Cutting Edge Research on Fibromyalgia with Dr. Jarred Younger
Inflammation in the Brain, Low-Dose Naltrexone, and the Science Behind Finding a Cause
- Could fibromyalgia be the result of inflammation in the brain? Find out what cutting edge science is discovering.
- A new tool for scanning and imaging the brain may help us finally pinpoint the pathology of fibromyalgia.
- The discovery of low-dose naltrexone as a treatment option occurred as Dr. Younger was testing his hypothesis on inflammation in the brain.
- Correcting inflammation in the brain can begin with simple (albeit difficult!) dietary and lifestyle changes.
- The hardest thing about running studies is getting willing participants — but that’s how we make the scientific advancement.
- Advocacy is having a tremendous effect on fibromyalgia research. It actually improves the scientist’s ability to create new information.
An objective test for fibromyalgia will change everything. As a researcher, Dr. Jarred Younger’s mission to figure out fibromyalgia has led him to study neuroinflammation as a primary suspect. “What I think is happening in fibro is an overly robust immune response, an abnormal reaction to low level, daily insults to the immune system.” Having seen so much suffering with no effective treatment options, Dr. Younger has become driven to solve the mystery of fibromyalgia by scientifically uncovering the root cause.
About Dr. Jarred Younger
Dr. Jarred Younger is the director of the Neuroinflammation Pain and Fatigue Laboratory at the University of Alabama in Birmingham. He is currently funded by the National Institute of Health to study new techniques for diagnosing and treating neuroinflammation, which is inflammation in the brain and nervous system. Dr. Younger completed postdoctoral fellowships at Arizona State University and Stanford University School of Medicine. Dr. Younger’s goal is to end the chronic pain and fatigue that is caused by inflammation in the brain.
Links & Resources
- Get free copies of Tami’s books here
- The Teal Pumpkin Project is raising awareness of food allergies through the addition of non-food trinkets and toys to your treats, making Halloween safer and more inclusive for all trick or treaters.
- The American Fibromyalgia Syndrome Association (AFSA) is the nation’s leading nonprofit organization dedicated to funding research that accelerates the pace of medical discoveries to improve the quality of life for patients with fibromyalgia.
- ClinicalTrials.gov is a database of privately and publicly funded clinical studies conducted around the world, a resource provided by the U.S. National Library of Medicine.
- Report.NIH.gov provides access to reports, data, and analyses of NIH (National Institutes of Health) research activities, including information on NIH expenditures and the results of NIH supported research.
- UpToDate.com is a tool used by many clinicians for finding treatment recommendations and other important information associated with the care of their patients.
- Below you will find both a full transcript and video of the episode, with the studies mentioned in the show linked in the transcription.
- Dr. Jarred Younger has conducted a number of research studies to advance our understanding of what causes fibromyalgia, including studies on low-dose naltrexone as a treatment option for fibromyalgia patients.
- Evidence of widespread metabolite abnormalities in Myalgic encephalomyelitis/chronic fatigue syndrome: assessment with whole-brain magnetic resonance spectroscopy.
You are listening to the Fibromyalgia Podcast with Tami Stackelhouse, Episode 21.
Welcome to the Fibromyalgia Podcast! I’m your Coach, Tami Stackelhouse.
In today’s episode, I am interviewing Dr. Jarred Younger, who is one of the researchers that is doing some really great work when it comes to fibromyalgia. My interview with Dr. Younger ended up being a little bit long, so I’m going to try to keep this introduction short.
[01:11] We do have a couple of things that I want to make sure and share with you before we dive into his interview.
[01:17] First, I want to give a quick shout out to one of our listeners in North Carolina. We got an email a week or so ago, and I wanted to share it with you because it might give you an idea that maybe you hadn’t thought of.
[01:32] She says, “Thank you so much for doing this podcast. Not only has it helped me start to research different things about fibromyalgia, but my husband started listening as well. He gets it now. He didn’t believe me about how much pain I’m in on a bad day. But once he heard your podcast, a few of your podcasts from the beginning, he treats me a lot different. He helps me more and doesn’t give me attitude when I’m having a really bad day and I end up sleeping the entire day. God bless you.”
[02:06] Thank you, so much, for sending this in and sharing how this has helped you in, maybe, some unexpected ways. I love this because that is actually my hope — that you would share these episodes with your family, your friends, your loved ones, to maybe help them understand a little bit better what you’re going through. So, thank you so much for that.
[02:31] The other thing I wanted to share with you in this episode, just really quick, because I know Halloween’s coming up in a couple of weeks. There is something I wanted to share called the Teal Pumpkin Project.
The Teal Pumpkin Project is exactly what you think it is. It is a teal pumpkin, and this particular color signifies food allergies. Whether you are someone who has kids, or if you participate in Halloween and have trick-or-treaters coming to your door, then I want you to have this information. If you don’t, that’s totally fine too. I would still love for you to listen in case there’s somebody you can share it with.
[03:18] The Teal Pumpkin Project was started from the idea that there are kids with food allergies, and they should be able to participate in fun things like trick-or-treating along with other kiddos. You probably know some kids who have peanut allergies, but there are also things like gluten allergies. There are kids who shouldn’t have too much sugar. There are just all kinds of things that are going on.
[03:48] The reason I’m bringing this up on the Fibromyalgia Podcast is because of the fact that we know if you have fibromyalgia, your first degree relatives, meaning your kiddos, are also more likely to have fibromyalgia and all the things that go with it. A lot of us do have food allergies. I think this is something that you guys are going to want to be aware of.
[04:15] The Teal Pumpkin Project is all about taking this cute little teal pumpkin and putting it outside your front door to let people know that you have non-food items available for trick-or-treating. Now, my parents have participated in this ever since I discovered it a few years ago. I interviewed my mom a little bit to find out what their experience has been using the teal pumpkin. I want to share that with you.
[04:48] She said that they have actually chosen to only give away non-food items because she feels that it makes the kids feel good to know that anybody who comes to their door gets the exact same choices. It’s so the kids don’t have to choose the right things, right? If you know from your own experience… maybe you shouldn’t have that chocolate cake, but having to make the choice continually to not have it can sometimes be trouble, right? Sometimes, we don’t make good choices. So, I love that my parents just give non-food items. They also have a sign that they post outside their door that explains that is what they do at their house.
[05:35] She said that the Teal Pumpkin Project is getting popular enough that she can actually hear some parents say, “Oh look, there’s a teal pumpkin!”
[05:46] Now, you might wonder what kids are going to think when they come to the door, and they don’t have the usual selection of goodies to choose from. I will actually post a few pictures that my mom sent in the show notes page for today’s episode. Just go to FibromyalgiaPodcast.com/21 and you’ll be able to see a few of those pictures. They include all kinds of different things when they open the door to trick or treaters. A lot of the things they use are fun pencils or cute little erasers.
Mom said that her favorite quote from one of the kids that came to visit them was from a junior high girl who came up the steps and she looked in the goodies and she said, “Oh stickers! I love stickers!” So, they’ve got stickers in there. They’ve got super balls and all kinds of different things in there, but just non-food items.
[06:42] The important thing to keep in mind if you want to go this route is, first off, you don’t have to go completely to non-food items like my parents have. You can actually have both. The point of the Teal Pumpkin Project is that there are options that are not food, not that you’re only non-food items. “I’m participating in the Teal Pumpkin Project” just means that you have options for kids who have food allergies.
Take a look. A great resource for you, if you want to participate in this, is just to go to TealPumpkin.org. I will also include that link in the show notes.
They’ve got a sign that you can print out, the one my mom said she puts outside the door, and they’ve got yard signs you can stick out. They’ve got coloring pages. You could actually give those away to kids. They’ve also got suggestions for some non-food items, and even for fun community projects you can do like, instead of buying a teal pumpkin… I actually got this one at Costco. Not Costco, I got this one at Target, for just a few dollars. A lot of places will even have them. You can also paint your own, if you wanted to do a jack-o’-lantern or something like that, you can actually do it teal! There’s a lot of resources at TealPumpkin.org and I think that with everything we’re learning, this also ties in to my interview with Dr. Younger.
[08:16] We are finding that the foods we eat affect a lot of things. It’s not just that idea of eating peanuts, going into anaphylactic shock and needing your EpiPen. It’s a lot of other things as well, and that can lead to inflammation, which can lead to stomach issues and not feeling good. Having other options out there, I think is just healthier in general, and just good all the way around. So, I wanted to share that with you.
[08:57] My mom said that a lot of the parents that come past their house will come up and thank them for having non-food options. Those of you who have kids who come home with bucketfuls of candy, and then you have to dole them out so your kids don’t go into a sugar coma. You can just see where it’s just kind of a cool idea to have a different option. So go take a look, TealPumpkinProject.org or just TealPumpkin.org, both will get you to the same place. There’s all kinds of information out there. If you haven’t already decided what you’re doing for the little spooks who knock on your door on Halloween, go take a look at that.
