[00:00:00] Speaker A: Welcome to the Heart Rate Variability podcast. Each week we talk about heart rate variability and how it can be used to improve your overall health and wellness. Please consider the information in this podcast for your informational use and not medical advice. Please see your medical provider to apply any of the strategies outlined in this episode. Heart Rate Variability Podcast is a production of Optimal LLC and optimal HRV. Check us
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Welcome, friends to the Heart Rate Variability podcast. I am excited to have an individual on that. I continue at the AAPB conferences just to have fascinating hour long conversations with, and I've been trying to get him on the show for a while. Finally, I think maybe a six hour sit down last day where we were having fun, I finally convinced my friend Nick to join us. So I'm excited to have doctoral candidate assumed to be, fingers crossed, Doctor Lackey, but doctor Nicholas Lackey. Nick Lackey, welcome to the show. I'm excited to have you. Like I said, we've just had some great nerdy conversations the last couple of years. So I'm really excited to share your work, specifically in this episode around your research around pain, uh, an HRV with our audience. But uh, give us a little bit of introduction into the man that is Nick.
[00:01:35] Speaker B: Well, thank you very much. Yeah, I am Nick Lackey. Um, well, uh, doing a clinical psychology PhD at Alliant International University, uh, at St. In San Diego. Um, as someone you've had in the podcast before, uh, doctor Pollard has been somebody who's been a colleague of mine since starting. Um, I actually interestingly started thinking I want to do neuropsych going at that aspect of how the brain just interacts with psychology and the body. But then after actually taking a course, of course, for doctor Richard Goodverts at Alliant, um, that door opened of the more medical side of psychology, health psychology, and how heart rate variability is a really good way not only to help with patients, but also I found to get that buy in with physicians to be like, this is a good physiological tool to connect with patients that helps both sides of the aisle physicians get the buy in of, oh, hey, there is something autonomically controlled that can help with that as well as be able to get that patient and buy in of just this is something you can understand about your physiological experience and everything like that. Um, got my start there clinically. Uh, my first practicum experience was that sharp chronic pain in San Diego, just treating a lot of patients with chronic pain, actually using that HRV or the thermobiofeedback there at the clinic. Unfortunately, it was at the height of the pandemic, so group therapy is not my forte.
But then was able to continue that using that understanding to do integrated primary care at UCSD for my second clinical placement. And that was definitely just really working alongside the physicians there. Um, really seeing the large amount of buy in and diagnoses you can work in, in those settings and where HRV even just explaining that understanding can help patients, even if can't directly clinically do it just for the, um, structure of, of a larger medical setting like that in a primary care practice. But, um, definitely very helpful nonetheless. Regardless if you're actually using their HRV or not, that buy in, that understanding of how emotional states can induce these physiological changes and that they can perceive those changes is just vastly helpful and important.
But yeah, that just a little bit about me before. I know, jumping in. Dissertation in a little bit.
[00:04:03] Speaker A: Yes. So one of the interesting, I think we've talked a little bit about it on the show in the past, but it's been a while, is HRV, biofeedback and pain. So let me, because I know what kind of brain I have on the episode here today, let's start out with what is pain from a nervous system perspective? Because obviously pain management, chronic pain, we're coming. We're still pretty much in a drug epidemic caused by our mismanagement of pain with the opiate epidemic, et cetera. I don't know if we've ever done a good job with it. So when we think about what is pain from your perspective, uh, how, how do we go about defining that, uh, that concept?
[00:04:56] Speaker B: So if you're.
I think it would be good to help define it more from the medical model right now. And so if we're thinking about pain, pain in general is just an experience that you perceive as noxious or just the fancy word for bad from a negative stimulus. Um, and that can be modified whether it's by the actual physiological state of your body or how you perceive it or your emotions, your actual cognitive and affective state at that moment. The International association for the Study of Pain, or IASP for short, has a much more eloquent definition that I have not memorized, but they include all of those components. Now, chronic pain is any pain that has now lasted for three months or more, that occurs more often than not. And specifically, when we get to that chronic pain, the game changes a little bit. It's not just about, oh, hey, you have a gash on your arm or you have a broken bone that is slowly healing and that process just isn't fun, but will eventually go away. There is something outside of the normal healing process that now is perseverated, is inherently bad for the body, and your brain starts perceiving it and changing the way that you perceive it. Um, yeah, without going into the full neuroanatomical correlates in the brain, which. That is a rabbit hole diagnosis dependent. Um, I think generally that's a nice small framework to be able to start with. And of course we then start now having all of the psychopathological issues, depression, anxiety, pain, catastrophizing, even trauma, starting to be able to change how you perceive it, your emotional reactivity to it, that can start perpetuating those outcomes more that are not directly related to the actual noxious stimulus in and of itself.
