As research continues to grow and evolve, it's becoming clear that the vagus nerve is far more complex than just simply being 'the longest cranial nerve in the body.' It is proving to be multi-talented, with sensory fibres crossing into many tissues making it a useful target for modification of internal physiology using external stimuli.
Today we're joined once again by Emrys Goldsworthy to continue the discussion about the emerging benefits of transcutaneous vagus nerve stimulation (TC-VNS). Emrys takes us through the recent developments in TC-VNS that are showing clinical promise in treating numerous inflammatory-mediated conditions such as rheumatoid arthritis, atrial fibrillation, migraine, Crohn's disease, as well as various neuroinflammatory conditions like Parkinson's and ASD.
Covered in this episode
[00:49] Welcoming back Emrys Goldsworthy
[02:00] Recap: The vagus nerve
[05:26] A sensory organ: sensing dysbiosis?
[09:52] Diving deep into 'gut-feelings'
[11:54] How the vagus nerve influences inflammation?
[26:12] Complex regional pain syndrome
[28:06] Gut-to-brain axis and down-regulating immune activation
[37:54] Auricular stimulation in ASD
[39:35] Can singing be therapeutic?
[41:46] Resources for further learning
Andrew: This is FX Medicine, I'm Andrew Whitfield Cook. Joining us on the line today, after a long sabbatical, is Emrys Goldsworthy. He's the director of Athletica Physical Health. He completed a Bachelor degree in health science, musculoskeletal therapy, which he attained at Endeavour College of Natural Health, Brisbane. He’s also gained a master's degree in sports coaching, focusing on classical ballet coaching at Griffith Uni. He worked in the position of senior lecturer in the department of musculoskeletal therapy at Endeavour College of Natural Health for over nine years, and now trains clinicians across Australia and internationally in vagus nerve stimulation. And his system of assessment and treatment called the functional neuro-articular system.
Emrys' interest in the body began while he was a professional classical ballet and contemporary dancer. And he's a graduate of the Australian Conservatoire of Ballet, which led to a career in the Royal New Zealand Ballet. And I warmly welcome Emrys back to FX Medicine, because he's going to blow my mind once again, I know. How are you, Emrys?
Emrys: It's great to be on again. Thank you, Andrew.
Emrys: Well, that was a while back. And back then I was kind of, in my opinion, wasn't quite as refined in my approach to doing vagus nerve stimulation, because we didn't know as much as we know now. And even now, we're refining still, but I can imagine in five years' time it'll be a different discussion about what's going on.
But so vagus nerve stimulation essentially is a range of different options of different therapies. We're going to talk about specifically one, but that other... stimulating the vagus nerve, specifically, either through electrical means or other kinds of means, it might be vibrational or whatever. But I'm referring mainly to electrical stimulation through the sensory branches of the vagus nerve and in particular the auricular sensory branch. That's the ear.
So the method that I use is called transcutaneous auricular vagus nerve stimulation. It's a bit of a mouthful. But that differs from another type, which is an implanted vagus nerve stimulator, which of course, is not what I'm doing. And the auricular stimulation has been shown in research, in plenty of papers, that are coming out, to be a lot more... how to put it? Less risk, of course, less risk of infection, because it's applied outside of the body. There's no surgery that's needed, and also it can be applied at home or in the clinic. And it's actually just as effective. So that's the great thing. It's not that one is better than the other. They're both just as effective.
Andrew: You know, I remember way back when I was a doubter of complementary medicine and things like that, and I used to pooh-pooh it. And I would have initially said, "What a load of poppycock. You can't access the vagus nerve, which sort of runs... It's a cranial nerve for goodness sake. You can't access that externally." But indeed, this vagus nerve has branches in multiple places.
Emrys: That's right. So the vagus nerve not only is innervating a raft of organs, particularly more on the up part of the viscera, but it's also innervating muscles of the throat, sensory areas of the throat as well. Even the tongue, the back of the tongue, and the ear. It's a multi-talented nerve like I would say. It does so much. And so when I say to a patient, "Okay, we're going to stimulate your vagus nerve, it does all these things, but we're going to do it through your ear," it's very perplexing for them. Because this nerve is unlike any other nerve in the body. And although it does so much, it is poorly understood.
People think that it's just having an effect on organs, but that's not even really its main role. The best way now to describe it for me, I've really come to the conclusion that the vagus nerve is not a ‘doer’. It's a sensor. It senses things. And it either gets really bad at sensing things and doesn't act appropriately, or we can ramp it up and improve its ability to sense what's going on, particularly in the gut, and act appropriately and accordingly with an anti-inflammatory effect. Suppressing inflammation which we’ll talk about soon.
