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. In today's deep focus, we are diving into my anesthesia and pain management protocol. These are very unique. They are not novel. I did not invent any of these things, but I have pulled in a bunch of cross-pollinated strategies to essentially create what I would want if I was having surgery. These are linked to every aspect of surgery from preparation through the optimized recovery. All of these play together to number one, be safe, be very protective of your brain, your neurocognition. I'm a high performer. A lot of you are high performers. You don't want to blunt your long-term neurocognition for what is essentially an elective cosmetic procedure with me. And then pain management. We want to be very thorough and effective with that, but do it in ways that maybe don't involve opioids or benzodiazepines, which are traditionally used for this, and they in and of themselves are not bad. I just think that there's better ways to do it, and there's things that we can avoid with those that are, again, essentially what I would want. Same with anesthesia. I don't choose to use general anesthesia. Not that general anesthesia is bad. As a matter of fact, thank goodness for general anesthesia as uh for surgery as a whole. There are things that you absolutely need that for, but with the types of procedures that I do, um I don't believe that you actually need them. They actually make general anesthesia makes my life easier because it it sets a very specific type of environment, but I just, it's not what I would want. It's not what I want to do for my patients. And there's ways uh that I can be essentially just do better anesthesia for my intents and purposes in a way that I would want it that gets very nuanced, and these are things that I'm obsessed with. I love diving into this topic. And again, it really plays into this my surgical philosophy as a whole, which is optimizing outcomes, keeping things natural, um, having all of the uh aftermath or all the things of this be benefits as opposed to having anything afterwards that is maybe sort of like borrowing from our future to look better now. And that includes our neurocognition and what we look like. We want things to be natural, uh, and that includes in the way that your brain functions afterwards. I want everything to be functioning as it should, from your face to what this looks like. So this neurocognitively protective, benzodiazepine-free, opioid-free protocol is really rooted in that same thing. And so when the rubber meets the road, what this looks like is I'm gonna jump

Neuro Inflammation

SPEAKER_00 2:27

into the anesthesia protocol first because um, you know, the uh a good counterpoint to this is that a lot of the um posto-operative cognitive dysfunction, that's what we're gonna call this POCD that comes after anesthesia. We know this is basically brain fog, that foggy state where you can't find words, you can't remember things. That POCD that happens afterwards is driven by neuroinflammation. There are some other minor mechanisms that might have to do with microemboli and things like that, but let's focus on neuroinflammation because even the microemboli, the little blood clots, can lead to neuroinflammation. That's ultimately where the rubber meets the road here. And surgery itself causes a peripheral inflammation that can have effects on our central nervous system. And that's what a lot of anesthesiologists will point to. And that's true. When there is peripheral tissue damage outside of the central nervous system, these damage-associated molecular pathways, damps, get activated. And these are actually uh signaling inflammatory cascades. These are things like heat shock proteins that we've all heard of that kind of go down a line to signal peripheral inflammation via inflammosomes that then affect our brain and communicate with our central nervous system. And they do so by affecting the blood-brain barrier largely. And once the blood-brain barrier is not necessarily knocked all the way down, but even just a little bit compromised, we can get some inflammation in the brain via these microglia. Microglial activation of the brain is sort of like the immune system of the brain being activated. So very truly, peripheral tissue injury can cause central nervous system inflammation via this very complex pathway that goes through that that involves cytokines and a lot of inflammatory signaling. Now, first and foremost, is even the procedure that I'm doing is trying to minimize that peripheral inflammation as much as it can. I don't know that a lot of surgeons are necessarily thinking this way, but choosing minimally invasive types of procedures, very being very delicate with my tissue handling, not only improves your recovery time from the procedure, creates less unnecessary damage to that soft tissue that I'm working on, but it also changes the way that your brain responds to the surgery. That's a whole nother benefit to it. And that really illustrates a lot of these tie-ins that I'll talk about is that the overall philosophy around my surgical approach also affects how our brain reacts to the anesthesia. And that's a prime example. So, no question that the surgery itself causes or can contribute to inflammation inside the brain, but there's so much more to it that than that. And that's where the nuances really come in is you have to get, when you look at the granularity of this, you have to get very fine into this to really understand it and to really optimize the way that it goes, because there's a lot of large studies in anesthesia that show essentially no difference between having general anesthesia and having uh maybe more progressive types of anesthesia on sort of long-term outcomes, but it's not very detailed and fine and nuanced. And when you're in my world and you see it all the time, you know that there's so much more to it than that. And so this is where we get into the next steps. Ways that we can minimize inflammation in the brain with the types of anesthetic agents that we use. The inhaled gases that are used for general anesthesia are notorious for causing this type of a neuroinflammation. Just straight up we'll leave it at that. I don't use those anyway. Uh, when we get into the types of IV sedation that I'm doing, there's a lot of different

