#11 Post-Pandemic prevalence of ME/CFS - what we can learn from the increase with Suzanne Vernon, PhD

[Music] Welcome to Make Visible, the podcast shining a light on complex chronic illness. 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. Hello and welcome to all of you. Before I bring you this conversation, I would like to respond to feedback that I have received that we have a bias towards long COVID, and I wanted to explain to you that that is the lens from which I'm able to discuss my experience, and I do not ever pretend to have the same experience of those that have suffered from MCFS for the past 30 years. But I would like to point out that there is a bias in the research towards long COVID, and that is due to the attention, the numbers, and the funding that has gone into this condition. And what we are trying to do, along with many of the scientists, is capitalise on this moment of attention to endeavour to take what we're learning in the understanding of these energy limiting conditions and apply it across the multitude of conditions that need attention and research. I never underestimate how fortunate I am to have only had this for five years and for it not to have progressed into MCFS. What I am trying to do is bring my personal understanding and apply it to our wider community by the selection of guests to whom we speak. And I hope that what I'm saying here will become more apparent to you from the following conversation. I am delighted to bring you the inspiring Dr. Suzanne Vernon, research director for the Bateman Horn Centre and part of the Recovery Initiative, who here discusses a later study exploring that crossover point of long COVID and MCFS. And explains how this work is instrumental in developing our understanding and treatment strategies for you all. You are a microbiologist, a virologist and a molecular epidemiologist. You have had a particularly varied career in terms of working with a CDC and structuring various non-profit organisations. Can you just encapsulate how that broad career has brought you to specialise in post-infectious conditions within your role at the Bateman Horn Centre now? Sure. I got interested in MCFS research when I was working as a full-time staff scientist at the Centers for Disease Control Prevention in Blana, Georgia. I started at the CDC as a postdoc researching HIV and opportunistic infections in women with HIV and particularly human papillomavirus and cervical cancer. And the opportunity came up to lead the biomarker discovery program of the then chronic fatigue syndrome program. So there was a peer review of the then chronic fatigue syndrome program at the CDC. It was about in 1995, 1994, 1995. And at the time, CDC was really focusing on the epidemiology of chronic fatigue syndrome. Just trying to define the cases and collect samples from population-based studies in order to be able to understand what was causing MCFS. But the challenge was that there wasn't a laboratory program dedicated to MCFS at the time, just several really good epidemiologists working on it. And so the opportunity came up for me to lead the MCFS program at CDC. And that was actually at the time when it was still chronic fatigue syndrome and we didn't have the sort of diagnostic criteria that came almost 12 years later, really, that it started to be more cemented into the current definition that we have of MECFS. Exactly. So the FACUDA, the International Criteria was published in 1994, right? So it was right on the heels of that case definition being published. But I think what really excited me about this was the ability to combine very powerful population-based epidemiology and identification of cases with the tools in the laboratory. And is that because when you're working with the CDC, you have access to that much more data and to a population wide. Is that correct? Is that how exactly good? Yeah. So at the CDC, you have the opportunity to study populations. And not only their data, but to be able to collect samples and combine that sample information with the epidemiologic information and the clinical information. So it was really very exciting to me to be able to have that type of multidisciplinary endeavor to really define what was causing MECFS. And before we get into your most recent paper, which is our primary focus for our conversation today, picking up on that work that you started in 1995. Where are we? How far have we come between 1995 and 2025? We're talking about 30 years in terms of that biomarker identification in MECFS. Because through those years, you have written multiple papers, haven't you, that have identified so many differences in the MECFS population. You're talking about reduction of IL-6. Mytochondral dysfunction, you can see all of these different things. Do we have one definitive biomarker that's come out of all of that research that you've done? No, we definitely do not. And I don't think there will be one definitive biomarker. I think there's going to be a suite of biomarkers, if you will, that help to define and subtype out the heterogeneity of MECFS, which has really plagued the field because we do know that MECFS can originate, can be triggered by a number of different triggers. And then we do know that it's the time between getting a diagnosis and participating in research studies, berries tremendously. And we do know that along the course of illness, a lot of things change in an individual. And so any time this very heterogeneous population is researched, you don't know where in