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

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Dr. Linda Bluestein: [00:00:00] 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 fashion researcher and physical medicine and rehabilitation doctor. When I was having so many problems with persistent pain, I kept hearing over and 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 [00:01:00] EDS and HSD?

And how can we treat things like myofascial pain? 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.

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.

All right. Super excited to chat with Dr. Wang today. [00:02:00] Dr. Wang, can you start out by telling us why fascia is such an important topic for hypermobile EDS? Yeah. 

Dr. Tina Wang: Yeah. Um, fascia. is likely the organ or the originating organ that is affected in connective tissue disorders like Ehlers Danlos Syndrome and hypermobile 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 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.

Dr. Linda Bluestein: Okay, Annette, you might have already answered this question a little bit, but for the purposes of this conversation today, can we talk [00:03:00] about connective tissue disorders in general, or do we need to separate hypermobile EDS versus HSD versus other connective tissue disorders? 

Dr. Tina Wang: It really depends on the lens of the scientists you speak to.

So depending on if you're speaking to, um, even camps of geneticists where they may or not, may or may not agree that HSD and HEDS are, uh, the same condition with different phenotypic manifestations or if they are within the same type of pathologic manifestation. Um, so there's also debate within those who work with EDS as well as geneticists.

And then if you speak about things on a microscopic level, on a small organ [00:04:00] tissue level, looking at the cells, looking at the, um, extracellular matrix, then you would have a different lens and you may or may not, um, then speak about hypermobility, EDS, HSD, as well as other fibrotic conditions, 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. 

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 [00:05:00] 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.

Dr. Tina Wang: 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 that also includes collagen, those then start to go awry. They become Myofibroblast is a transition into a more pathologic state.

And so we know these things occur, uh, we can't say that if that's the initiating event or if the extracellular environment, let's say, for instance, mast cell or even [00:06:00] being bathed in chi gene. TGF beta from stress responses, um, either psychological or physical. Uh, we can't say if any of these things are causative, rather we know that they're associative.

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. 

Dr. Tina Wang: Yeah. Um, well, the story is, um, much like you, I started working with performing artists and performing artists have [00:07:00] a higher, um, occurrence We find that they have a higher occurrence of either asymptomatic hypermobility or symptomatic hypermobility.

So many years ago, as a young student, this, these were the questions we started to ask ourselves. And I know that you were part of that conversation too. And it's such a mixed bag because hypermobility itself does not confer a risk. And that's, that was a bold statement back there, Ben. And then we would say, well, then 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 and what a risk for injury or a risk for, um, comorbidities. So then we have to go looking into [00:08:00] subpopulations. And then from working with performing artists, then started to dig into this world of hypermobility in general.

Um, I'm also a trained PM& R physician, so ultrasound and understanding of pain and myofascial dysfunction. So 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 parimysium that envelop as well as or substance of the muscle and myotendinous tissue. Um, even looking at tendon. So even those days, it was so primitive. We [00:09:00] didn't even think tendons were something else to look at. Tendons, ligaments, joint capsules, and over the last couple of decades with fascia research coming out.

So again, we talked about the lenses of what even connective tissue is and how that is defined. And that's defined differently based on the lens of the professional studying connective tissue and fascia. And at the fascia research society that I'm a part of, uh, where we look at fascia from the lens of function, So then this starts to have a lot of flexibility of what we include, and that includes nervous tissue that's embedded in a lot of the deep fascia diving in and out.

Um, it also can include bone. So as I was in parallel trying to understand and [00:10:00] treat people without EDS, people with chronic pain, and then also trying to understand what this hypermobility syndrome is, and then starting to see overlap. Um, I started to see that this is likely particularly With Dr.

Columbi's paper on the myofibroblast transition and the integrin signaling system, I started to realize that, um, 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.

Of course, I would ask my [00:11:00] 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. So I don't want to do the study. It takes so much effort and time, but they would encourage me to, um, start looking at, uh, the, 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. 

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 actually so often having to pay to get their paper published, you know, it's like.

And even people who are doing [00:12:00] excellent research, I mean, we know that there's ways that you can get things published if you're, even if it's not great science, but it used, I feel like anyway, it used to be that if you paid to publish something, it was not necessarily good science. But 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 that we end up, you know, Uh, you know, journals are probably really struggling in this environment and trying to make the information accessible and not just to subscribers. 