Benzodiazepines And Opioids

SPEAKER_00 5:48

ways to do that. The traditional ways is to use a benzodiazepine and an opioid together, uh, fentanyl and versette or something like that. Those are brand names that get put together, or one brand name, one generic name, but they get put together, and that's a very common uh IV sedation strategy. And I don't do that at all. I do not use any opioids or benzodiazepines during my procedures because we know that benzodiazepines in particular can lead to types of uh brain state changes, even like delirium after surgery. And opioids have a complex cascade in the central nervous system with some potential promotion of neuroinflammation, um, and also like a almost a central like hypersensitization that can happen afterwards, in addition to making you not able to go to the bathroom after surgery and causing just that overall brain fog that we have with them. So I try to avoid those in my, not just in the anesthetic immediately during surgery, but also in the posto-perative phase as well.

Dexmedetomidine

SPEAKER_00 6:48

So focusing on other agents. Um, one of them in particular, dexmetatomidine, is very interesting. Um, again, this is not a novel strategy, but the approach that I take with it and the mindset that I'm using with it is relatively progressive because dexmedatomidine is a central acting alpha-2 agonist. And what that really means is it affects an area of our brain called the locus ceruleus. And this locus ceruleus is really important because this is the main norepinephrine portion of our brain. This is the part of us that is excitatory, um, that controls our activation, basically. And so when we can blunt that area, um, when we can slow down the norepinephrine in that area, it's very much a sleep-like state. And if you look at EEGs of somebody who's having dexmetatomidine as their anesthetic agent, it very much resembles sleep with slow wave sleep specifically, like non-REM slow wave sleep. And these, you have sleep spindles that are happening there. This is very different than other anesthetic agents, mind you. And so with this type of essentially sleep state, um, we are controlling activation, we're controlling sleep. And in those deep stages of sleep, we're also protecting your brain. And what I mean by that is in deep stages of sleep is where our glymphatic system, our lymphatic system is the lymphatic system of the brain that helps clear out uh it's our anti-inflammatory clear out system. When there's gymphatic activation, we want our um we want this system in our brain, our glymphatic system, to clear out all the inflammatory mediators that are there, essentially. And dexmetatomidine helps with that. It also helps protect this uh brain-derived neurotropic factor, BDNF. And BDNF controls the neuroplasticity of our brain. Let's just say that. How our brain, how resilient our brain is to stresses. Exercise increases that at a baseline, but something like dexmetatomidine and anesthesia helps to protect and raise our BDNF levels. So not only are we causing less inherent stress on the brain, we're making the brain more resilient, we're mimicking these sleep-like states, which also helps to not disrupt your sleep after the procedure, which is a whole category that is so under-discussed, in my opinion, because we all know that your return to sort of normal sleep architecture, if we will, after surgery is going to strongly drive your recovery from this procedure. Not just uh where the rubber meets the road and what your results are doing, but also how you're feeling, what the experience is like, getting back to your sort of cognitive and emotional states of health. Your sleep's gonna really drive that. And Dexmetatomidine is hands down our best option to protect that postoperative sleep architecture intra-operatively, doing it. And so I mentioned this locus ceruleus specifically because the neuroinflammation that happens, uh, whether it's from anesthesia or from the peripheral surgery itself, has a few key areas of the brain that are very subject to that neuroinflammation or that get affected highly by it. One of them is our hippocampus, and this is like our memory consolidation area. That's probably the most strongly affected by it. Our frontal cortex, our executive function, uh thinking, and we can all relate to what that feels like after anesthesia, maybe. Um, and then this locus ceruleus is highly affected as well. So protecting that, um, that's again, this is our like activation state. Uh, protecting that helps us restore uh back to a you know kind of healthy state faster afterwards. Um, and again, the hippocampus, like the memory consolidation, that you know, that's part of the amnesia that can happen after surgery, and even not during the surgery itself, but for the days afterwards, often people don't remember the initial phases of recovery because of that hippocampal effect of the neuroinflammation of the anesthetic agents, and then again, that executive function, that kind of brain fog of not being able to function normally from our frontal cortex. So that all plays into it as well. And dexmetatomidine is sort of my particular baseline staple of my anesthetic protocol because of its very unique properties. It's very challenging to use. You have to be really adept with it and you have to be experienced. It's very safe, but you also want to have an effective anesthesia, and that's part of it. It works really well when you're doing a very delicate peripheral surgery. So, me doing surgery in a way that is very skilled and very respectful of the soft tissue, and also having really good local anesthesia on board makes this very important. And the local anesthesia cannot be understated. Local anesthesia is what we think of with lidocaine and things like that because essentially I am sending no stimulus in the first place. Because the area that I'm working is so well anesthetized peripherally or locally, right where I'm working with nerve blocks, the brain's never getting a signal of discomfort or pain. So there's nothing stimulating the brain in the first place. That allows me to keep the overall anesthetic agents, all of the ones that we'll talk about, very, very, very low. And this is a skill, honestly. Your local anesthesia is a skill, your tissue handling, your skill set with surgery, all these affect it. And if you're not very good with local anesthesia and you're not very good at the surgery you're doing and you're kind of rough handling the tissue, that makes general anesthesia a lot more appealing to do. But at the phase I'm at, I don't need those things. So I can do I could do the procedures, the local anesthesia only because of the stimulation is so low. But dexmetatomidine works really well in that particular type of a of a procedural flow and does really, really well. So the next

