Episode 70 – Autoimmune Dysautonomia with Dr. Schofield

00:00:01 Announcer: Welcome to the Standing Up to POTS podcast, otherwise known as the POTScast. This podcast is dedicated to educating and empowering the community about postural orthostatic tachycardia syndrome, commonly referred to as POTS. This invisible illness impacts millions and we are committed to explaining the basics, raising awareness, exploring the research, and empowering patients to not only survive, but thrive. This is the Standing Up to POTS podcast.

00:00:29 Jill (Host): Hello fellow POTS patients and most appreciated people who care about POTS patients. I'm Jill Brook, and I'm excited for today's episode of the POTS practitioners because my guest is someone doing such important work who has published articles that have truly changed my life for the better and have probably done the same for some of you. So, I'm going to try not to be too giddy as I get to speak with her because she truly is one of my heroes. Dr. Jill Schofield is a physician and researcher who is a leader in autoimmune dysautonomia and related conditions. She is founder and director of the Center for Multisystem Disease in Denver, Colorado. She graduated from the University of Colorado School of Medicine and completed her internship and residency in internal medicine at the Johns Hopkins Hospital. In 2014, she uncovered the important association between autonomic disorders and anti-phospholipid syndrome, which we will explain, so don't worry if you don't know what that is. Dr. Schofield has advanced training in multispecialty autoimmune disease and thrombosis. She is a founding and active member of the Masterminds International listserv, which means she is one of the very top experts, leaders, and educators in mast cell activation syndrome. Dr. Schofield has published numerous research papers and regularly presents her work at national and international meetings. Dr. Schofield was the recipient of the Dysautonomia Support Network Patients’ Choice Game Changer Award in 2019 for her work in the use of immunoglobulin therapy in autoimmune dysautonomias. And again, don't worry if you don't know what that is, we'll talk about it. And Dr. Schofield has developed considerable expertise in searching for the underlying cause of dysautonomia in both adults and children who fail to improve with conservative therapies. Dr. Schofield, thank you so much for being here today.

00:02:35 Dr. Schofield (Guest): Thanks for having me, Jill. I really appreciate it.

00:02:38 Jill (Host): And it is true - there's a particular article of yours from I think, 2018, that I take with me every time I go to the infusion center, and so really...

00:02:48 Dr. Schofield (Guest): Really? Good! I'm glad to hear that.

00:02:50 Jill (Host): ...have been discussed several times when I needed it. So you founded your clinic to specialize in disorders like pots and casts, EDS, Hashimoto's thyroiditis, celiac disease and other kinds of complex autoimmune conditions that affect multiple systems of the body. And we don't hear about very many clinics for multiple systems of the body, we usually hear about clinics for one system, like a cardiology clinic or a GI clinic or dermatology. So, I'm wondering, why did you choose to specialize in the complex things and why did you create a clinic for multisystem disorders?

00:03:33 Dr. Schofield (Guest): Well, one day I hope there will be training in multisystem disorders 'cause I think that formal training - formal fellowship - 'cause I think that's what we need, 'cause these disorders don't fall into anybody’s silo as they currently exist. It's a complicated story how I got into it because I got into it through anti-phospholipid syndrome and dysautonomia, which are both multisystem disorders. And then by doing that work, mast cell activation syndrome and Ehlers Danlos Syndrome quickly took over my practice because they are very prevalent, and...and all of these things, as you know, overlapped to tremendous degrees.

00:04:11 Jill (Host): So anti-phospholipid syndrome that you just mentioned, that is one of your claims to fame that you discovered a connection between I believe POTs and migraines and anti-phospholipid syndrome?

00:04:24 Dr. Schofield (Guest): Autonomic disorders and anti-phospholipid syndrome.

00:04:28 Jill (Host): Oh, OK.

00:04:29 Dr. Schofield (Guest): We described that association. Causation is hard to prove, but we published the first case series associating those two conditions and I think it's a really important link. It may not be the most common cause of POTS. Again, I'm using the term "cause" loosely, but it's one of the most important links I think, because if it's missed then there could be devastating thrombotic or clotting complications or devastating pregnancy complications that could be probably easily avoided.

