Why Are You So Exhausted? with Dr. Brayden P. Yellman (Ep 140)

Brayden P. Yellman, MD: [00:00:00] I wanna be clear, these surgeries are not a cure. You still have me, CFS, you still have the immune dysfunction, you still have the metabolic dysfunction that is behind. What we think is, is post exertional latest to the best of our understanding of that entity. But you may take away the primary driver of symptoms of dysautonomia, in particular if you remove those neuro anatomical complications.

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 we'll be speaking with Dr. Braden Yeoman about M-E-C-F-S. This is such an important conversation because. Chronic fatigue and me CFS are different from one another as he will be explaining to us.

But we see this so commonly in people that have symptomatic [00:01:00] joint hypermobility. So whether you have one of the Ehlers Danlos syndromes or some other type of condition, I think you're gonna find this really helpful. I. Dr. Yeoman serves as the medical director at the Bateman Horn Center of Excellence with a strong background in managing complex multi-systemic illnesses.

Dr. Yeoman began his career as a clinical rheumatologist focusing on conditions such as systemic sclerosis, inflammatory myositis, and vasculitis. In 2019, he shifted his focus to me, CFS, fibromyalgia, long covid autonomic dysfunction, mast cell activation, and other infection associated chronic conditions, recognizing the urgent need for specialized clinical care and research.

In these areas, Dr. Yeoman is dedicated to advancing medical education, patient care, and research, working alongside leading experts to improve diagnostic and treatment approaches for these underrecognized conditions. His work at the Bateman Horn Center has contributed to numerous clinical studies and collaborations with [00:02:00] major research institutions.

I'm so excited to have this conversation with Dr. Yeoman. As always, this information is for educational purposes only and is not a substitute for personalized medical advice. Stick around until the very end, Sue. Don't miss any of our special hypermobility hacks. Here we go.

Okay. I'm here with Dr. Yeoman and we are going to be talking about me, CFS and how that relates to hypermobility and connective tissue disorders like EDS. So Dr. Yeoman, it's so great to finally meet you. 

Brayden P. Yellman, MD: Thank you for having me. 

Dr. Linda Bluestein: So, um, can you start out by explaining to us, uh, what me CFS is and how that differs from general fatigue?

Brayden P. Yellman, MD: Yeah. So M-E-C-F-S is a term that stands for myalgic, encephalomyelitis or chronic fatigue syndrome as it was formerly called. Uh, we don't generally go by the name chronic fatigue syndrome anymore because that's sort of. [00:03:00] Understate the degree of fatigue and really functional impairment that patients will feel, uh, and experience with ECFS.

Um, this is a term that's been used to describe what we're now starting to call in the medical field infection associated chronic conditions. Um, but it really is referring to a longstanding chronic illness that, uh, develops after certain insults to the body. And specifically, we have identified insults to the immune system as triggers for this illness.

So many times that is an infection. It can be viral infections. A really famous cause of this would be. COVID-19 as a trigger for a chronic illness long after that Covid infection has technically resolved. Uh, but it can also be, um, bacterial. It can be parasitic infections, it can be other assaults to the immune system, such as a traumatic brain injury, uh, or certain major, um, [00:04:00] events, uh, in life that activate the immune system.

Uh, surgeries, for example. Even vaccines, uh, as great as they are and, and as well as they work most of the time, are designed to activate the immune system. And if it activates in an improper way and doesn't entirely shut down or calm down in the ways that we would hope it's possible that people can develop me.

CCFs, um, me CCFs is currently a. Kind a grab bag term that we use for a whole clinical syndrome, a full body multisystem illness, and it does not have what we would call a biomarker, which makes it a little harder to diagnose. We can't just send a certain lab test or get imaging that gives us this diagnosis.

So instead, we rely on the Institute of Medicine's Core Clinical criteria from 20, uh, 15, what we call the Institute of Medicine criteria. Um, that essentially captures five criteria that are present in all people [00:05:00] with M-E-C-F-S, and there's plenty of other comorbid conditions and other complications that people can have.

But these seem to be core criteria for those of us who've been treating people with me, ccf s or infection associated chronic conditions for our careers. Um, the first of those criteria is a severe. Profound fatigue that is unlike anything a person had ever experienced prior to becoming ill. Uh, they must have it for at least six months, but I think the important part here is that fatigue is functionally impairing to the degree where people cannot do the same things that they could do prior to their illness.

Uh, and we're talking about huge differences, inability to work, inability to go to school, inability to learn things. Sometimes it goes all the way to inability to perform normal activities of daily living. Um, it can become very severe, even to the point where people become essentially bedbound. The second criteria [00:06:00] is the presence of what we refer to as post exertional malaise or PEM.

Uh, this is really the core. Pathognomonic criteria for this illness. Um, and I'm gonna come back to that in just a second. The, um, third criteria is really non-specific, but always present. And that is unre refreshing sleep. So that can be, uh. All kinds of sleep disorders. But even when someone gets enough sleep, maybe they even spend 10 hours sleep no matter what.

They still are not refreshed by sleep the way they were before. We may also see problems with insomnia. People describe being wired but tired. Uh, the more tired they get, the more activated their sympathetic immune, uh, sympathetic nervous system is. Uh, we see people, uh, struggle with falling as, uh, falling asleep to begin with, with staying asleep, with waking up frequently, having nightmares.

Um, lots of different types of sleep disruptions. So [00:07:00] that's the third criteria is un refreshing sleep. Uh, the fourth and fifth, by the definition set forth in 2015 for the Institute of Medicine required that you only have one of the two. But I would say having treated this illness, uh, for some time now for over six years, exclusively, I would say almost everybody indeed has these two criteria.

Um, one of those criteria is a. Cognitive impairment, and this is sort of different than the cognitive impairment we see in a lot of other illnesses. It is waxing and waning. It is not progressive. Um, it is often very much, uh, focused on trouble with maintaining attention. Concentration and focus. So people will think they're having memory issues, but it's really that they're not encoding or paying enough attention to begin with or unable to process information.

Um, it will often manifest with people having significant word finding issues. They'll often describe brain fog or sort of the inability to just access thoughts and bring them forward. [00:08:00] Um, and it can manifest in a lot of other kind of waxing and waning ways. It's the only other kind of cognitive dysfunction that I can think of that's waxing and waning in this way is what we think of for delirium in the geriatric population.

Um, it can be a little bit like that, but it also has a lot of features in neurocognitive testing that are similar to how we define a DD or A DHD. Uh, and the fifth clinical criteria is that of orthostatic intolerance not functioning as well in an upright position, so either standing or sitting with your feet on the floor as compared to laying down supine.

