauna induces our intracellular heat shock proteins, which is a protective pathway. This would be one of these hormetic stressors, like enough stress to generate a response, but not so much that it's damaging on the damp end. This is a prime example. We've I always talk about sauna being one of these hormetic stressors. Fasting is a hormetic stressor. Exercise is a hormetic stressor. It's enough stress to induce healing and regeneration, but not so much that you're like completely crushing yourself or having this big inflammatory pathway. Exercise can cross over, sauna can cross over. They can all do that. This is a good example of how sauna before surgery can improve your heat shock protein levels. It can make you more resilient to your surgery. And there's direct evidence looking at this with thermal preconditioning of the skin before an incision. That means applying heat to the skin, inducing heat shock proteins, basically cutting into the skin and looking at it if you do thermally precondition or if you don't thermally precondition, and having better wound healing, faster wound healing with thermal preconditioning. This is a direct mechanistic lever to pull when we're talking about doing saunas before surgery or saunas for anything. Great thing. So uh it's very nuanced there, but I think that that's really

How My Surgical Process Has Changed

SPEAKER_00 19:13

important. This also changes a little bit of me understanding a study that I published with one of my fellows. So this is me taking a piece of literature that I put out into the world. This is a great example and saying, I don't actually exactly do that anymore. And here's why. The study was for upper eyelid surgery, one of my babies, right? Upper eyelid surgery, looking at making the incision with a scalpel, which we call cold steel in surgery, a scalpel, making it with a cutting cautery device, which is the lowest thermal load, the lowest spread of what we can do with a typical like cottery device, like you might think about in surgery, which is like we call that electrosurgery, and looking at a CO2 laser. So years ago, um, it got really sort of sexy to do this laser-associated upper blephroplasty, which is where you just used a hand piece on the laser. I have this on all of both of my CO2 lasers, have a hand piece where I can make incisions. CO2 lasers are ablative, all of them are ablative, even if it's fractionated. This is a commonly misunderstood thing. All CO2 lasers are ablative, and I can put a hole in your body with it all the way through. It's very powerful, right? And so we can use those in surgery to make an incision. And so it got really sexy to do that for a while. And I was always sort of like, well, is that heat bad? And I thought the same thing with cottery, and I thought the same, you know, versus cold steel. But the advantage when you use those other devices is there's not as much bleeding, right? So you're weighing all these together. So I did a study with one of my fellows, Dr. Carkoville, um, who also had a lot of, she was uh board certified and uh pathology specialty as well. So she was really great at looking under microscopes, and we did a series of cases uh of upper eyelid surgery where we used, and because these are all very accepted pathways with no clear evidence as to what was best, we did some with a scalpel, we did some with a cut and cautery, and we did some with laser. And immediately after we took the specimens that we would have thrown away and we looked at them under a microscope basically to look at, okay, how damaged are these cells after the basically after this heat was applied to them or no heat with steel? And when we looked in a nutshell, we found that of course the the scalpel had no thermal damage as expected, that but we looked anyway. We found that there was a little bit of thermal damage, but it wasn't too over the top with the cutting cautery. Uh and then we also found that with the CO2 laser that had the most, like the most visible cellular damage. Cells get a very distinct look to them when they've been damaged under a microscope. They kind of get this like spindle drawn out there, you know, the fluid comes out of them. There's a bunch of interesting things that happen there that have to do with proteins getting denatured, but you can tell basically by looking at them. And so for a while I was like, oh, I'm that's good to know. We looked at quite a few patients with this, and I was like, that's good to know that the cutting. Cottery actually doesn't cause that much thermal damage. And so for there was a period of time where I did use thermal cottery on cutting, which again a lot of my colleagues do, many do actually. But eventually I ended up migrating back to cold steel, back to a scalpel to do this. Because, you know, when we look at outcomes on the other end, because I'm looking at under a microscope and that's where this study ended, just sort of how much cellular damage was there. But when we look on the other end at scar scales, my opinion, none of the scar scales are really sensitive enough to pick up nuances. Like if there's five points on a scale, you've got terrible, you've got great, and then you've got three points in between. Well, what if it's like, what if we need a hundred-point scale to really pick up the nuance differences between things? So I've always thought that was scar scales and um anything that showed CO2 laser or cutting cottery, they didn't show a big difference. But uh part of me is like, I but there could be more to it. There probably is more to it. And I started gravitating back towards a scalpel blade because I knew in my head, I'm like, I just don't like this heat. Well, here we are, now rubber meeting the road with a deeper understanding of, and this was, you know, at this point, probably maybe close to five to you know, 10 years ago that I was like in that transition phase, and I've been with, you know, scalpel ever since. And this is the mechanistic molecular pattern that explains why. Cottery, even if it doesn't directly damage the cell to a great visible degree under the microscope, is causing these damage-associated molecular patterns, these dams to be released. Heat shock proteins are getting released outside of the cell. That's gonna cause not only systemic inflammation, but it's gonna cause local inflammation in that area. When we release these damps, you know, I mentioned some of the pathways, but things like macrophages, which are some of our like cleanup cells, get activated. You you activate a local inflammatory cascade as well, which was gonna predict probably worse wound healing. So, although we don't have scales maybe sensitive enough to pick it up, there's a mechanism here. It's plausible, it would explain a super detailed nuance to my eye. And so I'm gonna change that. And I did. And thankfully I changed it before I had made the mechanistic connection. But for me, this was a bit of an aha moment, actually, is like this is what I knew deep in my core that whole time. And so is this a confirmation bias? Maybe, but there's definitely a mechanistic plausibility as to why I gravitated back towards cold steel even versus cold cottery when I had visual evidence in front of my eyes that there wasn't much of a difference. But now at the next level, that's you know, first order thinking, now a second-order thinking about the molecular pathways or even third-order thinking that I've changed the way that I practice. And uh, and I published that study. So that's an interesting sort of evolution for me over time. The