00:05:00 Jill (Host): Yeah. So can you just tell our audience who might not know what anti-phospholipid syndrome is?

00:05:06 Dr. Schofield (Guest): It is an autoimmune clotting disorder. It's a cousin of lupus in that actually it was first described in patients with lupus and about 1/5th or so patients with lupus actually have anti-phospholipid syndrome. If it's occurring in association with lupus, we call it 'secondary anti-phospholipid syndrome,' but it was later learned that it more commonly occurs without an association with lupus, and we call that 'primary anti-phospholipid syndrome'. But the layman's term or the layman's name for it is sticky blood, or it's also called Hughes syndrome after Dr. Graham Hughes who's the rheumatologist in the UK who first described anti-phospholipid syndrome in 1983. And it's very complex because there are criteria, and in order to meet the criteria you have to have either had a clotting event - a clotting in veins like a pulmonary embolus, or a deep vein thrombosis, or a clotting in arteries such as ATA or stroke - and/or particular pregnancy complications which are quite severe and particular lab criteria. And if you don't meet those then you don't have the syndrome, but you're just said to have the antibodies. So that's kind of frustrating in it's another case of, you know, we wait until you have a what could be a catastrophic or fatal event before we diagnose you with something. So that that's frustrating, but the problem with the way that in which that arises is that the criteria - they're called research or classification criteria - were intended to capture a uniform group of patients and the worst patients for research purposes in what's a very heterogeneous condition. But there are no diagnostic criteria, so those research criteria get used for diagnosis and it just leads to a lot of confusion. But it's another of the systemic autoimmune diseases like lupus or rheumatoid arthritis or Sjogren's. It actually often goes together with Sjogren's, particularly in patients with POTS. There's often an overlap. So, it can have some of the similar symptoms that are seen in systemic autoimmune diseases like joint achiness and fatigue and whatnot, but the hallmarks are clotting in veins or arteries and severe pregnancy complications.

00:07:25 Jill (Host): OK. And do you have ways that you can treat it if somebody does have it?

