How EDS and HSD Impact Fascia and Pain with Tina Wang, MD

[00:42] Dr. Linda Bluestein: Welcome back, every bendy body, to the Bendy Bodies Podcast with your host and founder, Dr. Linda Bluestein, the Hypermobility MD. Today, our guest is Dr. Tina Wang. I'm so excited to talk to Dr. Wang, who is a fascial researcher and physical medicine and rehabilitation doctor. When I was having so many problems with persistent pain, I kept hearing over and over again that I had myofascial pain. And at that time, I didn't fully understand what the implications were. And I also didn't understand that fascia is actually altered in people who have conditions like hypermobile EDS and HSD. So I'm sure you're going to enjoy this conversation with Dr. Wang to learn about fascia. What is it? How is it altered in people with EDS and HSD? And how can we treat things like myofascial pain?
[01:29] Dr. Tina Wang is a board-certified physical medicine and rehabilitation medical doctor and is an assistant professor of medicine at Loma Linda School of Medicine, University of California Riverside, and the Southern California University of Health Sciences. She is core faculty for the musculoskeletal curriculum, including the use of ultrasound-based diagnostics and interventions. Her published research focuses on ultrasound characteristics of fascial dysfunction to improve the clinical understanding, diagnostics, and treatment of myofascial pain syndromes, Ehlers-Danlos syndromes, and hypermobility spectrum disorders.
[02:06] As always, this information is for educational purposes only and is not a substitute for personalized medical advice. Stick around until the very end so you don't miss any of our special hypermobility hacks, and let's get started.
[02:21] All right, super excited to chat with Dr. Wang today. Dr. Wang, can you start out by telling us why fascia is such an important topic for hypermobile EDS?

[02:27] Tina Wang, MD: Fascia is likely the organ, or the originating organ, that is affected in connective tissue disorders like Ehlers-Danlos syndrome and hypermobility spectrum disorders. It envelops all of our organs, including our nerves, our vessels, our muscles. It includes our tendons and ligaments, even our brain. So you can imagine that if the connective tissue and the fascia are affected by pathological differences, then all of the organs in our body cannot function properly, which is what we experience with EDS.

[03:18] Dr. Linda Bluestein: Okay. I know that you might have already answered this question a little bit, but for the purposes of this conversation today, can we talk about connective tissue disorders in general, or do we need to separate hypermobile EDS versus HSD versus other connective tissue disorders?

[03:36] Tina Wang, MD: It really depends on the lens of the scientist you speak to. So, depending on if you're speaking to even camps of geneticists where they may or may not agree that HSD and hEDS are the same condition with different phenotypic manifestations, or if they are within the same type of pathologic manifestation — there's also debate within those who work with EDS as well as geneticists.
[04:15] And then if you speak about things on a microscopic level, on a small organ tissue level, looking at the cells, looking at the extracellular matrix, then you would have a different lens and you may or may not then speak about hypermobility, EDS, HSD, as well as other fibrotic conditions like ankylosing spondylitis. Those then would have different pathophysiology based on what we're seeing in the tissue, or they can have similar processes. So it really depends on the lens of the scientist, the doctor, the specialist that is studying the connective tissue.

[05:08] Dr. Linda Bluestein: When it comes to these conditions, do we know why the fascia is altered and how that actually takes place? Because you mentioned the word phenotype, which we know is the clinical picture, right? And then we know that the underlying genotype or genetic code can be very different in different people. And of course, we know that the genotype for hypermobile EDS is yet to be discovered. We have some potential clues, but we really don't know what the causative genes are at this point.

[05:42] Tina Wang, MD: Similarly, with what is happening with our tissue, we cannot say that we know a causative factor. We can only say that we have associated factors. So fibroblasts — the cells that make the extracellular matrix, which also includes collagen — those start to go awry. They become myofibroblasts as a transition into a more pathologic state. And so we know these things occur. We can't say whether that's the initiating event, or if the extracellular environment — let's say, for instance, mast cell activity, or even being bathed in TGF-beta from stress responses, either psychological or physical — we can't say if any of these things are causative. Rather, we know that they're associative.

[06:40] Dr. Linda Bluestein: Okay, so actually, Dr. Wang, I think I'm going to back up a little bit because I feel like we jumped into this very deep scientific conversation, and probably a lot of people are already going, wait, wait, wait a second, I'm confused. I thought that EDS was a genetic condition and it was a condition of connective tissue, but now you're talking about fascia. Maybe it would help me and the audience if we back up and you explain how you got interested in this connection in the first place, because I think maybe that would help with our understanding.