And this is something that... I had to topsy-turvy my... It was my mind. It was the way I was thinking about things. Because we're so often thinking more about nerves coming out of the brain and innervating. Like, you know, our muscles, for instance. And yet we, of course know, that when we get a burn, there's the immediate arc that goes to our spinal column and straight back. The ‘ouch arc,’ right? Which is an automatic arc. And then you've got that "Ow that really hurts." That "I burnt myself." And that's a sensory organ.
And it's really interesting that we think that the sensory organs has to be a taste, smell, eyesight, touch, pressure, tickling... that sort of thing, but it can be from our gut.
Andrew: And this is where this whole range of research is coming from now. So it's really interesting me.
Emrys: Well, 80% of the fibres are sensory. So, you know, when we talk about the vagus nerve, we're really just talking mostly, about its sensory impact.
Emrys: And so when we understand at that point that the vagus nerve is sensing. The sort of, what's going on in the gut? Not just the level of lipopolysaccharides that are, you know, being translocated or whatever. It's also sensing what's going on in the microbiome. It actually is able to decipher dysbiosis. It knows... that's what the literature is indicating. And we're not quite there yet exactly how or what, but it's deciphering this dysbiotic change, and accordingly reacting to that.
So what that means for therapy? I mean, I'm now thinking it could be a really useful therapy for dysbiosis. I mean, it's certainly been effective in SIBO, for the traditional, like, colon dysbiosis, it may well be a very useful option. Of course, you know, we've really struggled to get good therapies for the more and extreme end of dysbiosis, and I know fecal transplant is one of them. But this might be one in the future that does assist. It might be an adjunct, it might not be the only one, but definitely could play a role.
There's lots of papers coming out about its role in the microbiome, and, of course, you know, microbiome research is exploding, so you can imagine that emergence of vagal research, vagus nerve research, and microbiome research they're going to start to interact with each other.
Andrew: Is this tied in with the... you know, we would be pretty much ofay with the, you know, you get butterflies in your tummy, and that's the gut-brain axis working. You know, when you get nervous, you feel it in your tummy. And that's the vagus nerve being innervated. But what you're talking about is intestinal permeability?
Emrys: Well, okay. We’ll go back to that. So that feeling of gut feelings. So a lot of our emotional center is actually... so part of our limbic system is actually devoted to sensory sort of, input from the gut.
So our limbic system seems to process a lot of gut-sensory information. What that exactly is, you know, it’s not well described. But some of the sensory input comes from the sympathetic nervous system, so this is where it gets complicated. Some of it goes to the vagus nerve. Okay? Some of it goes to the sacral nerve. It gets very complicated.
But a lot of it does go through the vagus nerve. And everyone wants to think it's all vagus and vagus. But there are definitely gut-to-brain axis through the sympathetic nervous system. And we like to... we all know that the nervous system is completely split. But the vagus nerve activates sympathetic nerves. The vagus nerve activates the HPA axis. Is that a bit strange? All right, isn't it a bit strange?
Andrew: I know.
Emrys: So, you know, that doesn't necessarily mean it's going to make... that it's activating stress response. It just means that it's activating parts of the stress system. It doesn't... That's why neurology or neuroscience is far more complex than you read in the textbook. It's not as simple and black and white.
But you're right. The gut feeling, the sensation of "That doesn't feel right." At least in part is vagal. At least in part. Because you get that feeling of sickness, you know, that feeling of nausea. Right? That is vagally mediated. So you're right in that regard.
Emrys: Yes. Well, it does. I don't know if they’ve... and you might be able to give me more information on this? I don't know if they have found a really good pathway to why stress induces it, other than the fact that as soon as the vagus nerve is not functioning, intestinal permeability runs rife.
So the vagus nerve, at a sensory level, and mode, like a sort of reflexive, efferent motor output, is able to attenuate any excessive permeability. So if it notices that there is, you know, permeability for an extended period of time, it's able to mitigate that, and actually close the tight junctions.
Andrew: Oh, that's it. That's really interesting.
Emrys: It seems to... how it does it directly? It seems to do it indirectly. I mean, it does it. That's for sure. That's been shown time and time again when they induce that in animal models. Vagus nerve stimulation prevents it from happening... how to put it? Vagus nerve stops it from happening to the extremes that it would normally happen when the stimulation is done prior to, say, the induction of, say, a toxin, or something like that. Or an intestinal injury. But it also attenuates it after the injury if it's applied.