Dr. Tina Wang: Yeah, it's such a challenge. Um, firstly, so because, um, when we have academic positions, so I have an academic positions, we are expected as part of the professional environment and the job to publish.

So then these journals know it's really lucrative because we're, our hands are tied. Um, the other issue is exactly what you bring up. Even if [00:13:00] it's a niche Subject like EDS and HSD, you want to be able to give as many readers access because this is not going to be a big moneymaker for the journal for people dying to get access.

to many people dying to get access to the research. It's more like the, 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.

more difficult than it is. 

Dr. Linda Bluestein: Yeah. I remember when I first was writing a paper with, I'm sure you know, uh, Pradeep Chopra, one of our colleagues, and I was writing a paper with him on the anesthetic implication 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, you [00:14:00] know, You know, big, big paper, because it's such, to me, it was such an important topic. And there's so many undiagnosed people that are going into the operating room. And instead, it was really, really hard to get that published. And you don't realize, I think, until you actually are in that position, how challenging it can be.

Dr. Tina Wang: Absolutely. There's a lot of discrimination and exclusionary behavior. And what is published in the big journals are what's Vogue. So, you can't 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. It's the same thing that I've experienced with just fascia research without the um, EDS and hypermobility component. And you put the [00:15:00] two together, my goodness, it's like we're a heretic or something. 

Dr. Linda Bluestein: Yeah. Yeah. Yeah. Oh, my goodness. All right. Well, getting back to fascia. So, what are the histopathologic changes that, uh, that you see in the fascia that lead to dysfunction?

Dr. Tina Wang: Yeah. So, the, one of the earlier studies that I had conducted with Antonio Stecco, a fascia researcher, we found that he, so he had done one of the original, um, papers and studies for his Ph. D. showing that. In people with head and neck pain, there is a thickening of the deep fascia layers, and for those of you, um, who are not in science, or those of you who are, but are not familiar with fascia research and nomenclature, which is Also been developing over the last 10 years, um, and is hotly debated amongst us at the Fascia Research Society.

That's what we do at our conferences is, um, have scientific arguments. [00:16:00] So the D fascia would be right underneath the skin. And it's this enveloping layer and depending on the, if it's in the limb or the torso, it can have different structures of, uh, organized tissue, um, interspersed with, uh, 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, the name is, uh, misleading. It's not deep, but that's what we call it because we also have the superficial fascia and what we can talk more about that, um, as well.

I'm doing a study right now on that, but getting back to the deep fascia, Dr. Steko 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 [00:17:00] even thicker. 

Dr. Linda Bluestein: And 

Dr. Tina Wang: I have access to elastography, which is wonderful. So I was also able to look at the stiffness of the muscle of this deep fascia.

And what I saw was that in people without hypermobility syndromes, they tended to have a differential. So that would be the trigger point. that we're feeling, or the, the stiff muscle underneath that we're feeling. However, in EDS, this stiffness differential is not quite there. So it's kind of the same uniform density.

So this, this deep fascia is thicker, But we're not gonna 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 [00:18:00] of tissue in different areas of our body for force transmission, holding our posture, movement.

So that was one of the initial studies showing that there's this densification. And the other pathologic change that we can see in connective tissue, regardless of if there's EDS or not, is gliding. So that in, um, and one of the landmark papers was by, uh, Dr. Elong Langevin. Um, she's now at the NIH and it was an amazing study on low back pain.

And she found that there was decreased gliding, interfacial gliding between muscle layers. in people with low back pain. And so we did a follow up study. And 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 [00:19:00] those with pain, um, but even more so in those with HSD or EDS.

So 61, 61 to 62 percent decrease compared to People with no pain and 48 percent decrease compared to those with knee pain without hypermobility syndrome. 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.

fight through this tissue that's not gliding. There's still force transmission, so you can imagine then That if we're yanking really hard, then there's a ligament tear, a tendinous tear, or a joint dislocation [00:20:00] as we're trying to properly transmit forces and the amount of gliding is changing on a daily basis.

depending on the environmental conditions. Um, and there's more here, but I'm going to pause to let you ask some questions. 

Dr. Linda Bluestein: So this is really fascinating. And I guess the first thing I'm thinking of, if there's densification of the fascia and if there's less gliding of the, of the tissues, then it seems to me that you would be hypomobile and not hypermobile.