[00:07:02] Speaker A: So how does that inform your thinking? Because, I mean, I think we could just skip right on to, okay, now, now what? But I think that that, that's, you know, especially talking from when we get to HRV metrics, right where we're getting, we're getting a number out of this and, and, you know, I don't want to skip quite over. Is it maybe, I don't know if psychosomatic is even a word we want to use anymore. I'm stepping out of my area of expertise here, but there's a more complexity than my back hurts.
What's going on there, especially with the chronic pain. So I, as you are kind of looking at somebody and helping some structure a treatment plan or a way to help them, uh, work through the pain, what are some of the ways you think about the psychological factors?
[00:07:53] Speaker B: So, and I think here is where it's going to be important to start directly classifying the three kinds of pains we now have. We used to only have two, and they're the very face valid ones that we used to have. First one, no. Susceptive pain, fancy term for actual peripheral physical damage that your peripheral neurons are picking up on many different types, several different kinds of fibers of how it communicates with your central nervous system, of very quickly or very slow, dull aches that are not myelinated, um, whichever ones you want to take. That nociceptive pain is that classical kind of pain. We think of the other one, neuropathic pain. The actual nerve damage now has its own set of classification. There's that actual nerve damage that is different than nociceptive pain. Pain because there's that lack of communication or it's now overactive because of that cell death. And that gets interpreted a different way in the brain, thinking of, like, burning things like that. We get the bands of pain, specifically of what you would expect with where those neurons innervate from. Um, but now we have actually, the IASP has ratified a new classification of pain, and this is called nociplastic pain. Hmm, fancy term.
But I think the easiest way to think about it is from what's called allodynia and hyperalgesia.
[00:09:14] Speaker A: So that's a much easier term.
I know, let's simplify it.
[00:09:22] Speaker B: But I think these two terms now describe the experience with the pain, and then we can get into, like, the archetypal diagnoses. So hyperalgesia is around maybe peripheral pain, uh, some sort of peripheral source. There is more sensitivity at that pain site than you would otherwise expect, given the stimulus, maybe a little bit outside of it. There's even more pain to touch, and directly touching it is way more pain than you would expect from a simple cut or a bruise or whatever it would maybe. Right. So first we have that, and then the allodynia is even in a place where you wouldn't expect there to be pain, and maybe it's on the other shoulder, you would touch it, and now there's that tenderness there. There is now suddenly pain there. And so this is now defined as nosoplastic pain because there's no effective peripheral or neuropathic pain source. But this pain still exists, or is there or is exemplified because of this.
For the. I'm sure it's the right term.
Curious listeners out there, you can probably already start thinking things like fibromyalgia, certain of these archetypal diagnoses, where this pain is exemplified and expanded upon. And that's actually right. The literature is now split. And for those curious, this is getting into my dissertation topic of how we evaluate this. We're getting into a collection of diseases known as central sensitivity syndromes.
Central sensitivity syndromes are defined as this process of amplification or central sensitization. There is something, whether in the spinal cord or in the brain, that seems to be amplifying the response to pain, or where even normal things going to the body are painful.
Yeah, said a lot about pain. Label the diagnosis that we could go into rabbit holes about specific diagnoses. We'll put those aside. Let's bring this understanding now back to HRV, because the unfortunate aspect from the get go is that we would not actually see a major HRV difference if somebody is in the throes of nosoplastic, neuropathic or nociceptive pain because the body is inherently responding to a negative noxious stimulus. So all of it is going to decrease hrV.
[00:11:51] Speaker A: Okay, so we will see that. Oh, the decrease though.
[00:11:56] Speaker B: Mm hmm, mm hmm, exactly. So you would see decrease with all of them. But could we maybe delineate between them?
I wouldn't put my money on that, which is actually why my dissertation didn't directly collect HRV. My dissertation is trying to help classify between nociceptive or nosoplastic diagnoses based on pain drawings.