So vagus nerve stimulation could be used in the patient if they have been diagnosed with intestinal permeability, and it's kind of like strengthening the system to be able to self-regulate again. So that's what I see intestinal permeability as. It's more of a failure of self-regulation.
Andrew: Yeah. Now, I think that would be a question to ask Professor Alessio Fasano.
Emrys: Oh, I wonder if he looked at it? I don't know. Of course, I'm not in communication with him. It would be very interesting, yeah. I do read his... I love his work. Yeah.
Andrew: Now, in our first podcast, we spoke about vagal nerve stimulation or VNS, and it's used on anxiety and other sort of emotional type disorders. But you also alluded to its anti-inflammatory actions, which we're talking about today. So how does the vagus nerve influence inflammation, specifically?
Emrys: Well, I mentioned that it's a sensor, so it senses when things are sort of changing. Where you might have immune cells activating, it senses this in the gut. And it appears that it can also do it peripherally. This is a new area that's being explored. But because it actually suppresses the symptoms of rheumatoid arthritis, they're wondering how it's actually doing that. There's ways in which they're doing that. There are ways in which they believe it's doing that.
But one of the ones that they know is that it does activate the HPA axis, okay? And it helps to release cortisol. Cortisol is anti-inflammatory. Okay? So there's an anti-inflammatory effect from cortisol. Additionally, it activates the coeliac ganglion in the enteric nervous system, and that actually then goes through the spleen, and then the spleen T cells communicate with the macrophages, and the macrophages get suppressed in their production of TNF alpha.
Of course, now that's an important finding. TNF alpha, you know, probably in cases of rheumatoid arthritis, the most important proinflammatory cytokine to consider. And you know, in a raft of other proinflammatory conditions. If we can suppress the TNF alpha levels coming from the macrophages in the spleen, and then systemically from that, then we are definitely having a huge effect on systemic inflammation.
Additionally, it seems to also work at the gut level. So it suppresses TNF alpha production by suppressing NF-κB in macrophages at the gut wall. And it also seems to work through oceliac ganglion, now we believe, at the joint level through local joint immune cells. And so it can suppress the production of TNF alpha there as well. That's how it works with rheumatoid arthritis.
So there's lots of different pathways. And so all of those pathways are considered the cholinergic, anti-inflammatory pathways. And when I describe it as the sort of sensory is feeding back, and into the motor output of suppression of inflammation, well that's the reflex. So I call that the cholinergic anti-inflammatory reflex. And that's what's dysfunctional in a lot of these auto-immune patients.
I'm not saying that's the cause, but it's certainly dysfunctional. And it's also dysfunctional in intestinal permeability, and it's dysfunctional in Crohn's. That's been established. And likely ulcerative colitis, although that's not been well researched, and definitely rheumatoid arthritis.
Andrew: This is just amazing stuff. So, you know, the day is going to come where people are being assessed, being diagnosed with these auto or other inflammatory conditions. And not only will they be receiving perhaps a personalised drug approach, due to their genetic profile, but also these adjunct therapies, diet, lifestyle. And also maybe a little bit of an electrical stimulation from the ear to help in dampening all of these signals that are worsening their condition. I mean, it's quite amazing this sort of stuff. Really is.
Emrys: Well look, I mean, these researchers... if you look up PubMed ‘vagus nerve stimulation’ or even more specifically ‘transcutaneous vagus nerve stimulation.’ These are not, in any way, alternative medicine researches. These are immunologists, rheumatologists, et cetera, neurologists, and they're from reputable universities. This is at the...
Andrew: It's cutting edge.
Emrys: For them it’s very exciting for them. You can imagine that they wouldn't be putting themselves on the line for this kind of research unless it was meaningful to them.
Emrys: And you see paper after paper, and one author, and they're going in different directions. You know, like you'd get one author focusing particularly on rheumatoid arthritis, the next on atrial fibrillation, the next one on Crohn's, the next on migraine or depression, and this is what's happening.
You're seeing these particular authors working on one condition. But the condition list goes on, and it keeps increasing. Like there's papers now coming out with autism and ASD and ADHD. And that's sort of a new area, but it just goes on and on and on.
And neuro-inflammation, we should talk about that today, a huge one, you know? Now, hopefully, one day it will show some great effect if it's done in the appropriate way or the appropriate setting for things like Parkinson's and Alzheimer's. I'm hoping that's something.
