#5 How our understanding of ME/CFS, fatigue and pain has progressed over the past decade with Lucinda Bateman M.D.

[MUSIC PLAYING] Welcome to Make Visible, the podcast Shining a Light on Complex Chronic Elness. I am your host, Emily Kate Stevens, and I've been living with an energy limiting condition since 2020. Here, I will speak to the world's leading experts to bring you the latest science, research, and insights into invisible illnesses, including MCFS, EDS, fibromyalgia, pots, long COVID, and more. Welcome to Episode 5. Whatever brings you here, your condition, your medical curiosity, your caring capacity, you're welcome, and we love hearing your thoughts and feedback. We are trying to create a regular schedule with this podcast, but when our timing slips slightly, please forgive us. We are a small team, the majority of whom suffer from chronic illness. And we try to practice the pacing that we talk about with these experts. I do not take for granted the position of privilege that I am in to speak to the people to whom I have access for this show. And this week, once again, it's one of those people that I met, and I thought, why can't I have this person as my doctor? This week, I had the absolute pleasure of speaking with Dr. Lucinda Bateman, the chief medical officer of the Bateman Horn Centre. She is an MCFS and fibromyalgia clinician, physician, researcher, and educator, and an absolute powerhouse of both knowledge and humility. The Bateman Horn Centre has been at the centre of MCFS and fibromyalgia research for the past decade, with Dr. Bateman guiding that ship. With intense experience gathered from seeing large numbers of chronicly ill patients across decades, Dr. Bateman here gives us an overview from her perspective of where we are in 2024 looking at the research, the medical community, and the lived experience of patients. Dr. Bateman, thank you so, so much for joining me today. Initially, your work came from a very personal place. I believe that it's from your sister actually suffering from, was it time, DEMI CFS at the time? No, nope. It was really called chronic fatigue syndrome, and it was just starting to be recognised at the time. And I was in a small group practice for internal medicine for most of the 90s with three other women and got exposed to the illness, including in my sister, and also fibromyalgia, and got interested, and then decided to change my scope in 2000. And I left my internal medicine practice and opened a small private practice for fatigue consultation. And that is what helped me get extensive experience just in the trenches with patients trying to make it diagnosis and figure out how to treat them. And then we grew to, including research, and gradually my private practice grew, as well as, I had started a small nonprofit that was called Offer, Organization for Fatigue and Fibromyalto Education or Research, that was a working board and very small, not much money, to really work on educational efforts and things that I couldn't do in the office, right, to help further the cause. And so in 2015, the board of offer and me, we talked and decided that we were going to combine my private practice rebrand the nonprofit as Bateman Horn Center, and the nonprofit would take over management of the Clinic Research Center and help expand the educational arm. So that's how the Bateman Horn Center was born in 2015. And then enable you to, I don't really see how you could have put much more time into clinic or into research, but it didn't enable you to take your work in a different direction. 'Cause you still see patients, but just doing PubMed search whilst I was doing my research. And I think I came up with, I think it's averaging about a paper a month that you have your name on over the past couple of years. So the work that you do is prolific. So setting up the Bateman Horn Center in the way that you did it, enable you to focus or diversify. - That's a great question. And my plan worked out pretty well actually. And it was to take the responsibility of financially owning this small business off of me, make it a nonprofit that can bring in other sources of income but also grow as a company. But it allowed me to bring on Suzanne Vernon as the research director and to hire people to help with communications and education and build a bigger research department. Our mission from the beginning was to be a small but nimble organization that would look for ways to further the mission. That's why we're on everything. We look for opportunities to join on to help scientists to help move things forward and because we're a nonprofit actually and because of the great support we've had and really the talents of people who've come to Bateman Horn Center. We've been able to get grants, join on to NIH funded studies. Be sure that lots of patients are enrolled in research. People don't realize that when an NIH researcher puts in a grant, they wanna do science but they don't have patients, right? - Yeah. - Yeah. - So what we have is this gift of a large number of patients who are eager to participate but they just need that ability to be channeled into different areas. And so especially since the NIH funded the three collaborative centers in 2015 that was a five year grant to three collaborative centers and we were part of two of them. - Right. - So we partnered with Jackson Labs as the clinical core so we were like half of that and supplied 150 patients for these in-depth scientific laboratory explorations to try to understand the disease. And then we were one of several sites at Columbia and we're able to do a lot of good there. So it allowed us to give input into the clinical presentation of MECFS and to enable researchers to carry out their studies. - Yeah. And you can see that on all of your papers, the collaborations that you have. There's a lot of overlap with your enancy climates who I had a fabulous conversation with her