But at the outset, without providing treatment, seeing HRV increases or decreases depending on those just at face value. If it's unregulated, their HRV is also going to be unregulated. We wouldn't see a specific decrease. More of one untreated group versus another untreated group.
[00:12:35] Speaker A: Gotcha.
More.
[00:12:38] Speaker B: We would use HRV for globally, and this is more for all chronic pain is thinking about with implementing normal clinical sources, maybe actin HRV, anything like that, to be able to help treat pain, increasing that acceptance in decreasing pain, catastrophizing, that can again flare up that perception of what's going on. They're catastrophizing all about their pain. My pain is going to be worse. Therefore, in some respects, a self fulfilling prophecy. Decreased HRV from the emotional aspect, let alone the pain that's already there, decreasing, not allowing that relaxation to come into the body. Um, we would still expect to see overall HRV two go up, but with somebody, maybe with fibromyalgia, we would expect to be more swings compared to somebody, maybe with well controlled, no, susceptive chronic pain.
[00:13:30] Speaker A: Fascinating. Fascinating.
[00:13:32] Speaker B: Does that make sense?
[00:13:33] Speaker A: It does. So, so I, I'm just thinking about, like, their triggers kind of traditional way when I've been in pain, um, athletic injury or something like that. The medical advice I have is sometimes, you know, and we're not throwing as many opiates as people anymore, though. I, I've had them in my medicine cabinet, uh, in the past, um, or take some aleve or tylenol or. So let, let's just kind of bring this. And I'd love to get your thinking on. Take this pill before an activity or when you feel pain. So kind of that medical model, and I'm not saying all physicians do. This is my experience, and I would assume the typical experience. I'm not, as a medical provider today, not kind of figuring out much. I'm just trying to get rid of the pain for you so, you know, you go on with your life. What does, like, that common treatment, whether it's just self treatment, is, hey, you know, my knee hurts, I'm going to take a few leave or like the medical model right now of giving people pills to deal with the pain.
[00:14:53] Speaker B: You're touching on a very interesting topic that I personally and hopefully can professionally explore one day, which is more of like that behavioral call and response, trying to make it go away. Yeah, I personally do not agree with the aspect of taking the pill to make it go away because if we think from a behavioral perspective, what is that training and priming the body in our psychology for? Yeah, as part of that I asked definition of pain, that perception and emotional state around it, that expectation that'll make it go away. You're kind of training the body in that respect to be extremely responsive to pain.
Pain is not created in the brain, nociceptive and neuropathic and no sublastic. All of those are interpreted by the brain with one of them being defined as how the brain is broadening that interpretation of pain. Um, without being medical providers.
[00:16:02] Speaker A: Yeah.
[00:16:03] Speaker B: Or direct biomedical PhD individuals. I can't talk too much going into the deep inflammation pathways, but I think in general there's minor amounts, again thinking short term pain, less than three months, that maybe that is adaptive, helpful, functional, telling your body hey, don't do this thing because it's painful or two. There's something adaptive, some stimulus that you're putting into the body that may actually be okay. That delineation between maybe like soreness, could we define that as one out of ten pain? Yeah, probably. But where's that adaptiveness for the body versus. Not very standard thing in chronic pain treatment is thinking, okay, there is a certain amount of get up and go that you have to be able to do, and then where is your physiological point that you can perceive a difference so that that way you've gotten enough exercise for the day. Because if we take somebody with standard uh, arthritis, something more. No susceptive in nature, if they sit for too long, don't move their joints, don't move their body, they're typically going to have more pain on the opposite side of that. If they do too much, if they go, if they decide to do an entire graduation day with no breaks, yes, it was a big day, but their body's going to pay for it a couple of days after that. So I think pills can be helpful to manage it. Maybe like if you're going to be doing a long, a full day of something, knowing your body's going to be out for a few days, but coming from the acceptance commitment therapy side, that is something worth it for you. It is within your goal oriented behavior to adapt your schedule after that, that can be great, but we're going more lifestyle management here. And what are your goals? What is your situation if we're defining it as more as you were, kind of going like the athletic sense, I don't know how directly applicable that may be compared to how we would manage chronic pain, for instance. Just chronic pain. We're expecting that pain already. So that. That way it's. Can you tell within your body where that switch is to where you need to do enough to engage your body, not let that perpetuate and sensitize for the next day or two, versus also not going so far as you now can't do as many activities the next two or three days after that because you push your body so far, there was a negative response, and we would probably also see a decrease in HRV in response to that.