[10:21] TS — Dr. Younger is the director of the Neuroinflammation Pain and Fatigue Laboratory at the University of Alabama in Birmingham. In their lab, they do a lot of different things. Primarily, they are studying right now neuroinflammation, which is inflammation in the brain and the nervous system. They use neuroimaging, imaging of the brain. They use some pharmaceutical and immunological techniques to understand and treat chronic diseases like fibromyalgia. Dr. Younger completed postdoctoral fellowships at Arizona State University and Stanford University School of Medicine. He was an assistant professor at Stanford for a while and is now at the University of Alabama at Birmingham.
[11:16] TS — Dr. Younger’s goal is to “end the chronic pain and fatigue that is caused by inflammation in the brain.” He talks a lot about that in our interview, about why he is convinced that a lot of what’s happening with fibromyalgia is the inflammation in the brain. He talks about the research they’re doing to both confirm that hypothesis, that it is true, but also track down exactly what’s happening there, not just to say there’s inflammation in the brain. Well, how did it happen? Why did it happen? How do we track that? How do we undo that? Those are all things that he is researching.
[11:59] TS — Listen through the interview, and at the end of the interview, do stay tuned. He mentions a few links, and I will recap those at the end and also tell you what you can look forward to in the next few episodes.
[12:20] TS — Welcome. Thank you so much for being here, Dr. Younger. I really appreciate you doing this interview.
[12:25] JY — Thank you. Happy to be here.
[12:26] TS — Awesome. As I mentioned in your introduction, you have been doing a lot of the exciting research on fibromyalgia for the last few years. That’s really the main reason that I invited you to join us, to give us an update on what you’re doing and what’s happening in the world of fibromyalgia research.
My first question for you is: Why fibromyalgia? What got you interested in THIS disease specifically?
[12:57] JY — Yeah, but we have to go back quite a ways to get to that. I was a postdoctoral fellow at Arizona State University, and I knew I wanted to do pain. I had done a lot of pain stuff in graduate school, and we were using different techniques, even things like hypnosis and things like that, which work in some people, but not everyone. I was really fascinated about how aspects of the brain can control pain.
[13:20] JY — I got to the postdoctoral fellowship. They were looking at rheumatoid arthritis, and they were looking at fibromyalgia, and of those two, I could see that with rheumatoid arthritis, we had a good idea of what was going on. There weren’t as many mysteries to solve, and also there were good treatments for it — but, at that time, there was nothing for fibromyalgia.
[13:40] JY — When I saw these patients with fibromyalgia as participants in the study, I realized they had no good treatments, no good options that their clinicians could give them. From a human point of view, there was a lot of suffering that needed to be solved. On top of that, scientifically, we didn’t know anything about what was going on, especially fifteen years ago. There was a great scientific need, as well. When I had those two options, I just gravitated toward the one that had the greatest need, and I’ve been doing fibromyalgia ever since.
[14:14] JY — My mission for that has been to figure [fibromyalgia] out. Wherever that is — if it’s in the body, if it’s in the spinal cord, if it’s in the brain… What is actually going wrong, and then, how do we fix it? That’s been driving me since then, and I’ve branched off into things like chronic fatigue syndrome, which I think are related and those are natural extensions from the fibromyalgia work, but it’s all the same thing.
Then, I focused on inflammation in the brain, because that’s where the results from the experiments have led me. I think we’re getting closer and closer. We start to hone in on the core problem, and then we can develop something that’s actually going to fix it.
[14:51] TS — Totally. I read a couple of interviews that you did leading up to this, just so I knew what questions to ask you. One of the things that you said, I really appreciated — which was that a lot of the strategies out there for fibromyalgia right now are simply to help us cope — but that you actually want to fix it.
[15:12] JY — Yeah. Right. That was what I saw, again, in the postdoctoral fellowship. They were testing things like mindfulness and yoga. And, yes, sure, you might get some benefit from that, but you’re just compensating for things. That’s not fixing the root problem. That’s great — or maybe not great. That’s good as a kind of a bandaid or something to do while we wait for the good treatment. But, obviously, if people are really going to lead full lives like they did before they were kind of stricken with these conditions, we have to correct that core problem. I believe it’s not going to be mindfulness or yoga or something like that. It’s going to be a physiological, thing or we’ve got to flip a switch or direct something, or take a cell and push it in another direction, to actually get people back to where they were before things went wrong.
[16:08] TS — I totally agree with that. One of the things I believe is that — if you’re really going to live your best life with fibromyalgia, there are three things, three areas to address.
- You know, we do have to talk about our lifestyle: how we eat, how we take care of ourselves. You know, if you live like I used to, pushing myself all the time, you know that’s obviously no good.
- We’ve also got to talk about things like mindset: how you talk to yourself, what you think about your body and your illness.
- At the same time, the third piece is exactly what you’re talking about. There’s really something going wrong in our bodies, and we’ve got to address that. We also need more than just that. So, yeah.
[16:53] JY — Yeah, absolutely.
[16:55] TS — So, tell us about some of the work that you’ve done, and the research that has sort of led you to inflammation in the brain. Take us on that journey. Tell us that story: 15 years in 15 seconds.
[17:13] JY — There is so much to talk about! You know, so you go on about this as a scientist. We basically sit there, and we read all the literature, and we’re like, “What’s the best guess I can come up with on what’s wrong?” At the very start, I was looking at all the fibromyalgia symptoms that are the most common. The musculoskeletal pain and fibro fog, the brain fog, with some memory, concentration, word finding, and things like that… the fatigue, the general malaise, some depressed motivation, depressed mood. I line those up on a page and then look to see what out there has those same symptoms.
[17:57] JY — I’ve told this story before, I don’t know if everyone’s heard it, but when I did that, basically they lined up one-to-one with something called the sickness response, which is what happens when you get the flu. These are the behavioral aspects of getting sick. They happen because our immune cells in our brain, when they activate, they release chemicals that change the function of neurons in our brain to make us feel sick. It causes headaches. It causes you to have increased pain sensitivity, fatigue, lowered motivation, lowered mood, the same thing. They lined up one-to-one.
[18:32] JY — So, my starting point was, if I’m going to look at something, this idea that these cells are activated in the brain just like when you get the flu, that’s a good starting point because it looks the same behaviorally. People report it the same. A lot of people with fibromyalgia will even say, “You know, this feels like a flu that doesn’t go away.” There’s a lot of similarities, so that’s not a coincidence. That’s a good starting point.
[18:53] JY — From there till now, it’s been systematically saying: Okay, if that’s truly what it is, if I do this experiment, what’s the result going to be? Then, I kind of go through this process of doing the experiment, seeing what happens, and then adjusting course. There are so many studies we could talk about.
[17:57] JY — Gradually, I’ve been getting closer and closer to the brain. With everything I’ve done, the results have led me to the brain and to inflammation in the brain. I started off in the body, but that’s mostly because it’s really hard to [look at] inflammation in the brain. If people are doing animal research, they can have their rat model or mouse model and they can actually get the brain tissue. I don’t do animal stuff and you can’t do that in a human. You’d have to remove the brain.
[19:41] JY — I did blood tests in the body first. And, you know, one of the things we found is that if you have fibromyalgia or chronic fatigue syndrome, when you have bad days for yourself — I mean, maybe you might consider all days to be bad, but for yourself on your worst days — the inflammatory signals in your body are heightened. That tells me it’s an inflammation thing. The signals we saw that were elevated were things that we know cross the blood-brain barrier and cause those cells in the brain to activate. Things like leptin, which is one of the primary things that we see that correlate with fibromyalgia pain and in chronic fatigue syndrome fatigue. I’ve just been following that line. We can talk about a lot of the different studies, but where it’s taken me to now is actually creating new ways to image the brain, so we can finally see the problem of fibromyalgia.
[20:36] JY — We can actually take a single individual, just like you, and do a brain scan for a tumor or something and say, “There’s the tumor.” We want to be able to do a brain scan and say, “There’s the fibromyalgia; there’s the pathology.” And I think we’re really close to that. We’re at the point now where we can use MRI, magnetic resonance imaging, or PET, positron emission tomography, and get the same answer with both of those completely different scans to show the neuroinflammation when someone has fibromyalgia. It’s taken me a long time because there were a lot of technical hurdles with that and it’s just, science is really slow. But now, it’s pretty exciting because now we’re getting to the point where we actually have that.
[21:20] JY — Once you have that objective test for fibromyalgia, that’s going to change everything. If you had a clinician who didn’t take you seriously, they will, as soon as there is a test that shows that. They’re not… I don’t think anyone’s biased against it. They’re just waiting to have something objective and something clear, and then everyone will be on board with it, and then that’ll indicate treatments. Once there’s a good treatment for fibromyalgia, yeah, every clinician’s going to want to use it. They’d be more than happy to make their patients happy. They’re just waiting for the right tools. So, that’s what I’m doing.
[21:55] TS — Right. Right. And one of the things I heard in what you were just saying, is that part of the journey and part of what’s taking so long is that you’ve actually had to also create the tools to study things. You know, not being able to actually look inside somebody’s brain while they’re still alive is a bit of a hurdle. Right?