00:07:29 Dr. Schofield (Guest): Well, I screen many of my POTS patients for it because I don't want to miss them. There are certain features that kind of make me think more that somebody might have those antibodies and make me more likely to test for the antibodies. I'm not answering your question directly, but I want it...I want to explain a little bit of background. And those are pretty severe refractory migraine, often with aura like visual phenomenon that occurred before the headache or the migraine, livido verticular, which is a lacy like pattern to the skin, most commonly found on the arms and the legs around the knees. People often notice it more prominently when they get out of the shower when there's a sudden change in temperature. Reynaud’s - that occurs, not the Reynaud’s that's in every finger, it's present from a young age that runs in your family, but the Reynaud’s it kicks off kind of together with some of these other things, such as together with POTS and with migraine, make one suspicious of anti-phospholipid antibodies might be involved, and of course any blood clotting or superficial thrombophlebitis or any kind of recurrent miscarriage or later miscarriage after 10 weeks, preeclampsia. And memory loss - it can be hard to sort out from brain fog that's associated with POTS and even mast cell activation syndrome, but patients with significant anti-phospholipid antibodies or syndrome, they often have blank spells in their thinking that a lot of times the patients can kind of tell it apart from brain fog. So in terms of the treatment, obviously, if somebody’s had a blood clot, they'll be on blood thinners, usually indefinitely if they have anti-phospholipid antibodies, because there would be associated with a higher risk of clotting again, if you have those antibodies. But what often happens in my practice is, I'm trying to identify people before they have a blood clot. So it becomes tricky because you're not going to put somebody who hasn't had a blood clot on a blood thinner for no good reason. But last year, I think it was last year, we published a paper of 75 patients who had refractory migraine, anti-phospholipid antibodies, and response to antithrombotic therapy - meaning aspirin - clopidogrel, which is another kind of a cousin drug of aspirin that also inhibits the platelets or/and and/or anticoagulation. And that was a phenomenon that was first described by Dr. Hughes but had never been published in a large group of patients, just kind of small groups of patients. He also had shown that some of these patients with...with anti-phospholipid antibodies who have refractory severe migraine - and by refractory, I mean they just don't respond to the usual migraine medications or they respond very minimally - go on to develop stroke. And so, over a period, often of several years of having the migraines that these were young people. And anyway, so he described this phenomenon and and he noticed it in the patients who had a clot that when he put them on blood thinners, he started hearing a lot of patients say, "My migraines I've had for 10 years are just completely gone now." And so, he actually started a heparin therapeutic trial many years ago where he actually did treat people with heparin and and that was before the new oral anticoagulants were available and showed that many people, their headaches did go away. So that's one way in which the presence of the antibodies might change management and I saw one of these patients this week who was on a blood thinner and we added Plavix 'cause she was having severe headaches and she actually had an episode of what sounded like a TIA transient loss of vision for about 60 seconds for no reason. And that, in the presence of she had multiple anti phospholipid antibodies, I added on Plavix and she noted then that her headaches completely went away from one a day to not within three days of starting the Plavix. So anybody where that's happening, that tells you that the headaches were due to sticky blood and probably a good idea to stay on the blood thinner and the Plavix, even though many doctors...even she had already been told, "You shouldn't take Plavix and the blood thinner." And so I show them the papers and we try to educate doctors one at a time because there is no patient that I've ever seen who's experienced that phenomenon, who would even consider going off the drug or drug that made their headaches completely go away when they have multiple of these anti-phospholipid antibodies. We saw very little bleeding in these patients - in these 75 patients. It was a retrospective study. You can sometimes draw the wrong conclusions, but it was 75 patients. It was a lot of patients. And I think that patients who have this phenomenon where they can tell on the occasional person with warfarin and for example, Dr. Hughes liked to describe, they could tell what their INR was, which is the blood test used to monitor the level of Coumadin 'cause it varies every day. They could tell, based on their symptoms, if their INR was good or not good. And that's...that's another part of the phenomenon that is seen so they can almost use their symptoms as a gauge to the right regimen they should be on. There is no blood test for overall blood stickiness, unfortunately. That would make our life easy if there was.

00:13:03 Jill (Host): OK. So are you saying that they're all around dysautonomia symptoms get better? 'Cause what was going through my head is if somebody has anti-phospholipid syndrome and POTS, do they have a double whammy of blood pooling, making their brain not get enough blood but also sticky blood? Or is it more the sticky blood is responsible for it, do you think?

00:13:25 Dr. Schofield (Guest): This is just my hypothesis. You know, the small fiber nerves are these tiny, fragile nerves, and they're actually perfused by blood vessels that are smaller in diameter than the diameter of a red cell. So if you had sticky blood, that might be an area that's more vulnerable. A lot of neurological phenomenon are seen in patients with anti-phospholipid antibodies. And we've demonstrated that they're due to sticky blood by their response to making their blood less sticky. But I think that if we can catch people early, like adolescents who are just starting with this phenomenon, it seems like getting on the right...usually it's Plavix, clopidogrel that they usually don't aren't as severe as the adults, who often might need both therapies that blood thinner and an antiplatelet agent. It seems like it stabilizes their POTS, but...and it may be because, OK, their nerves are kind of taking a hit by not getting enough blood flow, but they're not so far gone that they need more. It seems that way, but I don't know 'cause we published the paper with regard to migraines, 'cause we wanted to keep a uniform population of patients, but the other...there are a number of other symptoms that are listed in that paper that, and people who report, improve and some of them you're not sure how exactly those things would improve, but they do. But the second most common one is the memory loss that improves, too, often dramatically, and that's one way that people have been able to tease out, OK, this memory issue is from my sticky blood, and this one from my dysautonomia. There's a long list of symptoms I have on there, and POTS is on there, but it's not...it's not the striking improvement that you see, like with the migraine and the memory loss. I think that there's two phenomenon going on in anti-phospholipid syndrome. There's sticky blood that is treated with anticoagulation, but there's more going on with the immune system. There's complex issues with the immune system. And so, the people with severe autonomic neuropathy with anti-phospholipid antibodies or anti-phospholipid syndrome may need IVIG and they respond often dramatically to IVIG. And so there...there are many people who are on both or on IVIG and they're on antithrombotic therapy. But to answer your question about treatment, I mean that's the other treatment that I think, if there is the persistent presence of anti-phospholipid antibodies, it opens up the door to treatments like IVIG. They're not necessary in everybody with the antibodies, so my approach has become to start by treating the more conservatively, like treat the POTS with the Band-Aid POTS treatment, right? You know, like vasoconstrictors and salt and exercise and things like that, and treat any mast cell activation that's usually also present. And then if they're not improving with all of these drug trials, then to me it says, OK their autoimmunity needs to be treated. And that's kind of how it usually shakes out, but I definitely have people, even people who have four anti phospholipid antibodies who do not need IVIG, they improve by just targeting their POTS, targeting their mast cell with these more conservative therapies. So I always give like 6-9 month trial try to improve things with the more conservative therapies, 'cause IVIG is not only that is extremely expensive and hard to get approved, it's burdensome. It's an all day infusion on a regular basis.