And of course we know that some people with joint hypermobility do have problems, like you said, with the muscle spasming and so they can appear like they're hypomobile, but I'm just trying to wrap my brain around the densification of the fascia and the less gliding and if they are hypermobile, how that actually present clinically.

Dr. Tina Wang: Yes, it's, it's the, one of the top questions I get every, [00:21:00] um, scientific presentation I get. So, um, and so what I like in this too is, um, the, starting at the joint itself. So 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 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. So that 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 [00:22:00] will then limit how much mobility that's within that genetically given shape that you were given.

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 that you were born with, that shape you were born with. 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. And so if that tissue doesn't have integrity, you'll come right out of that joint because that tissue is not providing that structure to hold you in because the, the, those joints are pretty shallow.

And so you can imagine that if you're [00:23:00] 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 where you're going to give out. So along the chain, not along the joints, is where the hypomobility of the interfacial 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, contracting more to try to allow for proper force transmission. There is a study that I'm working on now, and in earlier studies we've seen this. Again, the research was mixed in early years, but there is a, [00:24:00] um, less stiffening in the tendons and ligaments in EDS.

And this will reduce force transmission because we need stiff tendons for that muscle to transfer forces. And 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 somewhere through that weakened joint. And that's where you'll get your dislocation or hypermobility.

Dr. Linda Bluestein: Okay. That's, that's really, really fascinating. And I appreciate that excellent explanation. Probably going to have to go back and listen to that one again. It's, it's, it's such a unique way to me of, of thinking about how all of this comes together, really. Um, so it's really, really fascinating. And, and are those changes distributed symmetrically throughout the [00:25:00] body, or do we see.

I mean, I know you mentioned the hips and shoulders, and I definitely, the shoulders especially, like you said, being a shallow joint and having such excessive or having such wide range of motion, even in a, you know, normal, the normal shoulder, right, is supposed to have incredible range of motion. Are there parts of the body that are more impacted than others, do you think?

Dr. Tina Wang: Yeah. Um, so clinically I can tell you. that they are. And then there's research going back through in the hypermobility that tries to tease out which joints are most affected. And those tend to be hips, um, shoulders. Um, clinically, if we're talking about fascial changes, In the fascial system itself, uh, clinically, I do see that there are chains that occur.

And so when we work with the EDS patient, they'll say, okay, yeah, when I'm down at the ankle, [00:26:00] let's, let's say I'm working on the, uh, one of, and it really depends on your training framework. So you might call it a kidney chi line, or if you're a physiotherapist, you might call it a posterior line or posterior chain.

So when I'm down at the ankle and I'm manipulating the tissue using a retro lateral chain along that retinaculum, they'll tell me I can feel that Right in the back of my neck. And it's these type of clinical responses and feedback that tell me, Oh yeah, that these are the chains that are affected. Um, and they do tend to occur differently for each person.

as well as differently based on their lifestyle. So what did they do when they went out for the next [00:27:00] month? What did they eat? What did they subject themselves to? What kind of stress they were under? Those will start to change some of the affected lines that I'm seeing clinically. 

Dr. Linda Bluestein: Yeah. I think that's one thing that's so fascinating about fascia is if I understand it correctly that it 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, right?

So I know people have talked about tongue tie being associated with craniocervical instability and I'd love to know your thoughts. on that, um, as well. So that is an example, right, of an area where the fascial changes or fascial planes could affect symptoms elsewhere. 

Dr. Tina Wang: Yeah, that, um, area is intimately related to the anterior cervical fascia, which is then connected to the dura [00:28:00] through the dural bridge.

So that area is deeply connected. And that's where, um, I, 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, look, you, you get this tongue tie release and everything will be hunky dory and amazing.

It's more like, look, 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. 

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 [00:29:00] pain.

Okay, we're back with Dr. Wang. So 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? 

Dr. Tina Wang: Yes. It is, um a wild output feedback system.

So what I most commonly hear from people with EDS is there's stiffness. There's a twisting. I don't have a freedom through this area. It's, it's not spasms. It's stiffness. I try to stretch or try to work it out. I try, try to rub it out and it doesn't go away. And it's pulling. That's the other adjective all here.

Pulling, stiffening. That is a common output system from the fascia because the fascia [00:30:00] is a sensory feedback system, but it's the, the deep fascia is, but it is not a fine touch organ like your skin is. So the brain will often have difficulty interpreting what is happening in that tissue when there's dysfunction.

