#18 Leading research, delivering hope: The Open Medicine Foundation’s mission with Linda Tannenbaum

[Music] Welcome to Make Visible, the podcast shining a light on complex chronic illness. I am your host Emily Kate Stevens. Welcome back. This week I have the humbling pleasure of introducing you to Linda Tannenbaum, the founder CEO and president of the Open Medicine Foundation. She is a remarkable force within the ME/CFS community, connecting the highest level of scientists with funding, research opportunities, and patients. I hope you enjoy listening as much as I enjoyed having the conversation. [Music] It's great that you're doing this. You've met a lot of people I see. I've met a lot of people. It's really exciting. I've failed really, really privileged. So there are good things to come from this illness, which is actually, now I'm doing something that I really believe in, and the people that I get to meet are just, it blows me away every time I get to have one of these conversations with these people who are doing so much in this space and so much. It's a wonderful community. It's amazing. It's a small community. We know most of us know each other. It's a small community, but it's a very passionate community. We're all working to get people better and in this complex area that we're working in, it's very complicated. But because of that, everybody's sharing and talking and communicating, and it may be different than, however, research is being done. But in this case, it's so complicated and there's so many people that are suffering. We need everybody to share and to talk to each other and work together. Most of us know each other and see each other at conferences or. Do you feel that that kind of collaborative approach has been something that has been there within the ME/CFS community for the, I don't know, maybe save for the last 12, 15 years, since you've all been actually working on bringing it into prominence. Do you feel like it's being collaborative in that way the whole time? It's a very good question. I mean, I actually started the foundation because there wasn't any collaborative work being done. And so I set it up with that premise that if we're going to be able to solve this, people have to talk to each other, people have to share, people have to have conversations and collaborate with each other. So we set the whole thing up as a collaborative effort. But I'm not the only one that's doing it. It really kind of sparked a movement where other people realize that we have to collaborate together and now people are collaborating together. But it took a few years for people to start doing that. And more importantly, it took a few years for more people to start researching in this area. And so we needed to have the critical mass for people to be able to do research and then find each other and then share with each other. And that's the way to move things forward is to collaborate. And do you feel that that shift towards collaboration has enabled better funding and better awareness for some of the research? I mean, we've got to take it right back to, right back in the conversation. But in terms of, in terms of the funding and in terms of what you are able to do in this space has that improved as you've brought in more collaborators. So yes, I mean, funding is always the critical question here. All of our funding is unfortunately from patients who are suffering our patients' families who are caregiving for the patients. So the funding is only coming from net, not from philanthropists or foundations or the government. And so since all of our funding is from patients, for us, they know that we're collaborating with a lot of people. We have some collaborative centers. We're not just funding one researcher, one researcher, one researcher, in silos. We're only funding people who are collaborating with each other. So I think that has helped us raise money because people know it's really a global effort. It's not just one academic center working on something. It's a global effort, which means that lots of expertise is pulled to it and research can move faster when there's so many people. We probably work with over 200 different scientists that are involved with this. And that's really propelled it. And I'm sure it's increased the funding because of it, because of the way that we're doing this. But that is unbelievable. You have no large philanthropic organizations funding you. Now it's all independent private funding. Independent private funding from people who are sick and unfortunately others are not. We've applied to many foundations and grants and large groups and nobody wants to fund this. So it's all people who are suffering from this unfortunately. They should not be the ones that are funding this, but they are the ones that are funding this. And you are the largest private global research organization for ME/CFS. What do you think is the reason that you can't get that philanthropic funding? When you see philanthropists funding all sorts of things, dependent on their political viewpoint, what is it about this condition? There's so much money raised for something like cancer. What is it about this condition that, and we can talk to the figures about the figures later, but that means that people are not investing? Yeah, it's a real problem. Before COVID, of course, most people have not heard of ME/CFS or chronic fatigue syndrome or ME, whatever you want to call it, it's got a few names. And it's really stigmatized because doctors aren't able really to diagnose. And so they've treated this through the years psychologically a lot of the times. And so because of that, it has a stigma that people say, well, chronic fatigue syndrome, the name of it also doesn't sound like it's a really serious disease either. And the problem is when a patient is well enough to go to the doctor as you might have been, you look okay. You may go home and be crashed for a month or six months because you went to the doctor, but they don't know that. They only see you and you don't look so sick when you get yourself out of the house. And so people are not believed. It's really a horrible, horrible problem that I will never understand. I never understand. I mean, when my daughter was sick, she was 16. I knew she was sick. I knew it was not a psychological problem. Immediately that somebody's lying in bed and they can't get up. They're not doing it on purpose when they used to live their life and do athletics and be with people and be social. And suddenly they're not, this is not a psychological issue, but many, many doctors can't help patients. And because they can't, then they call it psychological because they can't find a cause. And all the normal tests, laboratory tests look normal of the ones that they look at, not the research tests, which are abnormal. But the clinical tests, which always look normal. And so it's got this stigma and it's all over the world. I mean, still in so many countries, they just dismiss this and meanwhile people are home. And nobody knows at their home, as you say, they're invisible. They are not present. And that is one good thing to come from. Such a large way of people having developed a similar or a situation that has similarities in long-haired because of the attention that is now been drawn to it. It's obviously not a positive thing that there are more people sick, but perhaps the numbers, huge, huge numbers enable everyone within this community to be a little bit less invisible. Because yeah, as you say, most people say, well, you don't look sick. And the problem is that the majority of time these people are inside their houses, inside their bedrooms, inside their beds. No one is really good in the overview of how they look on the other side of that doctor's appointment. I