that whole timeline of illness, any one particular individual is being studied. And so if you have 10 people, 20 people in a research study, it could be a number of different time points, timeframes that they're in in their illness history. And yeah, it just makes it very, very challenging to study. And that, of course, is also complicated by the fact that so many of the studies are relatively small because we have not had much attention and funding to do the large studies that really get at the, that can really tease that signal out of a very, very noisy background from a pathobiology perspective. Yeah, because you've got that difference in times of time point, so the progression of the disease, but you've also got that potential completely different driver, not necessarily the mechanism by which it. influences the body. There was a paper, I'm just going to see if I can find it here, that you authored in, I think it was published in January 2023 where you were looking actually at the post-exational malaise in post-COVID and comparing it to ME/CFS. But what you reference in that paper is Ebola, Chitingunya and post-West Nile virus. And by pulling out those in the same way as we do with the post-COVID, you're identifying drivers of a post-viral condition. And what you've just mentioned about the heterogeneous nature of ME/CFS is that idea that potentially you're looking at things that have been derived from a different start point. Is that fair to say? It is. It really is. So how important do you find it in your research and your work in trying to understand what that start point was for each patient? Is there relevance or is it irrelevant because you have to treat everyone from the point that they come to you in a similar way? So I think from a research perspective, the pandemic provided an unprecedented opportunity to study a large group of people that developed ME/CFS from the same exact trigger. And that being SARS-CoV-2 infection. That is such an interesting thing that you have just said that essentially you have said those people have developed ME/CFS, which is the crux of your most recent study, which is looking at that cross-aver where this post-viral COVID becomes ME/CFS. Correct. So I have a drawing that I made pen to paper at the beginning of the pandemic when Cindy and I, Dr. Bateman and I were shopping around this idea of what we now call long COVID, that there was going to be a lot of post-SARS-CoV-2 ME/CFS. And so when I was drawing out this little diagram, I had like West Nile, Epstein-Barr virus, the original SARS, Ebola, and the possible pathways that would result in this signature constellation of symptoms that we now define as ME/CFS. And the starting point for all those viruses is different, right? So salivary gillian, mononucleosis is different than the SARS respiratory syndrome that is different from the West Nile infection. Is that different in the behavior of the virus, the way that the virus latches on the position that the virus takes within the body as well as the symptom set that it gives? Initially, yes, right? So that acute infection is all quite different, but after six months or so, if you do not recover and you end up with this constellation of characteristic symptoms, it's all this kind of common endpoint, right? Yeah. So all these different entry points into a disease that ends up kind of presenting itself very similarly with the symptoms that we know are characteristic of ME/CFS. That convergence. Yeah. So it's complicated. It's super complicated, but again, the pandemic, the SARS-CoV-2 pandemic, provided us with just an incredible opportunity now to look at this one entry way into ME/CFS. I'm actually finding this with multiple researchers that whilst obviously post-COVID condition is not optimal for those suffering from it, and no one is saying that it's a good thing. It is providing this wealth of information that enables you to study these illnesses with that specific start point. And you have then gone on to write so many papers simply in those last five years, looking at the differences and similarities between the post-COVID and what you define as ME/CFS. And before we start talking about this paper, where we talk about the crossover, I think it's important to just mention that one of the big things that we're dealing with here is almost a fresh infection. So people still coming to you, the research that you're doing is still, I think even with this recent recover one, was it between 2021 and 2024? Yes, it's still ongoing. So you're talking about a fresh infection. You're talking about a newly acquired post-viral condition. And that is incredibly different to the long-term ME/CFS people that you are researching a lot of the time. Does that make this kind of research harder or does that allow you a different view of the same illness? Well, I think those comparisons have yet to be done to see where the overlap between pre-existing or pre-pandemic ME/CFS or longer-term ME/CFS and post-pandemic ME/CFS, post-COVID, ME/CFS, you know, what are the differences in the similarities? My guess is that there will be some ME/CFS post-COVID ME/CFS that has a similar phenotype to some other post-infectious ME/CFS that occurred before the pandemic. Let's say, for example, maybe there's going to be some similarities between ME/CFS that was triggered by mononucleosis and Epstein-Barr virus, right? I mean, I don't know. I don't know, but let's just say, for example, that's where our post-COVID ME/CFS and maybe some mononucleosis, some