Andrew: You mentioned earlier, you spoke about other nerves that are being used for various conditions, and you just mentioned atrial fib, AF? Am I right in saying that...? Is it... was it the facial nerve that was being stimulated and having some effect on AF? Is that right?
Emrys: I'm not aware of that research...
Andrew: Any other nerve apart from vagus?
Emrys: Well, I mean, you've got certainly, sympathetic nerves. I mean, there are the nerves that you'll probably hear sometimes about that relate to similar structures and systems, autonomic, although this is not an autonomic nerve. They use the phrenic nerve for essential sleep apnea. I know it's not atrial fibrillation. I'm not aware of any other neurostimulation being done for AF.
Andrew: Got you.
Emrys: But for AF, the vagus nerve has been proven clinically for me, and in the research, have such a positive effect. You know, it has a really good effect on the refractory period during a heartbeat. So you have this, like, period of no beat, and it's extended during, like, from vagus nerve stimulation.
So when the vagus nerve is not working, you can get, like, little beats in there, and that's essentially where you're getting, like, an arrhythmia occurring.
Emrys: And it will suppress that activity. And that's been well proven. And it's not... There's not enough randomised control trials with huge numbers being done yet, but clinically, works a treat. It’s amazing to see people's heartbeat just go down as you're treating them in one session. Okay, you start in a bit of a tachycardia, and it just goes down to, like, 60 to 70 beats per minute within 10 minutes or a little bit longer. It's great to see the results immediately. And then it gets maintained. Often they'll come in two to three weeks later after, you know, a few weeks of treatment, and we're starting with a normal heart rate.
Andrew: Yeah. This is the thing that is really quite astounding to me is how quickly it acts. You know, we spoke about anxiety, and just how quickly it can have an effect on somebody who's extremely nervous, who's going through an attack.
When you're talking about inflammation and neuroinflammation, normally these are more smoldering-type conditions that take a long while to get a positive effect from therapy. That's measurable in bloods. So what about blood mark has chang from using this therapy? Do you see a... like a very quick drop like AF, or do you see something that tends to dissolve over a period of time?
Emrys: Well, I'll tell you, the recent paper that came out for RA patients, the rheumatoid arthritis patients that were also epileptic. So these are the ones that had the implanted device, epileptics... The implanted device has been used for epileptics for a while. It was the first condition which it was approved for.
But they're now using the research, and people have also had heart rate who've also got epilepsy. And so I'll tell you their markers. So they, at baseline, which was at day 21 to them, their average interleukin 6 was 7.7, and at day 42 was 5.6. Not a huge drop, but a significant drop. TNF alpha, which is the big one, was at 3,765 at baseline, and went down to 1,835.
Andrew: Wow, half.
Emrys: At day 42. And then CRP 12 to 6 in that time as well. So that's a significant number. That's almost within range. So CRP and TNF, they're the big ones there. And another one that... blood marker that got that changes thing in the paper you look at and what they're measuring is interleukin 10. So that's an anti-inflammatory cytokine. And that goes up, of course. And so that interleukin 10, from the research I've read, inhibits interferon gamma and TNF alpha. So, again, another cytokine that's sort of working in our favour.
And, of course, it lowers interleukin 1 beta, so that's a… your normal sort of proinflammatory cytokine. So CRP, interleukin 6, interleukin 1 beta and TNF alpha, all lowered. Interestingly, at a blood level, it lowers cortisol. Now, I wanted to mention this because the cortisol is lowered in the blood after, you know, weeks and weeks of vagus nerve stimulation. But it activates the HPA axis? How does it... why is it lowering cortisol in one marker, yet on a sort of efferent level it's activating HPA? My belief is that it's improving... It's reducing any cortisol resistance that might be there.
So cortisol resistance, you know, too much cortisol over time makes the body resistant to cortisol. and it must be sensitising the body to cortisol. Because I've used cortisol as a marker. So like diurnal patterns of cortisol, and you'll see like, patterns where people are just tired all the time and have high cortisol, and that doesn't really, you know, you'd think that there'd be a bit more ‘up’ than that. And I see that cortisol lowers, and the energy rises in them.
Emrys: There's like a lowering of cortisol and a sort of a homeostasis of their energy systems are occurring.
So that’s a really interesting thing. So cortisol resistance seems to be attenuated... At least maybe not directly from research, but it seems to be clinically happening from what I've seen.
Andrew: And are these blood markers changing in correlation with improvement in disease state?