[22:17] JY — Right. Yeah. There’s no tool for it. You cannot go to your clinician and say, “Can I get a brain scan for neuroinflammation?” Even though it makes sense that it exists, because we can measure inflammation anywhere in your body. Of course, it’s going to happen in people’s brains as well. But science has not developed tools for medical professionals to use as part of a screening. They desperately need that, because it’s not just fibromyalgia, it’s after traumatic brain injury — a lot of those people, clearly you’re going to have neuroinflammation, but you have no way to know that. We have evidence that as people get older the brain naturally, gradually becomes more inflamed, so a lot of their fatigue and cognitive stuff may be brain inflammation. All kinds of conditions we can look at, if we just get that available.
[23:07] JY — Now that we have developed something, we just have to validate it and make absolutely sure, so we can tell a clinician: “If you do the scan and you get this result, that means neuroinflammation, without a doubt.” We’re not at that point yet. There are a lot of tests you have to do. That’s what we’re working towards.
[23:24] TS — Oh, that’s so exciting. I think so many patients can relate to what you were saying a minute ago, about doctors not understanding. Because you can’t see it, and we look totally fine.
[23:39] JY — Yeah. Well, the big problem has been, you know, a lot of people with fibromyalgia, they hurt in their muscles. The clinicians and the scientists are looking in the muscles and saying, “Ah, there’s nothing wrong.” And that’s true. I don’t think there’s any pathology in most cases. There are some cases where people have polyneuropathies and things that could look like fibromyalgia. That can happen, but in most cases the body is fine, and they didn’t have the ability to look in the brain. As far as they could tell, everything looks normal.
[24:08] JY — I do understand, but you know, I wish clinicians, all clinicians, understood that our brain controls everything. You can create any problem with just your brain, because everything we experience has to funnel through that. You can absolutely create pain just with a brain problem, without anything wrong in the body. We know that as pain specialists, but not every clinician knows that.
[24:38] TS — Just to be clear for the people who are listening, you’re not saying it’s “all in our heads.” It’s not imaginary. There’s actually something wrong in the brain. It’s “all in our heads” in the sense that if we didn’t have a brain, you wouldn’t even be alive and there would be no experience.
[24:53] JY — Yeah. You’re absolutely correct. For an example, when you take a pen and you poke your finger, you feel it in your finger. Right? But that’s not actually true. That’s an illusion that our brain creates. You can’t feel something in your finger. We have a map of our hand and everything else that’s inside a particular part of our brain. When those neurons activate, it makes us feel like something hurts in our finger. Well, that means it’s being generated by the brain. If there’s some reason why those neurons are firing in that region, it’ll make someone hurt in their body when there’s nothing wrong with that finger. That’s what we’re talking about. Definitely. It’s not saying it’s a psychological event. It’s a neurological event. It’s problems in particular regions of the brain that can be corrected that are generating that pain experience.
[25:45] TS — Yes, exactly. I really wish more people understood that it is all in our heads, but it’s not imaginary.
[25:54] JY — Yes. Yeah, a huge difference. I mean, really everything’s in our heads, but yeah, that phrase has been kind of co-opted to mean something else, but yeah.
[26:04] TS — Right. Exactly.
When I first started hearing your name, it was actually back looking at the use of low-dose naltrexone (LDN) for fibromyalgia. I’ve mentioned that a couple of times on the podcast, and it’s an interesting enough thing that we probably should devote a whole episode to LDN only, but would you just talk a little bit about that as part of this journey?
[26:31] JY — Wow. Yeah. After I formed that initial hypothesis of the cells in the brain being activated, my next question was, “Well, okay, if that’s true, then if we give something that we know pushes those cells back into their normal state, that should make people with fibromyalgia feel better.” That was a hypothesis I had. Then I had to search for what could I test the hypothesis with. What is something that we could give a human that has been demonstrated to do that to those cells? I researched for weeks and weeks and weeks and weeks and came up with a list of about twenty things. Some of them didn’t cross the blood-brain barrier. Some of them had never been used in humans. So X-ing things out. No, no, no, no, no. What I was left with was low-dose naltrexone, which fit all the boxes I had.
[27:24] JY — There was enough research to show in animals and also in cultures — you can do cell cultures — that it did what I thought it should do to the cells. It’s been used in humans for other reasons for a long time, for opioid antagonism, and so it’s safe. We know it crosses the blood-brain barrier. So, I decided this is the thing that’s going to test. I originally didn’t think about it as a treatment. Originally, it was a test of a hypothesis. If someone with fibromyalgia takes this and they get better, that means what I thought was wrong was correct. The initial study was really small. I think we just did ten people in the first study, which is usually how I do it — to start small, and if it works, we get bigger.
[28:10] TS — When you did that, you weren’t actually testing low-dose naltrexone. You were actually testing: Am I right about this? Is there inflammation in the brain?
[28:18] JY — Yeah. Yeah, because you had to do both at the same time. But, yeah, that was too premature to test it as a treatment. When we did it, the response rate was 60%, so it worked better than I thought it would. We do these things in a really meticulous fashion, and so we take symptom reports — you can see this in some of the papers — every day. Not only can we say, “Hey, you feel better after you take the drug.” We can look at the trajectories. We can see how fast it drops, and that most studies don’t do. I could see the effect, and since it was placebo controlled, I could see when they were on the placebo, and I could see what happens when they switched over to naltrexone, and it was a true physiologic response.
[29:04] JY — Once I saw that, I knew that the hypothesis was correct, but then also realized we had a potential treatment that people needed to know about. That’s why we got some money from the American Fibromyalgia Syndrome Association to do the larger version. I was like, “Okay, we need to replicate this and show that it’s actually true.” We got the same results with the second study, and we got that information out there.
[29:27] JY — I have no idea how many people are taking low-dose naltrexone now. It seems like a lot, because I get questions about it, but I don’t know if it’s 100,000 or 500,000. I have no idea. Of course, we have advocacy groups, like in the UK that are promoting it. That’s a lot of it. It looked great.
[29:48] JY — I wanted to do more with it. The next step is to run it on 400 to 500 people, do a huge clinical trial. Once you do that, the clinicians feel more confident in using it. I know if I run that huge trial, they would do it, but it’s really tough to get money for those multimillion dollar studies. Usually drug companies do that. I knew at the time that there were a couple of drug companies that were looking at [low-dose naltrexone], and so I just let them have it. I said, “Well, I think my work is done. I can at least let people know this could help. Now, these companies are going to do it.” I was hoping they would get out a product [that doctors could prescribe], but they haven’t. I don’t know where that’s going. It might be time to come back and say, “Okay, if you’re not going to do it, we do need to try to get the money and run a huge trial that will kind of give the definitive answer for it.”
[30:38] JY — I’m convinced, because now we’ve done three studies, and I did one after that where we measured the inflammatory stuff in the blood, and we can see that low-dose naltrexone decreases it. [See Dr. Younger’s research studies here.] Every time I test it, we get the same results. I can never give medical advice. I’m a scientist, not a doctor. But if I had those symptoms, [low-dose naltrexone is] the first thing I would try, because I know from the participants that most of them handle it very well. There’s a good chance they’re going to respond.
[31:08] JY — Of course, not everyone does, so now what we’re doing is trying to find if naltrexone didn’t work for you, what else might? We’re halfway through a dextromethorphan trial. I don’t know if you’ve heard about that one, but dextromethorphan also changes the function of those cells that we think are abnormally activated. The cool thing about dextromethorphan is that it doesn’t interfere with opioid receptors. With naltrexone, some people are scared to take it if they’re on hydrocodone or oxycodone or something, but with dextromethorphan, you can take [opioids] with it. They don’t conflict. We’re going to have finished that trial in February, and maybe we’re going to have another treatment that people can use. I don’t know yet, but we’ll have an answer mid next year.
[31:53] TS — That’s cool. I personally have been on LDN [low-dose naltrexone] since 2011. I think it’s one of those things that the longer you’re on it, the better it works, and that it works for a bunch of different things. I also have Hashimoto’s, autoimmune thyroid, for those of you who are listening who don’t recognize that. It helps with both things quite a lot.
[32:23] JY — Yeah, that makes sense. It does have actions in the periphery, as well, because there’s cells — like the microglia in the brain, but in the body — that it can reduce, and when we look at inflammation in the body, it goes down. There are studies with Crohn’s disease or inflammatory bowel disease, and it responds to that, too. So, it looks like an anti-inflammatory, similar to how you would think of ibuprofen or aspirin, except it also works in the brain, not just in the body. Not exactly the same mechanism, but it’s a similar way of thinking about it.
[32:57] TS — Cool. With the studies that you’re doing now, looking more specifically in the brain and the scans, the technology to get there, what are you hoping to discover? What are you thinking this will give us?
[33:14] JY — Again, it’s just about a tool for clinicians, but what we’re hoping to find — again, I keep saying this, there’s so many studies, so I think about which one to talk about first… One of the studies is the positron emission tomography, and those cells they have been talking about are called microglia. They have different states. They actually change shape. When they’re in the normal state, they have these long kind of arms that look for problems. When they find a problem, they pull in those arms, they become circular and then they change the receptors on their surface and they start to pump out a bunch of chemicals that make us feel sick. The cool thing about them is when they change into that circular shape, that activated inflammatory state, those receptors change in a certain way that we can detect.