00:17:09 Jill (Host): Yeah, maybe we can talk about IVIG now because you are really one of the very top leaders on using that in dysautonomia. Do you mind giving us your high level when you use it and...

00:17:23 Dr. Schofield (Guest): You know it's a game changer therapy in the selected group of patients. Somebody who doesn't have autoimmunity, it's not going to do anything. If anything, it will probably make your mast cell worse. That is how I've come to define who needs it. It's the same concept, as you know, the people who have a structural issue like a CSF leak, or untreated severe cranial cervical instability. They often also do not respond very well to these band aid medications targeting POTS or targeting mast cell. They just don't respond to anything. So then if they’re to respond in any kind of meaningful way to things always is a light bulb that OK, we're missing something here. And in the case of the autoimmunity, I'm not usually missing it. I know it's there. I just know that not everybody who has autoantibodies needs IVIG, and the people who don't need IVIG, I always recommend Hydroxychloroquine or Plaquenil, and it doesn't do anything for COVID but it's it's a great drug for autoimmunity kind of stabilized autoimmunity. So, it's not like we're not treating that piece of it, it's just that it doesn't need the bigger gun of IVIG or occasion we use rituximab, which is another immune potent immune modulatory therapy.

00:18:40 Jill (Host): So to be clear, for people who are not super familiar with IVIG, it's not that it gets used on any old autoimmune condition, right?

00:18:44 Dr. Schofield (Guest): Actually, if you look up any autoimmune disease in the medical literature, you can find reports of benefit from IVIG. It's just that there are easier to give, less burdensome, time-consuming infusions like IVIG, and cheaper, less expensive medications that are used for most other autoimmune conditions and then there's just a few that have shaken out as where IVIG seems to be the best therapy. And so, there aren't really that many FDA approved conditions for IVIG, but three of them are immune mediated disorders of the large fiber nerves. So actually the very first case report of using IVIG in a patient with dysautonomia was thought to have a pure dysautonomic variant of Guillain Barre syndrome, which is one of the large fiber and mediated neuropathy for which it's FDA approved. So that was how it got approved and he had a dramatic response and he probably didn't really have Guillain Barre, he probably had small fiber neuropathy. But you know, as you know the the technology for diagnosing small fiber neuropathy is quite new, so people went undiagnosed. So yeah, some of the neurological conditions are FDA approved indications for IVIG. And then there's some dermatological conditions, too. It was just a few spattering of things. So most of the other autoimmune conditions are treated with other drugs. But...and another one called Kawasaki disease and kids is first line and therapy is IVIG. So I think, you know, that was how IVIG came to be the kind of go to drug for small fiber neuropathy, because once that case report was published then other ones got published in the...and you know then we ended up - Dr. Oaklander and and myself - ended up doing, you know, doing two large case series retrospective of our patients we had treated. And there is an ongoing randomized clinical trial that Dr. Romito is running at Utah Southwestern. It's a long process to get FDA approval. They want to see large randomized gold trials and that takes a long time.