Emrys: Yeah. So in that paper I mentioned, they directly correlate with a reduction in the joint pain, and in the improved, you know, movement of the joint itself. So those two... the blood markers... nearly always correlate with a reduction of pain and an improvement in movement.
Clinically for me, when I'm using it for someone who's got like a cortisol resistance, or, you know, HPA axis dysfunction. That kind of thing. Their stress levels go down. So their coping mechanisms improve. Their anxiety levels go down. Let's just say they've got poor energy in the morning or throughout the day, fatigue, fatigue seems to be attenuated.
Fatigue isn't attenuated in everyone. I guess it depends on the cause. You know, it's a non-specific symptom. You know, heterogeneity for fatigue, but fatigue is one that I often use vagus nerve stimulation for. I'm treating a few... There's a theory that the vagus nerve is infected, I don't know if this is true or not. We don't know yet. But in conditions such as chronic fatigue syndrome, it's a belief by some authors that the vagus nerve has been infected by some herpes virus. And it's causing a, you know, a fatigue-like state. I don't know how true that is, but I've found great results with chronic fatigue syndrome. Over time, over time, certainly not overnight.
Andrew: It being a rather confounding, multi-factorial condition, have you found that it sort of, you know, waxes and wanes and acts on certain aspects of, you know, pain and inflammation, rather than others? Have you found any parts where it acts better than others?
Emrys: Pain, I’d say because it suppresses inflammation when it's excessive, I mean, it doesn't suppress inflammation when it's appropriate. That's really important to remember.
So if you're having vagus nerve stimulation after an injury, it doesn't suppress the inflammation to the point where you don't heal. It suppresses it if it's excessive. Because the body is smart enough to know. So, for example, a joint injury that has too much inflammation, and that's causing pain and reduction in movement, the pain levels are the first thing that go down. And normally that is just soon followed by improvements in movement, particularly if it's to do with swelling.
But then when it comes to just pain alone, treatment for inflammation is very different in vagus nerve stimulation than for treatment for pain. If it's inflammatory pain, that's one treatment type. If it's centrally-mediated pain, like a neurogenic style of inflammation, which is different to primary inflammation, like immune-mediated inflammation, it's very different. That's more substance P related, CGRT, that's done differently.
So as the clinician, they need to know the difference between the two, and if you don't, you're not going to treat appropriately. And I can tell you now, if you treat someone in, what we call sort of, trying to down-regulate the pain centres of the brain, what's called the pain ‘neuromatrix,’ which is a very different parameter, parameters that are used. You won't get the same effect for an inflamed joint which has got pain if you use anti-inflammatory treatment. And that's really obvious, clinically. And it's really obvious in the literature too.
So why? I'm not really sure. Why is it that one, like, hurts for one condition is different, and for the other, it's like completely opposite. And yet they're very similar? And they're not at a physiological level.
Andrew: Well, this is, as I understand it, and it is not a great understanding at all. But things like CRPS, complex regional pain syndrome. Is basically a feedback loop that's gone awry, so it’s looping within itself. Is that right?
Emrys: Yep, yeah, yeah. That's a pretty complicated condition. You know, clinically, I've seen that's a very neuropathic condition as well. There's a big sympathetic component to it. Is it vagal? Certainly, I would never suggest that it's a vagus nerve problem by itself. Is the vagus nerve a problem in them? Certainly. You don't see a lot of them in clinic. They're not that common.
Andrew: Well, they're going to be stressed?
Emrys: Yeah. And, I mean, that's like, isn't that like, the holy grail, like reducing stress and the stress response. Sympathetic dominance. And that is eventually a pro-inflammatory condition. If you are chronically stressed, you're going to eventually be chronically inflamed. And that's something that we want to sort of reverse.
Most of the time, you'll see clinicians either working on like anti-inflammatory diet, anti-inflammatory lifestyle, reducing environmental toxins, all the sort of, usual suspects. Which are really important. But a lot of the time, the vagus nerve is just sitting there not being looked at. And online, you know, you go online and look up vagus nerve stimulation, you're going to get a raft of strange home exercises that are not really based on science. They're sort of based on opinion and a few small studies that aren't really very indicative of really, specifically vagus nerve. And you've really got to get it worked on the vagus nerve specifically in a way that's clinically relevant. Clinically mediated. Not... You can do all sorts of things at home like gargling and the mammalian diver's reflex, but they're not as good as a clinical approach. Sometimes feels like sort of like anything, isn't it?