So it'll spit out those kinds of sensations. Another common, um, adjective is burning. It's burning in there. Um, aching. So very common adjectives that we'll use and explore in fascia research when we are investigating The other common, um, which I didn't find in my study, but it doesn't mean that it's not true.

There was a, um, older study, um, and they injected irritant into the fascial spine. the D fascia and what they [00:31:00] found was that D fascial pain is more radiating. Um, I didn't find this so much in my study where I injected through the different layers as treatment. Um, however, I still use that, um, feedback when I'm treating patients.

If they're telling me, Oh yeah, when you touch there, it's radiating. Uh, 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? I can't tell you where it is, but it's probably in this, this vicinity. So your brain trying to make sense of pathology and a system that is not.

Innovated for fine touch. 

Dr. Linda Bluestein: Okay. So things that we tend to think of for, for example, uh, neuropathic pain being, you know, radiating, burning actually could be coming from fascia. Sounds like, 

Dr. Tina Wang: yeah, [00:32:00] it definitely can be. Um, in this, um, study that I had done injecting, not in EDS patients, but some of them were. 3 percent of this quote unquote myofascial pain originated with the deep fascia.

So it was in different combinations in the muscle tissue itself, it with the superficial fascia, with these different combination. 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 enveloped some of that connective tissue and then the muscle in 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 [00:33:00] can also arise in addition to the nerve. 

Dr. Linda Bluestein: And in terms of evaluating somebody and getting worked up, we know part of the challenge with people with hypermobile in particular is They get lab testing or imaging if they're, 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 I guess maybe two questions, how you assess in your practice and what people can potentially ask for if they're not able to come and see you? 

Dr. Tina Wang: Yes. Um, that's, um, that's one of the toughest, 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 flecks. We, we have to make sure that the cervical [00:34:00] instability, and not just cervical instability, that's the term we commonly use, but there can be spondylosis or just degeneration throughout, and it's pushing on the spinal cord.

And 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 people. in EDS from, um, the proprioception that's been, that's poor. So we're, we have patients who are running into walls, like I do all the time, even when I'm doing my therapy, running into walls, tripping over things.

And these are big, traumatic events to a neck. And we have to make sure that we're, we're catching these and monitoring that spinal cord, making sure that spinal cord is healing. And if not, if that it's so, uh, degenerative in there, then we have to send our patients to the surgeons to, to get that cleaned up and stabilized.

So that, that's [00:35:00] the first thing that I'm. Always thinking about in this population is, 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, then it's so easy to dismiss our patients and say, Oh, here you are again.

Um, so that physical examination is critically important to look for those upper motor neuron changes, um, as well as the lower motor neuron changes. So the weakness, the, the objective weakness, not the, I feel a little bit weaker. It's clear signs of any atrophying muscle wasting. In a dermatomal, myotomal, sorry it's a myotomal pattern for the muscle wasting, those things really have to be caught and that's where the imaging really comes into play and supports us.

If it's [00:36:00] 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? Um, and that is really hard to find because we're still sitting in the forefront of translational research from FASHA research into clinical practice.

In my university based practice, I am teaching my PM& R residents how to start to treat the fascial system, investigate and examine the fascial system, but this is still hard to find because it is at the forefront of that translational process. 

Dr. Linda Bluestein: Yeah, so in your practice, are you doing routine, uh, you're doing a detailed physical exam, of course, as you were just describing, [00:37:00] and then are you doing ultrasound of specific areas as, as well, where you suspect that there's more fascial dysfunction?

Dr. Tina Wang: Yes, I, I am. Um, 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 they, a lot of our normal values come out of the Steko lab. And then once that we have some normal values, then 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. I'm also looking at tendon stiffness. So there's, I'm still in the midst of all the data coming out of the tendon stiffness. What I'm looking at is the appropriate loading of the tissue. So if we're loading in a certain manner, how [00:38:00] stiff is that tendon compared to normal values that are out in the population and compared to people who might be loading the tissue in a different way.

So, uh, uh, good comparison would be low, uh, long loads versus quick plyometric loads. And the tendon we know from the research should be very different in quality. And so looking in 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 load for rehab that I want to want this patient to engage in that would be best for them because it's not all uniform. I'm finding some surprising results as well. So post surgery, there are changes. So maybe in that tissue, you don't [00:39:00] want long loads. Maybe you want a little bit more plyometric.