4 Takeaways

SPEAKER_00 24:50

gist here is that I am working during your facial surgery to minimize the inflammatory signaling I'm sending to the rest of your entire body. That includes your brain, but it's also your nerves, your muscles, your fascia, your heart. Um, and there's a few key ways to do this. If I were to summarize, I could think of four main things is number one is it's not just the incision, meaning it's not just the minimally invasive approach. And this was important for me to recognize because I do use, I do tend to really gravitate towards those minimally invasive incisions, which is part of it. But the second one is that the mechanical forces, the tissue handling, the gentle nature of what I'm doing that I've always gravitated towards anyway, that's part of the overall signal that we're sending. So you've got small incisions and gentle tissue handling, one and two, and we are in a good spot to really understand and minimize what's happening. And it's just kind of funny to me that those, those, I knew those in my core. And these are some mechanistic, you know, support of that. The third one is I want to have you enter with these adaptive signals already turned on. I want your surgery to come in so that the one, the inflammatory, some of this is the cost of doing business, if you will. We're gonna have some damp creation just kind of pay-to-play. You have to be able to have a little damage to get the healing going. But if we can have so much support on the other end of that by, again, having the resilience already rolling, having these adaptive factors high and going, whether that's myokines or BDNF, we're gonna be in a good spot to heal and do the repair that we need to do. And I think the fourth one is making sure, and this is a little bit easier for me with facial surgery, but making sure that our approach is allowing your muscular function to restore as quick as possible. You could imagine that if you're doing like an abdominal surgery, a chest surgery, that it would be a little harder to get your muscles functioning. But for me, this is one of the focuses with my patients is I want them walking as soon as they can. We want them exercising to an appropriate degree. We have to wrap our head around this is a conversation I talk about with all my patients very extensively. Um, I think that's a sampling error of my patients too, is when can I exercise again? It's one of everybody's first questions. Um, because those are going to be protective signals, like we just talked about, the myokines and the BDNF. We want those protective signals to continue after surgery as well, because the inflammatory cascade, like I mentioned at the very beginning, tying this all together, when I look with my patients over time and we watch their HRV return to baseline, it doesn't happen overnight. It takes a little bit of time. But these are some levers that we can pull to make that happen faster. And we have direct evidence and something like that to show what that time frame looks like a little bit is how much of that systemic inflammation is still happening, how much of it is positive and directed towards healing, and how much of it is just straight overflow, right? So we want our positive healing, we want to support that, we want the inflammation that's letting us heal. We want to minimize everything else. And there's a bunch of levers we can pull to do that. And

Outro

SPEAKER_00 27:49

I'm thinking very deeply about it. And I encourage my colleagues to do the same thing and push me on this and help me grow and think about this and find new ways. And I encourage my patients to do everything you can on your end, or this, and this applies to any surgery, not just what I'm doing with facial surgery, but you have levers to pull going into your surgery to have all the signaling elevated, to be as resilient as you can be and to be as ready to adapt as you can be. So thank you for taking a deep dive into what I think is a really important and interesting topic that ties in a lot of things that I love, from exercise to sauna to pre-operative conditioning, and then of course to surgery itself, and how I can make your experience as good as I can make it, make your recovery as fast as it can be, and achieve those next several results. If you have any questions or topics you would like me to explore further, please leave them in the comments. I read them all and they often help shape the future conversations here. If you would like to learn more about my surgical practice, you can visit clinic5c.com where you will find additional information on my approach to surgery, recovery, and performance focused care. I also want to be clear that the views shared on this podcast are my own and are not associated with or representative of my clinical teaching affiliation with the University of Washington School of Medicine, nor should this be taken as individual medical advice. Thank you for spending your time with me. I appreciate you being here, and I will see you on the next episode.