[34:02] JY — They’re called a translocator protein receptors. You don’t have to worry about that. What’s important is that there are chemicals we can inject, radio tracers, that go to that receptor. Since those cells really only express that receptor when they’re activated, if we inject it in your body and we find a bunch of the signal in your brain, that means a lot of the microglia were activated. Does that make sense? It means they’ve changed into that activated state, and they have those receptors. We’re doing that [study] first. We will bring people in with fibromyalgia, healthy controls, and see if their brains are kind of lighting up with a lot of this radioactive signal we injected. I know that sounds bad, radioactive. It’s just positron emission tomography. It’s less than an X Ray. So, that’s how it works. That’ll be pretty straight forward.
[34:53] JY — Another study that is more experimental… I can talk about it just a little bit. We think that in fibromyalgia, the immune cells from the body are actually breaking into the brain and causing the inflammation. We’re supposed to have immune cells for the brain and different immune cells for the body, and they’re not supposed to mix. The brain ones shouldn’t get in the body; the body ones shouldn’t get into the brain. But we think that’s happening in fibromyalgia. There may be some… a little weakening of the blood-brain barrier, and those cells are getting through. Once they get in, they don’t know what to do, because it’s not their environment, and so they get activated, and they can cause these experiences of being sick. We’re going to pull the cells, do a blood draw, isolate those cells we think are getting into the brain. Then, we can incubate them with another tracer, inject them back in the body, and then wait a few days and scan the brain to see if those cells made it into the brain.
[35:51] JY — If that works out, if we find those cells in the brain, that’s going to be huge. That’s going to tell us there’s abnormal infiltration of peripheral immune cells. The, we’re going to have a true target to go after. That means we can try to strengthen the blood-brain barrier. We could try to go after those cells. We can try to find out why they’re being called into the brain. That’ll be huge. We have no idea if it’s going to… if that’s what’s wrong, but we know we’ve got the scan working, and so we will probably… Let’s see, we should start scanning in January, and we’ll probably do it in five months. So, by summer of next year, I think we’re going to have an answer, whether that’s actually what’s driving the symptoms of fibromyalgia.
[36:33] TS — That’s fascinating. As you were talking, it made me think a little bit of leaky gut, where things get [outside the intestinal wall where they shouldn’t be]. So, we have leaky brain too?
[36:42] JY — Yes. Oh, absolutely. And, in fact, we knew there were leaky brains before we knew about leaky guts. If you have inflammation, the blood-brain barrier kind of creates these gaps, and then things can get in. That’s what happens in multiple sclerosis as well, which is a really serious disorder. The difference is, in multiple sclerosis the immune cells are actually attacking the neurons because it’s an autoimmune disorder. In fibromyalgia, we do not think that’s the case. They’re not attacking the neurons. They’re just kind of globally releasing proinflammatory stuff. Fibromyalgia is not as serious a disease, in terms of damage, as something like multiple sclerosis, as far as we can tell, when we scan the brain. Once we correct that inflammation, the brain is good. It will be as healthy as if you didn’t have fibromyalgia. Whereas with multiple sclerosis, you can’t really. And in Alzheimer’s and Parkinson’s, there’s actually damage occurring. So, you can’t say that as much.
[37:39] JY — That’s the good news about fibromyalgia: we think it’s totally correctable. But, yeah, with the leaky gut, I think this is all a series of things. If you have the wrong balance of — I don’t know if you’d call a microbiota or flora or however you want to refer to this stuff — and it turns inflammatory, and you have leakage of lipopolysaccharide (or endotoxin, really), that can lead eventually to brain inflammation. Now, gut inflammation has been linked to rheumatoid arthritis, and even inflammation in the gums has been linked to heart disease, and now it’s been linked to Alzheimer’s. We’re seeing all these links between peripheral inflammation migrating into the brain and causing even worse things. That’s a huge thing in terms of what you were saying about lifestyle changes. Anti-inflammatory…. Even if you can’t target your brain directly, if you reduce inflammation in your body, you’re probably going to down the line and help inflammation in your brain as well.
[38:38] TS — Right. I was just wondering: if you start making these changes yourself — looking at reducing inflammation, reducing all the things that contribute to inflammation — how long does that process take before you start actually seeing results of that? If we’re talking about things that are happening in the brain.
[39:03] JY — The research that we do suggests a minimum of three months before you start feeling it, if you’re directly targeting the central inflammation. For example, low-dose naltrexone should take about 2-1/2 to 3 months before someone can tell if something’s kicking in. As you mentioned, it’s a long process, and because you’re correcting fundamental processes, you should continue to get better the longer you take it. It does take a while. It’s not like I’m taking a painkiller for an injury or something which can work in 45 minutes, or something for a headache sometimes. It’s much slower, but more fundamental. With a lot of painkillers, you’re covering up pain. We’re talking about actually correcting the abnormal problem to begin with.
[39:48] JY — If you’re trying to correct it with dietary stuff, it could take longer because you’ve got more steps in that chain. You know that you’ve got to correct the peripheral stuff. It’s got to have time to move through that system, change what’s circulating in your system, and then eventually get to the brain. I don’t know, because I haven’t done that research, but, I mean, it could easily be something where you’re truly helping. You might not know until like six months later the true impact of that. I guess that’s an argument too. You know, once you’ve decided to embark on a particular lifestyle change, you have to stick with it. Even if after the first month you’re like, “This isn’t helping.”
[40:29] TS — Yes, that is one of the things that I’ve seen as I’ve been coaching people, is that we’re obviously desperate to feel better. Right? I think a lot of times we give up too quickly, you know. We’ll do something for a short while and say, “Well, that didn’t work,” but also not having the understanding of how long it should take. Right?
[40:52] JY — It’s a lot of effort. And if you’re putting an effort into something and you’re not getting any return, it’s just as for anything. It’s hard to keep that up. But you’re right. If we could actually say — if we could research some of these things and say — “Hey, we know that you’re not going to feel better until six months, but at six months you probably will start to feel better.” I think that would really help people. We need more of that type of research. We need more dietary change research. You know, reducing the fats and salts and sugars. What does that actually do for fibromyalgia? What if you did all that? What can you expect as a reward for all that kind of work of giving up those foods? There’s not enough research to know the answer to that.
[41:31] TS — Right. It seems like we end up with contradictory things, right? Especially when it comes to diet. We’ll have some people who are like, “Oh, vegetarian diet, you will feel so much better.” “Oh, what? You know, paleo, you will feel so much better.” When really it may be just about what you’ve removed, not about what you’re actually eating.
[41:50] JY — That’s a great thought. It could be. And it’s different for different people. That’s the problem. For someone, it could be some particular protein that’s in a set of foods that you don’t even know are linked because you don’t know what proteins are in them. Then, there’s some obvious ones like certain grains or some dairy products where you don’t have an allergic response, but you have an intolerant response to it. I think that could do it. Eliminating and tracking symptoms over time to see if there’s any variation. Then if you see, “Hey, you know, why on these days were my symptoms relatively better?” Then you can start trying to figure out what was different on those days. If you can find out what those things are, then maybe you could eliminate it, mostly. I’ve used that as an example before. If it was milk or something or dairy, maybe you have a coffee every day, and you have milk, and so you’ve got that kind of trigger. But on certain days you have more milk, and maybe you have cereal or something, and you have worse days. If you don’t track that, you may not realize that, but that could say, “Hey, eliminate all milk and maybe you’ll feel a lot better.” I’m not suggesting that, it’s just an example.
[42:59] TS — As an example. Yeah. I have a similar example. There was a client I worked with several years ago and we were trying to track some of this down. She kept a food diary and sent it to me every week. By tracking it, we were able to discover that every time she ate tomatoes, she had a higher pain day two days later. There was no way she was ever going to discover that without tracking. Because, like, two days ago, I don’t know what I ate.
[43:30] JY — Absolutely. Two days is a very logical physiological window, and, for a number of reasons, that makes it really hard for people to track. The other one is interactions. It might be when you have dairy or tomato and you physically exert yourself over a certain amount, or you do that and get into the sun to be two things. Then it’s really hard to figure that out. I submitted a grant to the National Institute of Health once. What I wanted to do was have a program you could have on your phone where you track as many things as you can, and then a machine learning algorithm analyzes everything, to look for the things you say. Is there any two-day lag between doing something and having effects? Are there any interactions? Way more than a human could do by looking at it. Then, it will send a report to you saying, “Hey, guess what, we found something that reliably predicts your bad days.” I thought it was a great idea. They didn’t fund it, so I don’t know. Maybe we’ll try again. I think it’s really hard to do, but now the computers are good enough to do that. We may revisit that and see, because you wouldn’t have to think about it. You just record what you eat, record what you’re doing, like what you’re already doing when you journal it. It’s just that a computer then goes through it to try to find patterns.
[44:44] TS — Yeah, it’s really pattern recognition that we’re talking about. And for those of us, like me, who tend to be good at that, I can help clients with that. That happens to be a skill I have. Not everybody has that kind of a brain.
[45:00] JY — Yeah. And they don’t have access to a clinician who thinks that way. I think that’s one of the major problems. I know a handful of people who can do what you’re describing and do it really well, and they can work wonders for their patients. Then their schedule gets filled up, and I don’t know where to send people in different parts of the United States for that. I’d like some more people to refer them to.