Or even sitting with your legs elevated, say, on a couch in a horizontal position. Um, and this is sort of a, a grab bag term that's really identifying the presence of dysautonomia or a dysregulation of the autonomic nervous system to control, uh, where blood flow is going and where it's getting to when you're in an upright position, when you're challenged with orthostasis.

Things that we don't have to think about normally, but become challenging when our, um, [00:09:00] uh, autonomic nervous system is, uh, dysregulated to begin with. So this is where things like the diagnosis of pots or postural orthostatic tachycardia syndrome or orthostatic hypotension or some of the other terms we use fall under this category of dysautonomia and orthostatic intolerance.

Uh, I mentioned I would return back to post exertional malaise. Uh, the second criteria, the pathognomonic criteria because it is so important. This is, um. This is a unique situation that really only occurs in me CFS, and it is characterized by a fatigue, uh, and impairment that is more profound and more long lasting and, uh, associated with significant worsening of all symptoms that a patient experiences in me FS as well as the presence of new symptoms.

And it occurs, uh, best we can tell as a result of energy expenditure that [00:10:00] exceeds someone's. Shortened or reduced limit for energy. So if you imagine something like a cell phone battery being at a hundred percent for normal healthy people, that cell phone battery may be starting out at 50%. For someone with M-E-C-F-S, and it may be a very old cell phone, the kind that, you can literally watch that battery tick down from 50 to 49 as you're using the phone, right?

Mm-hmm. Uh, just using very simple apps drains that battery quickly. That is what is happening to what we refer to as the energy envelope. Uh, for people with ECFS, they, uh, spend energy on physical exertional activities or even just on maintaining an upright position as compared to a supine position. In that orthostatic challenge, they may be spending energy, uh, on cognitive tasks, whether it's processing.

Things cognitively, whether it's social interaction or even whether it's emotional processing, right? On a [00:11:00] cellular level, uh, people still are spending a lot of a TP or energy to have emotions, good emotions or bad emotions. Even opening presents on Christmas morning is using a lot of a TP on a cellular level.

And so, uh, it's a different level for different people and it can change throughout the course of an illness, but there's this sort of limit on how much energy is available and if someone exceeds that limit, they can enter post exertional malaise, this totally different physiological status. And that's, that's the way to think about this is an entirely different physiological state where their function is severely impaired.

And I think it's important to point out post exertional malaise happens with a delay in onset. Uh, there is generally a 12 to 36, sometimes even 48 hour delay between. The energy expenditure that exceeds this limit. And when the symptoms of post exertional mala really kick [00:12:00] in, um, and that's critical because there are people with orthostatic intolerance.

As we've discussed, uh, who may have pots but maybe not ECFS, who may go out on a hot summer day like I used to as, as a teenager in Texas in 105 degree weather and mow the lawn. And, uh, you can start to get dehydrated, feel lightheaded and dizzy and have pot symptoms. And then you need to go light out 'cause you start to feel sick, right?

That is not post exertional malaise. Now that may still trigger post exertion malaise the next day. Mm-hmm. Or 12 hours later. But that is a direct response to the orthostatic challenge. So post exertional malaise is different and even more severe than that and an entirely different physiological state.

Um, there is a recent, uh, I, I just bring this up 'cause it's come up recently. There was a study that was done at the American College of Rheumatology looking for post exertional malaise in rheumatological conditions. And they published on kind of self-reported post exertional malaise in rheumatoid arthritis and in osteoarthritis and it [00:13:00] Sjogren's syndrome.

And I can assure you having. Practiced rheumatology, uh, that the, what, the fatigue that is experienced in those illnesses is nowhere near what we experience in post exertional is. It does not meet that definition. Once you've talked to someone and sit down and observed what this means for people, you'll never be confused again.

I wish people had a, a sense to talk to or the opportunity to talk to people who've been through severe post exertional malaise, um, because it's really an edifying experience specifically for clinical providers. Um, I would say one of the things that we think about when it comes to post exertional malaise, uh, one of the ways we sort of screen for it clinically, um, is by asking about.

Functional status in patients. I just don't think we ask that enough in clinical medicine. Mm-hmm. So, um, I was taught by Dr. Lucinda Bateman in these terms, and I've, I've always followed this, is we ask patients about their hours of upright activity, so very [00:14:00] specifically time in an upright position with their feet on the floor versus laying down or having their feet elevated.

Uh, and we ask about, um, good, uh, things that they can and can't do. So, uh, specifically there's sort of two states. There's what is your hours of upright activity on a good day, which is really maybe not a good day because they're ill, but it's their baseline status. It's the best day they may have in a month.

And how many good days do you have a month? Well, well, I have four or five days where I am. Doing okay, I can be upright for three to four hours and I can walk to the mailbox. I can have a conversation for 15 minutes. I might be able to, to drive 10 minutes, uh, to get my kids to school. But then they also still can't exercise.

They can't do three chores in a row. They can't, uh, read for more than 20 minutes before comprehension starts to go away. So we ask these type of questions, both with activities of daily living and just other things that are kind of core to living [00:15:00] life, and how can you do those things and how long can you do them before you start to fade out.

And then that same patient may say, I also have 10 really bad days per month where we assume they're in post exertional malaise. I am upright for less than an hour a day. I can get up and make it to the bathroom, but then I have to climb back in bed. If someone brings me a meal, I can eat it there, but I can't really get up and prepare anything.

I definitely can't walk out to the mailbox. I've heard people even say, you know, if the house was on fire. I think I could get out, I'm not entirely sure, and I wouldn't get any farther than the curb. I mean, this is not just mm-hmm. I'm tired and don't want to, this is an inability to do things. But yeah, getting the num, the number of hours of upright activity and what they can and cannot do on good and bad days is, uh, a very simple, quick way to get a sense of someone's functional impairment and the degree to which this is disruptive to their life.

And I would encourage all clinicians worried about me, CFS worried about long covid other infection associated [00:16:00] chronic conditions to ask these questions in clinic. 

Dr. Linda Bluestein: Those are great questions, and I know on your website there is a link to a video that goes into detail about the battery analogy, the cell phone battery analogy, and that's a great video.

We, we can link that in the show notes so people can check that out as well. For, for patients who are struggling to get a diagnosis or struggling to get their clinicians to pay attention to these kind of symptoms, and if they just listen to all of this and they're saying, oh my gosh, this sounds like me, but none of my doctors are taking me seriously.