know. I know. It's true. COVID, the only benefit we've seen is that it is brought to the surface. Not only MECFS in discussions and publications and some articles and some news reports, but many people have to people who have long COVID and are still sick with COVID have MECFS symptoms. And so it's brought to light that a virus can cause these symptoms. And it's brought to light that a virus can make people sick, not psychologically sick, but biologically sick and chronically. The estimates before COVID were maybe 20 million people are more in the whole world. And now there's way over 200 million people that are suspected to have this. I mean, they don't know numbers because they extrapolate numbers, but way over unbelievable 10 times more people having that these same symptoms. So it's brought to light and some more researchers are looking into it, more people are looking into it, more people are being able to talk about it because now when we say MECFS, we say, do you know anybody who's still sick from having COVID? They go, oh, yeah. And I go, well, that's what this is. It's the chronic part of that. So it gives a different conversation to it also. And I think that's one of the things that I've heard from multiple different researchers and scientists is this idea that because COVID is a specific infection that caused long COVID, it now gives some clarity of understanding to the idea that a virus can cause this kind of post viral consequence. Now it's something that your community was very aware of, but it's almost like holding up a magnifying glass and saying, look, this is the proof that there is a direct correlation. The problem obviously with a lot of the MECFS community is that they don't necessarily know what that one thing was that caused it, or even if they do or they suspect that they do, we don't have any idea of how to reverse it. So let's take it right back to the beginning. Prior to 2012 when you founded the Open Medicine Foundation, you come up this from a very personal angle, but you also come at it with a scientific background. So my understanding is that you have had previously 20 years experience in clinical laboratories, managing clinical laboratories, as well as degree in bacteriology, is that right? So essentially what you've done in what you've created here is you're now managing a huge clinical lab of incredible, absolutely incredible scientists and contributors to your organisation. Can you tell me about the way in which you initially formed it and how you have got to the stage in 2025 that you are now working with some of the most prolific scientists in this space? Well, thank you for asking. It's been a long road. When I was 13th year, I actually started this with a smaller foundation that I created called Neuroimmune Disease Alliance in 2010 and really started raising money with family and friends to what can I do, how can I start research, how can we, how can we work on this because I really realised when my daughter was sick and she got sick in 2006 that by 2010, 2011, I still didn't see any collaboration or research happening that was going to find a treatment or a way to diagnose this. And so I thought it got us through emotionally that when my daughter was so sick, I said, we're going to have to start a research foundation as soon as I'm not your caregiver anymore. So the plan was that initially when she was sick that someday we're going to start a foundation because I knew that something needed to be done on a larger scale when I found out that millions of people were sick. I mean, when my daughter was sick and other people get sick, they think they're the only one that has those symptoms until you learn what you have. And then when you start researching it, you'll realise so many people have it. So I started the other foundation for a couple years and realised I was not going to make enough money from family and friends. This was not going to be enough to solve a disease as complicated and more complicated than cancer and other types of diseases. So I started Open Medicine Foundation after I met with somebody who asked if we could set up a seminar, a gathering of some researchers together to figure out what research needs to be done if we had money. And so that person was in Europe and they said, I know you have a nonprofit, which was my neuroimmune disease alliance. I know you have a nonprofit in the United States. Why don't we do something together in the US and gather some researchers together to just talk this through? And that person had, and she likes to remain anonymous, but that person has had MECFS for like 25 years. So she was very involved with it. And so we got together with 20 researchers that she pulled together and we pulled in another researcher to kind of oversee this Andy Koldelnik. He had a clinic called Open Medicine Institute. And so we brought these people together, about 20 of them and many of them that you've already spoken to. That's where I started meeting some of them, Ron Davis and Nancy Climus and I don't have the list of those people who were attended in front of me. But most of the people that we all know at this point that are involved with this, even back then. And we got together for two and a half days at the Harvard Club in New York. And during that time, we came up and then we voted on at the end of it. What's the top 10 research projects that should be done if they could be done? And then we realized, I realized that there's no money to do this and the government is not funding this. How now we've spent these two and a half days doing this. Now what do we do with this? So I decided to start a foundation. And since we had, I started with Andy Koldelnik at Open Medicine Institute. I called it Open Medicine Foundation with Andy Koldelnik working with him and funding with Open Medicine Foundation, which is why we called it that. He asked us to call it that at the time. So I changed the name. I kept neuroimmune disease alliance that I opened and created a 501-C3 with Open Medicine Foundation. I started raising some money while I was trying to get the 501-C3. I used NIDA, we called it for short. I used NIDA to raise money to start Open Medicine Foundation and use that money to get lawyers and start with the proper way of setting up the foundation. And started funding research for the first two years through Andy Koldelnik's group. He had a clinic. He's a doctor. He's an MD-PhD. And while doing that, MET and continued to talk to some of the other researchers that I had met at the meeting. After two years, I realized that this needs to be taken to another level. We need to take this global. We need to raise millions. And I couldn't raise millions of funding one doctor. So I got together with Ron Davis, who is the director at, well, you probably know who he is, but director of the Stanford Genome Technology Center at Stanford. And he has a very sick son that you probably know about, but he has a very sick son. Knowing that he was a parent like I was, I thought we could do this together. And so we spoke. And he was at our initial meeting in New York. And we spoke and I said, if you bring the scientists, I will bring the funding. But I need to be able to bring scientists in to do this research and to be able to raise money for this research in a larger way. So we talked about, and so he said, yes, let's do it. Because his son was very sick. My daughter was very sick. We need to do something. And he was trying to do research and wasn't able to raise money on his own for MECFS. I mean, he had a lot of money for other projects, but not for MECFS. So we started a scientific advisory board. I asked him if he knew any Nobel laureates that we could bring on because that's the level of scientists that he is. And he said, yes, I