[45:27] TS — Yes, exactly. You know, that’s been a challenge for fibro patients everywhere. There just isn’t enough being taught about it. I don’t think that there are enough clinicians who really understand [fibromyalgia]. Not just like even diagnosing it and recognizing it. That’s one challenge. But then, now that you’ve diagnosed somebody, how do we actually help them get better? A lot of the things that I have found that work the best, things like low-dose naltrexone, just aren’t part of the average clinician’s world.
[46:02] JY — If anyone gets the opportunity to take a peak, you can see what the physicians are being told by looking at something called “UpToDate“, which is the physician’s handbook on what to do. When a physician who is maybe an internist or a family care gets a fibromyalgia case, they’ll go to “UpToDate” and it’ll say, try this first, try this second, try this third. Those three things are the FDA approved medications for fibromyalgia. That’s what you’re probably getting [from your doctor]. That’s totally fair, that those that went through a huge process to get to that designation. Then, there’ll be off-label stuff after that. So, you know, pregabalin didn’t work. Try gabapentin. And there’s these listed drugs. Be sure to suggest exercise. Then make sure to see if they can see a psychologist to see if there’s any comorbid. It’s right there. So yeah, you’re going to get that list, and if you don’t respond to any of those… Some people do, but if you don’t, then what happens? Once they’re at the end of that page in “Up To Date” and there are no more, they’re like, “I don’t know what we’re going to do.” That’s what we’re trying to do. I’m trying to create things to put onto that page they can try, that are actually going to work for a large percentage of the patients.
[47:20] TS — That’s awesome. That’s exactly what we need, more information out there, more options and being aware.
What role do you think genetics plays in all of this? We’ve talked about a couple of things that don’t work for everybody, which makes me think that there’s probably something genetically going on. I mean, if fibromyalgia is the same — which is a whole other topic of conversation! — I know there’ve been some researchers looking at genetic markers and things like that.
[47:55] JY — Yeah. I haven’t done a lot of that myself. Now I have started working with the team from HudsonAlpha Institute for Biotechnology, who are a real precision medicine group and genetic group. I’m learning a lot of their things. What we’re doing, more with chronic fatigue syndrome, that could work for fibromyalgia, as well, is… We do the genetic test, and then their algorithms go through, and we go through all the SNPs, all the pieces of genetic code. Then, it links back to encyclopedias in libraries, about what types of proteins those things encode, and the likelihood that an aberration in that would cause some symptoms. You feed in all the symptoms — fatigue, pain — it runs the genetics and it says, “Oh, wait, we found these two things that have been linked with these symptoms, and it encodes for this protein. If you’re missing it, you’re not going to get enough energy to fuel the cell,” or something like that.
[48:55] JY — It’s been wild. I mean, it’s my first experience with it, but we ran ten people, and for probably four or five of them, they found something that likely causes their symptoms. In some cases you wouldn’t even look at fibromyalgia, but it was actually some deficiency in something that muscles need to operate correctly, and it’s a rare mutation. I could go to that person and say, “We just found something that’s probably causing all your symptoms. It’s not fibromyalgia, it’s this other thing. You have a very rare mutation. If your doctor does this biopsy, and he can prove… If she can prove if that’s the case, and if it is, you can take this thing and you’ll feel better.” I think it’s really cool.
[49:37] JY — So, yeah, there are a lot of ways to answer that. I don’t think there’s one path to fibromyalgia. I do think that we’re going to find that some people have things that are mimicking fibromyalgia, and if we can do the genetics, we can find those for the rest. I don’t know. Yeah, there’s a lot of gene stuff that comes up. We know that those microglia I’ve been talking about, they’re supposed to have those receptors that should be the brakes to turn them off. And so we’re supposed to be able to turn those off and feel better. People with fibromyalgia are more likely to have a genetic variant where they don’t have enough of the receptors. They’ve kind of lost the brakes on those immune cells. That’s just one example. That was published a couple of years ago, I think.
[50:25] JY — I think what happens is, if you get too many of those, not rare but infrequent variants, and you get too many of those together, you get something that looks like fibromyalgia. If you have a little extra inflammation, but then you lack the brakes on the things that are supposed to tone it down, then you get like kind of constant inflammation in the brain. How much is it going to explain? I think it’s like you hear with a lot of stuff. It’s probably a combination of a particular genetic predisposition. Then the triggers come along. There may be some people that have the genetic predisposition of it, but [didn’t get it triggered] because they didn’t get a certain number of infections in a short period of time, or they weren’t exposed to a particular mold or environmental toxin, or they didn’t have stress at a particular time when their progesterone was low, who knows?
[51:13] JY — All those are feasible, and, you know, I’m not making those up. Those are things that can happen. That combination of susceptibility and those triggers at that unique time, is probably what leads to that disorder. And that’s why you’ll have people younger and then some people may get to 55 or 60, because they didn’t hit that particular set of triggers to set that in motion. So, yeah, I definitely think there’s a genetic predisposition, and I think it explains more than half of probably who gets it. But it’s not the whole story. I think it’s genetics plus something else.
[51:48] TS — I think we’re finding that with a lot of things with genetics, that you might have this particular gene, but if you are getting the right nutrients, if you’re getting enough sleep, if you’re managing your stress, then those things aren’t really factors as much anymore. Right?
[52:06] JY — Right. And the unfair part is someone else could do all those things wrong, but because they lucked out on those particular genetic things, they won’t develop the disorder. There’s definitely a familial component. If you have fibromyalgia, your family members are more likely to have a number of autoimmune disorders. I mean, you’re going to see more lupus and rheumatoid arthritis. There’s some general connection there. We just haven’t nailed down the particular kind of aspects of the genetic code.
[52:39] TS — If you were going to categorize fibromyalgia… It seems to come with a lot of other autoimmune type things, but it doesn’t seem to totally be autoimmune. Does it fall under rheumatology? Does it fall under neurology? Where would you put fibromyalgia, with everything that you’re learning?
[52:58] JY — Yeah, that’s really, really tough. We have to consider the system that’s involved, which I think is the brain. Which would lead us to neurology, because rheumatologists don’t look at the brain, usually. They wouldn’t be reading radiological scans. But neurologists are. I think it’s more appropriate in neurology — more than rheumatology. But what I really want to do is make this a disease that’s treatable by the primary care physicians. I would really love it if you didn’t have to see a specialist. We’re talking about six million plus people, and going to a specialist is tough. I really want something [that’s treatable by the primary care physicians], and I think that it’s totally achievable. I think we can make it where you don’t have to go to a rheumatologist or a neurologist.
[53:55] JY — Again, if it was something like low-dose naltrexone or dextromethorphan or some of those — and we’re testing curcumin and stinging nettle and a bunch of botanicals — you don’t have to go past [the primary care physician]. I do think that because we can’t find damage in the brain, I do think ultimately it will be something that, once we have the right tools, so one starts to get it early-stage, they’ll go to their primary care physician. You’ll get this [treatment or medication], and it’ll prevent [your fibromyalgia] from developing further. I really think that’s how it’s going to ultimately end up. It’s not going to be something where you need brain surgery or things like that, so it won’t require that specialist level [of care].
[54:29] TS — That’s great. That’s actually my dream for the world. That it’s not like it is now when somebody is diagnosed with fibromyalgia. They’re sort of told, “Well good luck to you. We don’t really have much to treat this. Things don’t really work. Life as you knew it is over.” It would be awesome if we got to the place where it was like, “Okay, you have fibromyalgia, but it’s not a big deal. Here’s what we do.”
[54:57] JY — Yeah. I think that’s great. We just have to wait. That’s the target. And, you know, I remind myself everyday that is the goal, and I know we have to go as fast as we can. It’s really frustrating to me how getting funding or getting regulatory approvals can slow things down so much, and the ideas I come up with are so fast. I’ve got like the next 100 things planned out, but it takes so much work to test even one step, and we have to be disciplined and go step by step by step to convince institutes like the National Institutes of Health to give us funding. If we go too far out, if I try to go for the far thing, they’ll say, “No, that’s too big of a jump. You need to shore up these ideas first.” And so I’m, “All right”. But it means when we get there we’re going to be REALLY confident. It just really slows things down.
[55:53] TS — Is there anything that we can do to help make that process faster? Is there anything advocacy-wise or donating funds or… Like, what would make that process faster for you?
[56:06] JY — Yeah, well, thanks for asking that. That’s nice. I’ve been amazed by the advocacy that has been growing. That is huge because the pressure that’s being put on federal government at the Congress level… You’ve seen a lot happening with chronic fatigue syndrome in the last few years. All that benefits fibromyalgia, as well, because when we run participants with the CFS study, half of them are going to be comorbid. They’re going to have both. And so we’ll say fibromyalgia only, chronic fatigue syndrome only, and both. So, all of this research helps everybody. Those things have been really great.
[56:50] JY — I don’t think the animal research is going to push us very far. That’s my personal opinion, because we really don’t have a model that mimics fibromyalgia or chronic fatigue syndrome. I think the most important research is going to be done on people. And that means we have to have participants for it. The hardest thing about running studies is getting willing participants, because it’s so hard if you have fibromyalgia to come into the lab and have these things done. But that’s how we make the scientific advancement. So, I’d encourage everyone if you can, if it’s not going to be a really absolutely disruptive event, to find out what studies are in your area and see if you can participate in them. That’s the big thing I think.