Andrew: Well, it's like anything. But I just think it's really interesting that there's work being done by using the twilight hypnotic drugs prior to surgery, majorly for the action of decreasing anxiety. And it's the feeling of stress about the forthcoming operation that gives them pain after the operation. Reduce the stress prior to it, and you reduce the requirement for hard-core pain-relieving drugs afterwards.
Emrys: That operation one is an interesting topic. So if you had vagal stimulation prior to surgery, you are basically preparing your vagus nerve to the onslaught that's going to occur, right?
Emrys: And preventing it from being... your immune system from over activating. And that's what happens. That's been shown time and time again. Vagus nerve stimulation attenuates overactivity in the immune system. That's essentially the role of the vagus nerve does, at least in this context.
So if you have it before surgery, you're at least reducing the risk for an excessive, overactive immune response after surgery, which can really suppress healing times, you know? And that's... although it's required initially, it can go on, you know. A little too long, and that often affects people's long-term recovery times.
The other thing is that when you talked about anxiety. We know that vagus nerve stimulation seems to normalise glutamate GABA levels. So GABA goes up, glutamate goes down, that kind of balance is returned. That's why it works well with epilepsy. And that's also why... most likely because it's suppressing neuroinflammation, which promotes that imbalance.
But it also it works on serotonin levels going up, norepinephrine levels and dopamine levels going up, which is a little indicative of an anti-inflammatory state in the brain.
Andrew: You know, I just see so many opportunities here. So far-ranging. Not just inflammatory, but let's look at the worldwide opioid scourge that we're seeing at the moment and the choices that are offered. The medication choices are, you know, more often than not, they're like an NSAID or a paracetamol, both of which have their own issues, not just bleeding but also toxicity, that we're seeing more and more an issue. And this might be something where practitioners of all walks of life can initiate a safe therapy that takes away that huge cost and social medical burden of not just the opioids, but the side effects from the alternatives.
Emrys: Yeah. So, I mean, you look at...I mean, this can go for a long time this discussion because the concept of how doctors are just giving out opioids, or opiates, be it for a chronic pain or a neuropathic pain or conditions that are just prolonged, and they're not really giving any other option. You know, we know that a lot of these people are going to have a lot of other systems involved, you know, depression, anxiety, gut problems, the list goes on, and environmental factors, and it's not being addressed.
And we know that a lot of these conditions are not, you know, single entities, they're multisystem, pro-inflammatory, systemic inflammation, you know, this kind of thing. And that's not being addressed. And so, you know, all naturopaths will say, “Start with the gut,” Right? And it's true. It really is true.
And we look at the immune... the majority of the immune system is there. And the vagus nerve is actually there being you know, the watchdog. Over what's going on. And acting to suppress it when it's inappropriate. This whole network of neurons and bodily organs is so important, and it actually likely... you know, a lot of authors are talking about fibromyalgia and gut problems being linked, and things like that. And, I mean, the term fibromyalgia to me is not really helpful. It doesn't really tell me what to do. It doesn't really tell me why they've got it. And I feel that often you'll get one fibromyalgia patient that comes in, and, you know, there are some kind of pregabalin or Gabapentin or something. And it's completely different to the next fibromyalgia patient. We got completely different set of secondary comorbid conditions, and that's the problem. They need to be treated as an individual, and that's just not happening. They're given the same drug. Hopefully, it works.
And the whole idea is, I think, and this is why I say use this in conjunction with your nutritional medicine, with lifestyle medicine, with, like, looking at environmental factors and so on. And they're going to get to the bottom of their condition, rather than just to try to suppress symptoms. That’s my last thing I want to do. I don't want to try to suppress. And that's not what the therapy does. It actually enhances the body's own endogenous suppression of inflammation, rather than just actively and directly suppressing inflammation, which is I think is a bit of a different way of approaching it.
Andrew: Yeah. But I think likewise from, you know, medications just being handed out, how many natural therapists would think of "treating the gut" by, and I don't mean this as glibly as it sounds, tickling the ear? You know, how many people would think about treating your vagus nerve rather than looking at things that go in your mouth to treat your gut?
Emrys: Well, most people would think that the gut to brain axis is a one-way street. And it is certainly not. And my argument would be that it's certainly either equally, both directions. But, I mean, even if you say, "Okay, the vagus nerve, it receives information from the gut, so it's the gut that matters." Well, we know that people who've had traumatic brain injuries, they immediately get intestinal permeability.