I really struggle to explain the degree to which I have these problems. You know, they may hear those questions that you just, uh, mentioned and then they could, you know, spontaneously provide that information to their physician. But do you have any suggestions for ways that they can, you know, really get this message across to their clinicians, how significantly these symptoms are affecting them?

Because I know delays for diagnosis are a really big problem. 

Brayden P. Yellman, MD: Yeah. You [00:17:00] know, prior to long covid, it was an average of at least five years to get a diagnosis of me ccf s that shortened a little bit because of a greater awareness of me. CFS being that long. Covid is often becoming me CFS or meeting criteria for me ccf s in patients.

So it's getting a little more notoriety I would say. We've gone from very few physicians understanding these conditions to what's a lot better, which is maybe 10% of the general physician population. Um, there's no one simple answer to that. It's, uh, something that we as a nonprofit struggle with every day.

How can we mainstream this illness more? How can we provide better care? What's the right specialty to care for? This is the medical system mm-hmm. Even set up to deal with complex chronic illness or is it all about acute illnesses and a chief complaint and you have 10 minutes to say what's going on?

Right. So a lot of our patients, uh, anybody with this illness kind of is given that. You know, 10 minute window to come in and express what's going on. Uh, what I would say is [00:18:00] it's easy to get lost in a myriad of symptoms, what we call a review of systems in, um, medical language, right, as doctors. Uh, and that's about, you know, what's going on cardiovascular, what's going on, respiratory, what's going on, you know, with the skin, dermatologically, et cetera, et cetera.

Don't get as focused on the symptoms. Bring in a good summary of the functional impairment. I used to run every day five miles. I now, on an average day, I have five good days. I have 11 bad days. I have days where I cannot physically get outta bed. I'm not, I'm, I'm certainly, you know, sad that I can't, I'm upset, but I'm not, not just depressed, I'm not just anxious.

Mm-hmm. Something else is going, I physically cannot do these things. This is the limit of what I can do in this situation or. I get a whole bunch of other symptoms, which I can tell you about later. But pa uh, physicians and providers will get lost in that review of systems. But if you can very clearly [00:19:00] state, this is how much time I can be upright, this is how long I can stand for.

I, I'm, uh, you know, I have an MBA and I've been to grad school and now I can only read for 15 minutes and I can't understand beyond that. I get distracted and have to pull over when I'm driving if I've driven for more than 15 minutes or when I'm in a specific sensory over. Sensory overwhelming environment, for example, giving those kind of examples.

This is where I was, this is how I'm impaired now. This is my functional status is really going to help get a physician's attention. Now, that's not necessarily gonna get us to the diagnosis. And that's where you have to sort of bring a little bit of, uh, extra information to the table. So for example, um, we on our website, not to plug the Bateman Horn Center, uh, necessarily, but it, we, we try to, as a nonprofit, have a lot of free resources for patients who are worried that they have this illness because clearly we can't take care of everybody.

There's a right, a test that we use, a passive standing lean test or what we've referred to as the [00:20:00] nasa mm-hmm. Lean test, which is a very simple test that you actually can do at home with some help from family members that you can bring in. We have a, a form you can print off and you can fill it out and bring that in to a clinician and show them what your vital signs do.

This is a test where we have people lay down. In a dark room, no phones for 15 minutes. We have them stand up, not wearing any shoes and lean against a wall. And their heels are about six to 12 inches from the wall. And they're just standing there, palms forward, leaning against the wall. And we measure using a pulse oximeter heart rate.

We use a, uh, blood pressure cuff to measure blood pressure. And we look at oxygen level and then observe what's happening to a patient. Standing and just standing leaning against a wall sounds really easy. Um, I have to admit, I have pots myself, thank goodness I don't have any ECFS or long covid. I couldn't believe as an athlete how difficult it was to lean against the wall.

Mm-hmm. And the reason is because it takes away [00:21:00] the impact of the skeletal muscle in the lower extremities. Mm-hmm. And that squeeze and its involvement. In venous return to the heart in preload to the heart, in actual circulation, uh, while also challenging you ortho ecstatically. And so it's a great way to elicit what we know is going on underneath difficulties with circulation, with getting blood flow into the brain, to the muscles, et cetera, in an upright position as compared to laying down.

So you will see people's heart rate go way up. That's where we make a diagnosis of pota, uh, raise and heart rate of greater than 30 beats per minute over the course. Of that 10 minutes. Uh, alternatively, we also see lots of changes in blood pressure, and one of the most common ones we see is a narrowing of the pulse pressure.

So that's the difference between the systolic pressure, the high number, when the heart is squeezing and the diastolic pressure. When the heart is relaxing, that pulse pressure gets smaller and smaller. So if you start at 120 over 80, kind of the traditional normal blood pressure, that may drop [00:22:00] a little bit systo, you may get.

110, but that diastolic is gonna go up from 80 to, you know, maybe even a hundred you might get, or 98, right? So 110 over 98. Mm-hmm. There's a narrowing of that pulse pressure. Um, and so one thing that's important to remember on that test too, it's, it's great to, to fill this out, to show what's happening to your body, to bring that into a physician, but also to explain to them that the pathology in this case is not the heart rate increase.

The pathology is not the narrowing of the pulse pressure. Those are your body's secondary adaptive mechanisms for the actual pathology, which is the inability to have adequate circulation in that upright position compared to low to laying down. And there's some great studies, uh, that show. There are ultrasound studies that show on a heads up tilt tip table test, which is very similar to an NASALINE test, that there actually is a global reduction of cerebral blood flow on the average of about 25% in those, with these infection associated chronic conditions compared to six to 7% in healthy [00:23:00] controls.

Um, so yeah, bringing a nasaline test in your clinician and showing them, look what my heart rate does, look what my blood pressure's doing just by standing up. That is something they can put in your chart. That is something that is objective in their minds because there's not a biomarker, right? So anything you can bring in that's some form of objective evidence, uh, is really helpful.

I would also say I. Uh, and this is its own discussion topic, but, uh, it's very common for people with these conditions to have something called mast cell activation syndrome. Now, that's not part of the mm-hmm. IOM diagnostic criteria, but it's very common among many patients with me, CFS and trying to identify symptoms of mast cell activation syndrome.

And, uh, objective evidence of those things and talking about, or showing pictures of rashes, et cetera, to your physician can also be really helpful. 

Dr. Linda Bluestein: And we definitely talk about the, the triad of, you know, EDS pots and mast cell activation syndrome a lot on, on this podcast. So I'm really glad that you mentioned that so, so early on, [00:24:00] it's very important.