[57:35] TS — Right. Because you can’t research anything if you don’t have anybody to look at. Right?
[57:40] JY — Well, yeah, we need all kinds of different people also. We don’t want to just study one type of person. We don’t want to have only 20-year-old college students, because that may not be the same for everybody.
[57:53] JY — That’s the big thing, other than that… The advocacy groups are great. I don’t know how those operate internally or what that looks like from the participant side or patient side, but I know that it’s changing things. I was skeptical a few years ago about the advocacy groups, but I can absolutely say advocacy is having an effect. It actually improves the scientist’s ability to create new information. I’ve been really happy with that. I think people can give money to labs directly, but now there are groups that collect that money, and they give it to the most promising studies, basically every study I’ve done that’s important. If you look back at low-dose naltrexone, that was started with a really, really small grant. That was enough to get that going.
[58:47] JY — Those groups that collected that money and then gave money to groups like me, those have been really important. I mentioned the American Fibromyalgia Syndrome Association. They just funded two new studies. The NIH probably wouldn’t do that because they’re too experimental, but these private foundations can take more risks. They allow me to do the kind of out there stuff that I think is going to help, but they’re not conservative ideas. So yeah, that’s really important.
[59:17] TS — That’s great. And I know from the people I work with, going back just a little bit to the advocacy — writing letters, calling your representatives, your senators, that really does help. It just takes longer than you think. Like everything, it all takes longer than you’d think it should, but I have heard from those people who are meeting with those individuals, that they really do listen to those of us, especially when they start getting enough [letters and phone calls]. So, if any of you out there are interested in helping to further the fibromyalgia research, those are some things you can try.
[01:00:00] TS — So, what research is exciting you the most right now when it comes to fibromyalgia? Yours or somebody else’s or both?
[01:00:11] JY — I, well, I know I can say… Which one? Wow, that’s actually hard. Even just focusing on ours, trying to think about which one I’m most excited to run…
Let me tell you about one because I was just meeting with the graduate student today, Christina Moeller, who’s going to be running the study. We’re going to get it started. We were just funded by AFSA, American Fibromyalgia Syndrome Association, so we’re going to start it. I think we’re going to run it basically in March of next year. It’s going to be a lot of regulatory stuff, but we’re going to run it in one month and I think it’s going to be huge.
[01:00:47] JY — There’s a chemical called lipopolysaccharide, or endotoxin, that mimics a bacterial infection for a very short period of time. When you inject someone with it, it tricks your immune system into thinking you’ve gotten a small immune insult like you might [receive] every single day.
[01:01:07] JY — What I think is happening with fibromyalgia, is every day we get exposed to a little virus, a little bacteria, not enough to cause an infection because our immune system kicks in and beats it down. What I think is happening in fibro is those normal exposures are triggering an overly robust immune response, including a central response. You’re basically getting sick all the time because your immune system is overactive. You’re not actually getting the infection because it gets beaten down, but you feel horrible. You’ve got this constant struggle between your immune system and either something in your body or something coming from outside.
[01:01:46] JY — We tested that by injecting people. We’d bring people with fibromyalgia into the hospital and we injected them with this little low level trigger, and we found what we thought we would find. The fibromyalgia patients had an overly robust immune response to it, and they were supposed to produce something called fractalkine to reduce that microglia response in the brain, and they failed to do that. The healthy controls, after about four or five hours ramped up that chemical to push down the response. The fibromyalgia patients didn’t do it. And so it looks like the fibromyalgia patients were lacking the brakes to turn off the inflammation in the brain. We are measuring that in the blood. So that looks great. It’s exactly what I thought, but now we have to prove that it’s happening in the brain. [See more of Dr. Younger’s research studies on Google Scholar here.]
[01:02:35] JY — What we’re going to do in March is that same thing, but we’re going to do it in the scanner. We’re going to take people, put them in an MRI scanner. We’re going to inject them with that chemical, activate their immune system, and what we expect to find is their brains are going to produce more inflammatory chemicals and not turn off when it’s supposed to. I’m almost certain that’s what’s going to happen, but we have to run it.
[01:03:00] JY — We have the scan that can measure brain temperature. I don’t know if you’ve seen that one. We’ve published one paper on chronic fatigue syndrome. We can measure your temperature all throughout your brain and when you get sick, your brain temperature goes up. We’re going to measure brain temperature, and we’re going to measure some chemicals, like lactate, that get released when you have brain inflammation. You should only produce lactate when your brain’s driving really, really hard, more so than you can do by thinking. It’s usually only neuroinflammation. Now we can measure that in the MRI scanner. So, we’re going to inject them, measure all these neuroinflammatory markers, and if we find that fibromyalgia patients have that big response in the brain and the healthy controls don’t, I think we have our answer right there.
[01:03:42] JY — It’s an abnormal immune reaction to low-level, daily insults to the immune system. So I’m excited about that, and I’m going to be running all those participants myself, which I usually don’t have time to do, but we’re going to do this in such a short period of time, and since we’re injecting some serums you have to monitor medically, we’ll all be there for about ten days, all day, running this study as fast as we can. So yeah, I’m excited about that because I really want to run a study that’s going to give that definitive, objective answer, that there’s no question. It’s like, YES, the patients did this, the controls did this. That’s what the problem is. And we know what that means.
[01:04:25] TS — That’s exciting. What you’re describing there makes sense to me as a fibro person. I’ve always thought of fibromyalgia as an amplifier, right? Like we can experience a normal thing, but then it gets amplified to high pain or high fatigue or whatever. This sounds like the exact same kind of thing.
[01:04:45] JY — That’s a good way to think about it. The only question, I think, is whether that trigger is external or internal. It’s possible you could have an infection, for example if you get chicken pox. That virus hides next to your spinal cord your entire life, and it comes out later as shingles, if your immune system gets suppressed. When you had chicken pox, you live your life with the virus. Our immune system keeps it in check all the time, unless you get immune suppression, but it has to fight to do that. It could be that way with some people who have fibromyalgia. What they’re feeling is that daily battle between the virus that’s always trying to get out and the immune system that keeps trying to tamp it down.
[01:05:31] JY — A healthy person has that too, but it’s not amplified, like you say. They don’t feel it. It just happens behind the curtains. With fibromyalgia, they may feel it every time that happens. Now, that’s just potential. We haven’t tested that, but we’re going to. We’re working with a group, I don’t know if they know, I can’t mention them, so I’ll hold off on that right now. But we’re going to send them blood samples of fibromyalgia patients over months, longitudinal samples, and no one else has a sample set like this. And they’re going to measure the levels of all these viruses that stick in our system, to measure those low level concentrations, to see if when fibromyalgia patients have flares, is that when that virus started to try to replicate. And wow. I don’t know what’s going to happen, but if that works out, that’s going to be really, really important.
[01:06:18] TS — That’s exciting.
So, what research do you think we should be spending more time and money on, besides just yours? What I should say is: What things do you think we should be studying and spending more time and money on?
[01:06:40] JY — I’m now mostly convinced that this is brain inflammation. Any approach to handling brain inflammation, those microglia cells research, going into — How do we get those microglia cells to the state where we want them in? That’s huge. Other than that, I want to see more research on the things that people can do right now.
So, I think those are the two things I want to see a lot of research on. How do we correct the fundamental problem? But then until we do that, what are the behavioral things we can do? What are the environmental things we can do to at least get people to the point where they can live functional lives and accomplish most of their goals? Because that’s what all this is about, without having to struggle every day with it.
[01:07:28] JY — I want to see more dietary things. I want to see more botanical options. Can you take these botanicals and reduce your symptoms by 50%? That would be a huge thing. What else is possible? There are all of these kind of interesting treatment options now. There’s a noninvasive vagus nerve stimulator that I’m really interested in. I don’t know if you follow that, but you know, we’ve known for a long time that if you have fibromyalgia, and you do a vagus nerve implant stimulator, that can really help. The problem was, it’s invasive and so it wasn’t worth it. But now there are noninvasive devices that you can accomplish the same thing with no implants. A person can do that at home.
[01:08:12] JY — Does that work for fibromyalgia? It should, because it is anti-inflammatory in the brain, and it can help correct sympathetic and parasympathetic nervous system ratio. Both of those can be very good for fibromyalgia for a number of different reasons. So yeah, we need to test that device. You know, you may be able to treat it without even taking medicine, use it once or twice a day and have sustained benefits. So we need to do those clinical trials on some.
[01:08:38] JY — I’m trying to get my graduate students to do them because they have to do their thesis and dissertation. I’m trying to say, “Okay, you’ve got to do a thesis dissertation anyway, why don’t we do it on a potential cool treatment? Let’s just do a clinical trial, try it out and see if we get something.” So, that’s part of my daily work to get the students doing some. We can run more clinical trials and get more things tested. Those are the types of things, and we’ll do some of them, but then, wow, there are so many people researching fibromyalgia, and there’s so much… I can’t even keep up with what everyone’s doing. That’s the good news, that a lot of people are dedicating their whole careers to fibromyalgia. It’s definitely got attention. I don’t know who’s going to come up with that answer first. There’s a lot of competition, but somebody’s going to do it.