could. So. Sure. Let me ask them. And so we brought on three Nobel laureates on our scientific advisory board in the beginning, along with some other researchers, really, obviously top, top level researchers. He was familiar with and peers with. And we started going out and raising money to be able to do research at Stanford and with our scientific advisory board, advisors and backing. And through time, we grew our scientific advisory board as I met more researchers and invited them in and some clinicians. And he had other researchers that were involved. And we, I now have 21 members of our scientific advisory board to be able to give us input and really engage with us and give us advice. But the first four years, we raised funds and started raising more funds because of what we were doing, trying mostly to let people know and patients know what we were doing because you had to reach the people who were going to be able to fund and donate and build a whole system. So for the first three years, we were all volunteer and then it got bigger. And I mean, we built some systems up and we started raising more money. So I started hiring my first person and fundraising. That was my first person of fundraiser. And then we built it from there and realized that we need to communicate. We're not having events because people with MECFS are not going to show up to events. So we have to do this online. So we needed to start a system had to communicate better and write newsletters and get to people and have people sign up and receive newsletters from us. So we started a whole communication group and then brought in somebody to do some communications with us. And we started raising money and we actually over those first four years raised about $10 million for Ron Davis' research at Stanford to really kick this off. And doing so while we were there and had our scientific advisory board, I was getting to know some of the other researchers and said that if we raised enough money, we would start opening up other centers to expand this research because again, it's not going to be solved by one particular academic center. So at that time, Ron Tomkins, and unfortunately he passed a few years ago, suddenly, unexpectedly. But at that time, but Ron Tomkins was Harvard. And I said, you know, if we raise enough money, I would love to set up a collaboration at Harvard if you're interested. And he said, yes, if we had funding, we would do that. And then the one one foundation grant that I got was a $5 million unexpected grant from a cryptocurrency person who in those years made money in cryptocurrency and contacted through Reddit and said, this was end of 2018. I made a lot of money in cryptocurrency and I would like to give my money away to nonprofits and Reddit. I would like to know which nonprofits you think community at large would like us to donate to. So we had a following already because we were four years in. We had a following already in Europe and in Europe, they saw this note first because of the hours and started writing, you've got to a lot of people. You've got to give this to open medicine foundation for MECFS research. So enough people did that before we even woke up that we were contacted and I got an email and I thought it was spam because I didn't know this was happening. That we'd like you to apply for this. All we need to do is have a few paragraphs. So it wasn't like a full grant application like they are these days. So we filled that in and then forgot about it because it was a little paragraph and we applied to so many other grants and didn't get them and we ignored it in December. In January, I get an email. We would like to tell you that if you could receive cryptocurrency, we will give you a million dollars. So again, I thought it was spam and I asked our fundraising person. I said, "You think we should answer this?" I mean, what is this? And I said, "Well, I'll answer it. I'm not opening any attachments, right?" So I can answer an email. So I answered the email. Yes, we can receive cryptocurrency. So we were set up to receive cryptocurrency already. And we would love to have you give us a million dollars. And so the person said, "Okay, give us your connect and we will put a million dollars in your bank account." And that's exactly as simple as this happened. And then when this happened, I saw that this group, the Pineapple Fund. They called themselves a Pineapple Fund because they wanted to be totally anonymous. So the Pineapple Fund. I went online and saw that this person was giving to other people and had given two others five million dollars and had given a few others one million dollars. And then we were there as one million dollars. So I emailed back and I said, "If we received four million more dollars, we would do XYZ, all these different things." And we need this for this for this disease. There's so many people who are suffering and really it was a very short email. The person answered me, "I have a few questions. Are you sustainable? And what would you like to do with this money if you got it? Please be brief." So I spent two days made it as brief as possible and said, "If you would like any proposal or any more details, I will give this to you, but this is the brief part of this. We've already been in existence for five years and we've done this, this, this, this. We are sustainable. And at that moment in time, the cryptocurrency was crashing. So the person said to me, "I will give you four million dollars." And then it was crashing at the time. So the person said to me on the next day, "Okay, I'm going to have to give it to you a million at a time because of what's happening in the crypto market, but I have promised you four million US dollars and literally four days in a row." Wow. And with cryptocurrency in a nonprofit, it goes from whatever the cryptocurrency is immediately into your bank. It's not something that you, it's not like a stock that you sell or any. It goes right into your bank. So if someone says they're putting it in your bank, it's in your bank and it's in your bank. So we got five million dollars. So I took that five million dollars and we opened up Harvard and the Harvard collaboration. And then we opened up Canada, University of Montreal collaboration. And then we opened up Sweden, Uppsala in Sweden. And then we opened up a University of Melbourne later on when we raised more money. And that's a whole other wonderful story about how we opened up Melbourne. So that's really how it grew in the collaborative space. Over what time period did that take you to go from, I mean, already building a nonprofit to that extent over the first four years is huge. But then to go to having six different research centers, how long did that take you? I started this in the middle of 2012, July 2012. And in 2018, I believe it was, we opened up Harvard and probably 2019 was Canada, the University of Montreal. And at the end of 2021, possibly I don't have the dates in front of me. Uppsala Sweden. And then at the end of 2020, right in the middle of the pandemic, we opened up University of Melbourne. So we've had anything. So we've had all of them by 20, we had all of them up and up and running with researchers under all these directors. You know, that's why there's really over 200 scientists that are working on this because each director has their own group of researchers under them. And so as we raised money, we started funding research projects at these collaborative centers. But then again, we had to continue raising money to be able to sustain projects that we were funding at these centers. Because that's the thing, you now have to sustain those all of their centers every single year, year in, year out. And you still have the center at Harvard is called the Ronald Tomkins Harvard collaboration