Ketamine

SPEAKER_00 12:19

one that we'll move on to that I really like is ketamine. And ketamine is very interesting because it neurobiologically works at a lot of different levels. Um, it is an NMDA receptor antagonist, which basically stops it from glutamate stimulation that can happen with neuroinflammation and things like that as well. And it is very important in the dose that you're using with ketamine. A lot of people have heard of ketamine, um, and it has, you know, this kind of like emerging world of benefits that come with it, but it also has sort of like a higher dose, darker side, if you will. And so the dose of the ketamine is very, very, very important, um, as is the timing of the ketamine. So one of the things that ketamine does really well is helps to, at low dose, specifically a low dose, is it helps to upregulate BDNF levels back to BDNF again. Uh it helps to control neuroinflammation. This it's stabilizing on our brain at low effects. And this is a lot, that BDNF uh upregulation is one of the reasons that it's like maybe shown some efficacy in depression, actually, is that particular aspect of it. But then in the brain stabilizing portions of it, when it's um sort of neurostabilizing, increasing our brain resilience, that is really helpful for the surgery itself. And it helps, like I said, everything's tied together, it helps to control our pain experience after the surgery as well. So now you've got an agent when we talked about dexmedatomidine that really helps restore your sleep, mimics a sleep-like state, and you've got uh something like the ketamine that's helping to control your postoperative pain. You could imagine that that's a really nice setup to handle any discomfort that might happen after the procedure. So let's say you've got a one out of 10 discomfort, and instead of needing to take a pain pill, you have the reserve and the capacity to deal with it because you're better rested and you have some central reduction of that pain experience already. So these are some really cool and important parts of ketamine. At high doses, ketamine gets um, you know, psychotropic, very dissociative, and causes some neural inflammation at high doses, has emergence phenomena. There's a lot of interesting things that happen with it there, and that's not where I tend to go with it. I tend to use it very sparingly, very focally, very minimally at various parts of the procedure. And with that, I get to take advantage of the low dose benefits of something like ketamine. Um, and so we have dexmetataminine is our sort of base of our foundation, the thing that's doing all the work. We've got ketamine,