[07:15] Tina Wang, MD: Yeah, well, the story is much like yours. I started working with performing artists. And performing artists have a higher occurrence — we find that they have a higher occurrence of either asymptomatic hypermobility or symptomatic hypermobility. So many years ago, as a young student, these were the questions we started to ask ourselves. And I know that you were part of that conversation too.
[07:44] And it's such a mixed bag, because hypermobility itself does not confer a risk. And that was a bold statement back then. And then we would say, well, if it doesn't confer a risk, then everybody's fine, that it's not something to look at, right? Except when we go digging into the nuances, what we see is that hypermobility associated with dysfunction and disorder does confer a higher risk — a risk for injury or a risk for comorbidities. So then we have to go looking into subpopulations.
[08:26] And then from working with performing artists, I started to dig into this world of hypermobility in general. I'm also a trained PM&R physician, so ultrasound and understanding of pain and myofascial dysfunction were already part of my toolkit. Back in those days, all we knew about was trigger points and muscle pain. And as we became more nuanced, particularly in the regenerative medicine lens and under ultrasound examinations, then we started to differentiate into the sub-tissues. So the deep fascia, the epimysium, the perimysium that envelop as well as form the substance of the muscle and myotendinous tissue. Even looking at tendon — in those early days it was so primitive, we didn't even think tendons were something else to look at. Tendons, ligaments, joint capsules.
[09:33] And over the last couple of decades, with fascia research coming out, we talked about the lenses of what even connective tissue is and how it is defined. That's defined differently based on the lens of the professional studying it. At the Fascia Research Society, which I'm a part of, we look at fascia from the lens of function. So that starts to allow a lot of flexibility in what we include, and that includes nervous tissue that's embedded in a lot of the deep fascia diving in and out. It can also include bone.
[10:20] So as I was in parallel trying to understand and treat people with EDS, people with chronic pain, and also trying to understand what this hypermobility syndrome is, I started to see overlap. Starting to see, particularly with Dr. Columbi's paper on the myofibroblast transition and the integrin signaling system, I started to realize that it is likely that this fascial system is what is particularly affected — or possibly the source origin tissue that is pathologic in hypermobility syndromes. And so that started this investigation as I treated this population to start answering these questions.
[11:23] Of course, I would ask my co-researchers and people who were doing some of these original fascial studies, and they would respond to me basically saying, well, you should do the study. And I didn't want to do the study — it takes so much effort and time. But they would encourage me to start looking at these questions that I had and investigating them further. And sometimes the answer is so unclear and contrary to what we might think, it does take a lot of time after the data is collected to digest what might even be happening.

[12:07] Dr. Linda Bluestein: Yeah, I think most people don't realize how complicated research is, how much bandwidth you need in order to do it. And then nowadays it's crazy with people so often having to pay to get their paper published. Even people who are doing excellent research. I mean, we know that there are ways to get things published even if it's not great science. But it used to be — I feel like anyway — that if you paid to publish something, it was not necessarily good science. Nowadays I feel like it's just because we want things to be open access. I guess that's part of it, right? We want things to be available to the general public, which means journals are probably really struggling in this environment trying to make the information accessible and not just to subscribers.

[12:56] Tina Wang, MD: Yeah, it's such a challenge. Firstly, because when we have academic positions — and I have academic positions — we are expected as part of the professional environment and the job to publish. So these journals know it's really lucrative because our hands are tied.
[13:21] The other issue is exactly what you bring up. Even if it's a niche subject like EDS and HSD, you want to be able to give as many readers access as possible, because this is not going to be a big moneymaker for the journal. The people dying to get access to the research are more like our patients who are suffering and the providers who are trying to help this population. Those are the folks who are trying to get access to these papers, and we want to make it accessible to them. We don't want to make their life any more difficult than it is.

[14:07] Dr. Linda Bluestein: Yeah, I remember when I first was writing a paper with — I'm sure you know Pradeep Chopra, one of our colleagues — and I was writing a paper with him on the anesthetic and surgical implications of EDS. And in my mind, I'm thinking, oh, this is going to be in the New England Journal of Medicine, this is going to be like this big, important paper, because to me it was such an important topic. And there are so many undiagnosed people that are going into the operating room. And instead it was really, really hard to get that published. You don't realize, I think, until you actually are in that position how challenging it can be.

[14:43] Tina Wang, MD: Absolutely. There's a lot of discrimination and exclusionary behavior. What is published in the big journals is what's vogue. So you can imagine that when it's a smaller population, like those we work with, and they're disenfranchised and they don't have a large voice and there's not a lot of money to be made, then it's never going to be the cool thing to publish. And we then have to really struggle to get the publications out. It's the same thing that I've experienced with just fascia research without the EDS and hypermobility component. And you put the two together — my goodness, it's like we're heretics or something.

[15:29] Dr. Linda Bluestein: Yeah. Oh my goodness. All right, well, getting back to fascia — what are the histopathologic changes that you see in the fascia that lead to dysfunction?