[01:09:24] TS — That’s a race I’m happy to support. That’s cool.
I thought of something while you were talking. A couple episodes ago I had the founder of Oska Wellness on and did an interview with him. They have a PEMF device, and I was curious if you have ever looked at that for help with inflammation. It’s pulsed electromagnetic fields. It’s the same thing they use for regrowing bone.
Is that done on a bed, body wide or is it…?
[01:10:07] TS — This is actually a small device. It’s something that people can use at home. I know that they’ve used it for years in doctor’s offices, but this is actually a home device. I’ll shoot you the links.
[01:10:19] JY — I can’t speak to that. I just haven’t looked at it. I have to read a published clinical trial and scrutinize it, and I don’t know if they’ve actually published on it yet. Certainly there’s a lot of neuromodulatory research like transcranial magnetic stimulation. That’s more powerful but you can’t do that at home. It’s like a $50,000, really, really strong magnet that goes right through your skull and changes neuronal functioning. Those can help. Then there’s transcranial direct current stimulation, that’s something you can do at home. And, of course, there are all kinds of stimulators. I think the question is what, where to put that? Is that vagus nerve? Is that spinal related? Do you go to the brain directly? If it’s the brain, where in the brain? There are many groups working on that angle. I’ve kind of left the neuromodulation to other groups because they’re doing such a good job, and we’ll get the answers on whether those work. But yeah, I don’t know how efficacious the PEMF is.
[01:11:23] TS — Cool. I just thought I’d ask.
Where do you think we’re going in the next, say, five to ten years? What’s your prediction for the future of fibromyalgia?
[01:11:41] JY — I believe that we’ve been researching this for a long time, but, in talking with my colleagues, I feel like a lot of the lines of research that were in their infancy a few years ago are now getting to their kind of pay off. I feel like five to seven years is the time frame where there’s going to be really big, groundbreaking results. And yes, people probably said that 20 years ago as well, but there really feels like something different [is happening]. There’s a maturation of the fields, whereas other people before were just throwing out ideas. Most of them were wrong. Now, there’s starting to be a consensus on what areas of the body to look at, and things are converging now. I really feel like we’re getting close.
[01:12:35] JY — I think one of the trends that have hurt the field in general is treating fibromyalgia as a single disease. When you do that, you look at patients versus controls. If only one third of the patients have that thing and you do patients vs. controls, you may not notice the difference because it may wash out if you have too many people. I really think the field is going to benefit from subgroup analysis and realizing that maybe for a third of fibromyalgia patients it’s some type of autoimmune. But maybe in a third it’s some type of chronic infectious thing. And maybe for a third it’s something else. And now enough researchers appreciate that’s the case. So, I don’t think they’re making that mistake of throwing away good ideas just because it doesn’t work for everybody.
[01:13:24] JY — That’s something we’re going to see change. I think there’s going to be a major breakthrough. But then, also, I think we’re going to get more sophisticated at chopping away at the patient group and saying, “Okay, we may not be able to cure 100%, but hey, this works for 25%. Now we’ve got them handled. Now let’s see what’s left. Here’s 75% what’s the next thing?” I think that’s the way it’s going to work because we’re going to find a handful of major things that are going to be treated differently that’s causing the same set of symptoms. We have to start thinking that way to really handle the problem.
[01:14:03] TS — Yeah, I totally agree with that. I’ve thought for quite awhile now that in my lifetime we’re going to see this thing called fibromyalgia being divided up. Just watching and working with enough clients over the last ten years and watching how different people respond. It just seems a little bit like, maybe, diabetes or something — where we’ve got two things that are called the same, that have similar symptoms, but actually are different.
[01:14:29] JY — That’s a good example. Yeah.
[01:14:32] TS — So, we might have different types of fibromyalgia [like Type 1 and Type 2 Diabetes], or we may come up with new names for new things we discover. I agree with you that we’re going to start seeing that divided up, and it makes sense that that would affect the research too, right? Because if you have a lot of this particular group over here and not as many of that group over there, and it just helps one of those groups, then it looks like it didn’t really work when it actually did.
[01:14:56] JY — Exactly. Yeah. And the problem is for large clinical trials, you have to have an overall group effect. You could have one third of people that have a great response, and that may not meet the FDA requirements. I think we need to change that thinking. I mean, if you have a drug that works for even 10%, that’s a lot of people. I think we should have as many tools as possible. As long as they’re not dangerous treatments to try, we might as well give them a shot. A lot of these have low side effects, and so we should give them a shot.
[01:15:28] JY — So, yeah, I think that’s gonna be true. I think, ultimately, I would love in 10 or 15 years to not even have fibromyalgia as a diagnosis because we’ve understood all the subgroups and we’ve given them appropriate names based on the pathology. That’s when we’re done, when there’s no more fibromyalgia diagnosis out there. It’s a chronic herpes virus infection or it’s a microglia activation dysfunction or something like that. It’s still a long way to go to that, and maybe there’ll be a group where fibromyalgia will always be descriptive. I mean, it’s still helpful, but I really want to carve those out to meet the promise. Divide and conquer.
[01:16:09] TS — Yes. I love that. There have been a lot of things that we’ve talked about for patients, like getting involved with studies, getting involved with advocacy. Do you have any particular resources that might be helpful for patients if they want to participate in some of this?
[01:16:29] JY — Sure, let me think of some ideas. One good place to start is ClinicalTrials.gov. If you’ve never gone to that, it’s a federal site. Any US-based researcher who’s being serious about their work should register their study with ClinicalTrials.gov and you should be able to search for it. If you go to clinicaltrials.gov and put in fibromyalgia, you should see all the actively recruiting clinical trials and find out if there’s something close enough to you to go to. That’s the best resource for that. If you’re not close to a major institution, an academic institution, it can be hard to participate. We, unfortunately, usually don’t have funds in the NIH budgets to fly people in. I wish we could, because we could get people from all over the country that would actually do that. It’s a lot of work to come in. We’d need the budget to do that. Some of the studies are kind of long, so that’s hard to do. So yeah, I would check ClinicalTrials.gov.
[01:17:33] JY — What’s another good resource? There’s a site called NIHreporter.gov. I can send you this, or you can put it in a link somewhere where you can see all the grants.
[01:17:51] TS — Yeah, I was just gonna say we’ll put it all in the show notes. So that’d be great if you want to send it.
[01:17:55] JY — That’s a site where every researcher that has received funding for anything is listed. You can check that by putting in fibromyalgia, and then you will see by geographic region, “Hey, there is an institution 45 minutes away that’s got this cool fibromyalgia study.” I think that’s the best way. There’s not a really good resource for connecting patients with particular clinical trials that I know of. Maybe they exist but we don’t use them. I wish we could improve that communication.
[01:18:25] TS — Yeah, that would be great. I know you guys have a great Facebook page. Do you announce your studies on there?
[01:18:35] JY — Absolutely. I know for sure if you want to stay on top of what we’re doing, the Facebook page [will help you] do that. Any new study I start, we’ll put the link for how you can screen, to see if your eligible for it. Then, we keep them up with news, and I put the preliminary data on there, so you can see the results there as much as I can talk about them first. That’s the idea. Just from my lab.
[01:18:58] TS — Okay, perfect. And for those of us with fibromyalgia, especially if they’re in your area — you’re in Alabama, right?
[01:19:05] JY — Yeah. Birmingham, about the center of the state. For most of the studies, if you’re within two to three hours, because sometimes there are a few visits, that’s usually pretty doable. Outside of that, it’s kind of a case by case basis, but definitely if someone’s in Alabama. We’ve got all these brain imaging studies coming up. We have clinical trials. There are a lot of things to participate in.
[01:19:27] TS — Awesome. Now, I know a lot of times when I talk to people about clinical trials, there’s some hesitation. Would you just talk directly to those people who are thinking, “Hmm. I don’t know.”
[01:19:42] JY — Yeah. That’s a good point. I guess they can sound scary. There’s a pro and a con to all clinical trials. The obvious pro is that you’re getting something that could really help before most people can ever have a chance to try it. That’s really cool. You could get something that can help you five years before it would otherwise be available to you. The downside is that it’s experimental, and so we don’t have all the information about what side effects could be or what it could do. I think the steps involved that you don’t see to get to that point where we’re doing a clinical trial on people… There are so many steps involved. There are so many government entities making sure that this is safe, that it is really hard to find something, like for fibromyalgia, that’s going to cause problems.
[01:20:35] JY — We detect [those problems] way before. Usually, there are smaller trials before in animals and in vitro proficiency and toxicology elements. So if there’s something on ClinicalTrials.gov and you’re thinking about participating, you’re probably going to be safe to do that.
Now, the downside of a clinical trial is, it’s not individualized to you. If you go to your physician, they can titrate your dose or raise it or lower it, because your clinician is about helping you as a person. Clinical trials are about finding out something from the population. So, we, maybe, can only give one dosage. We’re not allowed to change it, so it won’t be as tailored for you. So, there are some downsides, but I think, usually, when it gets to that point, we’re pretty confident that it’s going to do something.
