How Computational Biology Is Changing Disease Research
In this episode, Haylie Pomroy is joined by Dr. Travis Craddock, PhD, Associate Professor at Nova Southeastern University, to explore how computational biology and computer modeling of the brain are changing the way researchers understand and treat neuroinflammatory disease.
Dr. Craddock explains how his lab builds virtual models of the brain's immune system, simulates disease states before ever treating a real patient, and applies this theory-driven approach to conditions like myalgic encephalomyelitis, chronic fatigue syndrome, Gulf War illness, and Parkinson's disease.
Together, they discuss the ongoing investigation into Epstein-Barr virus reactivation in chronic fatigue syndrome, why the body cannot be understood as a simple cause-and-effect system, and practical findings on sleep timing, gut health, and mineral balance that support brain health.
Discover how theory-driven modeling is shortening the distance between research and real-world treatment, and why understanding the brain as part of one interconnected system may be key to reversing chronic illness, here on Fast Metabolism Matters.
If your body feels like it's running on empty, overburdened, or just not responding the way it used to, Haylie's latest book, Toxic Overload, tells you exactly what to do. Download your free digital copy today and start understanding what your body is trying to tell you.
Free Download: Get Your Copy of Toxic Overload 👉 https://hayliepomroy.com/pages/toxic-overload?utm_source=podcast&utm_medium=podcast&utm_campaign=travis_craddock
You don't have to figure this out alone. Inside Haylie's private membership community, you get personalized guidance and support, member discounts on supplements and shakes, and the ability to ask questions directly to podcast guests like Dr. Systrom. Join free for 30 days and take the next step on your health journey.
Join the Fast Metabolism Membership — First 30 Days Free 👉 https://hayliepomroy.com/pages/fast-metabolism-membership?utm_source=podcast&utm_medium=podcast&utm_campaign=travis_craddock
Dr. Travis Craddock is an Associate Professor in the Departments of Psychology & Neuroscience, Computer Science, and Clinical Immunology at Nova Southeastern University. His lab builds computational models of the brain's immune system to study neuroinflammatory conditions, including myalgic encephalomyelitis/chronic fatigue syndrome, Gulf War illness, and Parkinson's disease. By simulating disease states in a virtual brain before testing any intervention on a real patient, his theory-driven approach helps identify viable treatment paths more rapidly, bridging basic science, clinical research, and patient care at the Institute for Neuro-immune Medicine.
LinkedIn: https://ca.linkedin.com/in/travis-craddock-30918978
Haylie Pomroy, Founder and CEO of The Haylie Pomroy Group, is a leading health strategist specializing in metabolism, weight loss, and integrative wellness. With over 25 years of experience, she has worked with top medical institutions and high-profile clients, developing targeted programs and supplements rooted in the "Food is Medicine" philosophy. Inspired by her own autoimmune journey, she combines expertise in nutrition, biochemistry, and patient advocacy to help others reclaim their health. She is a New York Times bestselling author of The Fast Metabolism Diet.
Learn more about Haylie Pomroy's approach to wellness through her website: https://hayliepomroy.com
Instagram: https://www.instagram.com/hayliepomroy
Facebook: https://www.facebook.com/hayliepomroy
YouTube: https://www.youtube.com/@hayliepomroy/videos
LinkedIn: https://www.linkedin.com/in/hayliepomroy/
Edited Transcript:
Dr. Travis Craddock: If we want to transition someone from a state of illness to a state of health, we can run millions, hundreds of millions of simulations to try and predict what is the best way to do that. We've looked at FDA-approved drugs, we've run those; we've run nutraceuticals; we've done multi-drug interventions, different changes in order, dosage, and timing. We've looked at things even beyond that, such as how would a magnetic field or an electric field affect this region of the brain, depending on what system we're looking at.
Haylie Pomroy: Hi, I'm Haylie Pomroy. I'm the Assistant Director of the Integrative Medicine Program at the Institute for Neuro-Immune Medicine. And I'd like to welcome you to our podcast, Hope and Help for Fatigue and Chronic Illness. Today, I have an incredible guest, Dr. Travis Craddock. He is a physicist, get this, who builds computer models of the brain to find new treatments for neuroinflammatory illness. Dr. Craddock, thank you so much for being here today. I really appreciate it.
Dr. Travis Craddock: Thank you for having me, Haylie.
Haylie Pomroy: Absolutely. I'm going to start with, what does that mean? Help me understand what you mean when you say builds computer models of the brain.
Dr. Travis Craddock: Okay, so there's a lot of work in understanding how the brain functions, various things about how the immune system in the brain works. And there are a lot of theories out there. And so in order to understand how these things work, we have to put it into a computer and use equations of math and computer algorithms to describe how the brain functions and to simulate actually what it does.
Haylie Pomroy: You've been with us for 10 years.
Dr. Travis Craddock: 10 years, yeah.
Haylie Pomroy: Congratulations. Happy anniversary. A term that floats around that I learned actually coming here from you, which is computational biology. Is that the essence of what we just talked about?
Dr. Travis Craddock: It is. Computational biology is a very, very large term. Using computers to study biology in any way, whether that's analyzing large sets of data, such as in genomics, like with Dr. Nathanson, or building models of how a biological system works, from ant colonies and viruses to brains and humans and so forth.