So looking at these kinds of asymmetries, um, I'm starting to guide patients that way, looking at the tendons as well, but I'll be able to guide them a little bit better once the study is completed. 

Dr. Linda Bluestein: And I've noticed in a lot of my patients, a lot of them really have difficulty getting muscle hypertrophy.

And I'm wondering if that's, um, Part of it, if you're not able to get that load through the tissues that, um, 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 and everything that, that we need.

Is that fair to say? 

Dr. Tina Wang: Yeah, absolutely. And if there's a over, um, overworking, Because of the improper dispersion of forces as they are trying to, uh, get hypertrophy, then you might see a breakdown of tissue, um, [00:40:00] in addition, um, there's difficulty with, um, neuromuscular activation because of the pathology found in the tissue and the feedback system, so that we can release the tissue either with a needle, with injectate, or fascial, fascial manual work, um, but if we're not retraining the brain and the force transmission.

and doing it with proper, uh, prescribed load amounts, then we may never get that patient to where they want themselves to be. And then of course, there's so much GI issues, so that even if we're dumping tons of protein in, May not be absorbed either. So it's just so many factors. 

Dr. Linda Bluestein: Yeah, exactly. That, that makes sense.

So in terms of pain, does, how does fascia contribute to pain? 

Dr. Tina Wang: Yeah. So, [00:41:00] um, we talked a little bit about that study that I had done previously and, um, In the anatomical work looking at the fascial innervation, prior studies, uh, this is by Menz out of Germany, they found that 40 percent of the deep fascial system, the innervation consists of postganglionic sympathetic fibers.

So 40%, and it seems to be the case It's throughout the innervation that we often think of these C fibers, um, if, if people listen to the, uh, talk by Fraser Berling, he talks about these unmyelinated fibers and they are often responsible for pain and we can't test for them per se directly because they're unmyelinated, just, uh, difficult to test under [00:42:00] EMG or MCS, uh, nerve conduction studies.

And these unmyelinated fibers, 40 percent of that nerve are sympathetic. So you can imagine that if you're stressed out, so it's not all coming from your head, it's your body's response if you're stressed out, or if you have an injury, or you're having digestive issues. Because 90 percent plus of that gut innervation is sympathetic, then you're gonna start to see changes in the deep fascia.

And it's not just one way, it's not just Receiving sympathetic input is also the expression of the sympathetic response into that deep fascial tissue so that you have both a sensory response as well as a sympathetic response in this tissue. And you'll, you'll see [00:43:00] that with even people without EDS, they'll tell you how much worse their pain is when they have stress, when they're stressed out.

Dr. Linda Bluestein: Yeah, that's super interesting because I think that definitely happened to me when I was at my, 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? You know, I'm sure you get asked that too all the time, like, you know, by family and things like that.

And so, um, that's really fascinating to have a pathophysiologic explanation for why, you Psychologic stress could make our pain worse, uh, rather than just thinking that, well, we're just not strong enough, you know, we're just not psychologically strong enough. 

Dr. Tina Wang: Yeah, and it influences not just the innervation, like the input and output of the fascial tissue, but also the fibroblasts and the [00:44:00] myofibroblasts respond to.

So in a separate study we did in collaboration with Robert Schleif, one of our big, famous fascia research society rock stars, and 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, um, and, uh, pulling sensations, really this, um, this change to TGF beta is really one of the, um, possible sources of this.

I can't say it's causative, but it could be. And in that study we did together, looking at the abnormal gliding of tissue in EDS, he and his colleagues, um, found that there were myofibroblasts [00:45:00] present and not in the subjects without. um, HSD and abnormal gliding. So really a possible source of these pain and dysfunctional sensations that we all feel in our body.

Dr. Linda Bluestein: And could that also explain the pain begets pain type phenomenon that we often see? 

Dr. Tina Wang: Yeah, it's a vicious feedback that you're, you're, 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, our allergic responses or inflammatory responses start to go out of control.

And then our POTS start going out of control. And then we start feeling crazier. And then more TGF beta is released. And we're in this vicious cycle that, [00:46:00] um, we often, I know at the, in the earlier days at the EDS society, where That was really anti steroids, but after talking to you all, it's like, well, yeah, I think there is a place where we just sometimes have to blast the cycle and interrupt it.

Dr. Linda Bluestein: And when you're talking about steroids, are you talking about steroid injections? 