other post-infectious ME/CFS will be similar. But those comparisons are yet to be done. I think they're, they will be done in studies moving forward because that's a big question, right? What are the similarities? What are the differences? In order to be able to understand, you know, how something started and what it is progressing into, which is a classic natural history study, that is the way that you can identify therapies that get at that root cause of the illness. Yeah, because that trajectory and progression is just something that with the post-COVID, we don't necessarily know yet how that is going to move, whether that is going to converge even more with the ME/CFS. But let us talk about your most recent paper published earlier this month. It is entitled the Instance and Prevalence of Post-COVID 19 Myelgic and Sepulomialitis, a report from the Observational Recover Adult Study. And this is a study in which you looked at 15,000 patients who fulfilled three different groups. Right. So, recover is, there's a bunch of different sections of recover. We focused on the 15,000 adult participants that were enrolled as the Adult cohort in recover. What does recover stand for? I always forget that darn accurate. recover stands for researching COVID to enhance recovery. There we go. So, those 15,000 people included people that were acutely infected and enrolled within 30 days of their acute infection. So, they had a positive test, a positive SARS-CoV-2 test. Then there were people who got sick in the beginning of the pandemic, 2020. Those people did not necessarily have record of a COVID test. Maybe COVID testing wasn't even done, but they fit all the other post or being sick with SARS-CoV-2 criteria. But enrolled passed the acute infection. Those are, those are called the post-acute cohort participants. So, they were greater than 30 days passed their acute infection. And then there was an uninfected, several thousand initially, uninfected participants that enrolled, but they also got sick and so then they rolled over into the into the Cech cohort. And they actually end up being acute infected, right? 'Cause here you're seeing uninfected to infected, so you're capturing them in real time as acute infected. So anyway, so those three groups, acute infected, post-acute infected, and then uninfected, participants were enrolled. And you did not include people who had been hospitalized with the virus, am I correct in thinking? We did not. So you therefore were not looking at that severity of illness. - That was a decision, a conscious decision on the part of Cindy and I, to try to focus in on the people who consistently fall under the radar, right? And also to eliminate the possibility of clear organ damage or something that could be causing MEC of us eventually. So anyway, we excluded hospitalized people. And then we just crunched the numbers. I mean, the nice thing about the recover initiative is it's a longitudinal study. So all of these people are followed every three months up until now. I mean, I think they're still being followed. So the data that was published in this paper was actually a data dump from as late as September of 2024. So really super, super fresh data and just an incredible data set. And so the participants are asked these surveys every three months. So the magic number with MECFS is six months by definition, right? They have to have these symptoms of certain severity and frequency for at least six months and beyond. They had to have at least six months worth of data and nothing less and everything beyond was counted. So somebody could have gotten sick after a year being followed or a year and a half of being followed. It was whenever after six months they then met the criteria that we used to define MECFS. Which let's just talk about that diagnostic criteria for MECFS because the study does hinge on these people then meeting the diagnostic criteria. What are the key markers there? Are we talking fatigue, post-exertional malaise, unrefession sleep, cognitive impairment, orthostatic intolerance? Is that correct? That is correct. That is correct. So that is the criteria, the clinical diagnostic criteria that was recommended by the Institute of Medicine and now the National Academy of Medicine. And that is what we've been using at the Bateman Horn Center for both clinical practice as well as research studies. And there's something that sticks in my mind about the diagnostic criteria. With MECFS does it have to be over a certain proportion of the time that you are suffering from those symptoms? Is it 50%? So it's 50% or more. So more than half the time. - Yeah. - In frequency and at least moderate to severe in symptom severity. So the nice thing about many of the questionnaires that are used is that they do assess frequency in severity because that's important for them with everything, right? How long have you had this and how bad is it? So we were able to assess fatigue that is associated with physical impairment, the frequency and the severity of that. Recover used, I mean, thank goodness they actually asked about post-exertional malaise. And that's really thanks to a lot of advocacy from the MECFS community that was involved in the design of the Recover study. So there was a yes/no question about post-exertional malaise. Do you have it now? Did you have it then kind of thing? And then there was a frequency and severity question for sleep and that used a promise sleep questionnaire which is a highly validated, widely used