Emrys: So when the brain is injured, the gut suffers. What's that about? That's the brain to gut axis. It's not the gut to brain axis. And so we know that when you stimulate the vagus nerve, you're basically sensitising it. You're improving it’s feedback system, and its output system.
Okay. So it's both directions. And I think that if you're a clinician can really learn to work in gut to brain axis kind of medicine, which is kind of a new field. You need to consider both directions, and you need to have a legitimate therapy that basically works from the brain to the gut, not just from the gut to the brain. Okay?
And that's the whole role of this. And it's like the highway. If the highway is broken, if the highway is not, you know, functioning, it doesn't really matter what you do with the gut, for the most part. You know, it has to function to work as a sensory system. And if it's not working, you know, you can imagine a lot of those therapies that people are trying to do to improve, you know, gut to brain actions or work on inflammation in the gut. It might not work as well. Or at all, potentially.
Andrew: Now, you mentioned Parkinson's and other neuroinflammatory conditions previously. Tell us more about this, and just how effective can vagus nerve stimulation be in... I mean, there's a plethora of conditions here, but where does it fit? Where does it work?
Emrys: All right. So the main two findings in regards to neuroinflammation is one. Which, firstly, I should mention that the blood-brain barrier becomes more permeable in neuro-inflammation conditions, neurology conditions, and that is like one of the signs of neuroinflammation. Blood-brain barrier permeability. Basically leaky brain, you've probably heard of that?
Emrys: The other one is that the microglia go, they kind of, can turn into a pro-inflammatory state. So microglial activation. We’ll call it.
Those two particular areas are of key importance. Because vagus nerve stimulation in more than two papers has attenuated blood-brain barrier permeability. So it does it not only in the gut, but does it in the brain. And also it actually changes the phenotype of microglia towards what's called the M2 phenotype, which is an anti-inflammatory microglial state.
So you're changing the state of affairs. The sort of neuro-inflammatory milieu becomes more normalised in homeostasis. And goes away from that, you know, degrading state of inflammation, towards back to a building state. And that promotes things like brain drive neurotrophic factor which helps with…
Andrew: Neurotrophic… I was just going to say it.
Emrys: Yeah. And also all the neurotransmitters normalise in their levels when you have all these things heading in that direction.
So that's... It's a really useful technique for any neuro-inflammatory condition. And we know that there is, you know, ASD, you can see it in that condition as well. As well as all your normal types of dementias and so on. And so this is a new field. It's not as established as depression, although it may well be, you know, with neuroinflammation, depression may be a part of that. So there is a link there. But it's certainly one of the burgeoning areas in the research and also in therapy.
But I've had really good success with it, but by no means would I ever say any of these conditions will go away overnight. It's like training. You go to the gym, you train your arms, you want to build up your arm muscles, you're not going to get it overnight. It's going to take weeks and months of treatment and of exercise, and vagus nerve stimulation is exercising the vagus nerve. So it takes time for it to get good at what it does.
Andrew: What about, though, you mentioned ASD. That's really interesting to me. Have you seen effects, positive effects, with vagal nerve stimulation? And how responsive are these kids to the intervention of that thing on their ear?
Emrys: Yeah. Er, well, yeah, that is the issue. Some of it you're just never going to be able to do it. Their ability to withstand that kind of stimulation is not going to happen.
Emrys: So they're not appropriate for treatment, at least with this electrostimulation. Others, you know, they're a different part of the spectrum, and you're working particularly on frontal lobe activity. And so attention span and ability to sort of engage with another person, you know, eye to eye and not have a looking around the room behaviour. Or sometimes it might even be just cognition, so you're working on their cognitive function. And that's been shown to be quite effective, vagus nerve stimulation on cognitive function ASD in the research.
Every ASD patient is different, you know. Your kind of have to approach it, "What do we want to achieve? Okay, well, let's measure that. And then let's measure it again in a month or two after, you know, doing the stimulation on a week by week basis."
Emrys: And yeah. I've mainly seen it in attention and focus and cognitive function. They're the main ones that have changed. It's slow change. You know. ASD is very hard to treat, very difficult to treat, and I would say that you would look at it as sort of an adjunctive therapy in line with all the other sort of nutritional therapies that they're normally on over the course of the years, rather than months.
Andrew: Can I ask, though, you mentioned, or we've mentioned, singing, previously in the previous podcast. And I am quite interested. I can't say astounded, I haven't seen it used as a therapy, but I'm quite interested in the aspect that some people with this sort of lack of focus and even processing disorders, when they put some sort of accentuation rather than speech, some sort of highs and lows attributable to singing, it tends to stick with them. They can read more fluently. They can remember. They can process the story and have a more comprehensive outlook on it. Have you ever seen results yourself in this?