Dr. Tina Wang: I, I think, um, systemic ones, yeah, that's what I turn to if I really can't stop somebody's cycle, and you'll, 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, uh, the brain fog, the dysautonomia, uh, pain, dare to say pain, dislocations.

And when I'm unable to break this cycle with any of our tools, with manual therapy, with injections, um, whatever it is, then we turn to steroids, um, [00:47:00] at the great protest of patients because none of us like being on steroids. 

Dr. Linda Bluestein: And before we get into other treatment options, um, I just want to talk about a couple of other specific examples.

So with TMD or, um, temporal mandibular joint dysfunction, of course we know that that's also like in the vicinity and it can affect, uh, upper cervical instability and things like that. And then another area that I'm thinking of is, you know, this whole like coat hanger pain, right, that we see so commonly.

What kind of role does fascia play in those specific, those two specific. Phenomena. 

Dr. Tina Wang: Well, so it's not fair because I'm a fascial researcher, so I'll tell you everything is fascia, right? And then if you talk to a neurologist, they'll tell you everything is nerves. Right. 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, um, to properly and effectively effectively treat [00:48:00] the TM, uh, TMJ when there's TMD present. Um, we have to treat along the fascial system. So oftentimes we're going into the arms, we're going into the chest and then same thing with that neck.

There was a great, um, paper out by Jan Welke a few years ago. Um, and he released the ankle. and improve the neck range of motion. So I'm always going down into the ankle and then my osteopath colleagues will tell me pelvic floor and jaw are intimately related. So then going into that pelvic area. So really looking at the whole body, especially if your TMD is just so hard to control, you want to look at the whole body.

And then, of course, talking to my colleague, um, my dear colleague who trains with me in osteopathy, Rebecca Griffith, [00:49:00] she will tell me that it is just, uh, just a beast to treat. And just, um, years of of sessions and adjustments with her. Um, the safety autonomic system, the protection of the airway is a huge part of it.

So I'm, I'm always looking at sleep apnea, um, airway control in my patients with this dysfunction. And then for Finally balancing cervical stability with the TMD. My, some of my colleagues who don't do research, but who are amazing clinicians, um, out in other countries. And they will tell me that their patients with or without EDS, the 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 [00:50:00] perhaps They are crooked because they are compensating for other dysfunctions. So that if we go and force that jaw into a certain position, if that jaw, which most likely I think it is clinically compensating for dysfunction, then we create more stress on these other areas that are dysfunctional namely that cervical cranial 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. 

Dr. Linda Bluestein: I love that because I think too, so often we We, we hear that parts of our body are asymmetrical or there's some dysfunction somewhere.

And then of course, that also can plant a seed that can sometimes be not very helpful for us. Um, so I, I [00:51:00] love that line that, that you use. 

Dr. Tina Wang: Yeah. That's great. It drives me nuts, right? When we'll hear that particularly from patients who work with providers or, uh, who are not EDS aware. 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 no, it's that there's my, my osteopathic teacher, Dr. Jealous, would always say there is more health in the lesion, or as we say, dysfunction, there's more health in the lesion.

Then there is Lesion. In the lesion, there's more health. Mm. It's compensating. It's keeping us alive. It's keeping us functional. So let's, let's not go messing with it too much. It doesn't mean we don't treat you. Mm-Hmm. . But we also don't shoot for this idealized version of perfect. That exists nowhere.

Dr. Linda Bluestein: Okay. And. I want to make sure to talk about treatment a little bit [00:52:00] 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 of course that is, I know one thing that for me personally has definitely happened.

It feels wonderful at the time. Are there certain contraindications? Are there certain indications, contraindications? How does that differ from just like deep tissue massage? And is this something that we should be doing on ourselves? And I know that's like a, that's a long question and there's, and I have a couple other treatment related questions, but we can start with that one.

Dr. Tina Wang: Yeah. Um, and if, um, I don't answer part of that, just feel free to ask again. Um, so very common question that I get. So I always tell people, uh, there's a three pronged. approach. You know, of course, when you and I treat EDS and all of our, our, um, colleagues, it's much more complex. We're taking so many more factors into consideration, but this is [00:53:00] really meant to guide the patient.

who doesn't have all of these, um, you know, years of training like you and I do. 