[15:41] Tina Wang, MD: Yeah, so one of the earlier studies that I had conducted with Antonio Stecco, a fascia researcher — he had done one of the original papers and studies for his PhD showing that in people with head and neck pain, there is a thickening of the deep fascial layers. And for those of you who are not in science, or those of you who are but are not familiar with fascia research and nomenclature — which has also been developing over the last 10 years and is hotly debated amongst us at the Fascia Research Society, that's what we do at our conferences, we have scientific arguments — the deep fascia would be right underneath the skin, and it's this enveloping layer. And depending on whether it's in the limb or the torso, it can have different structures of organized tissue interspersed with less dense connective tissue. So it has specific structure. And then you'll run into the muscle layers. And sometimes between the muscle layers, you'll have another layer of deep fascia. So the name is misleading — it's not actually deep, but that's what we call it because we also have the superficial fascia. And we can talk more about that as well; I'm doing a study right now on that.
[17:10] But getting back to the deep fascia — Dr. Stecco found that the deep fascia is thicker in people with head and neck pain. And when I looked at people with HSD or EDS, that layer was even thicker. And I have access to elastography, which is wonderful, so I was also able to look at the stiffness of this deep fascia. What I saw was that in people without hypermobility syndromes, they tended to have a differential — so that would be the trigger points that we're feeling, or the stiff muscle underneath that we're feeling. However, in EDS, this stiffness differential is not quite there. It's a kind of uniform density. So this deep fascia is thicker, but we're not going to be able to always feel that trigger point. It doesn't mean that there isn't spasming of the muscle, but the overall elasticity of all the different tissues tends to be the same. And we need differential stiffness of tissue in different areas of our body for force transmission, holding our posture, and movement. So that was one of the initial studies showing that there's this densification.
[18:39] And the other pathologic change that we can see in connective tissue, regardless of whether there's EDS or not, is gliding. One of the landmark papers was by Dr. Helene Langevin — she's now at the NIH — and it was an amazing study on low back pain. She found that there was decreased interfascial gliding between muscle layers in people with low back pain. And so we did a follow-up study. It was a beast to do the calculations, just an absolute beast, really difficult. But we were able to show that there was a decrease in gliding in those with pain, but even more so in those with HSD or EDS — a 61 to 62% decrease compared to people with no pain, and a 48% decrease compared to those with knee pain without a hypermobility syndrome.
[19:49] So there's this densified, thickened tissue that's an issue, and there's improper gliding. And what we see then qualitatively is that there's going to be a strong muscular contraction as people with hypermobility try to force through this tissue that's not gliding properly. So you can imagine that if we're yanking really hard, there's a ligament tear, a tendinous tear, or a joint dislocation — as we're trying to properly transmit forces and the amount of gliding is changing on a daily basis depending on environmental conditions. There's more here, but I'm going to pause to let you ask some questions.

[20:41] Dr. Linda Bluestein: So this is really fascinating. And I guess the first thing I'm thinking of is, if there's densification of the fascia and if there's less gliding of the tissues, then it seems like you would be hypomobile and not hypermobile. And of course, we know that some people with joint hypermobility do have problems with muscle spasming, and so they can appear hypomobile, but I'm just trying to wrap my brain around the densification of the fascia and the less gliding, and how that actually would present clinically in someone who is hypermobile.

[21:20] Tina Wang, MD: Yes, it's one of the top questions I get at every scientific presentation. So what I liken this to starts at the joint itself. The joint itself and the surrounding connective tissue — the ligaments, the capsules — the integrity is not there. From changes in the fascial environment, from the hypermobility disorder itself, or from co-occurring conditions like MCAS or POTS. So the joint capsule and the tissues surrounding that joint are lax. And that can give you hypermobility. Depending on your ethnic and racial background, there are certain joint shapes, and that joint shape gives you your native range of motion. Then the capsules and the neurologic environment will limit how much mobility exists within that genetically given shape. So if that capsule and those ligaments are not strong, then you're going to be able to have much more range of motion within that structural joint you were born with.
[22:49] And if that capsule cannot hold you in — because that capsule isn't strong enough — for instance, in the hips and shoulders, those are big mobile joints where stability and mobility have to be really well balanced. And that's where we see a lot of dislocations, particularly the shoulder. If that tissue doesn't have integrity, you'll come right out of that joint because the tissue is not providing the structure to hold you in.
[23:23] So you can imagine that if you're not having proper transmission down the line for forces, and your muscles have to over-contract to force the glide and transmission of forces, then where the weakest point is, is where you're going to give out. So along the chain is where the hypomobility of the interfascial gliding is occurring. And where the hypermobility is occurring is at the joints themselves — where it is the weakest point that is overcompensating and moving more to try to allow for proper force transmission.
[24:14] There is a study I'm working on now, and in earlier studies we've seen this — there is less stiffening in the tendons and ligaments in EDS. And this will reduce force transmission because we need stiff tendons for the muscle to transfer forces. If those are not stiff enough, then you're going to really contract to try to transmit those forces, and then that force is going to come out through that weakened joint, and that's where you'll get your dislocation or hypermobility.

[25:01] Dr. Linda Bluestein: Okay, that's really fascinating. And I appreciate that excellent explanation. I'm probably going to have to go back and listen to that one again. It's such a unique way of thinking about how all of this comes together. So are those changes distributed symmetrically throughout the body, or do we see — I mean, I know you mentioned the hips and shoulders — are there parts of the body that are more impacted than others, do you think?

[25:45] Tina Wang, MD: Yeah, so clinically, I can tell you that they are. And there's research going back through the hypermobility literature that tries to tease out which joints are most affected. Those tend to be hips and shoulders. Clinically, if we're talking about fascial changes in the fascial system itself, I do see that there are chains that occur.
[26:19] And so when we work with an EDS patient, they'll say — and it really depends on your training framework, so you might call it a kidney qi line, or if you're a physiotherapist you might call it a posterior chain — but they'll tell me, "I can feel that right in the back of my neck," when I'm down at the ankle manipulating the tissue along the retrolateral chain along that retinaculum. And it's these type of clinical responses and feedback that tell me that these are the chains that are affected. They do tend to occur differently for each person, as well as differently based on their lifestyle — what they did over the past month, what they ate, what kind of stress they were under. Those will start to change some of the affected lines that I'm seeing clinically.

[27:38] Dr. Linda Bluestein: Yeah, I think that's one thing that's so fascinating about fascia — if I understand it correctly, it can be part of the explanation of why things that are felt in one part of the body are actually being caused by a different part of the body. I know people have talked about tongue tie being associated with craniocervical instability, and I'd love to know your thoughts on that as well. That is an example of an area where the fascial changes or fascial planes could affect symptoms elsewhere.