questionnaire. And it asks, is your sleep refreshing? And so it gets at both frequency and severity by answering yes or no and how much kind of thing. So it kind of turns around. It asks if your sleep is refreshing but what we define in MECFS with is unrefreshing sleep, right? And then it asks about orthostatic intolerance. This was one of the questions that was not asked really that well from a frequency and severity perspective. Although they recover, did use a large questionnaire about orthostatic intolerance that we did not use for this study. We just used a single question about orthostatic intolerance. And then we used a pretty sophisticated questionnaire called the NURRO QOL which assesses cognition and cognitive impairment and it's scored. So that got at frequency and severity of cognitive impairment. So those were the questions that we used in order to be able to see if someone met MECFS clinical diagnostic criteria defined by the Institute of Medicine. And your results are quite, I don't want to say alarming in terms of I don't want people to be shocked but they are quite revealing in terms of the difference in the instance of MECFS since the onset of COVID. Can you just tell me a little about what you have seen in that data set in terms of the changes? The ability to get at this, the incidence or the rate of new sickness, new cases that MECFS following SARS-CoV-2 infection was because of the design of the study of the recover study. Again, this is a natural history study of what happens to people once they get sick and do not recover or recover from SARS-CoV-2 infection. And the ability to study acute infection and see who actually becomes MECFS meets criteria for MECFS was just, I'm getting goosebumps thinking of it was just like, wow. Yeah, it was remarkable. It was, again, it has not been done because we have not had the opportunity like we had with the pandemic to do such a study of this scale. Another really interesting thing that's going to come out of this is to be able to compare these acute onset MECFS patients to the post-acute patients who also meet MECFS criteria. What are the similarities, differences, overlap there? But it is alarming and we knew it, we anticipated. Were you expecting before you started running this data to see quite the figures? Because you have a fairly good gauge on the number of people that are coming through your doors. But were you anticipating quite these figures to come out of this study? Yes, because of some other studies that we've done, some other post-infectious studies that we've done, I was anticipating between a prevalence of around 10% is what I was anticipating. About 10% of people would not recover and would develop MECFS. We identified 4.5% prevalence. And that is not just 4.5% of people who have post-COVID, long COVID syndrome. You are talking about 4.5% of those that were infected with COVID. Within this study, so I think we have to be careful about generalization because it wasn't necessarily a population-based study per se. I mean, it is a very large population, but there are various selection biases, etc. that occur when people enroll in studies like this. Yeah, of course. So of the people that enrolled in recover and were infected with SARS-CoV-2 and did not recover, 4.5% of them went on to develop MECFS. And that is higher than pre-pandemic prevalence. Prevalence are the cumulative number of cases. That 4.5% is about 8 times higher than previous prevalence pre-pandemic. prevalence estimates. Now the incidence, which is again the rate of new cases, which is an important differentiation, that is 15 times higher than previous incidence estimates of ME/CFS, which were done by the CDC, incidence studies are hard to do for chronic disease because you have to have a system set up in order to be able to catch a new disease, right? And this is what the pandemic gave us the opportunity to do. We had people that we knew were sick within this certain time window. Now we could just start following from that beginning point of their infection and see who stayed sick, who got ME/CFS, who got better. So one thing that I was actually very curious about was from that data, did you have people, and is this recorded, that did develop ME/CFS, fitted the diagnostic criteria for ME/CFS? At some point during this data set, and then subsequently recovered from that. So that study hasn't been done yet. We have that data. Oh, do you? Oh yeah. It's a super important question. How many people get better? And what are the factors in people getting better once they get an ME/CFS diagnosis or meet criteria? How long, and what are the factors involved with them actually recovering? Versus those that go on to become either more severe or don't get better. But we have that data. We haven't looked at that data yet. It's a very important question in terms of ME/CFS at large as to whether the importance of identifying that driver, that trigger point, that pathogen. So in this case, we know that it was or was not COVID. The relevance of that and the timeframe in which identifying that, because obviously we still do not have a treatment or a way of removing what COVID has done to the body, one single treatment. But there's the importance of, if you identify within X number of months and implement, I know the sort of programs that you offer people at the Bateman Horn Centre, which is really focused around addressing various of the things that we've talked about the sleep, the PEM using pacing. Identifying the timeframe in which that