Dr. Linda Bluestein: So 

Dr. Tina Wang: just keeping it simple. It's three prong. 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 tenosyte piezo, um, 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, your team of medical professionals that also, you know, include integrative health folks. So if you have a herbalist that you work with, an Ayurveda doctor, your primary care, your surgeon, your psychiatrist, your psychologist, they all fall into that [00:54:00] medical group.

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 that, um, you need to give them all equal attention, but care needs to be given.

And as, um, I I've heard Alan Hakeem, um, say this as your condition. starts to pacify or improve or even recede, um, which is possible, then the amount of attention you put into the pillars will lessen. And the amount of time you, and intensity you need to spend seeing and hearing. These professionals will also lessen and that's where home care is super important too in self [00:55:00] care.

So in terms of the manual therapy component, um, it's, you're, it's going to be hard. 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, even, I've seen an explosion.

Um, providers out there who are highly skilled. So finding one of these people who knows how to work with HSD, EDS, will be a first step. If you can't find that, then finding someone attentive. So this might be an acupuncturist working manually with needles on your tissue. It might be a massage therapist.

If It might be a structural integrator, the newer terminology for all firsts. They don't consider themselves massage [00:56:00] therapists. It might be any of these folks an, an osteopath, a chiropractor, a, uh, physiotherapist, physical therapist. who does manual therapy. So any of these folks and the approach. Um, and so this is one of my passions is teaching massage therapists how to approach people with HSD and HEDS because they are the first line.

So the, one of the earlier studies show that 81 percent of people with these conditions seek out manual therapy and 84 percent who do, do well with it. 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. Um, in my early years, um, Antonio Stacco said, Oh yeah, if you treat too many points, some people get fevers.

I said, what are you talking about? And [00:57:00] then I started treating people with EDS and not only do you get fevers, you get dysautonomia, you get diarrhea, you get, um, Brain fog, spells. I had a patient who went to sleep for, gosh, 24 hours. You can imagine the panic I had. Yeah. Um, so yeah. Wow. 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. So 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 [00:58:00] how your body responds and then starting to explore different depths of tissue treatment modalities. Um, and as you work with this person, that's the person you can ask, where do I treat? at home for my 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 this session? And I will show my patients where to treat a couple of points where I do not recommend. What I absolutely do not recommend is indiscriminately, you know, Going at your tissue, you will injure yourself, you will destabilize points, and I also do not, um, recommend, I, I had a patient who did this, going to get the textbooks and deciding where you're going to treat, you're really going to destabilize yourself, and it's, it's going to be a mess, and, and, you know.

I really caution against that. So really finding a [00:59:00] 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 tissue so that you can tolerate it. 

Dr. Linda Bluestein: Yeah, because sometimes it's so hard to tell while you're actually doing the activity if it's, if it's too much.

I mean, even for me, it's very hard for me to tell at that time. And I have one last quick question on the treatment before, well, I shouldn't say quick, we could do it probably an entire podcast episode on, on this question, but before we move on to the hypermobility hack and, and close up on 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. So in terms of prolotherapy, PRP, cell based injections, things like that. Um, do you have any thoughts that you're willing to share? 

Dr. Tina Wang: Yeah, absolutely. Um, I, I do the prolotherapy and the [01:00:00] PRP and So does, uh, Frasier Berling in our EDS Echo, and so we're often collaborating or having conversations about it.

So at the EDS Society, our last conference, we gave that fascial based talk together. And the idea behind the, uh, prolotherapy and the injectate using PRP or tetradecyl, for Dextrose is that we are stimulating the fibroblasts or the tenosites, which are specialized fibroblasts in the tissue to lay down more tissue.

After these injections, we really need you to load the tissue properly. So working with your movement professional, because now that we've stimulated the tissue, the cells, we need that tissue to lay down properly and with proper strength so that the, the loading is really important. So oftentimes when people come to [01:01:00] see me for it, I will recommend if they're not getting that injection in that session to please start their physical therapy or their movement therapy with their professional in preparation for the injection.

What I've heard from my colleagues is that, um, working with someone who is EDS aware is important because how we're all taught to inject, um, most of us are taught through the Hemel Hackett Foundation, um, both Fraser and I were. and others are maybe taught in their residency, and um, if there is, we're taught to inject a variety of tissue, and the protocol is just to inject everything, and we do not do that with EDS.

It has to be targeted and pinpoint this tissue is fragile, and we know mast cell is [01:02:00] occurring. in a lot of our patients. So we have to be cognizant of how many times we're sticking them into that tissue for our surrounding joint. Um, again, with the manual therapy, we saw that fever response and that dysautonomia.