[28:14] Tina Wang, MD: Yeah, that area is intimately related to the anterior cervical fascia, which is then connected to the dura through the dural bridge. So that area is deeply connected. And that's where I tend to be really cautious in terms of approaches. So it's not wrong to get a tongue-tie release. However, we need to be cognizant of the entire chain that's being affected to make sure that we're addressing all of the differences along that chain. So that we're not promising patients, "Hey, you get this tongue-tie release and everything will be hunky-dory." It's more like, this area may need to be released, and then let's see how your system settles in and compensates. There is a chance things can decompensate and worsen. Don't panic — we'll address them if they arise.

[29:18] Dr. Linda Bluestein: Okay. We are going to take a quick break, and when we come back, we are going to talk about the role of fascia with pain.

[30:22] Dr. Linda Bluestein: Okay, we're back with Dr. Wang. We are learning so much about fascia; it's so fascinating. And we are definitely going to talk about pain shortly, but I want to start by talking about what the clinical manifestations are of fascial dysfunction. Can you run through that with us?

[30:39] Tina Wang, MD: Yes, it is a wild output feedback system. So what I most commonly hear from people with EDS is stiffness. There's a twisting. "I don't have freedom through this area." It's not spasms, it's stiffness. "I try to stretch, I try to work it out, I try to rub it out, and it doesn't go away." And it's pulling — that's the other adjective I'll hear. Pulling, stiffening.
[31:12] That is a common output from the fascia because the fascia is a sensory feedback system, but the deep fascia is not a fine-touch organ the way your skin is. So the brain will often have difficulty interpreting what is happening in that tissue when there's dysfunction. It'll spit out those kinds of sensations. Another common adjective is burning. "It's burning in there." Aching. Very common adjectives that we use and explore in fascia research when we are investigating fascially mediated pain.
The other common one — which I didn't find in my study, but that doesn't mean that it's not true — came from an older study in which they injected irritant into the deep fascia. What was found was that deep fascial pain is more radiating. I didn't find this so much in my study where I injected through the different layers as treatment. However, I still use that feedback when I'm treating patients. If they're telling me, "Oh yeah, when you touch there, it's radiating," that is the brain saying, "I'm not certain where exactly this is, because it's not skin, but boy, does it seem to affect this area." So your brain is trying to make sense of pathology in a system that is not innervated for fine touch.

[33:06] Dr. Linda Bluestein: Okay, so things that we tend to think of for, for example, neuropathic pain — being radiating, burning — actually could be coming from fascia. Sounds like.

[33:17] Tina Wang, MD: Yeah, it definitely can be. In a study I had done — injecting not exclusively EDS patients, but some of them were — 73% of this quote-unquote myofascial pain originated with the deep fascia. So it was in different combinations: in the muscle tissue itself, with the superficial fascia. With these different combinations, the deep fascia was also responsible for pain generation in 73% of these different pain areas that were injected. The superficial fascia came next at 55% — and that's the fatty layer that envelops some of that connective tissue. And then the muscle at 43%. So it doesn't mean that we don't treat the muscle or forget about the muscle. It's just that these are all different tissues where pain can also arise in addition to the nerve.

[34:22] Dr. Linda Bluestein: And in terms of evaluating somebody and getting worked up — we know part of the challenge with people with hypermobile EDS and HSD in particular is that they get lab testing or imaging if they're lucky enough to get that. Sometimes they don't even get that. And of course, most of the time it's unremarkable or not helpful, right? So how do you assess, or — maybe two questions — how do you assess in your practice, and what can people potentially ask for if they're not able to come and see you?

[34:57] Tina Wang, MD: Yes, that's one of the toughest parts without a physical examination. That physical examination is so important, so critically important. And one of the big things I know that you and I look for are the red flags. We have to make sure that the cervical instability — and not just cervical instability, that's the term we commonly use, but there can be spondylosis or just degeneration throughout that is pushing on the spinal cord — we have to make sure that we're catching these. These are really, really important. And we know that there's a lot of brain injury in EDS from the poor proprioception. So we have patients who are running into walls, like I do all the time. Even when I'm doing my therapy, I'm running into walls, tripping over things. And these are big traumatic events to the neck. We have to make sure that we're catching these and monitoring that spinal cord, making sure that spinal cord is healing. And if not — if it's so degenerative in there — then we have to send our patients to the surgeons to get that cleaned up and stabilized.
[36:17] So that's the first thing I'm always thinking about in this population: am I missing something big? Because it's so easy to dismiss when a patient is in chronic pain and when there's a lot of autonomic dysregulation and the patient is really suffering. It's so easy to dismiss our patients and say, oh, here you are again. So that physical examination is critically important to look for those upper motor neuron changes, as well as the lower motor neuron changes — the objective weakness, not "I feel a little bit weaker." Clear signs of any atrophying muscle wasting in a myotomal pattern. Those things really have to be caught. And that's where the imaging really comes into play and supports us. If it's clean, then we can move on to conservative treatment. Then we can start to look at what are the fascial components that are being affected, what are the fascially-based approaches that can be taken.
[37:36] And that is really hard to find because we're still sitting at the forefront of translational research from fascia research into clinical practice. In my university-based practice, I am teaching my PM&R residents how to start to treat the fascial system and investigate and examine the fascial system. But this is still hard to find because it is at the forefront of that translational process.