previously. There are these heavy hitters within this space and I notice that you've collaborated with a lot of different people. So the number of papers that you have done is vast. Let's take it right back to where the MECFS and fibromyalgia research is right now as we head towards the end of 2024. And let's look at it taking it from 2015 when from the inception of the Bayman Horn Center. How far have we come? Where are we at this stage of 2024 in terms of our understanding, our diagnosis and our treatment of these, what you described as generally misunderstood pain and fatigue illness spectrum? - I think an important turning point for our field was the Institute of Medicine report that was published in 2015. It was an evidence-based report which gives it high credibility in the medical and scientific community. That means we reviewed all the literature and used the published literature to establish clinical diagnostic criteria. And it was very controversial at the time. We'd need another hour to talk about all the conflict and angst and fears about having that report. But I was joined on that committee by some amazing people including Nancy Climus and Ron Davis and Peter Rowe came on as a pediatric expert and it was really just an amazing effort. Through that report, we were able to document in a way that was accessible to everybody what the common core symptoms are and how a clinician can see a patient and start to learn how to recognize the whole point of that report was for regular clinicians to be able to make a diagnosis. And after that report, that's when the kind of the official term of ME/CFS started to be used. It had been used before that but it was adopted by all the federal medical and scientific institutes and it's been a really important guidepost. And then what followed after that was the funding of the three collaborative centers, right? Which was really, really important. And superimposed on this was this Centers for Disease Control study, the M-CAMP study, which is called the Multicite Clinical Assessment of ME/CFS. And this took a long time. I mean, it started in 2012 and spanned over many, many years. There were seven sites of ME/CFS specialists around the country. Nancy Climus was one of them. And we enrolled patients in this study funded by the CDC to gather information from them every year and how they were doing in the meds they were taking. And every year there were different things added like more cognitive testing or cardiopulmonary exercise testing. And this was a really valuable contribution to understanding how the illness presents. Well, I think honestly we were kind of disappointed. It took so long for the papers to start to come out, but they're finally getting published. They've published a paper about what the study was, what we've seen in terms of cognitive issues and patients, a look at natural killer cells, and then this recent one about chronic overlapping pain conditions. So all these efforts were going on. What is really, really apparent from what you have just said is the length of time, the time period over which you have been looking at these patients, trying to create a framework, a structure of treating these patients. And I think one of the most shocking things about ME/CFS is the length of time over which patients are sick. It's absolutely vast. Do you see people that you were following back then? Do people recover over the long term? That's a good question. We actually did a look back survey, four of us, where four of the seven centers joined this. We had a small amount of funding. And we tried to get 100 patients from each site and contact people who had been sick more than 10 years and query them about their current situation. It was hard. I mean, we carried it out on almost no budget and using students and help train them. But what I came away with was 90% of the people were still sick. 95% had never received an alternate diagnosis, you know, which we always worry about. Are we diagnosing ME/CFS when there's really some other problem going on? But that didn't happen in general. Quite a few people improved a little bit. But 90% said they still met criteria. You know, they still consider themselves to have ME/CFS. So that kind of validated our idea that while some people get better, once you're sick for a long time, the likelihood is you can to carry those limitations to some degree. As a clinician, I'm always hopeful that I can improve people's symptoms and improve people's function. And that's our goal, right, is to help empower people to live with their chronic illness better. Yeah. And the thing that's apparent here, I think it was in 2021 that again, with some of those people that you've talked about and Benjamin Nattleson, you did a complete review of all of the literature and so forth to date. And essentially then, and I think possibly still today, the parameters that we have essentially are treating the symptoms of these chronic illnesses, rather than us being able to actually cure or remove what has caused them. Would you agree with that? Yeah, I have to agree with that because those questions were made unanswered. That's true for long COVID, too, right? So it's more than just treating symptoms. I think the approach, especially in the last few years, has shifted to identifying comorbid conditions and aiming treatment at those comorbid conditions. And it's not just symptoms. It's a little more complicated than that. For example, if people have orthostatic intolerance, we can improve and support their orthostatic intolerance with a lot of interventions, which may improve their brain function and improve their function overall and reduce symptoms. So it's treating a piece of the real physiology that might be true if people have mass-selectivation syndrome, for example. So it's a step forward from just treating pain and insomnia that we did for many years. For years, my treatment