So, so I do Nassau lie tests in my office, usually at the first visit. And I do give people instructions also so that they can do it at home, um, if they, if they want, if, if we didn't have time or if they're, you know, consulting with me in a more informal fashion and they're gonna be going in for an appointment with somebody else.

So with deconditioning, you also would see some changes potentially. I mean, if someone even just had the flu or something Right. And they're, they're kind of still recovering. I know you mentioned that you need to have, uh, the, the fatigue and, um, post exertional malaise for at least six months. So that kind of takes out that, that portion of people maybe who are acutely recovering.

But I guess what I'm wondering is, with that Nassau Lean test, are there certain things that you're looking for that would help you determine if the results are. Um, indicative of ECFS versus pots versus deconditioning? 

Brayden P. Yellman, MD: Yeah, well, so somebody who's severely deconditioned could s could show [00:25:00] some notable, uh, dysautonomia on an CELINE test.

But even so, I would argue that they generally don't meet criteria for pots or orthostatic hypotension or have drops in their pulse pressure that are greater than 25% of the overall blood pressure, for example. So, um, mm-hmm. That's sort of a starting point. Uh, so it's, it's challenging, but when you put things with a medical history, I think it becomes a little more clear.

So if someone gets a viral illness, if someone has a head injury, if someone has a surgery and then they are never the same after that, they used to have no problems with conditioning. They were generally healthy people, and all of a sudden they're not. I think that's an important. Uh, clinical characteristic to think about.

Mm-hmm. Um, I would also say we get so worried about whether it could be deconditioning that we forget there's a person that's suffering in front of us either way. Mm-hmm. [00:26:00] And, uh, let's say just in a thought experiment that someone was just severely deconditioned again, that's probably only likely if they've been laid up in an ICU for a very long time where it would be clearly obvious that that's the case.

Um, but let's say that someone was deconditioned and, uh, uh, we mistakenly made a diagnosis of pots, as it were, or we, uh, started giving them orthostatic support. Let's say we gave them IV fluids in a situation where we knew they could handle it from a cardiovascular perspective. Let's say we gave them flu, cortisone, we gave them arterial support with midodrine, hydroxy dopa.

We used period asig to enhance venous return. Mm-hmm. We used compression clothing and they felt better. Are we really doing any harm to patients? Right? And then as they get better, if they do, especially if it's deconditioning, you can wean those therapies off. They don't have to be long-term therapies.

They can be a short bridge to someone actually exercising and getting better. In the case of deconditioning, [00:27:00] in the case of me CCFs, which I promise is gonna be way more likely, this is what we almost always see. Mm-hmm. This is what's actually happening. Those support measures are still gonna help people with their functional status.

The problem is you're just not gonna be able to quickly wean them. And I think this is a, an important point, uh, to bring up in this case too. It is. And you always have to be really careful how you say this. So I wanna be very clear to everyone. There is very strong evidence that exercise does help.

Dysautonomia does help in deconditioning, no matter the cause. However, and this is the huge caveat, it is not helpful if that level of exercise causes post exertional malaise. Mm-hmm. Which is why that is such a pathognomonic and important feature. If someone experiences post exertional malaise as a result of the exercise, and that may be very, very little exercise.

I may not even meet our definition of exercise, right? It may just be mm-hmm. [00:28:00] Walking one block or going up the stairs. But if that's gonna cause post exertional malaise, you're actually doing harm to patients, you're worsening their long-term functional prognosis, they're not able to see the improvements of exercise.

And so when I treat people with dysautonomia who have post exertional malaise, these therapies are designed to help extend that leash, extend that energy envelope to where they can do some things without experiencing post exertional malaise. And I would say generally, in the first year of therapy, even for people who are very responsive, and not everybody is, but for people who are really responsive, we need that.

Pharmacotherapy support. We need that exogenous fluid and salt support to really help people learn to live within their energy envelope and learn to live without experiencing post exertional malaise. And then only then when they've stabilized, when they've been able to avoid PEM with those supports, can we start to ask, can we pull back on therapies?

Or alternatively, should we start by [00:29:00] introducing careful, um, observable exercise, trying to keep a max heart rate below a certain range, trying to be very careful about avoiding post exertion laser. But can we introduce a little bit of physical therapy or exercise safely without triggering PEM and gradually make improvements.

A lot of times we can, but that is just never first line. It's never something I think that we really successfully get to in the first year of therapy. That comes later. We'd love it to come sooner because, hey, it's non-pharmacological, right? It sounds like it's a great first line therapy, but it never really works that way in those who have post exertional la.

So if you have pots, if you have dys adenoma, if you have deconditioning, does exercise help? Yes. But only if you don't have post exertional mala as a result. 

Dr. Linda Bluestein: So we are going to take a quick break and when we come back, we are going to talk about, uh, the ve there's no biomarkers, but are there some laboratory tests that can be helpful?

And I also wanna ask you about upper cervical [00:30:00] instability and if that impacts the, the clinical picture and genetic testing and a few other things. And so we will take a quick break and we'll be back in just a minute.

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This helps us reach so many more people and spread the information to everyone. [00:31:00] Thank you so much again, and enjoy the rest of the episode.

Okay, I am back with Dr. Yeoman, and I know you mentioned that there were no biomarkers for me, CFS, which is a huge problem. And there are no biomarkers for hypermobile EDS or HSD either. So these are all clinical diagnoses, which really, really makes it so tricky. Um, are there any lab tests that can be beneficial?

I know that I've read some things about natural killer cells and that those can be, uh, the function of those can be impaired in me. Ccf s 

Brayden P. Yellman, MD: that, that's very true. Uh, I generally think of those specific kind of tests, those immunological panels as being helpful in the research, um, arena, but not so much in clinical medicine.

Um, they're hard to know exactly what to do with. They could theoretically be supportive if you really have concerns about making a clinical diagnosis, but I generally do not order them. Um, I would say it's important to do a basic. [00:32:00] Traditional lab workup for someone who is presenting to you with symptoms of chronic illness.

So anything that you would think of that would go on that workup should go into an M-E-C-F-S workup as, uh, a basic way to make sure we're not missing something else, right? Mm-hmm. Um, so basic CMP and CBC, maybe inflammation markers with ESR or CRP. Definitely looking at thyroid, hemoglobin A1C. Sometimes we'll check.

Cortisol, although, um, there's sort of a debate back and forth about how helpful that is. It's sort of low normal or sometimes high normal, depending on the clinical circumstances and how physiologically stressed that patient is. But it's, it's important to make sure someone doesn't have, you know, say Addison's disease.