really, really makes a difference if you can get on top of people's illness. That's right. Some studies early on by the CDC indicated that the sooner someone is diagnosed and treated, the more likely they are to recover. And then there's been research studies that have shown some pathogenesis differences, potentially some phenotypic differences between people who have been sick for less than two years, less than three years, less than four years compared to people greater than five years, greater than 10 years. The underlying pathology is changing. It's different and it's progressing. It's the body's adapting. So the ability to have this recover data set and all the samples that are being collected on it. And now the identification of people that meet MECFS criteria within this data set to now look at all of these molecules, look at all these signals, look at all of the clinical data in the context of how they're defined is just going to be. I hope it's going to reveal a great deal about not only what is causing MECFS, but again, how it can be treated. And what are the different targets that we can look at for treatment? That essentially is what you set out to do at the Bateman Horn Centre, identify objective diagnostic measures and implement evidence based treatment, implement treatment, help people to actually live their lives. And not one of your things is you're dedicated to actually trying to be able to for people to get their lives back. So hopefully this can go some way. Now there has been a lot of criticism of the recover program. More broadly, I think amongst not necessarily involved patients, but patients and actually I have heard it from researchers in the US who have said that they did not necessarily include sufficient people either with lived experience or with the depth of knowledge of post viral conditions when they were designing their teams and their studies. You obviously in terms of the data that you have been able to gather from the recover program have found it immensely useful. Can you tell me your thoughts on the way that it is structured and the information that you felt that recover should be able to bring us. So in the recover initiative, I just want to digress for a minute. I'm going to go back. I'm going to go back to when I was at CDC and I was invited to give a talk at the infectious disease Society of America. And it was me and another MD. We talked about post infectious MECFS, gave presentations on that. And it was really quite stunning to me to in this room, the room was full. The room was full. There was probably at least a couple hundred people on the room. And then afterwards there was the opportunity to talk with both of us that gave the presentations. And there was literally a line for both of us in answering questions one on one with with these people. Most of the people that were in line talking to me were MDs and practitioners, infectious disease docs that just came to this big infectious disease meeting. And we're looking for answers for how to treat patients, these post viral patients. So there was a lot of interest. So I think there's a recognition out there for the most part in the world that there's this post viral post infectious phenomenon that happens to people that practitioners need to want to know how to identify and help the patients. So I think when recover was put together. And it's an NIH funded initiative. So the academic world is what the NIH funds. And so they were really kind of spearheading the whole design. And I think NIH has also made a conscious effort to make sure people with lived experience are. Are involved in the process. And I think that really kind of stems from the whole PCORI initiative, which is the patient centered outcome research initiative that's been going on for for many years now. Anyway, so it was a large group 200 plus investigators initially together with the NIH and people with lived experience involved in the design. Bateman Horn Center was one of the only groups that was involved in recover that was actually I think funded to some level to be an investigator in there. So there was MECFS research and clinical expertise involved. But it was, I mean, it would at least it was there wasn't a ton. I think what has happened over the past couple of years now with our involvement is that Bateman Horn Center has had an incredible opportunity to inform and educate people at all levels in recover. And it's not always easy, you know, you can't always just convince somebody that what you're researching or what you're doing or what you've been studying or what you've been caring for is the right way. But I think we've made incredible progress at helping people understand post COVID MECFS is there is important and needs to be part of the research. And that's evidence by the fact that look at all these these people on this paper from academic institutions that I could have never have even imagined to have had the opportunity. to work with. And these are all people that now, it's like, wow, this is ME/CFS, this is something, this is important. That again comes from this horrific situation that we have in terms of huge numbers of people being affected by post-COVID. But the way in which the medical and scientific community and researchers have come together in this is quite phenomenal. And not just from an outside perspective, but I've noticed it in the people that I speak to, how much each one of them have gained from being part of a wider community and this more open conversation