Emrys: I don't use singing a lot. It's sort of a hard thing to sort of introduce to some people.
Andrew: What's singing?
Emrys: Singing. Exactly. Embarrassment and things like that.
Andrew: Yeah, in my instance it's screaming. Yeah.
Emrys: But I think it's healthy to sing. And I think that it's likely going to improve your vagus nerve function. Because the vagus nerve is controlling intonation, majority of it is vagally mediated, so, speaking. And singing, you know, really stimulates it. And you see that with people who, you know, have vagus nerve problems often who are singers, so their voice has been affected by a vagus nerve problem that they have. But singing again as a therapy, you can imagine it as being a potential. Particularly, I... My opinion would probably be more operatic, or at least where there’s more vocal range, rather than, yeah, that kind of singing. Maybe group singing is obviously a really good way of getting people to do it, less embarrassing, I guess than trying to do solo work. But I think...also, anything, where you're in a group setting, is going to be helpful for your anxiety levels, unless you've got group anxiety. But, you know, I would say that that's generally quite a positive therapy for most people, and long-term it can really help the health outcomes.
Andrew: I've harped on how important this is for practitioners to link into and they need to know what they're doing to know. They need to know how to do it properly. Where can they learn more about this? Because I know you do courses.
Emrys: Yeah. So I have three portals over which I advertise my courses through. Facebook, Emrys Goldsworthy BHSc, which just stands for Bachelor of Science, that’s my credential. And then also emrys_goldsworthy_bhsc at Instagram, and then emrysgoldsworthy.com is my website.
And so all of it that will be on there. Instagram seems to be the one that I update most often, and so you'll see I'm doing courses on vagus nerve stimulation all around Australia at the moment, and next year I'll be taking it to Europe. So it's a pretty exciting time, and I just recently did one in Canada, which was great.
Emrys: And, yeah, everyone's loving it and it's great. Because I've got a Facebook group of all the different clinicians that have done the course, and it's great to see some amazing treatment outcomes that they've had. And conditions that I've never seen in my own clinic. They're seeing, and they're getting great treatment outcomes. And I'm so excited about the potential once more people learn how to use this therapy.
Emrys: So, yeah, I do a certification program in the method that I teach, in the method that I use, and just look up in those sites for more information.
Andrew: And I also understand you've... Is it you've just done or you're just about to do a talk with the Australian Traditional Medicine Society, the ATMS. Is that right?
Emrys: Yes, I've recently done a webinar with them, and yeah. So that webinar has been recorded, and it's available on the ATMS website.
Andrew: Emrys, thank you so much. Again, you've blown my mind.
Emrys: Well, it’s great to be back on.
Andrew: Seriously, well I keep looking at these opportunities that we're just not thinking about, and we just... we really need to hook into this, because it's a safe externally applied therapy that everybody could learn to use. It just needs an appropriately trained clinician to take them through how to do that. And so that's where we really need to get the word out there.
Emrys: Indeed. I hope everyone who listened today will see the benefit and can see how they might be able to implement this therapy in their own practice. And, yeah, hopefully, they can come and attend one of the certifications.
Andrew: And we've certainly got a legion of references to put up on the FX Medicine website so that people can follow through, you know, some of the research strands that are going on. It's quite comprehensive.
Emrys: Indeed. And if you're just wanting to research, just go PubMed, and put in ‘vagus nerve stimulation’ and ‘vagus nerve.’ ‘transcutaneous vagus nerve stimulation,’ and I'll give you a year to read through all of those papers.
Andrew: Well done, Emrys. This is FX Medicine, I'm Andrew Whitfield-Cook.
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Zhou H, Liang H, Li ZF, et al. Vagus nerve stimulation attenuates intestinal epithelial tight junctions disruption in endotoxemic mice through α7 nicotinic acetylcholine receptors. Shock. 2013 Aug;40(2):144-51.
Koopman FA, Chavan SS, Miljko S, et al. Vagus nerve stimulation inhibits cytokine production and attenuates disease severity in rheumatoid arthritis. Proc Natl Acad Sci U S A. 2016 Jul 19;113(29):8284-9.
Kaya M, Orhan N, Karabacak E, et al. Vagus nerve stimulation inhibits seizure activity and protects blood-brain barrier integrity in kindled rats with cortical dysplasia. Life Sci. 2013 Mar 12;92(4-5):289-97.