following his death. Who now runs that or how has that, how has that morphed? And you still able to sustain that in the same way. Yeah, it's a good question. Yeah, we named it that when you passed. I wanted to give his name and honor. So I changed the name at that time. And then we at the time, Ron Tomkins was working with Wenzong Zau at Harvard. And Wenzong Zau is our director of our computational center, but he also was part of the Harvard collaboration. So with Wenzong Zau, we then brought in Dr. David Sistrum. And you may know his name from your research as well. And Dr. David Sistrum has been seeing patients in the cardiopulmonary area. And he's been seeing patients for several years before I brought him on and asked him to join us and see if we can do some clinical work with him. And so he's the one who, which has been, excuse me, fabulous. He's the one who's been doing is doing our lift trial and doing a muscle. Yeah, it's a dream. That brings us on to one of the main things that we'd like to talk about, which is, and it's both of them, it's when Wenzong Zau and David Sistrum, who are overseeing that study. Yes. Now, but this is the lift study, it's not just something that you plucked out of the air. This is actually works that they previously did together or some of the basis of this, I believe, is work that they previously did together with your support and they were looking at Mestanon in MCFS. So they have this groundwork of looking at Mestanon. And there was also some subsequent work that was going on looking at electronic health records that I was reading about on your website. But looking at Mestanon and now you have taken that on to look at a trial of Mestanon in combination and sometimes not in combination with LDN, Lodo's Nell Trexon. Yes. Explain to me, this is heralded as the first OMF clinical trial. If I look at your work, you have been involved in so many different pieces of research and trials. So explain to me how this is your first OMF clinical trial. Yes, good question. All the other projects that we have funded and we have funded, I think, over 67 of them, 68 of them so far. I mean, tried to do my research into your project. There's a lot of, there's a lot of. Was. Yes. Yes. Thank you. Sorry for all that. To be sorry, it's absolutely amazing. Yeah, I mean, there's been a lot of research and there's right now we're funding about 30 of them. So right now there's a lot of research happening. But a lot of the research in the beginning days, we're looking for needle in a haystack. So a lot of the research in the beginning days are looking to see where do we look. So our first project that we did was with the severely ill patients and thought that if we look at the sickest, let's look to see if anything stands out like a marker. What stands out in a person who's so sick? And so we did like a thousand different tests on these on 20 patients and did not find any pattern. So we thought, okay, we're not looking in the clinical world and the clinical laboratory testing. Nothing is standing out. So now where do we look? So a lot of the work has been. Most of the work has been looking at the molecular cause. What's going on in the metabolomics and the proteomics and at the molecular level? We didn't know enough to do a clinical trial. Okay, so we knew of some treatments that people were trying, but we didn't know enough scientifically and evidence-based information to do an actual clinical trial, which because they cost so much money, we want to make sure that whatever we're doing makes sense and we'll help the most people. So while that is all happening and people are doing all and the researchers are doing all these phenomenal research work and we're learning and we're really coming to the point of not looking for needle in the haystack, but really focusing on where do we see the abnormalities that are showing up that are measurable and testable in the blood and in the urine and in spinal fluid and what can we learn from all of this while that is all happening. The clinicians coalition developed by the Cindy Bateman Horns Center and Mary Dimmick and they put together this clinicians coalition to bring clinicians together that are in this space and talk about what treatments and what diagnostic information can we all share together because each doctor really treats patients' personalized medicine indifferent and we wanted to know what is what can we learn from each other. So during that time we took a vote if you could have one clinical trial, what would you say would be the most impactful for your community and that was low-dose naltrexin and the doctors who were giving LDN to their patients were seeing more of a symptom reduction than other types of drugs at the time. So I always knew if we were going to do a clinical trial we wanted to do a LDN trial first because that's what they really significantly wanted because so many other people go to other doctors and they can't get LDN because there is no evidence anywhere and we wanted to be able to do a trial to show that it helps some people and then people can bring that paper, that publication, whatever when it happens to their doctor in their local area and say can I have this drug it may help me. So it took years to be able to raise enough money to do that kind of thing and to get the right people together and so with David's system then being on one of our directors he was involved with that and giving LDN into his own patients and giving Mestinon to his own patients and then we did the Mestinon study looking to see with Mestinon is it sustained or are the improvements sustained with the first study in Mestinon. And then over time basically we wanted to do a clinical trial and start looking for treatments because Initially, when I started this, of course, I wanted to look for a cure. And then I realized through time that while we're looking for the cause and a cure, we need to start helping people. So I said, now we need to focus on clinical trials so that we can start helping to reduce symptoms for people while we are looking for the Holy Grail to solve this disease. So originally, we were thinking of doing another trial, but then run Tomkins passed in the middle of all this. So I won't get into those details. And so we decided instead of doing that, which would have been under him, we would do it with David Sistram. His expertise is right in this area with LDN and Meston. It was perfect. He did the right type of testing. He had the patients that he was looking for with orthosatic intolerance. It was a perfect combination for him to do our first clinical trial. So we started raising money for that. And then we raised enough money not only for the trial, so the trial itself is very important to see who responds to LDN, who responds to Meston and what percentages are helped by it. And also is there an added benefit to do both LDN and Meston because it really treats different symptoms. And then of course, placebo because we wanted to do a proper study, double blind placebo study, it's the largest study, 160 patients. It's one largest study at that time when we were gathering it all together in this space. But most important from the study, from the lift study is the additional money that we raised to do testing on responders versus non-responders because we know some people will respond. We know that people have been improved by this. So we want to see what is it? Is there any measurable so that we can pick up from the blood to see what changes in a person when they respond versus if they didn't respond? So we can predict who can be helped by this and so we can look at there's any markers that are affected in a person who responds versus doesn't respond. So it's almost like looking to see if everyone who had high