between organisations and between scientists, often sharing knowledge that previously was not really the crossover between body systems, the crossover between different types of illnesses, between different specialties. That sharing of information has been quite phenomenal in the way that you've all been working in something like recovery, but also in the other organisations that have formed, these groups that have formed as a result of something that was really not idea. Yep. I must say it has happened in other epidemics, like with West Nile, with SARS, the original SARS, with Ozeca. The interesting thing is that, so the initial kind of surge of attention happens and this intense research happens and the need to develop diagnostics and understand the pathogenesis and then get treatments or vaccines or whatever. So that happens. I think what's been an interesting observation for me is that once the acute scenario goes away, the funding and the interest goes away too, because there's no more funding, so how can researchers do it? So that again, one of the things about this pandemic as horrific and as tragic as it is, it has forced us to pump in a bunch of money and to figure it out because so many people, there's there's not one person really that hasn't been not touched by this pandemic in some way, shape, perform. So before pre-pandemic, you could say, MECFS and people are like, huh? What's that? I'm never, oh, you're just tired or something like that. And now you say long COVID or you say MECFS and you're bound to find, be talking to someone who has either known someone or has been affected by it. Yeah, it's very rare now to speak to someone who does not know of it. And so I think that there's also within your profession, whether or not people are dealing on a day-to-day basis with people that haven't, they've also all had personal experience of it, which definitely adds to the way in which people are being treated. Yeah. Do the results of your paper suggest the majority of us that have long COVID are categorized now as having MECFS? No, it does not. That's a really important point because one of the reasons we did this was to really determine our long COVID and MECFS the same thing or are they different. I think what our research right now indicates is that MECFS is the more severe subtype of long COVID. So if you have, and I'm going to just generalize because I don't remember the exact numbers from the paper, I'm actually going to go back to the paper that was published by recover by in JAMA last year, the first case definition paper, where they showed the four clusters, how long COVID patients clustered into four different groups. And when Cindy and I saw this cluster, this heat map, we both said MECFS is going to be in the most severe cluster, the most symptomatic cluster. And that turned out to be true. So if you think of a Venn diagram, here's long COVID, and then here is MECFS, it's embedded, it's a subset of the whole umbrella. And most of it, 90% of the MECFS fits within that long COVID bubble, but there's 10% that doesn't. Does that make sense? Yeah, absolutely. There's something that I've since I started researching the MECFS much more, it's something that's really interested me because the diagnostic criteria that I'd mentioned earlier that requires 50%. Since I read that, I've always been wondering, well, therefore I don't think I meet the diagnostic criteria for MECFS because I probably have it about 40% of the time that it's completely cripplingly debilitating. And then the other part of the time, it's just niggling symptoms. That's an interesting point in itself either for people with long COVID or MECFS in terms of whether you need to fully fit into a criteria to subsequently be able to gain disability benefits or things like that that might enable you to live life and whether having only crippling disease 40% of the time means that you are just then left to live your life. Just because it's just over 50%, then I'm classified as being a K. And I think that's just something that we need to be really aware of in terms of the way in which people are treated. Yeah, totally. With MECFS as well because there will be people who are just borderline in terms of that criteria and it doesn't mean that it's easy for them to live their life. Totally, totally. It's a really important point. Yeah, it's just fitting into diagnostic criteria. You can't encapsulate everyone, you have to have cut off points but then I think it is the way that you look at people and treat people at the Bateman Horns Centre is you look at the individual and you speak to the person and you're trying to find ways in which those people's lives can be improved, whether or not they fit into boxes. Yeah, I guess to me the diagnostic criteria was there and we know it works, right? We know we can diagnose people with MECFS using the IOM diagnostic criteria. So it just seemed logical to us to just operationalize it, use it to identify the people that we could help. Yeah. And so it's interesting to put it in that framework. Everybody needs help. Everybody needs to get the diagnosis. Everybody needs, we were just focused in on MECFS because it's kind of what we know, what we do. Could I ask you what you are most excited by either in terms of the research that you are currently doing yourself and with the team at Bateman Horns Centre or out there in the field. What are you seeing that you feel like might really make a difference in this space? I'm really excited that this paper