[00:18:28] Speaker A: Evan? Yeah. Yeah. So. So let's talk about your work now with bringing a heart rate variability into the realm of pain. So let's talk about your thinking, your research. Uh, what gets you excited about. About this topic?
[00:18:45] Speaker B: So what gets me excited about this topic?
Everything. But then again, I would be getting a PhD in clinical psych if I don't think I was getting excited about it.
[00:18:56] Speaker A: Yeah.
[00:18:56] Speaker B: Um, so my dissertation, although unfortunately, distinctly lacking HRV, is specifically evaluating a scale that tries to measure the central sensitization symptoms an individual may be experiencing.
[00:19:12] Speaker A: Okay.
[00:19:13] Speaker B: Now, the issue is that there is no direct way for us to measure central sensitization. There's theories and animal models about.
We believe this mechanism to be the way, but there's no consistency across these diagnoses that we're expecting. So my dissertation was just asking, do we get another incremental validity above and beyond what we already know about the scale, which is it's psychosocial related depression, anxiety, pain, catastrophizing, and trauma symptoms. Um, do we account for more with adding in a pain drawing or not?
Um, so can you.
[00:19:51] Speaker A: When you talk about pain drawing, let. Let's. Let's define what. What we're talking about here.
[00:19:56] Speaker B: Yeah, sorry. Um, so pain drawings is just literally a drawing of a person front and back. And patients, uh, would just fill in where they're currently experiencing their pain. And so we would expect if people have more peripheral sources of pain, they're going to be a bit more localized, no matter the intensity of the pain. If it's arthritis, let's say maybe it's specifically in the rinse wrists and specifically in the knees. If it's myofascial pain. Um, per a Trevelly and Simmons book on myofascial trigger points, we would expect specific areas of pain, of referred pain from specific trigger points. If it's neuropathic pain, which is an exclusion, I have a scale for exclusion in my study, but we would expect specific dermatome maps for that kind of neuropathic pain and descriptors thinking more like the burning and things like that.
But then for nosoplastic pain, we would expect it not to follow these dermatomes and to be more expansive than you would otherwise expect given the nociceptive input. So you can kind of see that, especially in collaboration with other providers. As all the studies these days show, multidisciplinary work is going to be the best working with PT and psych and physicians. So definitely want to get that cross trans diagnostic help is always the mainstay for, or should be the mainstay for chronic pain treatment these days.
With all of that, it turns out that the one skill that we have, the central sensitization inventory, yes, it's getting cs related symptoms, but pain drawings seem to be separate than the scale.
And we also know that with things like myofascial pain. So let's take myofascial fibromyalgia. Myofascial pain may have light I'm using quotation marks for people who aren't in the podcast or aren't seeing this quotation mark light central sensitization symptoms. But we also know that people who have anxiety and myofascial pain, their pain gets worse with sympathetic onput or the parasympathetic withdrawal. So that might be autonomically explained within that. But with fibromyalgia, it's kind of defined in that collection of autonomic dysregulation disorders or central sensitization syndromes. Thinking Ib's, chronic fatigue syndromes, maybe even pots, is a new one, kind of being put all in this collective group.
And there then what's the differences there? What's actually helpful or not? And this scale seems to be, at least from my study, 62% of the variability of this scale was accounted for by those psychosocial things and nothing more by the pain drawing. So the pain drawing may be an effective, helpful way to delineate between those now, taking a step back, why is this going to be helpful? And thats because of treatment and treatment outcomes for no susceptive pain things. Maybe some of the pain medication may actually be helpful. Getting back to your point earlier, thinking about opioid epidemic and things like that, where even maybe some nsaids and other things may be helpful. Again, not a physician being very clear about that, that is a medical provider conversation. But still some of those medications may work, because we know from the literature that opioid medications do not work for conditions like fibromyalgia or things, because those are mechanisms of cs or something like it, that we don't yet fully understand, where the opioid system and other systems are not being interpreted correctly by the body. Not a thing trying to say it's your brain making or creating the pain, that's not it at all. But the way that is processed by your brain that is also affected by your emotional circuitry and everything else seems to be the issue. And therefore the opioid system isn't helpful, whether it's not tamping down the pain effectively on a chemical, molecular, neuronal level, or just being processed differently with everything else going on. And that's where it's like the literature is very interesting. We don't know pathophysiologically exactly where the delineation is. There's no consistency in the brain region changes or even the activation patterns. But there is a consistency based on the diagnosis for which treatments you can give that's going to be helpful or not helpful. So it's tricky. And this is why my dissertation is a thing.