glucose, when you lowered the glucose, they were better. We're looking for something, a marker of some kind, we're always looking for a biomarker, we're always looking for something to measure. So in this case, we actually raised a million dollars for the study and then we raised another million dollars to do the testing because the testing is as important as the study. And so this is a very, very important clinical trial to do first because we know some people will be helped by LDN and we want to learn from this as well as a clinical trial just looking to see how what percentage of people respond to this drug. So it's a very significant. The hard part is, of course, it's placebo. So you have to wait till the end of the study in order to break the code and then do the testing. So it will be a couple years for this. But it's going. It's already moving. It's already we're already giving it to patients. It's already moving. It's amazing. I do still find it shocking when I looked at the study protocol submission that you said the first line by, I guess the background it says, MCFS is a complex chronic disease with no FDA approved treatments. No FDA approved treatments. It still absolutely shocks me. It is. It's shocking. With this size of community, no treatments. Yes. And what you're suggesting here actually very sensibly is the repurposing of two drugs that you have seen not only anecdotally, you have also seen in other research that they can improve to go deeper into it. Maybe I should speak to the people involved in the in the trial. But can you tell me about the idea of possibly combining them because you've got four arms. You've got the people who will be just placebo. You've got the Mestanon with placebo LDN with placebo. And then LDN combined with Mestanon. Talk to me about that idea of combining the two. Is it the idea that they are treating different angles of the disease simultaneously? But presumably that they have been shown to not have bad interactivity? Or what is it about the combination of those two that you're looking at together? So good question. We know that they treat different symptoms. So they do treat different symptoms. And Mestanon is really for orthostatic intolerance. And LDN can help many things actually, but it can help fatigue and brain fog and sleep and other things that Mestanon may not be able to help. But LDN has been known to help some of those other symptoms. And many people have both all of the above all of those symptoms. So it's important to test them separately. But together they might be synergistic that the interaction of the two of them might be greater than than one plus one. But even if they're not greater than one plus one, we hope they are. At least you would be able to help with both drugs help more symptoms than one or the other. So they have been given together in patients a lot. So we know that they can be given together. That they're safe to give together. And so many of the doctors just immediately as soon as they have a diagnosis try those two. And so of course it's the doctors that don't know anything about it that we want to teach about this. And that's why we're doing this. So it made sense to do both of them together in a clinical trial. And when you can do multiple drugs in a clinical trial, of course you save money than doing them separately. So it made sense. It's also quite hard to get that across the line though, isn't it? Because the more variables you add to a trial, the harder it is to actually get it passed. So the design of the study is clever to actually have managed to get it through. Well, that's why it was important to do them separately and together. So that way you have all the parameters covered there. It's important because we may have some good outcome measures on one of them separately, but not together. We don't really know right at the end of the day. But it was important to do them. The hard thing is is that it costs more to do that because you're adding more arms to it. And you have less patients. Like if we were going to do 160 patients, of course, now it has to break it down into four. So four groups rather than two groups. So you have less patients in each group. And then when you want to do female and male and you add all these subsets that diminishes the numbers and you really want as many as possible, but it's cost prohibitive to do that many more. So we did what we could afford. It's really exciting one. Particularly the LDN is one of these that has been with the long-cabird has been discussed since about 2021 that it's had positive effects. But most people are still getting it off label or however, by whatever means possible. Well, it actually appreciates it. We'll be a couple of years. Yeah. It will be, but it won't be an FDA approved drug. It still won't be. It's an FDA approved drug, but it won't be an FDA approved drug for ME/CFS. It is an FDA approved drug because you can get it easily. And the best thing is it doesn't cost a lot. So it's reasonable compared to other types of pharmaceutical interventions. So people hopefully can afford it if it's going to work for them. I hope. Yeah. Let us talk now about, okay, there were two that I really, really want to get to. And one that I think is really interesting for the community. And obviously every single trial, every single piece of research involves patients and members of the community. But you're treat me study. You actually took information from almost 4,000, 3,925 patients to try and establish what actually is working for patients. Now, this, you can't compare it to a clinical trial in the way that we've just been talking about the lift trial because it is about patient reported outcomes without the control of a trial. It's a very different big. However, you've got information from almost 4,000 patients. And from that, I think has come some quite interesting information about potential treatment avenues. And this goes back to what you started in 2012. What are the top 10 research areas? What are the possible things that we need to look at that could help people? You from this have established various different treatments that are making a difference for people or lifestyle management that are helping people. You've established similarities between long COVID and MECFS and where there is a divergence. Can you tell me what for you really stands out in the information that you gathered from that study? That's a good question. I mean, it's really important to get information from patients because they're the ones that are the people who know the most about this disease and what helps them. The hard thing about it is is they only are able to take what the doctors or they've been able to gather themselves. So it's not the end all answer of what is going to cure this disease because people haven't called us and said I'm cured. So they answer questions and which then we analyzed for about a year and a half or so to try to give the 400 questions of my Russian thing. Yeah, like the more than, you know, like 420 or something like that. It's really remarkable that any MECFS pays now through one of the questions. Well, we were really worried about that, but we said they can take all the time in the world that there was no deadline at the time. And because we did this this over like a two year period. And Martha Ecky who created this. this whole thing is just brilliant in the way that she did this. She did this on her own before I met her. And then when we met her and I saw her survey, I said, we have got to analyze this and then share it with the world at large. And can we do this because you've spent so much time creating this fabulous survey that she actually shared on Twitter on X. And she was getting some people to answer it. And she was giving them some