Propofol

SPEAKER_00 14:46

and then we've got propofol. Propofol, a lot of people have heard of um, it is different in the way that it acts. It acts via GABA. Um, and it's more along the lines of what we'd think of as like a traditional anesthetic, meaning when it puts you to sleep, it's actually not a sleep-like state in particular at all. Ironically, uh there's some very famous cases of people using it for sleep, which it is not mimicking at all, right? And so that makes me very cautious and careful with the amount of it that I use. But the beautiful part about it is it is very reliable in what it does. So we can very much micro, micro, micro-dose this essentially, um, and have it be very reliable in what it's doing when it's very quick on and very quick off. And that's very, that's an important part of how this particular agent works. So it can be a focal supplement to the overall protocol and have high reliability and very low doses. At high doses, it can essentially be a general anesthetic if you do use a lot of it and a lot of total intravenous anesthesia, T I V A, Tiva, will use something like propovol as one of its main aspects to cause essentially general anesthesia through the IV. Um, so when I use it, I'm very cognizant of the dose that we're using of it. It becomes a supplement to our overall, but it's an important mention in here as far as like one of the agents that goes into it. And so it's also very amnestic. So as far as like controlling uh memories of things afterwards, it's it's an important aspect there. So we have this whole profile that sort of builds in to be protecting your sleep architecture, priming you to manage any discomfort afterwards, minimizing discomfort as a whole, even the local anesthesia part of it helps to minimize the experience of discomfort after the procedure by stopping the peripheral pain signals from ever being sent to the central nervous system. Even under general anesthesia, if you do, if you cut somebody's skin when they're under general anesthesia, there's a pain signal sent from the periphery to the central nervous system. It's just not registered there, basically. But that sending of that signal opens up some pathways, kind of primes these pathways. If you stop it, if you stop the pain signal from ever being sent in the first place, there's less of those open peripheral pathways to the central nervous system to uh that mitigates the pain after surgery, meaning even with general anesthesia, using local anesthesia during the procedure makes the postoperative experience more comfortable, even with something like general anesthesia. So take that little nuance and apply it to essentially no pain signal ever being sent at all during the entire procedure with very gentle tissue handling, and we have the perfect setup for pain management afterwards. So the very last thing that I do in a procedure, the procedure is over, it's done. We've done a lot of our regenerative stuff. I'm using on my PRP and my PRF and you know, stem cells and all

Long-Acting Local Anesthesia

SPEAKER_00 17:38

the things that we're doing. Quite literally the last thing of the procedure that I do is I go to the key peripheral nerves. In our face, there's some very reliable nerves that we can block, and I'm using a long-acting local anesthetic. That long-acting local anesthetic, it's called liposomobivacaine, I put right around the nerves, and it lasts up to 72 hours. Um, I would say I see an experience of more like 48 to 72 hours of essentially stopping any peripheral pain signals registering to the brain at all. Now, I usually kind of word this to my patients, it's not perfect. It's not like everything is rainbows and puppy dogs afterwards, but we have significantly blunted the pain response from the procedure to your brain after the afterwards for two or three days, which is when a lot of the normal postoperative discomfort happens in the first place, right? And so in doing that, we have significantly reduced the peripheral to the central. So we don't need to block much centrally, right? That's where opioids work. They're working on the central portion. There's also a new medication that I really like to use called

Suzetrigine

SPEAKER_00 18:40

suzetrogen. When I say new, it was approved in early 2025 in the US, and it works on peripheral sodium channels, blocking pain signals from being sent to the central nervous system. Sounds a lot like what I just said with local anesthesia peripherally, and interestingly, local anesthesia also works on sodium channels. This suzetrogen just works on a very specific sodium channel to stop the communication of pain from the periphery to the central nervous system. So another peripheral option, that's good. That means your brain's protected, your brain's functioning, your central nervous system isn't blunted, and we're having a nice, sort of comfortable type of recovery. Very low side effect profile, like an incredible option. I think that we're going to hear a lot more about it as time goes on with it, but I've been loving it and what it does for my patients. So now you've got a peripheral nerve block, you've got a peripheral medication working very well.