paradigm was to manage symptoms. And it started with prevention of post-exertional malaise, which is doing something to prevent symptoms. And then it was treating pain, treating sleep and helping people manage their cognitive and secondary mode symptoms. Then it kind of shifted to a new plane, right? Of identifying comorbid conditions, including viral reactivation or mass-selectivation and the things that might be causing autonomic dysfunction or the static intolerance, which has really taken us to a new level. But it's still not a treatment aimed at the primary driving problem. But I will say that's true of a lot of diseases, right? That's why diseases are chronic. Any condition that's chronic, we lack the ability to reverse whatever the problem is. That's creating it. Yeah. So similar to something like diabetes that people then just have a lifelong management strategy, right? Rather than a cure removal of the disease, right? I mean, we'd all like to understand the underpinnings, you know, using diabetes as an example, when I was in grade school, the only way we had to monitor diabetes was a urine test strip. And you have to have blood sugars over 300 to even have urine show up. So it was a very rough tool. We've come so far in diabetes and be able to prevent complications by managing blood sugar and renal function and all the things that matter, even though we haven't been able to conquer or prevent what causes, especially type one diabetes, we're a little better at prolonging and improving type two diabetes. But those things still matter if you can do early intervention and management of the progression of disease and management of symptoms in a way that improves quality of life and function and maybe delays worst need of the disease on that subject. One of the things that you found in a study that you were doing in January 2023 is that long covers, if there was an early diagnosis or early intervention, you could see improvement over a year in long covers, where you do not in ME CFS or the idea that if we intervene early with long covage, you could potentially prevent it progressing to ME CFS. Is that the case? Yes, but let me add some parenthetical things. Okay. One of the biggest differences between our observation of long COVID and our observation of ME CFS is that by definition, especially it's getting less this way, but by definition, we're looking at early onset disease long COVID. We're looking at people in the first one, two or three years of their illness. But in ME CFS, we know that people don't get a diagnosis right away. They make old years and particularly when they get to studies and to specialists, they've often been sick many years. So to me, this was less like huge aha moment, right? When we started understanding long COVID and that is, this is our chance to fill in some of the gaps about what is happening in the first year, two, when people have a post infectious condition. So we don't know in ME CFS how many people spontaneously recover from their infectious insult and how many go on to have chronic illness, because we haven't available to do that research. So yes, there's the element of how many people spontaneously recover in the first year or two, as well as can you improve their prognosis by intervening early, right? By making a diagnosis, by changing things. So it's a little bit of reality. We don't have yet and a little bit of the hope that early diagnosis and intervention will create much better long term outcomes. And hopefully within that, so long COVID is obviously really shown a light on these post infectious chronic conditions and maybe bought it more prevalent within the media within the mainstream, rather than people who were very much marginalised in terms of having ME CFS because it's not a disease that you really have the energy to shout about. But the thing with ME CFS is that historically, there wasn't ever this deluge the way that we've had it with long COVID. It's just always been sporadic. I think there have been cluster cases. There have been cluster cases, but lots of sporadic cases as well. And also because you, in terms of the pathogenesis, we don't have one thing. Do we with ME CFS to say it is caused by this? You've got mono and you've got EBV reactivation and you've got various other pathogens and various other potential mechanisms. Definitely, definitely. the literature tell us and show us that many different pathogens can lead down this path. So the beauty of studying long COVID, mine is still complicated, right? But at least we think we know what the pathogen was in this case. But the more time that goes by the less we know that, but the list of things that could be causing ME/CFS and causing long COVID is almost the same. It's a post and is the infection still there? Are there still pieces, you know, antigens of the infectious agent there? Is it causing viral reactivation for like Epstein-Barr virus? Is it creating some kind of an aberrant immune response? Either a dysfunctional immune system that is causing chronic inflammation or allowing more infections or even autoimmunity? The list, this has just been striking to me as I've watched because we've struggled with these questions for 20 years and now a completely separate group of scientists are starting to ask the same questions about long COVID. And so far, none of them have been answered. Exactly what are the parts that play one thing or combinations of those things that keep it going? Now that's an interesting point that you've just made that it's a completely different group of scientists. Now I know that there are a lot of people within the ME/CFS medical community who have actually turned their hand to long COVID because of the similarities and because they were almost best placed to have a starting point for long COVID. There has been criticism of the NIH Recovery Programme and people have said that they haven't necessarily