[00:24:35] Speaker A: So I don't know if it is there any more we need to unpack. I want to get into your work and thinking about heart rate variability and hrv biofeedback with this, but is there anything we need to unpacked there? I think what just blows me away is what we still don't know about pain. Even though we focus to so much about pain. It's like it's been such a key point of discussion, chronic pain, all the different things you mentioned. Anything more coming out of your dissertation? Before I move us to heart rate variability, biofeedbacks specifically.
[00:25:18] Speaker B: I think without getting on a pedestal and trying to talk about extensions of what it may mean, I would say as a relatively conservative statement is the literature right now needs to be careful at how it is interpreting these papers about cs, because we right now do not actually have a way to measure this, nor do we have a way to delineate between normal psychosocial increases in pain and perception in our emotional states versus these actual physiological mechanisms of CS. Or are they intimately intertwined? Or is it just they interact together?
We don't know any of those questions. We do. It's kind of like a black box. We know input of if were thinking fibromyalgia, there was probably trauma as a child. They were always kind of sensitive. And then you have this pain diagnosis coming out on the other side where we have CBT and act and some antidepressant and other treatments that seem to be relatively efficacious. But its now going to be a lifelong diagnosis. Or again now going back to the myofascial pain syndrome idea where theres specific trigger points, whichever physiologies understand. There's a couple different theories in there, but still this kind of integrative theory of there are specific peripheral mechanisms, there can be some CS mechanisms that are treated with peripheral treatment. So we kind of know how to treatment. There's been HRV done with it through doctor geverts for again it's effective treatment so we know it can get better even if it is modulated by the anxiety. So again we can see what the diagnosis is, we can then effectively treat it. But what's the actual exact thing going on?
You don't know. And that's kind of like the interesting thing of there seems to still be this black box of that transition to chronic pain. What's that exact delineation is we have medical definitions, we have diagnostic differences, but the pathophysiological, maybe there's specific diagnosis that from the medical side are more understood, but we only have treatment delineation that truly helps us between these diagnoses. From my view on the literature, specifically with this new ideology of central sensitization, it's unhelpful and leaves a large swath of things kind of unsaid. We're definitely getting there, don't get me wrong, but its not there yet and I would hope that we handle it carefully so we dont restigmatize people with fibromyalgia, IB's, these medically unexplained symptom individuals that have been beaten down by the medical system. Thats kind of the issue that I see. So were trying to make efforts, but we need to make sure those efforts help understand rather than kind of just say the same old it's in your head. Which is why I'm being very careful about that argument and understanding now, because that's where it can go all too easily of oh, it's just this phenomenon that requires behavioral treatment again. And it's like, let's not go down that road again.
[00:28:35] Speaker A: Yeah, fascinating stuff.
Because I think like I guess call me a layperson on this issue.
I would have thought we had this more figure out. I guess so. It's really fascinating for me to see those gaps still exist in this area that has gotten so much. And I do a lot of work in communities that just been devastated by the opiate epidemic. So I mean, obviously you see the trauma coming out of this thing. I at least thought we knew what we were doing when we prescribed some of these. The fact that we may just have been throwing pills at things we didn't really understand just hurts my heart in a whole different level with this.
[00:29:29] Speaker B: Yeah, yeah.
Going back to the conference that we went to, we had a keynote by Doctor Stephan, him talking about the impact of chronic pain. And it's really thinking about those stress viewpoints on pain and how that can amplify pain in and of itself. Again, going back to that definition, it's about. About the emotional state, the physiology and everything else on top of what the actual pain stimulus is. It's one of those things where yes, opioids tamp down the peripheral stimulus, but what are your neurons doing to modulate that response or reacting to the downregulation of the pain by the onset of opioids? Yeah, so yeah, we definitely.