finally got published. I think it's evidence that we've been needing for a very long time. I'm also very excited by the recover initiative because we have not had a study of this scale ever, ever. And now the number of people involved and the range of expertise involved in this multidisciplinary study, it's just bound to come up with answers that will get us at treatments for this community. And it will also get the attention of pharmaceutical companies because pharmaceutical companies have not necessarily been interested in post-infectious MECFS or long COVID because there aren't biomarkers, right? There's not things that they can measure and say, "Okay, we fixed that or we've modified this, we've had this effect." So recover has the opportunity, I think, to really provide that type of evidence base that has been really sought after by the pharmaceutical companies to get involved. Do you think the way in which recover works legitimizes listening to your patient? Because for example, a lot of your study, it is done on huge numbers of people, but a lot of it is to do with patient responses. To be backed by something like recover and therefore the NIH does that legitimize. When patients are saying, "I have improved, I have not improved." It's not something that historically in terms of scientific studies was necessary taken to be sufficient ever Does it legitimize that? - Let's share his help. Diagnosis is important, right? So people want to understand what it is that's going on with them. So a long COVID diagnosis or MECFS diagnosis is important to have. And then the ability for a physician to understand how they can manage that pay-out. It can manage that patient is also important. I think if there's, I'm not a clinician, I'm a scientist. So I think if we can make it easier and more efficient to diagnose with objective outcome assessments, you know, objective measures. So that physicians in general can just say, I think you have this. And oh my goodness, this is the worst part of this thing that you have. You know, you orthosetic intolerance is bad. I can fix that or I can help you manage that. That's super important from a clinical perspective. And then from a research perspective, being able to identify patients that fit certain types of criteria, whether the study, the trial, for example, really wants to focus on viral reactivation or orthostatic intolerance or cognitive impairment, to be able to have the ability to zoom in on the disease characteristics that you want to will also be very important. And I do think that recover is helping the world, the physicians, the US to appreciate that. You know, they have trials now that are designed targeting very, very focused areas. Immodulatory trials, they have metabolic trials, they have viral persistence trials. So I think, yes, it's just going to take time. I know it's exasperating how slow stuff moves. I mean, again, this darn paper took me two years. So I hope it does. And I hope things begin to move faster. You know, I think we're snowball, right? So I think it's just getting bigger and bigger and faster and faster and we'll make a difference. And again, I hope this paper, which has been picked up by a lot of different media outlets, really helps people appreciate the magnitude of the problem that we have at hand and the attention that it needs. Fantastic. I think that is a really lovely point on which to end. Thanks for having me, Emily. I hope that you enjoyed that conversation and that what Dr. Vernon is researching and the way in which she and the team at the Bankman, one center are applying their some 30 years of knowledge of treating these patients is being fed now into this better funded space. With the hope that we can develop strategies for everyone living with these energy limiting conditions. One of the other comments that I have received is that we've not yet had full episodes into various of the conditions that we're hoping to explore. Along with some of the symptoms sets and subjects that you have requested, please do stick with us. We are only 11 episodes in and this is a project that we're building piece by piece. We feel like we are doing something unique here by trying to encompass all of these conditions. What I'm trying to do is jump on some of the latest papers as they come out or bring to you some of the most influential researchers in these conditions as they have new findings and new work to share. There is so much going on out there, but I can only work as fast as I am able with my condition. So we would love it if you could bear with us stick with us, keep feeding back because we really, really appreciate knowing the direction that you want us to take this. And I read all your comments and try to take all of them on board. Whether you have been affected for 30 years or for one year with one of these life limiting conditions, your particular experience is valid and respected. And we all weather and choose to react differently to our situation. One thing I implore you is to please be kind to each other. How you deal with it is your choice. There should be no preaching, but there can be ideas shared. We all have our own paths to navigate. Please take from the people that I speak to what aligns for you disregard what does not fit. But always try to stay open to possibility to new information and open to hope. 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. To find out more about what we're working on and how Visible could help you, visit our website at makevisible.com.