[38:10] Dr. Linda Bluestein: So in your practice, you're doing a detailed physical exam, of course, as you were just describing. And then are you doing ultrasound of specific areas as well where you suspect that there's more fascial dysfunction?

[38:25] Tina Wang, MD: Yes, I am. And part of that is guided by the normal values that we have in research. It's guided by the areas that I have researched, and then it's guided by the additional areas that are being researched — particularly a lot of our normal values come out of the Stecco Lab. And once we have some normal values, we can start to use them in clinical practice as well. So those are the areas that I might look at for deep fascial densification.
[38:59] I'm also looking at tendon stiffness. I'm still in the midst of all the data coming out of that work. What I'm looking at is the appropriate loading of the tissue. So if we're loading in a certain manner, how stiff is that tendon compared to normal values out in the population and compared to people who might be loading the tissue in a different way? A good comparison would be low, long loads versus quick plyometric loads. The tendon, we know from the research, should be very different in quality. So looking at that and the cross-sectional data — am I seeing this in my EDS patients? And then looking at the tendon stiffness of the patient in front of me and guiding the load for rehab that I want this patient to engage in, because it's not all uniform. I'm finding some surprising results as well. Post-surgery, there are changes. So maybe in that tissue, you don't want long loads — maybe you want a little bit more plyometric. So looking at these asymmetries, I'm starting to guide patients that way, but I'll be able to guide them better once the study is completed.

[40:36] Dr. Linda Bluestein: And I've noticed in a lot of my patients that many of them really have difficulty getting muscle hypertrophy, and I'm wondering if that's part of it — if you're not able to get that load through the tissues, maybe that's why some people have so much difficulty with getting muscle hypertrophy, and then that doesn't provide the protection of the joints and the joint capsule that we need. Is that fair to say?

[41:02] Tina Wang, MD: Yeah, absolutely. And if there's overworking because of the improper dispersion of forces as they are trying to get hypertrophy, then you might see a breakdown of tissue. In addition, there's difficulty with neuromuscular activation because of the pathology found in the tissue and the feedback system. So we can release the tissue either with a needle, with injectate, or with fascial manual work. But if we're not retraining the brain and the force transmission and doing it with properly prescribed load amounts, then we may never get that patient to where they want to be. And then of course, there's so much GI involvement, so that even if we're taking in tons of protein, it may not be absorbed either. So there are just so many factors.

[42:07] Dr. Linda Bluestein: Yeah, exactly. That makes sense. So in terms of pain, how does fascia contribute to pain?

[42:17] Tina Wang, MD: Yeah, so we talked a little bit about that study I had done previously. And in the anatomical work looking at fascial innervation, prior studies by Menz out of Germany found that 40% of the deep fascial system's innervation consists of postganglionic sympathetic fibers. So 40%. And it seems to be the case throughout the innervation — we often think of these C fibers. If people have listened to the talk by Fraser Burling, he talks about these unmyelinated fibers, and they are often responsible for pain. And we can't test for them directly because they're unmyelinated — just difficult to test under EMG or NCS, nerve conduction studies. And these unmyelinated fibers, 40% of that nerve supply, are sympathetic.
[43:31] So you can imagine that if you are stressed out — and it's not all coming from your head, it's your body's response — if you have an injury, or you're having digestive issues, because 90%-plus of that gut innervation is sympathetic, then you're going to start to see changes in the deep fascia. And it's not just one way. It's not just receiving sympathetic input. It's also the expression of the sympathetic response into that deep fascial tissue. So you have both a sensory response as well as a sympathetic response in this tissue. And you'll see that even with people without EDS — they'll tell you how much worse their pain is when they're stressed out.

[44:26] Dr. Linda Bluestein: Yeah, that's super interesting because I think that definitely happened to me when I was at my worst. And I was led to believe — and I also thought this myself — like, oh, that must mean that I'm imagining things, because if my pain gets worse when I'm stressed, then is my pain real? I'm sure you get asked that too, by family members and things like that. So that's really fascinating to have a pathophysiologic explanation for why psychological stress could make our pain worse, rather than just thinking that we're not psychologically strong enough.

[45:07] Tina Wang, MD: Yeah. And it influences not just the innervation — the input and output of the fascial tissue — but also the fibroblasts and the myofibroblasts respond too. So in a separate study we did in collaboration with Robert Schleip, one of our big, well-known Fascia Research Society rock stars — his original research found that if you bathe the fascial tissue in TGF-beta for longer durations, more than an hour, you start to see contraction through the tissue. So if you talk about feeling stiff and pulling sensations, this change related to TGF-beta is really one of the possible sources of that. I can't say it's causative, but it could be.
[46:04] And in that study we did together looking at the abnormal gliding of tissue in EDS, he and his colleagues found that there were myofibroblasts present — and not in the subjects without HSD and abnormal gliding. So really a possible source of these pain and dysfunctional sensations that we all feel in our body.

[46:30] Dr. Linda Bluestein: And could that also explain the pain-begets-pain type of phenomenon that we often see?