00:20:58 Jill (Host): Right, right. And we all have our fingers crossed for that because it'll make it so much easier to get it approved by insurance.

00:20:59 Dr. Schofield (Guest): Exactly

00:21:02 Jill (Host): So, have you had any patients who were on IVIG and getting good successful results who were then able to wean off of it?

00:21:14 Dr. Schofield (Guest): That’s a great question. I've been treating people - I don't know - for up to 10 years. And that's about as long as almost anybody. So, we're like very early days in this where there aren't studies in this group. But we can draw from CIDP, which is like chronic form of Guillain Barre that has been FDA approved indication for IVIG for a very long time because it's diagnosed with EMG nerve induction testing. And that's been around forever, so it's very easy to diagnose. I think when I've looked at that data in the past, my recollection is about half of the patients who respond to IVIG are eventually able to get off it, but many it takes many years of therapy. The best way and the way they do it with CIDP is to try stopping the therapy and if the symptoms come back, you have a plan in place to get back on it. And I've had a number of patients where therapy was interrupted because of the insurance company saying they're not going to approve it anymore, and we have to spend several months trying to get it reapproved. And if it's in the first year, those patients always get...100% of the time have gotten worse. So, that's something that I think it's very reasonable and my rule of thumb is once somebody has been on the dose - their optimal dose, which takes time to figure out - for at least one year. So usually not until someone's been on it for at least about a year and a half. And then most of the people get worse who've tried it, and they end up back on it. I had one patient that I thought might might be able to get off because she got diagnosed very quickly. She just happened to live in Denver. She just happened...she was a nurse and and she she found me. We got her in quickly and she had four anti-phospholipid antibodies and five novel Sjogren's antibodies. She had a lot of antibodies. And her case was kicked off by a viral illness, the classic story of somebody would autoimmune POTS - was perfectly well, got a virus. In her case it was gastroenteritis and she recovered from that but then developed this new constellation of symptoms that was like POTS and she and she was taken seriously, unlike many people, and she got all the tests, appropriate testing got quickly diagnosed with POTS. So she got on IVIG. She she was a nurse so she did her drug trials of the other agents pretty efficiently and quickly, and she wasn't responding to them. So she got on IVIG maybe within six months of diagnosis. So I thought she had a good chance to get off, but she...she, well, she got off but she got worse after maybe six months. And IVIG has a long half-life, so it sticks around in the body for four months, so that kind of fit the right time course of what you might expect.

00:24:14 Jill (Host): For people who don't know, I think that IVIG is a whole bunch of donor antibodies, correct?

00:24:21 Dr. Schofield (Guest): 10,000 different donors pooled immunoglobulin, because it was actually first used over 30 years ago for what you would think it might be used for, which is immune deficiency. So patients who don't make enough antibodies for whatever reason their immune system is kind of the opposite of autoimmune, they're not making enough antibodies. So they got pooled antibody and the reason for the pool from all the donors is to try to get broad coverage of any possible infection that person might come across. So that's the reason for all the donors. So it's not really intuitive at all that it would work for autoimmune disease because if you have too much immunity, why would we give you more. Too many antibodies, we're going to give you more. That doesn't make sense, right? But nobody did try to use it for that in the beginning. But what happened was, as often happens in medicine, is somebody noticed they had a kid, they had one patient, he had immune deficiency plus ITP, which is immune thrombocytopenia - autoimmune attack on the platelets. So they noticed every time he got IVIG for his immunodeficiency that his platelet count went up. So then they got some other kids and they said, "Yeah, we saw the same thing with these other kids." So then they started studying another autoimmune conditions and found that [inaudible] people did better from an autoimmune standpoint, if they had a higher dose. So there are about 10 different complex mechanisms of how it might modulate the immune system in patients with autoimmune diseases. And just kind of the simplest one is to say it's negative feedback. This probably isn't at all correct, but is just a way to think about it. Every system in the body has negative feedback regulation to keep things in check. So, if you flood the body with...with antibodies, then that might tell the immune system get slow down, stop making so many antibodies. It has a great advantage over every other immunomodulatory therapy except plasmapheresis, in that it doesn't suppress the immune system. And Plaquenil is also in that category where it modulates but doesn't suppress the immune system. So that's the one advantage it has particularly, you know, in the time of COVID when people were nervous to use rituximab. And so that that is the one advantage that IVIG has, but there are the disadvantages of just being long infusion times and very expensive and stuff.