summaries of things that she'd seen. And we really wanted to take it to another level when we had fun at about it. And so she worked very hard with our team to work and analyze this data in order to be able to share it with the public because that's what's most important is to be able to share with each other. So what we learned for that really kind of led us to one thing, one specific thing that came out of it for the low dose naltrexan trial to tell you the truth. They were able to in this particular survey, not only to say what has helped you, but what has it helped. And we had thought we would mostly be looking at LDN for fatigue and pain. And that our outcome measures should be for fatigue and pain. And what it showed us from this treatment survey was that brain fog cognitive dysfunction was one of the most things that were helped by people that were taking low dose naltrexan. So we added a test to test for cognitive ability as one of our outcome measures. So we actually learned that from this study and did not know that. And because most of the people who were taking LDN years ago were for five of myelia, which was for pain. So we had thought that was the focus. But here it showed that more people were helped with their brain cognitive ability. So anyway, we have an outcome measure because of that. But it showed how people who are under doctors care and or are learning themselves, stowed again and again and again, that pacing is the best way to help yourself get through at the day and not improve your symptoms, but prevent crashes. And it showed in the list of what is helped the most with fluids being number one and pacing being number two. That's because that's some people that's all they have. But it also is significant. It is very significant for people to get fluids and for pacing and pacing more than anything else if we train doctors on anything, is to teach people not to exercise their way to health, but to pace themselves and to understand that what they're doing may be harming them if they do too much and they need to stay under there with what we call their threshold, but figure it out for themselves. What it is that crashes them and try to do less at a time rather than more at a time. And rather than building up your endurance, you need to pace yourself to not go over and cause yourself a crash. So the results actually showed that as well, that people are really mostly improved on their symptoms by learning how to pace themselves. And then basically-- - It's a cool thing for you to then filter out because it's one of those things that is, you can't say this is the regimen, this is the dosage. It is so personalized to every single person's activity and their severity level. It's also not something that any pharmaceutical company can come in and take a lot of money from. - No, no. - You know, the problem then comes in terms of trials and studies is that you're not really going to get people wanting to, you're not going to have that pharmacological money coming in. - Right, right. - Well, again, it's not a cure. It just helps prevent you getting worse if you can pace yourself. But there's a lot of people who are in bed that pacing doesn't even make sense because they're not doing anything anyway and they're not getting any better. So pacing is for the people who are up and about and may think that doing more might help them when doing more may harm them. They need to know that. Although I think that this is an interesting area for discussion because I think a lot of the time people consider that pacing means purely physical, whereas actually from experience, from my own experience, cognitive pacing, I don't know if it's actually to do with the glucose uptaken, the energy used by your brain, but cognitive pacing is almost as important as the physical pacing for someone like me in terms of managing my symptoms. And so I think that we do need to help people understand that pacing is about everything. So if you are flat out in your bed, not physically doing anything, but you are working or scrolling social media or answering emails on your phone, that still takes its toll in terms of your pacing. And we do need to make sure that people have that awareness that we're not just talking about, don't go for a run. - Exactly. - I agree with you totally. - Yes, yes, absolutely. - But interestingly, that was one of the things. So you, the pacing was and the fluids were the most effective in both ME, CFS and long COVID where they not. - Yes, but again, because most people are not getting certain medications for the illness, it's probably also what most people are more aware of and able to get. But yes, and it is the two items that everybody can do, hopefully, I know in some places you can't go and get fluids, but you can actually make sure that you are to stay hydrated yourself if you can't get IV fluids, then you can stay hydrated yourself and try to help yourself that way. But yes, I mean, it showed up in the numbers with people answering the survey and us doing the analysis. - And it came up with, I think 150 different treatments that people had tried. Were there any in there that actually surprised you in terms of their efficacy that you had not necessarily registered that number of people were using? - Not really, because we talked to so many patients and so many clinicians, we've heard of people taking these things, which is also why when Martha created this, she created this with the knowledge from patients of which drugs to include in the question here. So the question wasn't open ended, what are you taking? The question here was, are you taking this particular drug? - Okay. - So what dose and what symptoms help? And so it's a little bit biased that way. - Okay, so it wasn't something out of them. - Interesting me. - Graded exercise therapy, which is a very contentious subject still. - Yes. - Actually, was the only thing that really, really came up as such a detrimental treatment strategy for people that there was no other treatment that actually caused so many people, I think it's over 75% of people to feel worse. Whereas everything seems to be making incremental gains. Some people obviously didn't get on with certain drugs, but you're generally looking at it, you know, a couple of percent. But the Graded Exercise Therapy really. - Yes, it just proves that again. And sadly, people answered that because it's probably many people were advised to do that from their doctors. And so they know that it made them worse. And so they were able to answer that question that it made them worse. So it just proved it once again that Graded Exercise is really harmful for many, many people with this illness with both long COVID and MECFS. And so it made sense. In fact, when people get COVID, one of the first thing I tell them is is just you need to rest. Don't try to work it out. When people have the flu or they have another virus, they might, once they're feeling a little bit better, think, well, I should start getting up. I should start walking. I should start getting out. When they have a virus like this, a serious virus, our first recommendation to them is you need to rest it through and just get over this and rest because you don't want to make it worse. And you don't know what's going to happen later. - I think that might be good advice across the board when people get sick, then not to have that. So urgency to get back, particularly to hard exercise. - Well, your body responds in a negative way when you're sick, unpurpose to make you rest. It's kind of evolutionary, I think. It's just some people don't listen to their body and think that I should work through this and really into rest. - I think that's our society, isn't it? We say a program now to push and not necessarily listen to our