So we're, we're trying to reduce that reaction. The, um, other thing to be cognizant of is the mast cell flare up. So, um, to people's dismay, I will turn them away if the mast cell's not under control. I, it doesn't matter what they say to me. It has to be under control. So I don't, that's the other thing, I don't, um, Depending on the doctor out there, you know, in my early years, um, I would take them 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. 

Dr. Linda Bluestein: Mm hmm. 

Dr. Tina Wang: Now, I want my patients controlled. I [01:03:00] want them on their medications. Do not come off your medication because that medication, those supplements, they're not are modulating your immune system. And I want you to go into this injection with your immune system properly modulated for the best response.

You're, it's a long way to come see me. It's a lot of time. It's a lot of effort. And I want I don't want to waste your time and I want you to have the best response, especially if you're going to sit through a session like that. 

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, but you preoperatively, right? And it's like people might have their migraines extremely well controlled with magnesium or you know, some other supplement. And it's like, no, just stop everything. It's like, no, there's specific guidelines that you can use so that we can be very specific about what supplements need to be stopped for what surgery.

And yeah, [01:04:00] when, when we don't, uh, take a little bit more time and slow down and think it, it can be very frustrating. Yeah, absolutely. I like to end every episode with a hypermobility hack and you could probably give us a hundred or hundreds of these. Um, but what hypermobility hack would you like to share with us?

Dr. Tina Wang: Yeah, when, um, there is a joint that is unstable and you just can't seem to get it back into joint with stability. All your tips and tricks. Then what I recommend is, um, first, first, always try to calm down that nervous system because there's a great sense of panic. For me, frustration, either panic or frustration, like I don't have time for this.

Gotta go on to see the next patient. 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 [01:05:00] how that's 90 percent of the battle fighting that nervous system. So just giving your nervous system a little break, a minute or two of extended long exhales, 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, kind of 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.

Dr. Linda Bluestein: Okay. I like it. I like it. Okay. And, uh, before we, uh, wrap up, of course, we also need to know where to find you. And I just am so grateful to you for coming on the podcast today and sharing your, your vast knowledge and, and wisdom with [01:06:00] us. It's been such a great opportunity to, to finally chat with you. I've wanted to do this for such a long time.

Dr. Tina Wang: so much for having me on, um, one of, um, 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. So I'm a deep meditator, yoga practitioner. So I do try to not spend so much time on social media, but I will occasionally post there.

So it's still alive. It's Tupelo Point, um, or Tina J. Wang. There's two of them and you can find information there. I will be having a book on this science EDS coming out. So that I will. probably post to social media as well as on the website when it's out. [01:07:00] Um, I'll probably self publish it so I can update it as the science continues to move at such a fast pace.

Um, I'm also on the board of the FASHA Research Society. So if you like to learn more about FASHA 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 as well. I'm on the the scientific committee and I'd love to see some of you present your work at the congress and that will be next year in New Orleans.

So those are all the different ways to find me and then, um, you know, I just, I'll 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. [01:08:00] extroverted, uh, uh, extrovert activity type.

So really just a million things for doing, doing this on all of our behalves and advocating for all of this scientific and medical work that all of us are doing, but you're the face of it. Thank you so much. 

Dr. Linda Bluestein: Oh, well, I, I really appreciate those extremely kind words. It's, it's one of those things where We know that not everyone can, you know, travel to come see you or travel to come see me.

And so 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. Right? It's really huge. So, well, thank you so much again. Uh, this was a long time coming. We'll have to have you back on once your book is out and, uh, be able to dive deeply into that.

And I'm sure people will be very, very excited to get their hands on the book [01:09:00] and really learn a lot more about this, uh, topic that, uh, I've talked to, I'm sure, you know, Jill Miller. Yes. Um, so I've had Jill Miller on the podcast twice and I have her book actually on the shelf behind me and she's, 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. So I just am grateful to you for taking the time to come and talk to me today. 

Dr. Tina Wang: Absolutely. Thank you so much for the opportunity.

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, and you just kind of quickly got through it. In anatomy dissections, you kind of quickly got through the fascia and 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 [01:10:00] conditions like EDS and HSD. 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 bendy bodies podcast.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. If you'd like to meet with me one-on-one, check out my available services options on the services page of my website@hypermobilitymd.com.

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