00:26:45 Jill (Host): So you had mentioned plasmapheresis, which I believe is a procedure to remove antibodies from the blood. Why did they use that instead of...it seems like a lot of trouble to collect donor antibodies from 10,000 people. It seems just intuitively easier to hook up a machine that would take out the antibodies. So why is IVIG preferred?

00:27:05 Dr. Schofield (Guest): Well, it's just the plasmapheresis is a big deal 'cause you have to have a catheter going into your artery and a catheter going into your vein. So it's like a dialysis catheter, and occasionally there can be fatal complications from those lines. It it's just a very transient effect, so you have to keep that line in indefinitely. So it's not really a good long term solution. It could be helpful diagnostically to say, you know, if you're not sure if something autoimmune and you try that and it doesn't work, then it doesn't rule out the possibility that it's autoimmune, but it makes it a lot less likely. I have only used it on extremely rare occasions, I just think IVIG a more practical long-term solution. The other thing is, you know, people can do that in the hospital or can get it, it'll get approved if you're in the hospital, that kind of thing. And for Guillain Barre, either is considered an acceptable acute treatment for Guillain Barre in the hospital.

00:28:00 Jill (Host): OK. So you are a real expert in nerves and neuropathy, and I think small fiber neuropathy is a common factor in a lot of the conditions that you specialize in, and I guess I'm wondering what's up with small fiber nerves. Why are they so fragile? Why are they getting damaged by all these different conditions? And can I tell a quick, funny story, which is that during the pandemic, my neighbor who is a music teacher, decided to give a bunch of us ukulele lessons. And so we were having fun, she got out the little kid ukuleles. And after the first lesson, we had all had a real ball. But one of us couldn't continue because we had neuropathy from a breast cancer treatment, one of us had neuropathy from small fiber neuropathy from autoimmune neuropathy, one of us had it from Type 2 diabetes, and all of us had, you know, we couldn't feel our fingers. And so, there went the ukulele lessons. [Laughter] Jeez, what's up with these small fiber nerves? Is there any way to protect them or heal them faster?

00:29:07 Dr. Schofield (Guest): That's the million dollar question, Jill. I think you bring up a really important point that which is that like if you get a skin biopsy and it shows you have small fiber neuropathy, it doesn't tell us anything about what caused the small fiber neuropathy. In my practice, I’ve long thought that mast cell activation syndrome was the most important cause. And again, causation is hard to prove. So, I was very excited when a few months ago somebody published a paper linking mast cell activation syndrome and small fiber neuropathy. Maste cells love the small fiber nerves so they in the normal state line up along small fiber nerves. They're sending messages back and forth to each other cause the mast cells they line up at the environmental interfaces, but they use nerves and blood vessels kind of to communicate to the rest of the body that they were under attack, if there's a foreign invader identified. So I don't know. I've heard too many patients say - let's say they ate something with red dye and they have mast cell activation syndrome and the red dye fires up their mast cells and they say, "I get this immediate burning all over my whole body and then I take a Benadryl and it goes away," there's no other good explanation besides the mast cells got activated by the red dye or dumping mediators on those nerves or in some way irritating those nerves, and the Benadryl’s calming it down. I just hear that story so many times. And some of the small fiber nerves remember are sensory. They control pain, itch, and temperature sense, and some of them are autonomic, and in my patients that I've done skin biopsies on, I would say about 2/3 of patients have issues with both maybe 3/4, and occasionally someone just has only autonomic or only sensory. And it doesn't always align perfectly with their symptoms, probably because, you know, it's a patchy process. But, there are many causes of large fiber neuropathy, too. I just think nerves are vulnerable to insults. Small fiber nerves are more fragile. They're not protected by that coat of myelin, they're just...they're small. They're just seem like they would be fragile and more susceptible, but thankfully they can regenerate.