You don't wanna miss something like that in a fatiguing illness. Mm-hmm. Um, you wanna make sure that there's no signs of malignancy or a chronic active infection, and those are just gonna look really different. And I think we're all, as, as clinicians, uh, trained in identifying those things. But I would not make this an extensive, what I [00:33:00] used to call in rheumatology, like the shotgun panel where you're just looking for everything and you're testing every auto antibody under the sun.

You know, at least for rheumatological conditions, and I think this is true of, you know, neurodegenerative conditions as well, they have a way of presenting themselves. They're pretty obvious on clinical exam in the way that they're gonna present. And so I would really encourage clinicians to trust. Their physical exam to trust their history, uh, to trust clinical medicine.

Um, so you can do the basics, make sure you've, you've dotted your i's and crossed your T's, but it doesn't have to be an extensive, uh, ridiculous, you know, extremely difficult to conceive of laboratory evaluation. And same goes with with imaging. Um, there's, there's some of these conditions that I think some clinicians will refer to as diagnoses of exclusion.

And I think me, CFS and infection associated chronic conditions get seen in that sense. Like you have to exclude [00:34:00] every other illness under the sun to make a diagnosis. And that's just not true. This is a diagnosis to be made. And if you look at those, um, IOM criteria, if you really know how to ask about post exertional malaise, if you.

Assess hours of upright activity. If you assess good days and bad days in a functional questionnaire. I mean, we do this just screening patients to even come into our nonprofit to make sure we're serving the patients that we're really trying to serve. It's, it's really easy, honestly, to make these diagnoses.

Mm-hmm. And this sense that we need to rely on a biomarker for a clinical diagnosis, I think is misplaced. Would it be extremely helpful for research? Would it make it easier for clinicians who are not well versed in infection associated chronic conditions to make a diagnosis? Certainly a biomarker would be great, but it, it is not really there right now.

And I think these extensive workups slow the, uh. The, the opportunity to get to a diagnosis [00:35:00] and start actually doing something about it for patients. And, and again, you know, doing something for patients can be as simple as giving them a diagnosis and perhaps supporting a little time off from school or a little bit of extra support at work.

Like, these are the things people need now. They need to start pacing and realize that they can't keep pushing themselves into post exertional malaise and they need accommodations. Any clinician can do that. So this is a diagnosis to be made. Getting hung up in a lab workup, I, I think is a, is a fallacy. I.

Dr. Linda Bluestein: And I think that for a, any clinicians listening to this, I'm also going to link in the show notes. There's a paper that you are a co-author on, and there were multiple other co-authors that have also been on this podcast. Um, David Kaufman, I, Irene Ruy, um, Tanya Dempsey. And in that paper you had a, a great table with some pretty extensive, uh, questions so that you could really could get a sense of someone's post exertional malaise and that kind of thing.

So I will link that in the, in the show notes as well so [00:36:00] people can access that information. And, and what about genetic testing? Is that something that, that you ever find to be helpful? 

Brayden P. Yellman, MD: Yeah. Well, so, you know, with hypermobile spectrum disorders and HEDS, which is really our most common version of presenting with a bendy body as it were, this is a, a multigenic, uh, situation, right?

And it's, there's not a single genetic test that is going to guarantee you have this particular illness. And I think it also, uh, doesn't take into account the environmental impacts of that genetic background and how things change over time. How insults to the immune system may activate, uh, mast cell activation, which is theoretically implicated and actually progressing hypermobile spectrum disorder.

Right? There's this interaction that we're still trying to learn about, about whether those are even two distinct entities and how they right. How they affect one another. Um, so when I see a patient, uh, I'm certainly assessing for hypermobility on exam. I'm certainly [00:37:00] looking at the bit criteria. I'm certainly looking at the EDS society, uh, diagnostic, clinical criteria, although those are somewhat insufficient and I understand are being reviewed for consideration of mm-hmm.

New diagnostic criteria. But I don't send an extensive genetic. Panel. That being said, mm-hmm. There are situations where you do want to make sure you're not missing vascular EDS, which is a very specific type of EDS where there's a really high risk of complications, um mm-hmm. Including complications for surgery.

So if I have a patient, for example, who I've been with for several years, who we are really worried about. Their neuroanatomy. Maybe they have cranio cervical instability or a tethered cord and they're looking at getting a surgical intervention for that. Then I might test for vascular EDS to make sure we know we're not getting into a more complicated surgical situation that could have a bad outcome.

I think that changes management. Mm-hmm. There is an argument to be made for testing for vascular EDS or other [00:38:00] subtypes, um, or even, you know, Marfan syndrome or Sickler syndrome, uh, when you are helping a patient say apply for disability. But the problem is the absence of those things doesn't really mean that they don't have functional impairment.

And so I think that can be its own kind of tricky web that should go down. So do I do it? Sometimes? Yes. But it's certainly not something I think that has to be done. Again, from the perspective of clinician caring for people. Is it more important as we continue to research? Uh, yeah. It's 

Dr. Linda Bluestein: in terms of. Upper cervical instability.

Have you made any observations in your patient population in terms of, you know, how often they, you see that overlap and if you see sometimes if they do have severe enough, um, upper cervical instability and they actually go for fusion type surgery if their me CFS actually improves. 

Brayden P. Yellman, MD: Yeah, that's a, uh.

That is a sort of newer topic that is entered into the care of these conditions. So, uh, upper [00:39:00] cervical, uh, instability as you're referring to, we often call cranio cervical instability. So that's where the skull sits on C, the C one vertebra. And then there's also issues with atlanto axial instability, which is C one upon C two.

And so we're talking about an area that should be very stable with the surrounding connective tissues and not be moving around a lot. And when there is a connective tissue disorder, perhaps when there is active mast cell activation in these areas, these connective tissues may become more lax and there can be more motion at these sites.

That can be horizontal motion, it can be vertical motion, it can allow for things like the brainstem to sink down a little bit more with gravity and upright positioning. Uh, but ultimately we think that in some of these cases of instability, uh, and, and in certain. In certain pressures, uh, with certain volume statuses for patients, and these are all dynamic conditions that can affect the symptoms, that there can be neurological.

Uh, irritation, impingement pressure [00:40:00] upon areas of the brainstem or the cranial nerves that actually drives symptoms of ECFS that actually drives, for example, dysautonomia based symptoms, whether that is vascular, dysautonomia, and orthostatic intolerance, whether it's gastrointestinal, dysautonomia with severe gastroparesis and nausea and vomiting, uh, et cetera.