employed people with the most experience in dealing with these chronic conditions but you are someone who has experience of dealing with these chronic conditions and you have been involved with the Recovery Programme since 2022. Is that correct? Yes. So can you tell me about how you became involved in that and what your feeling is about the way that that program has been put together in terms of do you feel that there is involvement from the correct people? Yeah that's a complicated question. What I see in Recovery is a mirror image of what I deal with throughout my career in dealing with people in academic medicine and other places. So let's just say historically the people that have been most difficult to convince about ME/CFS have been people in major academic institutions because they're so far removed from the community level where patients are diagnosed and there's no pathway for patients with ME/CFS to make it up to specialists because there aren't any specialties. So the more people are embedded in academics the more removed and protected they are from exposure to patients every day with ME/CFS and fiber myelotive. This is a little bit true with COVID. So what happened with COVID is the experts in COVID were people who were in hospital in the ICU. So when they started designing clinical trials people around the country and academic institutions submitted grant applications for recover clinical trials and the ones that were picked were the most outstanding in their fields but that doesn't mean they had long COVID experience. I've consulted in my role and recover on many of the protocols that have come out mostly as an ME/CFS and long COVID clinical provider but particularly to be a voice for ME/CFS and post-exertional malaise and that kind of thing and I found that academic people that I work with to be a wonderful people they just have a whole different world they're from a whole different world right and they're well without patients. Yeah and fewer patients and a narrow selection of patients that can make it through that process it's like cherry picking and they don't do it on purpose but they get the patients that sit their paradigm when you're in an academic situation and then everybody else kind of gets left by the wayside. What I've learned in energized for example I'm working with these amazing PIs you know they submitted this grant their experts in cardiology and pulmonology and rehab but they really they started at a disadvantage right they were thrown in and told to create these clinical trials when we knew almost nothing about long COVID so all they could do is take their prior knowledge and their experience and design clinical trials even those of us in the field don't know exactly what kind of clinical trials would be best I mean he is still challenging even those of you who have that length of experience as well right in the field right I mean to be honest I mean there are things we'd like to try but so recover set out to design huge multi-site clinical trials to test hypotheses but it's hard to know what to study in those trials so they picked them the best they could there are really good aspects of these clinical trials I totally understand the criticism that's come because people want to move more quickly and clinical trials of this magnitude they just move slow that must be hilarious for you as well that people once moved quickly you have been dealing with people with these illnesses I mean you reference there that you've been you went back to study people who have had this illness for longer than than 10 years you've been studying these chronic post viral conditions for a long time so do you feel like they are actually moving quite quickly in some of the recover or some of the clinically controlled trials that are beginning to come out compared to what you've seen in ME CFS oh yeah right I mean I'm in I'm in hog heaven right because where I had no voice to talk to anybody in academics I used to have a little button that said infiltrate academics right and part of my mission is just to maintain respect so that I have a voice but sometimes the opportunities don't come up so for two years I've had great conversations I mean I'm like a teacher within the system having great conversations with all of these really outstanding academics in their own fields it's been great and yet compared to never having any studies you know now we have a chance to design trials and learn from them I think what's frustrating for a lay person is you can learn from negative results of a trial so for example let me just take the cardiopulmonary exercise trial you know there were a lot of people that said don't hurt people you know you're gonna main people my argument is if we design the trial right so that we're screening and observing and being honest with what happens there's no better opportunity than this to learn about post-exertional malaise it's about designing the trial correctly so that you say oh my gosh look these patients can't do this without relapsing but if you didn't plan the trial you'd never know to me the sin of a trial is when you ignore the results or exclude people or design a trial just to focus on the people who respond to your trial but if you design a trial well it can change history in terms of how we approach these illnesses and I think that's an interesting point that you make there because actually if you go to the patients and say would you be prepared to be part of this trial that might induce post-exertional malaise you'd probably find that if people feel like that it is ultimately going to provide benefit or move us forward in terms of the research they would gladly do it I had this conversation with the cardiologist who didn't want to do the exercise testing on me for fear of inducing a crash with my long-handed so um but I was asking for it right there is something definitely to be said for asking