Gross generalization. Stating that up front. GROSS generalization. But even if we know like 50% of rheumatoid arthritis then is going to be well regulated with certain medications, diagnoses, some lifestyle factors, but then there's always that other 50% that for whatever other reason, human variability are more reactive, may fit under this Cs realm more even if we don't fully understand it. And again, fibromyalgia is considered under the rheumatological diagnosis still within rheumatoid arthritis, or like under that umbrella with rheumatoid arthritis and these other things. So it's like a lot of those things we still don't know. Ib's, which is considered one of these syndromes as well, is also handled by GI specialists and things like that. So we just, we don't know. It is a possible mechanism, but it's related to emotions, affective states, all of those different things kind of combining together, modulating and interacting with how you perceive your pain.
[00:31:14] Speaker A: Awesome. So let's talk, because we've had geverts on the show, it's been a while, so don't feel like you're retreading on any. Talking about his work, I believe with children in Irvael syndrome, which was some fascinating and really promising research that he talked about on the show, but I'd love for you to retread over that ground, or tread on some new ground about how maybe heart rate variability, heart rate variability, biofeedback could be potentially very helpful for the populations we're talking about.
[00:31:52] Speaker B: Yeah. And so just to reiterate, because I like being repetitive with my arguments, within the realm of central sensitization syndromes, it feels as if there is this autonomic regulation again, whether it's like the interactive components with it, where you're integrating your physiological information or not, that response is then reflected in HRV, or even if maybe somebody's overall okay, but they still have these symptom flare ups. HR, HRV Biofeedback still seems to be helpful at symptom management, learning that allowing your body to adapt to its own states better.
I wish we had more data on how it's interacting with the brain or things like that, but unfortunately we don't have that. But we do have that data. We published a paper on disorders of the gut brain interaction, DGBIs in pediatric settings of just, again, using HRVB, along with act and hopefully other disciplinary treatments as well. But just being more efficacious to where, if it allows the body to pick up other aspects of treatment, better be better respond, whether to the relaxation techniques or better implementation the lifestyle changes that's inherently going to be better. Um, that logic extends to fibromyalgia, that logic extends to, hopefully the new literature coming out, still very new, but still thinking about pots as an autonomic dysregulation disorder that's just coming out in a very different way there. Um, utilizing HRVB in those situations to augment the other treatments going on overall, seems to be another way to tackle it, given the interconnectivity of these brain regions. Presuming, again, and this is with the presumption that this is the interaction of these information sources and processing in the brain that HRVB can help tap into when you are in resonance frequency.
[00:34:02] Speaker A: Fascinating. So, and we can enter the world if we, if we say we're speculating, we can speculate, but what do you think is, you know, kind of going on with those brain connections? Well, what is your best? And again, if we want to call it a best guess, you know, we won't hold you to it in the future, but just kind of love to get, I'm sure you've obsessed on this a little bit over time of what's going on here. Why are we getting these results with pretty simple non intrusive breathing exercises.
[00:34:45] Speaker B: There's one thing that actually hit me when I was in undergrad, when I was studying the brain. I did the b's in more biopsych at UC Davis for my undergraduate.
And in one of those courses, I think it was my actually developmental psych, where it was a very biological perspective of looking at development, brain development, even in the context of other animals. And when things develop in that class, of all classes, surprisingly, the entire brain is always going all at once. We can't think about it of like a typical cpu where it's like one core on at a time, right? No.
[00:35:29] Speaker A: Are we only using 20% of our brain?
[00:35:33] Speaker B: Oh, that's. No, definitely not.
But the level of interconnectivity and parallel processing going on at the same time, I think is really the way to think about this and that, even though we don't know, we have a good idea of the white matter tracks.
For those not as caught up in the lingo, where specific neurons in the brain connect to other neurons in the brain and then therefore interact with each other, we have a good idea at the overall general track. So it's been mapped for a while, but the actual activation patterns and how they integrate and the length of time at which they take to respond, we just don't know. There is clearly some integration of that, that we can understand from other sources.
Again, with chronic pain already, where you can think about the cingulate cortex, which is a lot of area, um, where that emotional integration comes in, that also lights up with the pain processing regions. We also know that with CBT treatment for chronic pain, there is a study or two that has found gray matter and activation changes with CBT treatment for chronic pain. So we know that there are some of these things from control to people in specific diagnoses like fibromyalgia, we have seen these differences there. So we know that there are some integration changes on top of.