Um, I would also throw in real briefly a close association between cranio cervical instability, ano axial instability, and something called acquired tethered cord, which is the base of the spinal cord getting tethered to the surrounding soft tissue structures, uh, creating sort of a downward pulling pressure and a little bit of tension in that spinal cord, perhaps even anchoring, um, the.

Brainstem into a neuro anatomically disadvantageous position where you're actually, uh, contributing to this type of worsened dysautonomia. Um, so that is often found comorbid, uh, with it. And then of course, in the background we have some kind of emerging understanding of [00:41:00] how the venous and lymphatic vasculature also affect these conditions and are mm-hmm.

Dynamic and changing and making things more complicated. Um, so these are. These are complicated diagnoses to make. There's really no agreed upon, you know, type of imaging that is sensitive and specific for it. Uh, different specialists of which there are very few, uh, can have very reasonable arguments for different ways of doing things.

There's no standard of care. Mm-hmm. Uh, and yet when you're caring for these patients over time, there are many patients who, for example, uh, aforementioned have bad orthostatic intolerance. And if you treat aggressively enough, you can significantly improve that orthostatic intolerance, um, with pharmacotherapies behavioral therapies, et cetera, support therapies.

And then there are others that you will provide all the same therapies that work across populations. But, and even though each therapy individually seems to move the needle a little, you see that that patient in their overall functional status is not getting better or perhaps even slowly [00:42:00] getting worse over time.

Mm-hmm. And at some point you come to this realization that there is a subset of people who have something upstream. Of their dysautonomia that is preventing clinical progress with all of the therapies we know otherwise work. That's when I start to consider or look for neuro anatomical reasons or complications, uh, that could be driving this inability to move forward otherwise.

So I don't generally like see a new patient say, let's start looking for cranial cervical instability. I really think of it as something that we wanna save for when we can't make any further progress with all the tools we have in internal medicine that to help people first. Uh, when there's something clearly still not moving forward.

That's when we go looking for these neuro anatomical complications. That's generally when we find them. So of course I'm gonna have a, a bias about how often I find it because I think I'm looking at the right people. Um, and yes, in those circumstances when we do find Tether Co. When we do find CCI, uh, and we cannot move [00:43:00] people forward clinically otherwise.

I do see some of these neuro anatomical interventions make an enormous difference in PA patients' lives. And I wanna be clear. Surgeries are not a cure. 

Dr. Linda Bluestein: Mm-hmm. 

Brayden P. Yellman, MD: You still have me, CCF s you still have the immune dysfunction, you still have the metabolic dysfunction that is behind. What we think is, is post exertional is to the best of our understanding of that entity.

Uh, but you may take away the primary driver of symptoms of dysautonomia in particular if you remove those neuro anatomical complications. Um, so sometimes that does involve a cranio cervical fusion, which is a really, really big deal that we wanna save. Mm-hmm. Only for the most severely ill patients that are just not making any further progress.

Uh, but sometimes if you also notice that there is a concurrent tethered cord, I have seen a lot of cases now where people will go for a tethered cord release and upon releasing the tethered cord, which is a, a way safer, easier to do surgery, relatively compared to a CCI surgery. Uh, when you do that [00:44:00] tethered cord release.

Their disautonomia symptoms get better over time. In other words, that anchoring of the spinal cord may not be pulling the brainstem into quite as disadvantageous of a neuro anatomical position. And while CCI still exists, it may not be as, uh, unconquerable as far as its constant ability to exacerbate dys adenoma and, and drive symptoms.

So, for example, if that tethering goes away, the brain stems like slightly shifts to a point where it's not as irritated, you can then layer on very specific, careful physical therapy to help provide better cervical support. Um, there are things that people can do from a positioning perspective, motion perspective to try to protect or prevent the brain stem from getting back into those neuro anatomically disadvantageous positions.

And they can live with CCI without the same severity of symptoms they had prior to that Tether quarterly. So I often look for that first and try to do that on a slightly more conservative basis. Um. All of [00:45:00] this is, you know, on, on a, you know, uh, tens of patients, not, you know, hundreds. Right? We still have a lot to learn about, right.

Uh, these situations. But, um, there are, there are times when people get stuck. There's no way to move forward otherwise. And that's when we start looking. And I think we're learning more about how to have good outcomes in these situations. Think it's important to point out, I would never send someone to one of these surgeries without really, uh, feeling that I've done a great job controlling mast cell activation.

I think that's important to clinical outcomes and to, to, um, 

Dr. Linda Bluestein: definitely 

Brayden P. Yellman, MD: healthy recovery. Um, so there's a lot, we're still learning. It's really complicated. There's, there's no standard of care, but it is relevant and we're gonna be learning more about this in, in the upcoming years. 

Dr. Linda Bluestein: And actually it, it's funny timing 'cause the episode that came out yesterday, now this will be released obviously in a few weeks, but the episode that came out yesterday was with Dr.

Petra Linga, who obviously, um, is a neurosurgeon, does lots and lots of tethered cord surgeries. And I, and I've also interviewed Dr. Polo Boase. And [00:46:00] so I'll link both of those episodes also in the show notes so people can learn more about tethered cord and, uh, cervical instabilities, um, at CCI and a a i, um, as, as well.

And I wanna talk about treatments. So you have already mentioned flu to cortisone, midrin, um, IV fluids, a a number of different things. So, so these are, there are no FDA approved treatments for ECFS. Correct. And so these are all off-label, which is, I mean, that's the same thing for, um, EDS. There's no on-label treatments for EDS, so everything's off-label.

Um, so could you talk about, you know, how you approach the treatment of these, um, of these symptoms and, uh, what you find most effective? 

Brayden P. Yellman, MD: Yeah. So, uh, I agree that most of the tools that we use are in some ways considered off-label. Uh, but I, I would actually point out that if it's, if it hasn't already happened, and forgive me if I'm not as up to speed as I should be, but I know that there've been studies, um, from David's work [00:47:00] that have shown that period of stigma mean absolutely helps in me ccf s uh, and long covid situations.

Um, they've been reviewed, I know they were under reviewed by the FDA and we're relatively certain at some point, if it hasn't already happened, that that will become period of stigma will become an f FDA approved or, uh, recognized treatment, um, for me, ccf s mm-hmm. So I did wanna point that out. Mm-hmm.

Really start with. Comorbid conditions, right? You don't look at someone with me CF s and just treated as me ccf s you have to start breaking things down into sub components. And I think this is true in the care of lots of complex chronic illnesses. I think it's true of, you know, my rheumatology colleagues when they're looking at something like lupus, which is a multisystem illness, and what systems are affected and how are you going to help with those specific issues.