[46:41] Tina Wang, MD: Yeah, it's a vicious feedback loop. You're releasing this TGF-beta, myofibroblasts are now spitting out all this dysfunctional tissue and then signaling to our mast cells. And then as it's laying out all this dysfunctional tissue as well as other inflammatory mediators, our allergic responses or our inflammatory responses start to go out of control. And then our POTS starts going out of control and then we start feeling worse and then more TGF-beta is released and we're in this vicious cycle.
[53:24] And I know that in the earlier days at the EDS Society, I was really anti-steroids. But after talking to you all, it's like, well, yeah, I think there is a place where we sometimes just have to blast the cycle and interrupt it.

[53:24] Dr. Linda Bluestein: And when you're talking about steroids, are you talking about steroid injections or systemic ones?

[53:24] Tina Wang, MD: Yeah, systemic is what I turn to if I really can't stop somebody's cycle. And we'll see that where all the co-occurring conditions start to flare out of control — so now the gut's out of control, the pain's out of control, the brain fog, the dysautonomia, dislocations. And when I'm unable to break this cycle with any of our tools — with manual therapy, with injections, whatever it is — then we turn to steroids, at the great protest of patients because none of us like being on steroids.

[53:24] Dr. Linda Bluestein: And before we get into other treatment options, I just want to talk about a couple of other specific examples. So with TMD, or temporomandibular joint dysfunction, of course we know that that's also in the vicinity and can affect upper cervical instability and things like that. And then another area I'm thinking of is this whole coat hanger pain phenomenon that we see so commonly. What kind of role does fascia play in those two specific phenomena?

[53:24] Tina Wang, MD: Well, it's not fair because I'm a fascial researcher, so I'll tell you everything is fascia, right? And if you talk to a neurologist, they'll tell you everything is nerves. So I think it's intimately related. And those of us who use manual therapy or injections or treat the fascia will tell you that to properly and effectively treat the TMJ when there's TMD present, we have to treat along the fascial system. So oftentimes we're going into the arms, we're going into the chest. And then the same thing with the neck — there was a great paper out by Jan Wilke a few years ago, and he released the ankle and improved neck range of motion. So I'm always going down into the ankle. And then my osteopath colleagues will tell me the pelvic floor and jaw are intimately related. So then going into that pelvic area.
[53:24] So really looking at the whole body, especially if your TMD is just so hard to control. And then talking to my colleague Rebecca Griffith, who trains with me in osteopathy, she will tell me that it is just a beast to treat. Years of sessions and adjustments, with the safety of the autonomic system and the protection of the airway being a huge part of it. So I'm always looking at sleep apnea and airway control in my patients with this dysfunction.
[53:24] And then, finally, balancing cervical stability with the TMD. Some of my colleagues who don't do research but who are amazing clinicians in other countries will tell me that their patients' dysfunctions really started to arise after orthodontic treatments. So we willy-nilly go and try to straighten those teeth — we want them to look great — but perhaps they are crooked because they are compensating for other dysfunctions. So if we go and force that jaw into a certain position, and that jaw is most likely compensating for dysfunction, then we create more stress on these other areas that are dysfunctional — namely that craniocervical junction, that upper cervical area. And so we have to be cautious when we're treating to really balance people's dysfunction. I always tell my patients that they're perfectly dysfunctional the way they are.

[53:24] Dr. Linda Bluestein: I love that, because I think too often we hear that parts of our body are asymmetrical or there's some dysfunction somewhere. And of course, that also can plant a seed that can sometimes be not very helpful for us. So I love that line that you use.

[53:24] Tina Wang, MD: Yeah, it drives me nuts when we'll hear that — particularly from patients who work with providers who are not EDS aware, and they'll try to force them into a posture. It's like, no, that posture is compensating for something. And yes, over time we would like to see improvement in that, or a little bit more symmetry. But my osteopathic teacher, Dr. Jealous, would always say, there is more health in the lesion — or as we say, dysfunction — than there is lesion in the lesion. There's more health. It's compensating. It's keeping us alive. It's keeping us functional. So let's not go messing with it too much. It doesn't mean we don't treat you, but we also don't shoot for this idealized version of perfect that exists nowhere.

[53:24] Dr. Linda Bluestein: And I want to make sure to talk about treatment a little bit before we wrap up here. So you mentioned myofascial release, and probably a lot of people have experienced this and have gotten some benefit. Maybe it's not sustained necessarily, because I know that's definitely happened for me personally — it feels wonderful at the time. Are there certain contraindications? How does that differ from just like deep tissue massage? And is this something that we should be doing on ourselves? I know that's a long question, and I have a couple other treatment-related questions, but we can start with that one.