I know Doctor Gebert has brought this up, this specific study is not going out of my brain. But there has also been some prefrontal cortex, the regulatory region of the brain changes with HRVB practice going on. So we know that HRVB can induce some changes, and it seems as if those changes coincide with the autonomic regulation in general. So then face valid would then make sense that given those are autonomic dysregulation diagnoses. And we know that HRV induces some change, that the change that HRVB induces is to reregulate, regulate those autonomic areas that are dysregulated.
[00:37:57] Speaker A: Gotcha.
[00:37:58] Speaker B: We could go on and on whether it's genetic, social, environmental, because it's always environmental and genetic at the same time. You can never truly disentangle them even if we like our categories because we have to somehow study it. But like there's clearly something there. We have our neurovissal integration theory, we have our porges polyvagal theory, we have arguments back and forth between them. We know it's also socially regulated within all of that aspect too. It's infinitely complicated. And yet at the same time there seems to be this increased uptake in multidisciplinary treatment that is induced by the inclusion of HRVB. And that's what getting back to our paper that I started this rant on.
That's what our pediatric HRVB review just kind of did of. It seems as if when we include HRVB along with other things, the uptake of the, of other treatment seems to be more helpful, whether it be the lifestyle. In the specific case of the. I know the study doctor Gewirtz was trying to bring up was it was with kids with uh. Functional gastric disorders at the time. Um. And we, there was one group where um. Adding the fiber supplement, one with fiber and CBT and one with HRV. Fiber and CBT. And the ones that did the best of course were fA. Uh, fiber, HRV and CBT. So it seems to be that whatever interactive effects seem to be most helpful. And I would say that is generalizable course validate within every diagnosis.
Then combined with the nuance of just. Is it more nociceptive or no sublastic to where that from a lifestyle perspective, if it's fibro, the CSS is it's going to be a lifestyle thing when, if it's just nociceptive maybe some quick HRVB with trigger point therapy might help somebody with just that myofascial pain. But we're still diagnosis dependent right now. We're not pathophysiology capable yet. And I think we need to evaluate our diagnostic sources right now to be just ask the questions. What's truly helpful because the literature is going down this central sensitization viewpoint right now when it's. Its outcome, it's treatment dependent right now because we don't yet have the understanding we're making strides. But it's still associations, we can't directly measure the physiology. So just like HRVB, I very clearly love it, study it and am saying that it can be really great. But do we know exactly why it's helpful?
As you said, this is us kind of standing on our pedestals right now being able to say I think this is where it's going. And I think that's kind of a good general conceptualization of where HRVB can be helpful within the context of chronic pain. It is a helpful treatment modulator that can help engage lifestyle factors and engage it in a way that helps re regulate the autonomic system to better implement, amplify and hopefully perceive those changes in our patients over time.
[00:41:08] Speaker A: Well that's kind of what I was pulling out. I mean you just summed it up beautifully is we have a regulated autonomic nervous system. Any additional like for as mental health therapists, it's like the best homework we could ever give someone. Because what I'm doing, especially around trauma work, is to help to regulate a nervous system that's been dysregulated by trauma and even maybe developed differently if it was in childhood. And like here is something that's helping to regulate that, that people are doing on a daily or you know, at least a few times a week. You know, it makes sense at least. And again, this is why I love interviewing people like yourself, because we got to have the data right. It's just because math thinks it makes sense. Doesn't necessarily mean it makes sense, but it's that real. It makes, it does make sense. At least in Matt's mind is a regulated nervous system is probably going to make any treatment more effective because you know, the treatment's not necessarily even working against something. You know, where, you know that dysregulation, inflammation, all that stuff is going to work against most treatments. And this at least addresses some of maybe those barriers and I would imagine promotes health, you know, bonus benefits on top of it as well.
[00:42:31] Speaker B: Yeah, yeah, it's.
I. As a heuristic I would probably compare it to like needing to do exposure therapy for anything where the. You're kind of needing to adjust the neurons and so you need to expose it to decrease the strengths of the stimulus. I kind of again baked even to the definition of chronic pain. It is a physiological and emotional perception of a noxious stimulus. It's not just the noxious stimulus in isolation. So if you're hyper reactive to that noxious stimulus, you have to find a way to decrease that reactivity. Now whether whatever component it is, as we just said, HRVB seems to help decrease that hyper reactivity. Even if it's something else in the treatment that's causing it. This helps in that implementation.