And so are there, you know, FDA approved or recognized treatments for POTS and orthostatic intolerance? Yeah, I mean, that's where IV fluids and compression clothing and oral fluid and salt loading and fluidic, cortisone and midrin and [00:48:00] Dr. Dopa really come in. Um, so, so those are kind of recognized for that comorbidity.

Um. We have a long way to go in our understanding and sort of dissemination of knowledge when it comes to mast cell activation syndrome. But if that is present, we actually have a lot of tools that are known to be mast cell stabilizers. Uh, and that can affect mast cell numbers, et cetera, and can really help reduce the symptoms, uh, and secondary and tertiary comorbidities associated with that illness.

Uh, I screen patients for. A degree of what I kind of generally refer to as a sympathetic overdrive. This constant activation of sympathetic nervous system. And yes, sometimes that is directly a result of the, uh, physiological stressors that they're undergoing into denomi, but there can be an additional component of it that's really difficult to treat.

And so I will use things that we know, calm down the sympathetic nervous system, right? Clonidine has been used for years and years for blood pressure, especially things like an ER [00:49:00] situation. 'cause it can really drop blood pressures when they're raised because someone's in neurosis or having a heart attack because they have high cortisol levels, because they're under physiological stress.

It's, it's an alpha blocker. It's blocking sympathetic signaling, saying with beta blockers. That's really why we use beta blockers, not because slowing the heart rate is a treatment for pot. Specifically, it's reducing cortisol response, catecholamine response, the overall secondary symptomatology of that, that huge surge of, uh, physiological stress that people are experiencing.

Um. It sounds blasphemous. A lot of people disagree with me, but this is a field where I think benzodiazepines are really helpful for sympathetic overdrive. Mm. Um, you know, we always refer to them as, as not being great medicines because they, they don't address the core underlying features of anxiety.

Right. It's the neurotransmitter levels that are different, but when someone's having pot symptoms, when they can't be upright in their bodies. Sending distress signals that peripheral, you know, the dirtiness of, of benzodiazepines, that peripheral nervous [00:50:00] system effect is beneficial. It helps people tolerate other medicines that they don't otherwise tolerate.

I've seen people, uh, who take a Tylenol and don't sleep for two days. Right. And, and is that the pharmacologic, uh, response to acetaminophen or is that a, like a hypersensitive, neurological response to it That can be mitigated with tools we have? Absolutely the latter. Um, you know, I, I assess for the impacts of hypermobility of small fiber polyneuropathy, of fibromyalgia, of gastrointestinal dysmotility, of possible vascular complications like may turner's or nutcrackers or median arcuate ligament syndrome.

I assess for the neuro anatomical, uh, complications we just assessed for, and you kind of break it down into those components, uh, and try to, uh, provide individualized treatments for each of those. Comorbid conditions. Um, and yeah, some of those are FDA approved, some of them are just sort of accepted in the field, and then there is a lot of stuff that's still off label, but [00:51:00] also.

Safe. Also things we've been using for 30 years in, in medicine. So for example, uh, I'm thinking about use of very low dose aripiprazole, two milligrams or less. Seems to be really helpful for reducing sensory sensitivities to bright light, loud sounds. Multiple things going on in a sensory environment around us.

We know that two milligrams of aripiprazole or less is generally safe and well tolerated. We use dextromethorphan over the counter dextromethorphan up to 15 milligrams three times a day, sometimes less. And some people find that it helps reduce the incidence or duration or intensity of their post exertional malaise.

It helps them avoid post exertional malaise To begin with is, is this as an off-label treatment, something that, because it's off-label, that clinicians should feel scared to use? I mean, it's dextromethorphan. Um, mm-hmm. So there's, there's a lot of examples, uh, like that off-label that are still really helpful and I think that we can, can use without fearing harm to our patients or fearing, uh, [00:52:00] legal retribution.

Dr. Linda Bluestein: And when it comes to benzodiazepines, given the, the potential, uh, risks for, you know, dependence and things like that, are there any certain precautions that you take or do you dose them in a certain way to, uh, help mitigate that? 

Brayden P. Yellman, MD: You know, um, I, maybe I have a unique position on this as well, but, uh, I, I will say in treating people with me, ccf s and using benzodiazepines, do people develop a, uh, physical dependence?

Of course they do, but they also develop physical dependence on all kinds of medications. Look at venlafaxine, for example. Mm-hmm. How hard it is to get a patient off of that. What I haven't seen, I have not seen psychological addiction or psychological dependence. I just haven't seen it in me cfs.

Patients with these drugs. Um, they, it sounds bad when they say, oh, I take Lorazepam and then that really helps my symptoms. But, uh, if you really get down to why are you having the [00:53:00] symptoms in the first place, in what ways is it helping? If you're really paying attention to how they're using it, uh, when they're using it, giving them clear, uh, instructions on that, I just haven't seen, I.

Misuse of these drugs at all. Um, so yeah, of course a physiological dependence is not great. Is there an association with long-term benzodiazepine use and potentially earlier dementia? Yeah, there are concerns here. Um, but I would argue if you have a patient with untreated orthostatic intolerance for years and years and you don't identify that and there's actually globally reduced cerebral blood flow, might that ultimately be a risk factor for cognitive decline in the future?

We don't have the data, but I think it's reasonable to assume it could be. Um, so, you know, I, I would say the same precautions we would have for using benzodiazepines in any other circumstance, but just not this, this terrible fear, this idea that they have no place in medicine anymore. I just, mm-hmm. I liken it to.

NSAIDs and to opioids, right? For at one point, NSAIDs were the greatest, and then they caused gastrointestinal ulcers and renal disease, and then you can't use 'em at all. [00:54:00] And then you use opioids. And now we find out how awful opioids are, right? There's a time and a place for everything to be used responsibly, and you just have to consider the circumstances.

So I sort of take that approach to benzodiazepines as well. And, and again, this is not to say this is the only treatment or the major treatment, um, but it's a tool that, that we've been using for years and years and years in medicine that we shouldn't forget about. 

Dr. Linda Bluestein: Yeah, no, I think that's an excellent point because the pendulum tends to swing so far in one direction and then so far in the other direction.

And, and you're right, I think, I think a lot of people are, you know, tend to, um, look at things very black and white. But these, uh, these cases are so complex and, uh, patients have. Such poor quality of life in so many instances. So we have to really weigh the risks and benefits of everything that we're doing and really think about, you know, the person in front of us and how can we really help them to, to feel better.