00:31:19 Jill (Host): Are there any ways to make them regenerate faster?

00:31:22 Dr. Schofield (Guest): You know, that's a whole field of study outside of my world, but nothing that I know of today in 2022. But treating the underlying cause is what we try to do. If it's mast cell activation, try to work on treating the mast cell activation. If it's autoimmune, treating the autoimmunity and that's again how you know if the autoimmunity needs to be treated, if you treat the mast cell, treat the POTS, and the person is not getting better, that means, you know, there's some ongoing insult to the...presumably to the small fiber nerves. Other things, you know, are those stealth infections like Lyme, bartonella, babesia...those are also potential causes, HIV, hepatitis C...there's a number of causes. Vitamin deficiencies. So, I always try to check US Preventive Health Services Task Force recommends all sexually active people for HIV and hepatitis C, which both can cause small fiber neuropathy. So, I'm always screening for all those causes, and sometimes there's more than one cause.

00:32:27 Jill (Host): OK. So, there's just little tiny, delicate threads that, I guess....

00:32:33 Dr. Schofield (Guest): I feel like that's right.

00:32:35 Jill (Host): ...it doesn't take a lot to hurt them. So, I know that you've been working and publishing on some long COVID patients. Do you feel like long COVID is teaching you anything about dysautonomia?

00:32:48 Dr. Schofield (Guest): Not really, because I just see it as another of the potential insults, of which we've been seeing many other ones all along. I think it's really helpful though, and that it's brought to light to the NIH, for example, these problems that we see. But I feel like, you know, there there's many other potential viruses. For example, a gastroenteritis that caused that nurse’s...kicked off her illness that looked exactly almost the same as another patient I had where it was kicked off by COVID. So, it's long been known that to get an autoimmune disease you have to have a genetic predisposition and then you have to have an environmental insult or trigger. And there probably in reality, I would guess, are more than one trigger like and whatever those triggers are you know might lead one person to get lupus and another person to get anti-phospholipid, another person to get rheumatoid arthritis within the same family. So, I don't really see it as any different than any of the other triggers, really. My approach has been to treat the long COVID patients the same as my other patients, same way, and they usually respond in the same way, at least the subset that I've seen. And I think there can be different subsets of long COVID probably, so it's unsure thaty heterogeneous and patients with more cardiac issues set, but I don't consider POTS a cardiac issue, I consider a neurologic issue. But hopefully it will...it will lead to advancements in the field because of increasing awareness.

00:34:27 Jill (Host): Yeah. So I think maybe more than other physicians you mention lifestyle approaches. Do you mind just taking a minute to talk about what lifestyle approaches you think are important and...

00:34:42 Dr. Schofield (Guest): You have to exercise if you have POTS and Ehlers Danlos. Like, those two conditions are...it's you have to do it. You won't get better if you don't figure out a way to do that. There's the occasional person where exercise...they have severe post exertional malaise and they just cannot exercise. But that is the minority in my practice, extreme minority. And if you have to start with one minute a day on a recumbent bike or 30 seconds or whatever you have to start with, do what you can. Next week try to do a little more, next week try to do a little more. But diet has been so huge. I think it's important for mast cell activation syndrome much more than autoimmunity. I mean, I know there's it's touted more as an autoimmune diet, but my experience is that the people it seems to really help is the mast cell patients who are so sensitive to chemicals and not all of them, but the vast majority just getting on an anti-inflammatory non-processed mostly organic diet - getting rid of all the chemicals. And that's a major lifestyle change for some people, most of the people who come to my practice are already eating that way. But if you eat the SAD diet - the Standard American Diet - is like hot dogs and fries, like not only is there no nutritional value in that "food", but it has also a lot of toxins in it. It's just all these chemicals that mast cell patients are much more sensitive to. And then, many do better with a gluten free and/or dairy free. Some people, it's both some people, it's one or the other. And a low histamine diet - or figuring out what high histamine foods are triggering for you - is also very helpful for many patients with mast cell activation syndrome. So my preference is always for people to do those things first, because the key to treating mast cell activation is figuring out what the triggers are and eliminating them, if you can. So, sometimes people are just so unwell we start with drug trials, but eventually I try to get people to do those dietary things. I've just seen so many people dramatically improved just with those two things.