[00:43:22] Speaker A: Awesome. Let me get you out of here on this question. Because this is just for our audience coming out of the blue. So if you need a second to think about it, but let it, let's say I got $20 million, granted. And I'm saying you know, Nick, you've got, let's just say whatever funding you think you need because you might want to get a functional MRI or something like that. So just like you know, I have a check, you can fill it out for whatever you need.
What would Nick go to next? What would you, with all this information and expertise in your brain right now, what would, what would you want to study next? What would you want to figure out next?
[00:44:08] Speaker B: Okay, I am going to go two directions here. First, im going to keep internally consistent with chronic pain as per our topic for the day. And the other one is just going to be me expanding. If were specifically looking at chronic pain, staying in the line of my dissertation, and I had 20 million or honestly probably a lot more for this idea. Doctor Justin.
[00:44:30] Speaker A: Yeah, its a blank check.
[00:44:32] Speaker B: Yeah. Um, I think we would need to get at least a thousand individuals of each central sensitization diagnosis as well as a couple of other hand picked nociceptive and neuropathic disorders and be able to stick them in the scanner and get their heart rate variability.
Um, I know this is something actually that doctor pepper even brought up to where that statistical significance in some respects doesn't even really matter when you get down to it, it really is about the effect size. So at 1000 people per disorder, with getting fMRI data and heart rate variability data and all the psychosocial data, were going to find significance. I think were going to want to look there at the magnitude of the effects. Can we actually see a crossing of the brain regions holistically and consistently in a singular study without needing to take that larger step back and do it meta analytically where theres just the fuzziness in the data because its different participants, different scanners, different um, techniques of how you're doing the brain, it's not whole whole brain, maybe it's specific regions you're looking at. I know I'm nerding out in the neuroanatomy and stuff, but I do think that level of research and specificity will help clinical psychology and all of the rest of us as well, because we can then say what is in the realm of things we know can be changed through this kind of therapy versus what actually is more predispositions like we think there is in the central sensitization syndromes.
Like that would be a holy grail if we could do something that big, having that much data, because then we could just really dig into that data to say, where are these differences? Hopefully we could have some treatment effects within that as well. But that is like 25 year study, if we're being brutally honest with that. So, yeah, that's just impossible. But I think my now for the kind of other one is thinking about my future careers. I definitely want to stay in the health psychology in general.
I want to use heart rate variability and biofeedback in general, just even any biofeedback in that respect, because I think that's a really good way to cement us alternatives, unfortunately, is I personally feel we're still considered a little bit of alternatives in the current models.
I want to be able to get ourselves more integrated. I know there's a great call right now for medicine having us in there. I myself want to get board certified and clinical health psych just to give myself that weight, to advocate for ourselves in those spaces, even if there's a shortage of us. I think advocating for ourselves in that way, and from a research perspective, then saying we can account for that last 10% of the variance, maybe 90% of disorder is medically understood, but there's always that 10%. Even in that keynote with Doctor Stefan, again, talking about stress and chronic pain, placebo effects are real. If we can be the ones, on behalf of the physicians and nurses stepping in to maximize that placebo effect for the body to uptake medicine, have those even larger effect sizes, just because that perception is there, that it may be helpful that they are being cared for, that social connection that does account for a certain amount of outcomes, even if it's only five or 10%. That five or 10% at a population level clinics worldwide is necessary to account for. Now, unfortunately, yes, some of those get lost at a population level, and I can't deny that. But I do think to maximize our system, that's where the research and where I kind of want my career to go. Again, my personal bias is going to be the biofeedback, hence being here on the podcast. Um, but I really think that that's where we can be helpful in the long term.
[00:48:42] Speaker A: Awesome. Well, I know that I could ask questions of you for another three or 4 hours, uh, but we'll get you back on the show sooner than later. Nick, I really appreciate you in your work. Like I said, I've had some of the most energizing conversations, wide ranging conversations. You're one of those people that I know I at least need like a half hour with one on one at the conference. At some point just to, I think we kicked around AI for an hour or so just between talks, and that's what I enjoy about you and just excited to share your expertise with our audience. So I appreciate you and look forward to our next conversation.
[00:49:26] Speaker B: Thank you very much for having me on. I very much agree. Conversations are very fun and I just love being able to talk, use heuristics and see where the logic goes.
[00:49:37] Speaker A: Awesome. Well, as always, you can find show notes and other
[email protected]. dot Nick, thank you so much and we'll see everybody next week.