the patients what they are prepared to put themselves through and I think that with long-covid you have seen a lot of people going to quite extreme lengths with the things that they have paid to put their bodies through or the the risks that they have taken to be able to get better do you think there's enough patient involvement in the child's designs? Actually yes the NIH has done a really good job of them in including lived experience people. And I think they're in a difficult spot because they're representing all those people out there but most of our meetings have had lived experience people there to to and I see they're particularly the NIH actually has a commitment to listening to the patient voice I think academics feel a little more old-fashioned they're kind of like okay why is this patient telling me this right but they've been doing the best they can and I do think that sometimes when you're outside the system and you don't know what's going on it's very distressing and it's easy to be critical when you're inside and you see the work and the process that goes into it and you have more insight then you realize the effort that's going on but it's sometimes hard to communicate to other people. One of the biggest problems is that the community, it's not a problem, the community wants to move more quickly and you do smaller, quicker studies to test potential treatments. And the recover took a very conservative, broad-based way. They wanted these platforms to be, once the first rollout got done, then they would put more and more trials into the same general platform and it would save a lot of time down the road. So we'll see if that happens, but it's been slow. Going back to I was just mentioning trials or looking at post-exasional malaise, I know that you have done some studies into actually comparing post-exasional malaise in long COVID to post-exasional malaise in ME/CFS. And historically you've obviously looked extensively at post-exasional malaise in ME/CFS. It is one of the things that is defined as a, is it a marker? It's one of the things that you have to have to fit the diagnosis criteria of ME/CFS, I believe. Right. And that's gotten more and more crystallized over time. So some of the case definitions that have been criticized didn't require it. Right. But those of us in the field say, "No, no, this is the group we should be studying for chronic disease," the ones who have post-exasional malaise. And how do you define that post-exasional malaise? Or how do you measure it? Is it patient reported? In a clinical setting, you know, you just have a discussion with patients about what happens with their activities and what the consequences are because it's really a tool to help them adjust. It's hard to come up with a very specific diagnosis or paradigm for what it is. I mean, essentially it's illness relapse from activity that would otherwise be normally tolerated, cognitive, physical, orthostatic activity. And the weird thing about it, it's not always delayed, but it can be delayed. You can do something on a Sunday and have symptoms show up Monday or Tuesday from what it is you did. You can also do a little bit too much over several days and then have the post-exasional malaise come crashing down. So that study that we did comparing post-exasional malaise in Long COVID to ME/CFS followed a first study we did that we published in 2021. It was published in fatigue, biomedicine, health, and behavior, which is not listed on Publ-Met Med. But what we did is we made our own questionnaire for post-exasional malaise that's kind of detailed and we would give it to patients when they were coming to clinic. And so we learned a lot about their post-exasional malaise and published this paper that dissecting the nature of post-exasional malaise. Then when COVID hit, we took the same questionnaire and gave it to our Long COVID patients. And so that paper that you're talking about in 2023 was comparing the answers of our long-term ME/CFS patients about post-exasional malaise to this new thing with Long COVID. It was super interesting. I mean, first of all, we learned that Long COVID, lots of Long COVID patients have post-exasional malaise and all the data suggests that. Another thing I learned is that in Long COVID patients, there's a big overlay of their emotional distress from being sick. They're in the first one to two years of illness and their lives are being decimated and they're anxious and they have huge amounts of grief and loss and they haven't adapted to post-exasional malaise. So my theory is the ways that they differ shows that adjustment and adaptation that ME/CFS patients do once they've been sick for a while. It's just so tragic thing because you're basically saying that it's just been over such a long period of time for these people. Right. And they've had to learn to cope on their own. And if they don't, they're a mess. So by hook or by hook, eventually people start to learn over time what they can do and what they can't do without crashing and without making their symptoms worse. But that's why the overlay of mental health problems is so much lower in ME/CFS in my opinion because we're studying people after they've gone to the steps of grief. Yeah, the grieving process. Yeah. I had such a grieving process. And I still, when I talk to people about the Long COVID, there's just so many elements to that grief. But I think that must be awful for these people with ME/CFS because they have never really been allowed. It was almost like for so long they were denied that they were even ill. Right. So then they've got this grief of not even being, I mean, I know that some people still don't believe the Long COVID exists. But I think in the majority of cases, it's been accepted that that people are sick. Yeah. Oh, totally. You know, it adds horrible insult to injury to not be believed, to have these huge losses from your illness. And