[53:52] Tina Wang, MD: Yeah. And if I don't answer part of that, just feel free to ask again. So very common question. I always tell people there's a three-pronged approach. Of course, when you and I treat EDS and our colleagues treat EDS, it's much more complex — we're taking so many more factors into consideration. But this is really meant to guide the patient who doesn't have all those years of training. So keeping it simple: it's three prongs.
[54:30] One is manual therapy. One is movement therapy — you have to load that tissue and you have to load it properly. The fibroblasts respond to load. They're alive. The Nobel Prize was on the tenocyte piezo receptors' response to loading and how the tendons stiffen in response to proper loading. So this is crucially important. And then the third one is your team of medical professionals, which also includes integrative health folks. So if you have an herbalist that you work with, an Ayurveda doctor, your primary care, your surgeon, your psychiatrist, your psychologist — they all fall into that medical group.
[55:19] But I also want you to really think about the manual therapy and the movement. You can't have a lack of any of these pillars. If you are not caring or being attentive to any of these pillars, then the care will be lopsided. It doesn't mean you need to give them all equal attention, but care needs to be given. And as I've heard Alan Hakim say, as your condition starts to pacify or improve, or even recede — which is possible — then the amount of attention you put into the pillars will lessen, and the amount of intensity you need to spend seeing these professionals will also lessen. And that's where home care is super important too, and self-care.
[56:19] So in terms of the manual therapy component: it's going to be difficult to find someone who thinks in a fascial chain kind of framework. They're out there. And from the advocacy work that you've done and the EDS Society has done over the last five years, I've seen an explosion of providers out there who are highly skilled. So finding one of these people who knows how to work with HSD/hEDS will be a first step.
[56:56] If you can't find that, then finding someone attentive. This might be an acupuncturist working manually with needles on your tissue. It might be a massage therapist. It might be a structural integrator — the newer terminology for Rolfers; they don't consider themselves massage therapists. It might be an osteopath, a chiropractor, a physiotherapist or physical therapist who does manual therapy. And this is one of my passions — teaching massage therapists how to approach people with HSD and hEDS, because they are the first line. One of the earlier studies showed that 81% of people with these conditions seek out manual therapy, and 84% who do, do well with it.
[57:56] So when you go, just make sure that it's a short session, it's light. You have to see how your body responds to it. In my early years, Antonio Stecco said, "Oh yeah, if you treat too many points, some people get fevers." I said, what are you talking about? And then I started treating people with EDS, and not only do you get fevers, you get dysautonomia, you get diarrhea, you get brain fog spells. I had a patient who went to sleep for, gosh, 24 hours. You can imagine the panic I had.
[58:37] So being very cautious with your first couple of sessions with the manual therapist — whatever their background — so that they can get to know you and you can get to know your response, seeing how long it lasts. And then as you start to get your treatment plan together and you get to know your provider better, then you can start to explore more aggressive treatment. If you're a person who does really well with deep tissue — which is not that many people; many people think they do well and then they'll tell me, "Oh no, actually when I pay attention, there's a huge flare-up afterwards" — so really knowing how your body responds and then starting to explore different depths of tissue treatment modalities.
[59:19] And as you work with this person, that's the person you can ask, where do I treat at home for homework? I don't want to see you every week; I want to see you every two weeks or every three weeks. So what can I treat in between sessions? And I will show my patients where to treat. I do not recommend indiscriminately going at your tissue. You will injure yourself. You will destabilize points. And I also absolutely do not recommend — I had a patient who did this — going and getting the textbooks and deciding where you're going to treat. You're really going to destabilize yourself and it's going to be a mess. So really finding a trusted provider and working with that person on where to treat. And the same goes for the loading — really working with somebody who will slowly get to know your body and how to properly load your tissues so that you can tolerate it.

[1:00:34] Dr. Linda Bluestein: Yeah, because sometimes it's so hard to tell while you're actually doing the activity if it's too much. Even for me, it's very hard to tell at that time. And I have one last question on treatment — well, I shouldn't say quick, we could probably do an entire podcast episode on this question — but before we move on to the hypermobility hack and close up: regenerative medicine. This is something that I get asked about all the time. I don't perform these procedures, but I'm always looking for options for people. In terms of prolotherapy, PRP, cell-based injections, things like that — do you have any thoughts you're willing to share?

[1:01:14] Tina Wang, MD: Yeah, absolutely. I do the prolotherapy and the PRP, and so does Fraser Burling in our EDS ECHO. So we're often collaborating or having conversations about it. At the EDS Society's last conference, we gave a fascial-based talk together. And the idea behind the prolotherapy and the injectate using PRP or tetradecyl or dextrose is that we are stimulating the fibroblasts or the tenocytes — which are specialized fibroblasts in the tissue — to lay down more tissue. And after these injections, we really need you to load the tissue properly. So working with your movement professional is important, because now that we've stimulated the tissue and the cells, we need that tissue to lay down properly and with proper strength. So the loading is really important. Oftentimes when people come to see me for it, I will recommend that if they're not getting an injection in that session, they please start their physical therapy or movement therapy with their professional in preparation for the injection.
[1:02:33] What I've heard from my colleagues is that working with someone who is EDS aware is important because how we're all taught to inject — most of us are taught through the Hackett-Hemwall Foundation, both Fraser and I were — the protocol as taught is to inject a variety of tissue, and we do not do that with EDS. It has to be targeted and pinpoint. This tissue is fragile, and we know MCAS is occurring in a lot of our patients. So we have to be cognizant of how many times we're sticking them into that tissue surrounding the joint.
[1:03:27] Again, with the manual therapy, we saw that fever response and that dysautonomia. So we're trying to reduce that reaction. The other thing to be cognizant of is the mast cell flare-up. To people's dismay, I will turn them away if the mast cell activity is not under control. It doesn't matter what they say to me — it has to be under control.
[1:03:58] The other thing: in my early years, I would take patients off all sorts of medications. Take them off this, take them off that, because "this doesn't promote healing, can't be on the fish oil." Now I want my patients controlled. I want them on their medications. Do not come off your medication, because those medications and supplements are modulating your immune system. And I want you to go into this injection with your immune system properly modulated for the best response. It's a long way to come see me. It's a lot of time, it's a lot of effort, and I don't want to waste your time. I want you to have the best response, especially if you're going to sit through a session like that.