00:36:48 Jill (Host): So you're located in Denver, the Mile High City, very high altitude, thin air. What do your dysautonomia patients say about changing altitudes?

00:37:00 Dr. Schofield (Guest): I don't think it's a POTS thing, I think it's a mass cell thing again. And I I have a number of people they can tell exactly where they get worse. And we have a number of people leave Denver because they feel better at lower altitude. I think I have two patients who feel better at high altitude. You always see yin and yang in mast cell, right? Like somebody, this makes it worse. Someone that hot makes him worse, the other pretty cold makes him worse. You know, you see all these opposites, but it's very clearly in - at least in my anecdotal experience - activates mast cells. And the mast cells are just sensitive to, like, barometric pressure change, temperature change, and it’s just like finicky, right? So that's what I think it is. I don't think it's POTS.

00:37:40 Jill (Host): Well, we love listening to you about what you've heard from other people. I just have one more question: is there anything on your mind that you wish more doctors or patients understood about POTS?

00:37:54 Dr. Schofield (Guest): Well, we're grateful that most doctors have now heard of POTS, which is just so exciting, because - what - even five years ago, that was not the case. So the next step that I...I have a dream one day people will say they'll treat POTS the same as, say, anemia. If somebody has pots that's severe enough to keep them, you know, they're 20 years old and they can't go to school, they had to drop out of college or go live with their parents, just the same as if someone had anemia that was severe enough that caused that kind of functional limitation. Any doctor of any stripe would say, "You better figure out what's causing this anemia." Do they have a bleeding ulcer? Do they have autoimmune attack on their red cells? Do they have leukemia or, you know, what do they have? And let's treat that, instead of just pumping a bunch of blood into them every week. And I, I think that today people have heard of POTS. They know that it can cause disabling symptoms. They know about giving salt and exercise, and then it just maybe try a couple of medications and that's it. They don't think this could be a presentation of an autoimmune disease, this could be due to this, this could be do that. So, that's what I hope one day people will understand. I think that to move forward, we have to get insurance companies to recognize that there are complex patients where there needs to be more time spent with one doctor who's focusing on all these things, but also in order for that to happen is we have to develop some sort of training program for doctors to have a formal way to be educated about these conditions instead of where we are today, which is learning...learning from each other, learning as we go, learning from the physician Listserv, which is invaluable, as you know. So, those are the two things that I hope one day will change, 'cause you can't figure out POTS in a one hour visit, you just can't.

00:39:47 Jill (Host): Amen! Well, we thank you so much for being that person who's looking at the big picture and helping to educate others and putting the puzzle pieces together, 'cause not very many people are. So, like I said, some of your work has directly improved my life, so I'm just so grateful.

00:40:03 Dr. Schofield (Guest): I’m so happy to hear that.

00:40:04 Jill (Host): And we thank you for the time that you take to volunteer for Standing Up to POTS on the Medical Advisory Board. And I'm just, you know, so happy that your brainpower and your compassion is on our team. So, thank you.

00:40:20 Dr. Schofield (Guest): Thank you. And the same to you for sharing your expertise and pouring all of your time and energy into helping other people have an easier time than you did some years ago.

00:40:30 Jill (Host): Oh, well, thank you. Thank you very much. And hey listeners, as always, this is not medical advice. Please consider following us because it helps us get found by more cool people like you. Thank you for listening. Remember, you're not alone and please join us again soon.

00:40:48 Announcer: You can find us wherever you get your podcasts or on our website, www.standinguptopots.org/podcast and I would add, if you have any ideas or topics you'd like to suggest, send them in. You can also engage with us on social media at the handle @standinguptopots. Thanks for listening and we hope you join us. This show is a production of Standing Up to POTS. © 2022 Standing Up to POTS. All rights reserved. [Transcriber’s note: If you would like a copy of this transcript or the transcript for any other episode of the POTScast, please send an email to volunteer@standinguptopots.org]