Caffeine

SPEAKER_00 19:31

There's a few other nuances that I like with my patients. Um, with a lot of my patients, I'm using caffeine. Um, actually, in the pre-operative period leading into the postoperative period, this works really well with my coffee drinkers, but caffeine has a few benefits to it. Uh, it helps our emergence from anesthesia sometimes, kind of by stimulating those areas of activation that we were talking about prior, but it also uh has been shown to have an analgesic benefit, meaning helping the postoperative experience of pain afterwards. And it goes beyond just the uh caffeine withdrawal headaches, which is another important aspect. If somebody's a daily coffee drinker and they're not getting their caffeine for a little bit, this helps with that as well. But then there's another medication called gabapentin. And gabapentin has, we don't need to go too into this because it's more of a select option, but um, it has a bit of uh peripheral, uh, excuse me, a bit of central stabilization that happens. So that's kind of our first discussion of a central stabilizer. We're gonna go into more central stabilizers here in a little bit. But that can be used in very select cases, um, and

PONV (Post-Operative Nausea And Vomiting)

SPEAKER_00 20:32

I really like that as well. I would say another just like side nuance if we were to put a pin in those conversations and move on is uh postoperative nausea and vomiting. Um we call it P-O-N-V in medicine. And post-operative nausea and vomiting is not necessarily related to anesthesia or pain directly. In fact, uh propofol, the medication that we talked about, is a very strong anti-nausea, which we call an anti-emetic. So it's another important avenue for propofol in the overall, in the in the overall milieu of what I'm doing and the mix that I'm doing. But um there's some preoperative medications that I like to use as well. One in particular is called amend, um, and that helps really with our post-operative nausea and vomiting. So just another aspect of something that could be, I guess, unpleasant that we have taken away. There's also uh issues with post-operative nausea and vomiting. I don't want my patients vomiting after surgery just simply from a blood vessel standpoint and getting their blood pressure up in their face. So that would be a side note in that sort of overall. As we get

Post-Operative Protocol

SPEAKER_00 21:30

into the things that we're doing in the post-operative period that are controlling pain and helping our neural inflammation, it's worth mentioning uh just the overall basic recovery protocol that I'm doing for my patients anyway. And this includes their type of IV nutrition that they're getting, which is quite literally customized to every patient based off of their laboratory work, their genetic profile, the procedure that we're doing, kind of what they need basically. But that helps with our inflammatory states after our procedure, which is our brain is part of that as well. Restoring a blood-brain barrier, minimizing our glial activation in our brain, and helping with our post-operative cognitive dysfunction. So something like the IV therapy helps with that. The hyperbaric oxygen does not get enough mention for this. I'm using hyperbaric oxygen to help with all of the aspects of our recovery, with the long-term results that we're getting, with our fat transfer survival, with the swelling and the edema and the healing, and basically making the things that we want to happen happen really fast and really effectively, but it's also helping with our postoperative cognitive state, you know, by reducing our neuroinflammation in the brain. So an unsung hero may be of this as well. And the same goes for all of the aspects that are controlling the inflammation after surgery. And that could be our PEMF, post-electromagnetic fields, whatever we want to throw in there. Anything that's helping our peripheral inflammation is also helping our postoperative cognitive dysfunction or our brain states after surgery. So that's definitely worth a