then not have your doctors validate you and sometimes even your own family members, not believing the suffering you're going through. I just can't even imagine the emotional devastation. And I've said many times, I wouldn't want to wish this on anybody. But if people had any idea what the cost of this illness is, they would be dealing with it totally different. The caretakers. Yeah. There's also the element of that with the grief and with the emotional toil of this feedback loop in Long COVID. In ME/CFS, you see the same thing that cognitive and emotional overexertion also leads to symptom worthening. It varies person to person. There's some people who have predominantly trouble doing physical activities or predominantly have orthostatic intolerance as their limiting factor. But there are a lot of people I know that really susceptible to cognitive and/or emotional stress. And it's sometimes varies at different points in the illness too. I know someone who has had ME/CFS for a couple of decades who couldn't stand up more than four minutes in our orthostatic test date without feinty. Now she can exercise. She's working with a little bit of accommodation. She doesn't have those problems, but she still has brain fog and she can still be triggered by both emotional and cognitive work. So I just say go figure, right? I don't judge that this heterogeneity exists. And what we have to do is adapt to the person and just help them on the places that are more malleable, the parts of their illness that respond. We work on that and then we're gentle on the areas that can still trigger post-exertionalize. What you have just said shows the extent of knowledge of the clinicians require in dealing with these conditions. And I don't necessarily know that you can have that from a general practitioner because obviously every single illness is specific to that person, but there are so many specific facets to ME/CFS or Ceylonkavid. In terms of the symptom set, in terms of the exacerbation and because we don't necessarily know the pathogenesis, you need such knowledgeable clinicians. And I don't know how we get to the point that people have access to them. Yeah, that's really my whole life career, right? Is how do we get access? How do we get patients access? I firmly believe that if clinicians just see patients, they will learn quickly, but you have to see a lot of patients and you have to listen to them. Listen. Yeah. And that listen problem is missing because of all the pressures in our medical system to be efficient. I think plenty of doctors would like to take more time, but they're not allowed to. And then they learn not to. They learn to be efficient. But if you can listen to patients, you can learn everything you need to know about these illnesses. I know this because I work with a lot of long COVID specialists now and they get it. They see patients. They're trying to help patients and they're like, wow, this happens, right? And I'm like, yeah, been there, done that. I'm part of an educational program funded by the Centers for Disease Control to teach physicians about long COVID and ME/CFS and other post-viral conditions. So we have a faculty of people across the board and it's been so fun for all of us as faculty to share our insights and I go on and talk about what I've known about ME/CFS and they're like, oh, yeah, that works. I'm going to try that. It's been great. It's been a great collaboration. You mentioned of the CDC takes us back to the paper for which I originally contacted you, which was your very recent chronic overlapping pain conditions study and actually the researchers from the CDC, I am going to speak to them as well. Can we just talk about some of those chronic overlapping pain conditions in terms of ME/CFS and do those chronic overlapping pain conditions bring fibromyalgia into overlap ME/CFS. So this is a complicated question, okay, because I've been a fibromyalgia specialist all of this time too. Yeah. And we all kind of use these cases. case definitions, but we use them in the way that makes the most sense to us. And the way I divide someone I call fibromyalgia only, and ME/CFS, is the ability to return to exercise, and the nature of the flare of symptoms after you do more activity. And I'll tell you what I mean by fibromyalgia alone. Yeah, please. So fibromyalgia, I mean, I have hundreds of fibromyalgia patients that need help with symptom management. They need help with sleep, and they need help with pain modulators. And they usually have a lot of stressors going on in their life. I think of fibromyalgia as a almost purely stress-induced illness. Physical or mental stress? All stress. Okay. Yeah, I think mental stress too. You can not separate them very well, right? If someone is a single mom working nights and in a job where she doesn't have any control and has a hard time making ends meet, what are the stressors? The night shift? Is it not getting sleep? Is it, you know, you can't separate them or ours? Yeah. But over time, I'm just stunned by my fibromyalgia patients and what they've been through, and they're just strong people who have trudged through difficulties. It's weird because it's not like they're weak people. It's like they're people who wouldn't lie down when things got hard. So they push themselves through very difficult conditions and develop widespread pain and fatigue and sleep problems and brain fog and stuff. But the difference is, and the literature holds this out, if you take someone who has fibromyalgia and you gradually help them rehab physically, they get better control over their illness. They can't do hard exercise, but they do moderate movement and strength training and low-impact exercise. Doesn't make their illness go away, but it helps their mood, it helps their sleep, it helps their fatigue. And they get an overall better management of their illness. They don't really get post-exertional malaise. They