[1:04:50] Dr. Linda Bluestein: Yeah, it used to drive me crazy when some of my colleagues would just indiscriminately tell people to stop all their supplements — well, they still do — preoperatively, right? And it's like, people might have their migraines extremely well controlled with magnesium or some other supplement, and it's just, "No, stop everything." But there are specific guidelines that you can use to be very specific about what supplements need to be stopped for what surgery. And when we don't take a little bit more time and slow down and think, it can be very frustrating. Yeah, absolutely.
[1:05:26] I like to end every episode with a hypermobility hack, and you could probably give us hundreds of these — but what hypermobility hack would you like to share with us?

[1:05:35] Tina Wang, MD: Yeah. When there is a joint that is unstable and you just can't seem to get it back into joint with all your tips and tricks, what I recommend is first — always try to calm down that nervous system. Because there's a great sense of panic, or frustration — like, I don't have time for this. So I encourage you to first just collect yourself, do some breathing, long exhales, to get your nervous system under control. And you'd be surprised how that's 90% of the battle — fighting that nervous system. So just giving your nervous system a little break, a minute or two of extended long exhales.
[1:06:31] Then think in opposites. So if it's your shoulder and you're trying to shove that shoulder back in, you might go to the other side and try to release something there, stretch that out a little bit. Or you might think far away — so you might go into the hand and stretch the hand out a little bit and see if the joint doesn't just reduce itself, come back in.

[1:07:02] Dr. Linda Bluestein: Okay, I like it. And before we wrap up, of course, we also need to know where to find you. I just am so grateful to you for coming on the podcast today and sharing your vast knowledge and wisdom with us. It's been such a great opportunity to finally chat with you. I've wanted to do this for such a long time.

[1:07:24] Tina Wang, MD: Thank you so much for having me on. You can find me at my website, tupelopoint.com. I'm not so active on my social media, but you can also find me there. I do try to post periodically — I'm a deep meditator and yoga practitioner, so I try not to spend so much time on social media, but I will occasionally post there. It's still alive. It's Tupelo Point, or Tina J. Wang. There are two of us, so you can find information there.
[1:08:02] I will be having a book on this science as it pertains to EDS coming out. I'll probably self-publish it so I can update it as the science continues to move at such a fast pace. I will post to social media as well as on the website when it's out.
[1:08:25] I'm also on the board of the Fascia Research Society. If you'd like to learn more about fascia specifically and all the dense science that comes with it, I encourage you to join, or to come to our Congress, or to submit your work for presentation. I'm on the scientific committee and I'd love to see some of you present your work at the Congress — that will be next year in New Orleans.
[1:08:57] And I just want to really thank you, Dr. Bluestein, for all of the advocacy and this social media outreach work that you do, because us cerebral types really have a hard time with this extroverted activity. So really, just a million thanks for doing this on all of our behalves and advocating for all of the scientific and medical work that all of us are doing — you're the face of it. Thank you so much.

[1:09:38] Dr. Linda Bluestein: Oh, well, I really appreciate those extremely kind words. And it's one of those things where we know that not everyone can travel to come see you or come see me. And I felt like this was a good way to reach a large number of people, because we know the number of people that are suffering and that are impacted by these conditions is just vast. So, thank you so much again. This was a long time coming. We'll have to have you back on once your book is out and be able to dive deeply into that. And I'm sure people will be very excited to get their hands on the book.
[1:10:23] I'm sure you know Jill Miller — yes — so I've had Jill Miller on the podcast twice, and I have her book actually on the shelf behind me, and she's brilliant as well. So I think maybe that's part of being in the fascia space: you have to be a certified brilliant person. I'm just grateful to you for taking the time to come and talk to me today.

[1:10:43] Tina Wang, MD: Absolutely. Thank you so much for the opportunity.

[1:10:47] Dr. Linda Bluestein: Well, that was such an excellent conversation with Dr. Wang, and I hope you enjoyed it as much as I did. Fascia research has come such a long way from when I was in medical school and we just saw fascia as something to be discarded — you just kind of quickly got through it in anatomy dissection, threw it in the trash, and went on to the muscles and tendons and things like that. So it's really, really fascinating to hear how fascia is involved in conditions like EDS and HSD.
[1:11:19] And I want to thank you so much for listening to this week's episode of the Bendy Bodies Podcast. I hope you found it informative and empowering. If you loved what you learned, follow the Bendy Bodies Podcast on your favorite podcast player and subscribe on YouTube where full video episodes are released each week at Bendy Bodies Podcast. Visit bendybodiespodcast.com to access transcripts, show notes, or leave us a message. Please help spread the word about joint hypermobility and related conditions by leaving a review and sharing the podcast.
[1:11:52] If you'd like to meet with me one-on-one, check out my available service options on the services page of my website at hypermobilitymd.com. You can find me, Dr. Linda Bluestein, on Instagram, Facebook, TikTok, Twitter, or LinkedIn, all with the handle hypermobilitymd. You can find Human Content, my producing team, @humancontentpods on TikTok and Instagram. To learn about the Bendy Bodies Program disclaimer and ethics policy, submission verification and licensing terms, and HIPAA release terms, or to reach out with any questions, please visit bendybodiespodcast.com. Bendy Bodies Podcast is a Human Content production. Thank you so much for being a part of the community, and we'll catch you next time on the Bendy Bodies Podcast.