I mean, are we really doing them a disservice if we don't prescribe something just because we're afraid of, of, uh, you know, potential [00:55:00] problems like that? So I think those are excellent points. Yeah. I mean, you can make 

Brayden P. Yellman, MD: the same argument for how we, I think are perhaps under treating pain now with our fear of using opioids.

Mm-hmm. You know, in the acute setting that's very different than chronic use. That's another conversation. 

Dr. Linda Bluestein: Yeah. Yeah. No, definitely. And I, I, I definitely have witnessed, but yeah, we could talk about that for a while. I've, I've, I've seen some really ridiculous things and it's just, it, it really is crazy. So, uh, before we wrap up, I just wanna ask if there's anything in particular that you're excited about from a research standpoint or any particular, uh, projects that you're doing, anything like that.

Brayden P. Yellman, MD: We have, we always have several, uh, projects cooking in the background. It's, it's hard to say too much until we get a little further into them, but I would say in general, sure. Uh, a couple things I'm, I'm mostly excited about, um, one of the black boxes in this field has been how do we address. And you probably haven't heard me say anything about it yet.

The [00:56:00] metabolic aspects of this illness, the, the clear inability to provide as much a TP to have as much aerobic metabolism before we switch into anaerobic metabolism. And that is clearly part of the illness. Is it the driver? Is it, is it, uh, secondary? We're still trying to learn that what's its role in PEM?

Is it why we have PEM? These are all things to still be discovered. And there's been a lot of great research done in that field. But I would also say we are finally starting to crack the egg just a little bit on some treatments that might be beneficial for improving just the overall weight of fatigue that just the heaviness, the absence of energy.

Um, and so that's a really exciting kind of area that we may see some progress in in the next five years. And then I think in general, as horrible as COVID-19 was acutely, but also from a long covid perspective, I. There's a silver lining and that is that it is mainstream and legitimize these illnesses, more clinicians are aware of, of this type of [00:57:00] symptomatology.

More clinicians are ready to listen to patients, to not dismiss them, to not just say you have the yuppie flu, or you're, you're just being lazy, or you're just tired, or you're just depressed, or you're just anxious. There's a tide changing and um, people with these illnesses are gonna be treated. Like they should have been treated all along with a little more respect.

Mm-hmm. And with some, uh, real, um, empathy for, for what they're going through and will start to receive even at, at a very basic level, like we talked about before, just support from their clinicians to have time off of work to, uh, to not feel like they're crazy in their head when they can't do things. To, to have their family members be, you know, speak to the clinician and, and sort of understand what their family member's going through so they don't gaslight their own family member or loved one.

Um, there's a real change happening there as well. So those are some things to be excited about. 

Dr. Linda Bluestein: And the gaslighting is definitely a huge problem, uh, you know, that people really suffer from. And, and I [00:58:00] always like to end every episode with a hypermobility hack. Uh, do you have a hack that you can share with us?

Brayden P. Yellman, MD: Um. So this is really for patients, and when you're talking to your clinicians, and I think it's gonna help all of us learn a little bit more about the dynamics of hypermobility, and that is when you have a symptom that is intermittent, or that waxes and wanes, or that's worse versus not as severe, think about.

Your position in space, what is your body doing? Are you upright? Are you partially reclined? Are you laying down? Are your legs elevated? Are they on the floor? Is your back flexed or extended? Is your neck rotated? Are you flexing or extending your neck? Um, seems to be important for, for patients that I see being in Salt Lake City, Utah with altitude, are you at altitude or are you at sea level?

What is the barometric pressure? These type of details when you have [00:59:00] symptoms that come and go that worsen and get better. Or things that we found to be relevant. And there's different relevances for relevancy for different patients, but you know, understanding, hey, the longer I'm upright as the course of the day goes on, these symptoms get worse.

Uh, or I wake up with severe headaches, but as I get into an upright position, things start to improve. Looking for those kind of patterns. And how position and biomechanical, uh, just arrangement in space, what your posture is, what, where, where your head is rotated, et cetera. These are details that can really help clinicians figure out what's going on in a very dynamic, uh, situation, in a situation that is, you know, the anatomy's different to some degree for everybody with connective tissue disease.

So think about those variables when you're looking at your symptoms of how they affect those symptoms. 

Dr. Linda Bluestein: I, I love that. And I, and I'm in Denver, I'm right now in Littleton, so I'm a little less than 6,000 feet and, and [01:00:00] just had some friends here and this guy's super fit, and we went up to about 8,000 feet and oh my gosh, it was amazing.

The, the difference in, um, you know, like you said, altitude and, and different environmental factors. And so I think that's, those are great tips. I really appreciate that. And where can people learn more about you and the fabulous work that you're doing? 

Brayden P. Yellman, MD: So the best place to learn more about what we've talked about today is probably our nonprofits website.

Uh, this is the Bateman Horn Center of Excellence. Um, so B-A-T-E-M-A-N-H-O-R-N-E Center. Um, and we have all kinds of YouTube videos and educational resources that are designed for clinicians, for families, for patients. We have links to how to do the NASA lean test at home. Um, you could really lose yourself on that website.

And I think, uh, you know, as a nonprofit, it's really our mission to try to get this information out so that more people can access it. Um, it's all [01:01:00] free. It's, it's, uh, we're always updating it. So please take a look there for, uh, any. Additional learning that you may want to purs, um, pursue. 

Dr. Linda Bluestein: Well, I'm so grateful to you for taking the time to chat with me today.

I know that you're very, very busy. Um, I know people are really going to enjoy hearing this conversation and we'll find it really, really informative. So, so thank you again. 

Brayden P. Yellman, MD: Thank you, Linda. It was a pleasure.

Dr. Linda Bluestein: Well, that was such a great conversation with Dr. Yeoman about me, CFS, something that I feel like is so misunderstood, and we know that delayed diagnosis is really, really common and very problematic. So I hope that you'll share this episode with other people who are potentially suffering from M-E-C-S-F, or clinicians who might be seeing this population.

And I wanna thank you for listening to this week's episode of the Bendy Bodies. With the Hypermobility MD Podcast, you can help us spread the word about joint hypermobility and related disorders by leaving a review and [01:02:00] sharing the podcast. This really helps raise awareness about these complex conditions.

If you would like to dig deeper, you can meet with me one-on-one. Check out the available options on the services page of my website@hypermobilitymd.com. You can also find me, Dr. Linda Bluestein on Instagram, Facebook, TikTok, Twitter, and LinkedIn. At Hypermobility MD you can find human content. My.

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