can get post-exertional pain amplification. Right. So if they exercise too hard, all the muscles can hurt and that kind of thing. So they have to kind of be careful because they have a pain amplification problem. So that's one group and I love seeing patients with that because I can totally help them get into a much better place. It's very satisfying. On the other hand, or what I consider ME/CFS and other conditions where people are vulnerable to developing chronic pain conditions like we're mentioned in that paper. If you have ME/CFS and you have post-exertional malaise, you can't implement what we would implement for a patient with fibromyalgia, even if you meet fibromyalgia criteria because you can't exercise. And exercise sets you back. So to me, that's the big difference and they're not completely separate illnesses. Think about what happens to someone with post-barrel injury. They lose sleep, they lose their job, they go through all these stressors and sometimes they don't have pain initially but they go on to develop chronic widespread pain or pain conditions. And maybe it's because of how horrible it is for them in the first year. All those stressors, the same things that can cause widespread pain. I don't know the answer. But what I want to say about that paper is the most important thing about that paper isn't saying, look, clinicians, there are many things you can treat in people with ME/CFS. So identify these comorbid conditions and take what we know about chronic pain management and start to treat your patient. And in that just for our listeners, we're talking about the overlapping chronic pain conditions of lower back pain, migraine, headache, insuficial cystitis, irritable bowel syndrome and temperament debular disorder. Yep, TMJ. TMJ. And that also goes back to what you were talking about earlier in terms of dealing with orthostatic intolerance or. Exactly. So you're trying to address these comorbidities as a method to alleviating some of the problems of ME/CFS. Right. Exactly. And one of the reasons pain was left out of the IOM criteria as a primary criteria. So the IOM criteria, they have those core criteria that everybody has to have. And then they say, oh, and there are a lot of other common symptoms of pain, chronic pain is down in that list of other symptoms. And it's because there's a broad spectrum of how pain affects people with ME/CFS as this paper demonstrates. And I know there are some people who don't really have pain who have ME/CFS unless they're in post-exertional weight. They don't have pain all the time, but if they overdo, then they get a flare of pain. And then there are all these pain comorbidities. And our thinking in making this case definition is we already have a great literature for chronic pain and fibromyalgia. We don't have to redo that with the IOM criteria. And that didn't go over very well with a lot of people who appreciated the comorbid pain conditions and included them in the case definition. In terms of the differences that you were just citing between the fibromyalgia and the ME/CFS, going back to your 2021 paper, I think, about the diagnosis and management of ME/CFS, I think it was still at that time or only just then that the graded exercise therapy and cognitive behavioural therapy. And that was removed as some of the primary management strategies for ME/CFS. And presumably that plays into what you've just described. So graded exercise therapy. Is it something that you. is that what you do with fibromyalgia? Is that graded therapy or is that something completely separate that we should just remove from the ideas of treatment for these chronic conditions? So to me, the term graded exercise therapy implies that there is a regimen that you follow strictly that escalates. Regardless of your fibromyalgia. Regardless of how you feel. Which is detrimental in any of these things, as we've just said, patient-takers. And it's actually not really the way most physical therapists rehab people anyway. And I can say, let me go back to the recover cardiopulmonary exercise trial. Just built into that trial lots and lots of information to the therapist about how to observe their patients and get feedback and ratchet down the treatment if they're having post-exertional malaise. They're individually taught to talk to the patient and adapt the therapy and change it. And that's why I feel like I know people are upset about it, but I feel more confident that we could learn something from that trial if we can complete it. But as a clinician, I don't tell people not to exercise. I tell people not to induce post-exertional malaise, right? And I usually tell people, you can do as much as you want as long as you're okay the next day and the day after. You need to figure out how much you can do on average that does not cause any relapse symptoms the day after or the day after that. And sometimes that's hardly anything. And people have to learn how to add up all the different exertions they do because sometimes you don't realize you're doing a whole bunch of cognitive or you're doing a whole bunch of upright and adding it in. And so if you have a busy day in one way, you have to do less than the other. The problem with some people is they wait till they develop post-exertional malaise to rest. And the real key is to learn how much you can do without inducing it. And if you do induce it, you stop immediately and rest and recover until you're better. And so I hesitate to give anyone a formula to give a group a formula or even an individual. I put it back on them and I say, this is on you. You have got to pay attention and keep a record and try to understand your body and what you can do and what you can't do. And how to make your episodes of post-exertional malaise less frequent and less severe and less prolonged. And the better they can do that, the better they're overall help will be. Do you tend to find