bodies. I think if there's anything that having chronic illness teaches you, it's too listed really, really hard to your body. And actually, if you do like with the pacing, if you do listen to your body, it's quite good at telling you quite good at telling you what it needs. It's unfortunate that sometimes that is just that it needs to stay in a dark room for a long time. - No, no, yeah. - Let us touch on a new study. I don't know how far you have got with this now, but a new large-scale study that you are working on and that is the BioQuest Study. You've previously done at least 11 Biomarka Studies, 11 Studies to try and find a Biomarka. And as I mentioned before, you're looking at the multiomics, you're looking at metabolites, kind of running, you're looking at mitochondrial function. There are so many areas of our systems that you are looking at. Can you tell me a little bit about how you are approaching the BioQuest Study, which is to try and find a Biomarka for MECFS? - That's a good question. Specifically, the other studies were really for looking at the molecular cause and the molecular basis of the disease, hoping that something may show up as a biomarker or diagnostic versus an actual project searching for a biomarker. as his bioquests. The reason we want to do bioquests is most of the studies that have been done, including ours, but including everybody's, have been with like 20, 30 people. And we wanted to do something in a very large scale, so that way it would have meaning and really looking for more of a biomarker signature, we know it's not going to be a biomarker, like one thing. But looking for a biomarker signature and looking for patterns and with AI, we think that with these new tools, looking at it like we've never been able to look at it before. So it's now a good time to do a large scale study like this and then have AI work it to look for patterns across Metabolo, Mix and Proteol Mix and cytokines. You might have these three things are low and these three things are high and together, it's a biomarker signature. And before with our eyes looking at the answers, we might not have been able to pick up those patterns as much as hopefully AI tools will be able to pick up some patterns that we would not normally have done. So the purpose of this of course is to test as many samples as we can at the same laboratories. So we get rid of the variables between laboratories, which we have seen because different researchers test the different laboratories, different mechanisms, different technologies, different results come up. So we want to take about 1,000 or 1,200 samples, half of them being ME/CFS. This will be an ME/CFS biomarker discovery study and take a look at half people that have the disease and then a lot of people who have different diseases that need to be differentiated with the disease. Like if a person walks into a doctor's office with symptoms, we want to know what the doctor needs different, differentiated from. So we want to use that as well and then healthy to come here to healthy. So the advantages is we have enough samples that are already collected. And so from our studies that we have done in Uppsala, Sweden and frozen away in biobanks and from studies that has been done via other institutions that are now housed by NIH, we have access to samples that are already frozen away and collected. And this saves a couple years of collecting and recruiting and all the other work that needs to be done in doing that. So it's really low-hanging golden fruit that we just couldn't pass up in this. And no one's ever done anything in this scale. So we want to take that many and do all the testing, take all the samples, collect all the samples together in one place and then test them all on the same system, same technology, and then compare the results and see what happens. So this is something that we are just in the process of tweaking which tests to do and how much the budget will be. We've already raised a million dollars to work this. Because everybody knows this is so important to have a diagnostic signature. And this scale, if we can't find it within this, then we will stop looking in the blood this way. There's other people who are doing things and we are also also doing electronic medical records search, which is another part. So the bioquest itself is literally testing samples and then doing a validation later on whatever biomarker signatures we find, then doing it prospective either in another cohort that's already collected or depending on the results or actually drawing new patients and seeing and validating it that way. So there obviously is a whole other area that's going to have to happen on the validation site. But additional to that and at the same time as that, we have actually three of our centers looking at the electronic medical record of patients and seeing if there's anything we could learn from the electronic medical record of all the tests that are been done. And those are the clinical tests, of course, not the research metabolomics proteomics. So it's looking at two different paths. One is the clinical side, pathology side, where the doctor has ordered tests and the results have come into the electronic medical record. The doctor has done an assessment. The doctor has written if a person knows that they had an initial viral infection or they had an exposure to mold or they had something else that triggered it that they think might have started this. But we will learn a lot from the electronic medical record as well. And again, because AI is with us now with these tools, we're able to gather all of these de-identified information from electronic medical record now and really massage it and see if there's questions we can ask it and see what other patterns might show up. And there's a whole other world that's going to open up with us. We are very, very excited about the new scientific AI tools that are coming up. So these two together are two different paths looking to see what we learn and what we can learn in their different subsets or biomarker signature. What can we learn when we look at all of these? It's incredible that we're doing this now. We, you, I mean, I was saying we as a globe, but it's incredible that you are doing this. Of course. Now, at a time when we actually have the access to that, because that is changing what you are able to pick up. And you're now able to find things that you didn't know you were looking for because of the nature of the way that a human brain has to go through and see, I'm looking for this. But the AI approach is just absolutely fascinating. And the scale to which it can be done is absolutely revolutionary. My one question with that with the looking at all of the multi-omics, that research side of it is if you find a biomarker signature, how do you then roll out something that involves that level of testing, that research level of testing rather than the normal pathology level of testing? How do you create something then that is actually able to scale out to your average patient? Perhaps once they've been to see the general practitioner, what do you call that in the States? Primary care doctor. And then perhaps they get referred to a hospital. How do you have that biomarker signature that is then relevant to those patients who get to that stage who are not in a specialized clinic? So that is the million dollar question, literally. But we do know people that are interested and able to take if we have something that's validated, to translate it into a commercial type of test. And it depends what it is. It depends what the results are. If there's something that can be done and to scale and we're able then to, and it'll be a long process. But the first benefit, of course, will be in research, because then you'll be