[01:21:24] JY — I know for our lab, we won’t put forward any treatment that has any serious adverse events. That’s not what I want to do. I don’t know if other groups would do that, but if there’s any evidence that it’s actually going to cause problems, then that’s a no go. I think most people at our clinical trials have a really good experience. We try to make it really easy. You’ll get capsules of something. You may not know what it is. It may be a placebo for part of the time, and it may be the active drug. That may be a downside, “Am I on the drug or not?” But you can trust us. We’ve set it up. When we’re at the end, we can tell you, “Here’s when you were on placebo; here’s when you were on drug; and here’s how you responded.”
[01:22:07] JY — With a lot of clinical trials, if it ended up working for you, there are ways where you might be able to get that medication, even though it’s not commercialized yet. Certainly, if someone goes through our clinical trials, we try to find a way to get them that drug, if it worked for them really well. I think the pros outweigh the cons for the individual. The real big thing is, if people don’t participate in those trials, we can’t go forward with treatments. I mean, that’s the end of it. We have to do those to get the information out. So, it’s critically important to developing new treatments.
[01:22:47] TS — Absolutely. I think that… I hear so many fibro patients who are all saying, “We need better options”, but we can’t have better options unless we show up as patients for those tests. You know, to let you guys use us as Guinea pigs to try those things out. Like, that’s the only way it’s going to happen. So, for those of you, if you’re near Birmingham, make sure you connect up with Dr. Younger. We’ll also have those other links out on the show notes so that you can check those out. I think that’s really important.
[01:23:23] TS — Any last thoughts that you have or you want to share about the work you’re doing or researching?
[01:23:30] JY — Wow. There’s so much to talk about. You know, we touched on some really good things. I think we did a good job talking about some of the focus on the new things that are coming up, which is what I like, as a scientist. It’s what I like to focus on. I think in terms of a kind of an overall thing. I still, and I’ve said this before, through different venues, but I look at brain images all the time and all kinds of different ways, different modalities, and I have still never seen anything that suggests that there’s any true damage occurring that’s lasting. I’m saying this as someone who actually goes in and looks at the function of the brain.
[01:24:20] JY — I truly believe that once we reverse that process in someone, they can go back to being the way they were before. You may have heard of a couple of imaging studies where they say, “Oh, the brain is shrinking faster or something.” But that’s kind of hyperbolic. When I go in and look at it, it’s nothing like what it’s being reported to be. Extremely minor stuff on small sample sizes. In the collective evidence, I don’t see anything suggesting it’s neurodegenerative, it’s destructive. It’s not even like rheumatoid arthritis where you get joints breaking down. It is a physiological thing. The amplified signals can be corrected, and then you will feel better again. As soon as we can get that tool to people where they can use it, I think we’ll just wipe out the problem.
[01:25:12] TS — That’s awesome. I’m really glad you brought that up, because I do talk to a lot of people who are worried, especially with the brain fog that we get, where we can’t remember things and we say the wrong words and we put our keys in the fridge and it’s like, “Oh no, am I, is this something like Alzheimer’s?”
[01:25:30] JY — Right. And that’s not the case. If someone who doesn’t have fibromyalgia gets a horrible case of the flu, you can’t think, you can’t plan. That is a chemical thing. It doesn’t mean that your neurons are being killed or anything. It’s just that’s what those microglia do, to force you to not want to do anything. That whole process you feel when you have fibromyalgia, that is an evolutionarily conserve process to make you want to get in bed or lie on the couch and rest. It makes it hard to do everything, but it’s just a chemical thing. There’s nothing being destroyed. It’s designed to get you to lay down so your body can fight off this infection. But in the case of fibromyalgia, it’s activated when it shouldn’t be. So your body’s acting like it needs to fight off an infection even though there may not be an infection. And so you feel like you’re sick all the time, and you suffer all those consequences. But if we get those cells back to the normal state, those symptoms go away. That includes the cognitive symptoms as well.
[01:26:28] TS — That’s awesome. I love that. And I’m one of those people who always uses that as an example, when people say, “Well, what does fibromyalgia feel like?” I always use the example of those days when you have the flu and your hair hurts and your eyelashes hurt and you get tired just going from your bed to the couch. That’s what it’s like. And you’re saying that actually is what it is.
[01:26:51] JY — Yes. I’m almost totally convinced is the same thing. It’s just chronically turned on in fibromyalgia.
[01:26:58] TS — Hmm. So fascinating.
Well, we’ll go ahead and wrap it up here, but I just wanted to say: anytime, you are welcome back. Anytime you want to share new research, or if you are looking for people, do let me know. I would be happy to share that on the podcast and let people know that you’re looking for people.
[01:27:17] JY — Great. Will do.
[01:27:19] TS — All right. Thanks.
[01:27:23] TS — I hope you guys found Dr. Younger’s information as interesting as I did. I think he is doing a lot of really good work for us on fibromyalgia. I really appreciate his focus and his passion and all the work that he’s doing to not just find ways for us to cope but actually find ways for us to get better — which, as you guys know, that’s the whole focus of this podcast.
[01:27:51] I just wanted to reiterate a couple of the websites that Dr. Younger mentioned. First is his Facebook page. And to be honest with you guys, it’s a really long link with several words and even a few numbers at the end. So rather than trying to give that to you by audio, I would love for you to just go to FibromyalgiaPodcast.com and go to episode number 21, so FibromyalgiaPodcast.com/21 and you will find all of the links including the link to his Facebook page, the Facebook page for the lab.
[01:28:30] Another website he mentioned was UpToDate, which is the website that doctors use to look up different treatment protocols for different conditions. They do have subscriptions out there, including subscriptions for patients and caregivers. So, if you’re interested in that, the website is UpToDate.com. Just all spelled out: UpToDate.com.
Dr. Younger also mentioned a couple websites where you can find out about potential research studies. One of them is ClinicalTrials.gov. That’s where you can go out and look up if there are any trials in your area.
He also mentioned the NIH Research Report, and that website is actually Report.NIH.gov. Which is a little bit different than he said in the interview. So, that is the National Institutes of Health Research Portfolio Online Reporting Tools, is it’s official name. Again, that website is Report.NIH.gov.
He also mentioned the American Fibromyalgia Syndrome Association, which is the organization that has funded some of his research studies. If you are interested in checking them out, their website is AFSAFund.org. That’s AFSA, as in American Fibromyalgia Syndrome Association, Fund, like fundraising or to fund a project. That is AFSAFund.org.
[01:29:16] We also talked about a lot of Dr. Younger’s research studies, and we will have links to all of those on the show notes page as well. So just FibromyalgiaPodcast.com/21 you will see those links out there, including the links to the research he has done on low-dose naltrexone, the research on inflammation in the brain. All of those things will be out there.
[01:29:43] Keep in mind that some of the research Dr. Younger mentioned hasn’t actually been published yet. If there are any things we discussed that you don’t find in the show notes, that is probably why. Some of the research, such as the studies that are coming up in the spring and summer, obviously, there’s nothing I can link to yet. So, just stay tuned. We will likely have Dr. Younger back on here at some point to discuss the findings of those. But remember, you can also follow him and his research on his Facebook page. So, again, FibromyalgiaPodcast.com/21 to get all of those links, both to the research and to be able to follow him on Facebook.
[01:30:31] I also wanted to mention a couple of episodes that are coming up.
Next episode will be your holiday survival guide. I know for some of you listening, your holidays may have already started, if you are outside the U.S. or depending on your family traditions and religious followings. Some of those have already started, but we are going to be talking about ways that you can get through these next couple of hectic months with Thanksgiving and Christmas and New Year’s and all the things. We’ll be talking about that next episode. I want to give you some tips and some tricks and some ways that you can plan out your holiday season in a way that both serves your heart and your body. Things that are both kind to you and manage your fibromyalgia and also provide what you need emotionally, physically, with your family. So, we will have that next episode. Episode 22 will be your Holiday Survival Guide.
[01:31:41] Episode 23, if all goes as planned, I have several of my coaches coming out for our annual alumni retreat that is happening in just a couple of weeks. While they are here, I plan on doing some interviews so you can meet a few of the coaches that I’ve trained here, about the work that they’re doing, the work that they do with their clients, and the kinds of things that they’ve been able to accomplish with their clients in helping them feel better. I’ve got some really great gals coming out who have very different kinds of things that they do with our clients. I’m looking forward to having you guys meet them virtually by way of interview here on the podcast in the next couple of months.
[01:32:33] Of course, we’ve got New Year’s, which will be a great time to talk about things like setting goals and exercising with fibromyalgia. It seems like in January everybody gets the urge to head back to the gym. I just wanted to let you guys know that there are very specific ways that you should and shouldn’t exercise when it comes to fibromyalgia. We will definitely be discussing that in a future episode, probably around the new year, and we’ll be talking with a professional athlete who has fibromyalgia about her journey and the work that she does, helping fibromyalgia patients get stronger again and exercise properly. Your doctor is right: exercise does help fibromyalgia. However, your doctor has probably not told you how to do that properly, and there really is a good and a bad way to exercise with fibromyalgia. So, we’ll be discussing that and giving you some tips on how to do that in a way that helps you and not hurt you.
[01:33:47] All right, thanks so much for tuning in this week and we’ll see you again next time. Bye.
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