Hypercapnic Tolerance

SPEAKER_00 22:57

mention. But some of the things that, you know, I have my patients do leading into surgery, like I would call now we're getting into sort of more of these very unique aspects to me, something called like hypercapnic tolerance or CO2 buildup. And I've talked about this before. And this is something that I like my patients to do from an activity and an exercise standpoint that increases their metabolic flexibility, their metabolic resilience, their ability to tolerate elevated levels of carbon dioxide. This can be something as simple as like going on a walk and nasal breathing, or doing nasal breathing through like a zone two exercise. And for about two weeks, that's all we really need leading into it. If you're exercising regularly, you have some good hypercapnic tolerance. But if we're doing a little bit focused on this leading into surgery, something simple like nasal breathing, you know, a few times a week leading into surgery, you know, maybe, maybe three to five times a week for two weeks leading into surgery is going to increase your hypercapnic tolerance. Now, why that becomes important when we get into recovery and anesthesia is that during your anesthesia, again, I have you as I have as little anesthesia on board as possible. And in that, I'm really controlling. We, when I say I, this is myself and my anesthesia team. Uh, we are really controlling your vital signs, your ventilation, your respiration. And a lot of times when people have a little bit of buildup of CO2 and their respirations get low, they have this hyperventilatory response, which is very activating to your sympathetic fight or flight nervous system. We don't want that. Um, that can exacerbate your inflammation after surgery, increase your postoperative cognitive decline theoretically, or dysfunction theoretically. So we don't want that to happen. So the better sort of shape or that you can tolerate the hypercapnia elevated CO2 levels that will kind of fluctuate during surgery, uh, the better you're gonna do with your anesthesia and your recovery. So very simple mechanism to do that. Seems like that's a kind of a no-brainer for any type of anesthesia, but I think it's pretty rare for a surgeon to talk about that. And then you get into even some things that would be very sort of more on the esoteric level of um

Sunlight Exposure

SPEAKER_00 25:05

exposure after surgery to something like the sun. Now, my retreat homes where my patients come and stay has a specific area of them that is outside, is upstairs, is private. And it's meant to be sort of a sunning deck, if you will. Um, it faces where I'm at. I'm in the northern hemisphere in Cordelaine, Idaho, and these places specifically face south. They look at water, they look at mountains. So you have fractal patterns and nature that kind of help your sort of neural state there, side note, but they also give you a beautiful exposure to the sun, uh, regardless of the season. Even in the lowest part, this for us in the winter, the sun is very low in the south, you still get the sun. And so that means your circadian rhythm is being helped at a baseline. I could do a whole podcast just on that and how that works. Um, but you're also getting UV exposure. And I want this on your skin. So part of this privacy is important here. Um, and again, I'm not trying, I'm not promoting like excess UV exposure or sunburns, but UVB on our skin, specifically on keratinocytes, these cells in our skin, helps all kinds of things with our vitamin D production and things like that, but it also uh stimulates our beta endorphin levels. Uh, beta endorphin is sort of our endogenous opioid system, if you will. This is why people in the sun get this sort of euphoric feeling. You feel great when you're in the sun. This is there's a mechanism as to why that happens, and it has to do with this beta endorphin release. But that beta endorphin release also changes your subjective perception of the recovery or pain from your surgery. So UVB light uh hitting your skin can make your surgical recovery more comfortable. In addition to helping to circuit the sun as a in general, helping to circuit reset your circadian rhythm and making you feel great, there's benefits to that. It's interesting. The mechanism by which that happens is when it hits the keratinocytes, it upregulates or triggers this sort of P53 cascade, is what it's called, which is actually a damage or apoptotic cascade. Um, but in that you get a release of something called POMC pro opio melanocortin. And when that gets cleaved, one of the things is beta endorphin, and the other one is a melanocyte stimulating hormone. So the same stimulus that makes you get tanner also makes you release this beta endorphin level. And so um I'm very counterculture, I would say, just general overall in my world, um, where we're talking about like faces and skin and things like that, uh, because I do think that the sun is very good for you and very important for you for your skin and for your eyes. And that that doesn't illustrate it. I don't know what does I'm not promoting sunburns, getting red, uh, things like that. But in general, we need to see the sun as a whole. And my retreat homes, the way they are set up and designed and laid out and um the furniture and the direction that they face is all very centered around this type of recovery, including uh the ability to see the sun, which is going to help your overall experience make you more happy. Um, just one of the many nuanced little details that go into this sort of overall experience. So if