able to do it in research and be able to know exactly what patients you want to test because you'll be able to use this as a diagnostic. And it will either be an algorithm that some of our researchers are looking into, there will be an algorithm of do all this testing and this algorithm will be the identifier for a group of tests that you go and get an enemia panel or a thyroid panel. And this is an MECFS panel, which is the dream that we would like to have. So it will be a path, but there are people who take information, like there's people in pharmaceutical companies to make a drug. There's people that want to take the information of the laboratory results and create a commercial test. But it has to be something that can be commercialized. So there's some studies that are being done that may show a suggested biomarker, but it's not something that can be commercialized. And we need something that can be commercialized, and not just in the research lab. So we're looking in this area specifically in metabolomics and proteomics, because you can take proteins and metabolites and make a commercial test and cytokines and make a commercial test out of it. So it depends what happens, but there are people that we will then approach and have them take it. And we hope that they make a billion dollars on this later on, right? I mean, we want that to happen. But this is it. And then we share it and say, now you can get a test for this. Go ahead and get a test for this and let people know about it. Because then our most exciting forward issue would be, how do we disseminate this information that this is available? And then that's what we hope we will be able to do and focus on later. Getting it in the hands of doctors, getting it in the hands of patients. And it would really start if we had that with letting the patients know about it, because then the patients will want the test. And with they start wanting the test, their doctors will start learning about the test. And it will go viral, as you say. But it will be a big process, but it has to start. It's not something easy. We've all looked for something easy and it's not something easy. So we have to go and look and see and then get a company to take this to commercial. But we have people who have approached us and said, if you had something, we would love to commercialize it. Because there's always people who want to set up a business and a startup to do that kind of thing. So that is so exciting. I think that is just really reassuring for the community. Because I think that there are a lot of people who have the best world in the world to find something or to create something. But without really that through line of how do you bring it to the people that need it? And I think that just exemplifies your approach. Because you came to this from wanting to work out how you could help your daughter and people like her, you've always got that idea that at the end of this, there is a patient who is a normal person who needs to have access to the treatment care cure. So I think that that approach of thinking, almost top down, bottom up. Flipping right. And I've read it wherever you mentioned. And I think in your six that turn everything, it gives hope. You bring hope to patients. And thank you. Yeah, I wish you the absolute best of luck with that. And you're other 50 studies, 50 research projects that you can't really have on going. Yeah, thank you. Thank you. It's a lot. It's remarkable. I mean, just to give hope to patients, I mean, researchers when they get together do really feel like we're close to a breakthrough because there's been a lot of research happening. And there's been a lot of discussions happening. And I think they're getting close. I mean, I think they're getting close. And so we're there right with there with them. But we have to continue this on. You know, we have to keep going and we have to scale up what we're doing. We'd like to do multiple clinical trials at the same time because on the other side, we hope to learn about a diagnostic from the treatments because if the treatments start working, then we start looking, why did that treatment work? And then that may be an indication of what the mechanism is that's going on the body. And then might lead us to a diagnostic. So yes, from ground up and from top down on that way as well. You know, so we need to all the all at once. You know, we really need to look both both areas. We have to keep looking both areas because my daughter, we had to take to 20 different doctors and no one knew what she had. So we want to diagnose it that you can go to your primary physician. And you don't have this side of the other, but you have ME CFS because you've you've you've you've had a positive result on this particular panel. And that would just be the dream because most people can't go to multiple doctors. You're just written off. And we need to stop that process so we can get people if you're diagnosed early. You might be able to get improved early and hopefully we'll have some treatments to suggest people. And this goes your meeting that you had where you've got some researchers together in the Harvard Club in 2012. You still do that every year, don't you? I think is it October this year that you're pulling everywhere? Is it is that right? Am I right in thinking you're doing it in October? September. September. It's always the yeah, now it's the day after Labor Day that week we try to keep it consistent so that we people know to leave that and then we have a Stanford. We now have a Stanford group running it. They run it. And we bring sometimes I think a hundred and forty hundred and sixty researchers together. Yeah, it's now virtual. Which is why we can bring people from all over the world. The one the other thing that COVID helped is we had it in person for four years and we got we had like six the seventy researchers in person but it cost us a fortune to run that and then we had a community day. And then when COVID hit and we did it online, we realized how many more researchers could join from all over the world. And so now we do that. We're going to keep it virtual and Stanford runs it. And we have many researchers. We have four full days on virtual members of the MACFS community can join or can people watch? We actually don't have that yet. We actually don't are enabled to have that because we have so many speakers. We didn't want to just pick a few speakers for that day. So, but but Emily, instead since we don't do that, we do have webinars with some and do videos with our researchers instead. So we backed off and did individual videos and and then we do webinars instead of that. That is amazing. That is so exciting to have that. Let me just finish by saying thank you so much for giving me your time today. Absolutely inspiring. Thank you. You as a person and the work that you do. Thank you Emily. Thank you. And I thank thank you from the patient community from everyone for just trying to get a handle on these some conditions. It yeah, it's amazing. Thank you. Well, thank you so much. And thank you for doing this. It just helps with awareness and and you're an excellent interviewer. So I appreciate you. You're very easy to talk to. So thank you so much for doing this. I really appreciate it. I have provided links in the copy of this episode as I do with all episodes. So that you can look at some of the work that this fabulous organisation is currently undertaking along with past studies and research. And we look forward to future conversations with the OMF scientists and collaborators sending you all the very best. 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 a hundred thousand people measure and manage their complex chronic illness. 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