that? Most people have to find that threshold. They end up slightly pushing it into the PEM before they then are able to pull it back, tailor it back to being within their threshold. Yeah. But in an individual setting, when I meet with people, I say, what are you doing to keep from getting weak? What are you doing to keep your core body muscle strong? What are you doing? And then individualize what they could do that's safe. Yeah. If it means getting out of bed every hour and walking to the bathroom and back, that's something. If it means little crunches, but it's amazing that you could do more than you think sometimes. Now, I know there are many gradations of how severely ill people are. But to really do things that will help you be stronger and less physically deconditioned is hard because you have to do it in these tiny, observed increments, right? But it can be done. And helping people learn about PEM, not be scared of it, but get control over it so they know what they can do and what they can't do. Most people get better and better at avoiding PEM over time, just by their experience. And do you think that we can obviously the people who have had MECFS for decades, there is so much to undo. in terms of the severity of their illness and how far down that path they've gone. But do you think that the earlier we can get to grips with that pastexasian malaise and earlier that we can get to grips with how much we can do, that that actually enables us then to move forwards and increase our activity somewhat? - Or do you see that it just puts a limit on it? - I'll tell you honestly that after about 10 years of practice, when I was trying to formulate my treatment protocols, I said the only thing I've ever done to alter the trajectory of illness in a patient is to teach them how to pace their activity and avoid post-exertial malaise. The next would be helping people sleep because sleep can unravel the whole illness. But I would say by far the most effective thing I can do as a clinician is help people realize how to not crash and not constantly be in illness relapse. And I am absolutely sure that the better they do that, the more their potential for improvement exists. I can't say for sure that people will get better and better, but they for sure have a more stable plateau and they are likely to drift up into a better plateau. - Okay. That is hopeful. That is a note of hope, but it is also one that takes discipline in terms of all of us actually listening. - We all talk about the clinicians not listening to us, but we have to all listen to people like you who say small increments just take small steps. There are so many more things that I could discuss with you. I've got so many of your papers printed out here, but I think for now, I think in terms of an A of U of where we are, I guess the only other thing that I could ask is what would be your hope right now, your immediate hope in terms of the direction that we need to be heading in terms of research. - I'm gonna say that even more than research and this is reflected in Batemanhorn Center's mission is we need all clinicians to recognize all of these illnesses. So we've just put this huge effort into provider education. And I think everybody needs to join this. Every patient should teach their own clinicians and engage them and share with them and find ways to teach them one-on-one about the cell list because there's no point in doing research if people don't get diagnosed. We can't carry out research and we can't complete research if there are people to study. - That's such an interesting point as well that you can do all the research that you want, but if that's not then filter it out. - Right, right. - Among patients, it's fatty futile. - Right, so what I would like to see, I like the direction long COVID research is going, looking into those various potential causes of what's causing the syndrome, whether it's persistent virus or whether it's secondary reactivation or what the aspects of immune dysfunction are and are there microclots and are vascular damage, really there's a lot of great discussion in the long COVID community. What I'd like to see is that they include ME/CFS patients and other chronic illnesses infection associated chronic illnesses in these trials so that we can compare. And I'd like to see more recognition to the fact that we're looking at different stages of a post-infectious illness. We're looking at relatively new disease in long COVID and we're looking at long chronic disease in the other patients. They're the ones who didn't get better. So we're kind of blinded with the long COVID community because it's full of people who are probably going to slowly get better, especially in the first six months and then in the year and the longer people stay sick, the more they start to look like people who aren't gonna get better right away. But just recognition of that. And also it's pretty complicated, but now at this point, when someone develops ME/CFS, we don't really know what caused it. - Yeah. - 'Cause everybody's getting COVID, everybody's getting viral reactivation, everybody's now exposed to new things. And when someone comes down with it, just 'cause you had COVID, we don't even know if that's why people get sick anymore. So we really just need a large umbrella and a very good science to try to delve into what these common processes are. - I'm anything. Thank you so, so much. Thank you for listening to Make Visible. Please do like, follow or subscribe to listen to our next episode where we'll be uncovering more insights into complex chronic illness. This was brought to you by the team at Visible, a group of scientists and engineers whose lives have been affected by energy limiting health conditions. We're building wearable technology that's helping 100,000 people measure and manage their complex chronic illness. 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