Outro

SPEAKER_00 28:03

I were to summarize this in general, um, you know, this opioid-free, benzodiazeprene-free anesthesia protocol and recovery protocol fits into the overall theme of everything that I want for you in your surgical and your surgery and recovery, which is reliability, safety, outcomes, um, and not having any long-term negative effects of doing this at all. I don't want you trading anything important like your neurocognition to, you know, align how you're feeling and how you're looking a little bit better, right? I want to do that all uh in a way that is sort of like as low penalty as possible. And this is what I would want for myself. And, you know, it fits into this idea of, you know, kind of like knowing what you're gonna get when you come here and knowing that I'm thinking along the same lines that you probably would be if you had the same intimate knowledge of it. I'm thinking about your sleep architecture afterwards. I want you sleeping better because, you know, all these big studies looking at the different types of anesthesia, I think that's one of the things that they're missing. Um, I'm using this hyperbaric oxygen therapy, not just for your recovery from your physical procedure, but I'm thinking of how it's helping your brain when I'm doing the surgery itself, um, the gentle tissue handling and things like that. Those have multiple benefits from your recovery to the results that we get to how that peripheral damage is affecting your central nervous system and your postoperative cognitive dysfunction afterwards. Um, and then, you know, not using the opioids and the benzodiazepines is just making your recovery experience better on every facet from how your brain is working, how you're thinking, your executive function, how you feel, to how you go to the bathroom and move. And um, you know, it's a much more pleasant experience that way, uh, not to mention all the addictive potential that we've avoided with that. So, you know, there's a lot to it. It's highly complex on some level. Um, it's a little bit, you know, uh cohesive and controversial at the same time. Cohesive meaning I've taken a lot of different things that already existed. None of these things I invented, but I have taken sort of the things I like about a bunch of different strategies and put them together. Um, the way that I view tissue handling and even the hyperbarics and things like that, those are pretty novel to this space. Uh, but overall, I've tried to compile the best information, the best protocol that I can that's truly challenging to execute. I mean, this isn't easy uh to do. It's not simple like flip it on, you know, the person's under general anesthesia, you know, slam them all the way down and then keep them alive. This is very different than that. It's very high touch, takes a very in-tuned team to do this, but it's much more safe and that has a much better recovery afterwards. And so it kind of fits into a very high-touch thing. And this is why you're probably not going to find this in a lot of insurance-based anesthesia settings. So I'm lucky that I live in a world where I don't have to rely on getting reimbursed by insurance for what I do. It's a total side note to the healthcare system, but so I can be as innovative and progressive as I want. Uh, this is a much more expensive way to do anesthesia if you look at it that way. So if you're a hospital system, this doesn't pan out as well on your ROI, uh, on your returns, you're going to get the same same uh insurance reimbursement for doing very basic, simple, inexpensive anesthesia as you would for something that's highly complex like this. But I would argue that in my world for patient outcomes, if we get really fine and granular with it, I think that we would and do see a difference here if we really get into the nuances. If you look at just like a you know bimodal yes or no system, you know, I don't think that that does it justice. And nonetheless, even with that, this is what I would want because it gets into a lot of theoretical nuances of neurocognitive protection and uh sort of long-term benefits that, again, things that I get obsessed with. And it fits into this overall profile of like, okay, you're gonna come out of this like looking great, feeling great, not paying a price with your brain for it in the long term, and it's gonna be a positive experience as you get there. Um, I think this sort of personifies a lot of me as a whole. Um, I love when my anesthesia colleagues pipe in because there's some people that are like, oh my gosh, I love this, and others that um get a little bit more defensive and well, disagree. I are we're already doing this, and these are not new things, and there's no evidence showing this. And I think if you really get into the nuance of it and kind of think about what you would want, um, it gets a little bit interesting to think about it this way. So uh a fun challenge to everybody out there. I hope you learned something from this, uh, got a little bit of insight as to what this looks like from my end. And uh again, thank you for your interest. 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.