Haylie Pomroy: But that's what we use, right?
Dr. Travis Craddock: Yes, correct. 100%.
Haylie Pomroy: How is your computational biology lab very specific? I'm going to take that big, long sentence that I just gave. How does it work to study neuroinflammatory disease, neuroinflammation?
Dr. Travis Craddock: Like I said, we focus specifically on the brain and how the immune system works in the brain. We look at how individual cells talk to one another and how they initiate inflammatory processes. And then when we build a model, it follows some sort of algorithms and rules. And when we put those into the system, into the computer model, it follows those rules, and we compare that against various experimental data to make sure that we're recapitulating or reproducing what we see in experiment. And then we know we have a viable model, a model that actually can do what we see in actual experiments. Once we have that, we can then play around with it, and we can do things that you wouldn't normally be able to do to somebody.
Haylie Pomroy: So like? Give me an example.
Dr. Travis Craddock: Like, so if we have a model of the brain or the neuroinflammatory process and we can tweak it to either look like a healthy person or an ill person, if we make it look like an ill person, we can start basically simulating ways to treat them. We can throw a host of different drugs at them in different combinations.
Haylie Pomroy: But when you say them, you're talking about a pseudo-human being.
Dr. Travis Craddock: I'm talking about a virtual.
Haylie Pomroy: This is like AI in medicine.
Dr. Travis Craddock: Kind of, yeah. Larger scale.
Haylie Pomroy: Yes.
Dr. Travis Craddock: But when I say the simulation, I'm not saying it's a person. It's just this brain compartment that we're looking at.
Haylie Pomroy: Got it.
Dr. Travis Craddock: As we build up, we add different things. And hopefully one day in the far future, people will be able to simulate the whole human body.Right now, small bits.
Haylie Pomroy: Okay. I have like 80 questions flooding my brain right now, but I'm going to try and land the plane here for a second. What types of diseases fall under that category? When we talk about neuroinflammation, we talk about setting inflammation in the brain. What do we see it manifest in the patient?
Dr. Travis Craddock: Any disease of the brain has neuroinflammation. Depending on what aspects we add into the model determines what kind of disease that we're looking at. For example, I primarily do research in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), Gulf War illness, Parkinson's disease. And each of those has, they all are based on the same brain, obviously, and the same inflammatory system. But there are key aspects that you'd want to focus on. For instance, in Gulf War illness, we believe it's associated with something that's gone wrong in the cholinergic system, the acetylcholine system.
Haylie Pomroy: Okay, say that again. With Gulf War illness, we believe that something's gone wrong, and I'm just going to—because it's probably going to be 15 different podcasts, which I love, but I want to make sure that we walk away with that. Is that a part of the brain?
Dr. Travis Craddock: Gulf War illness, 1990-1991, Gulf War, troops came back, about a third of them had this unexplained illness. And one of the leading theories is that it was due to overexposure to these chemicals that altered the cholinergic system, which is to deal with acetylcholine. That's a brain signaling molecule. It's in certain parts of the brain. Overexposure to these organophosphates or—
Haylie Pomroy: Like pesticides.
Dr. Travis Craddock: Pesticides and nerve agents.
Haylie Pomroy: Metals and chemicals
Dr. Travis Craddock: Yeah, I think it messed up that cholinergic system. We believe that it sets up these problems in the brain. That, when we're doing a Gulf War project, is something we want to make sure that we have in the system. We want to make sure that we're dealing with acetylcholine and how that signals in the brain. Whereas for something like Parkinson's disease, Parkinson's has been tied to molecules like alpha-synuclein, which is a misfolded protein in the brain.
we want to make sure that we include that within our models. And so that way we take that general neuroinflammatory system and then tie it into specific things that are disease-specific.
Haylie Pomroy: People don't just land in this field for no reason. Overarching theme in the Institute is we believe you. We're in your corner. We have empathy for what you're going through. But what I'd like to know is: what drives you? What's your passion? How did you get into this? Because you work tirelessly, all of us watch. And with such a drive, where is this coming from?
Dr. Travis Craddock: Originally, I started out in a field completely different than this. My first master's, which I didn't complete because I thought I didn't want to go down that road, was in subatomic physics. I was looking at radioactive beta decay and how electrons are shot at a nuclei or whatever. I was like, that's not for me.
I started getting interested in the brain and how the brain works. And in specific, how does the brain, from a physics standpoint, produce something like subjective experience and consciousness? And so I started looking into modeling things like proteins in the brain and how it contributes to overall brain function in order to try and understand this very, very large concept. Consciousness, okay.
In that process, once I got into the area of trying to find funding. A lot of people don't want to fund basic consciousness research. Research into illnesses is where a lot of the funding goes. I moved from consciousness to memory and started looking into things like Alzheimer's disease. That kind of went from Alzheimer's disease to neurodegenerative diseases in general, Alzheimer's and Parkinson's. And then because of the tie-in with neuroinflammation, that's how I got into neuroinflammation. And then eventually I came down here.
Haylie Pomroy: Do you feel like it's a little bit full circle because consciousness is such a significant part in getting well in chronic disease?
Dr. Travis Craddock: Of course. Yeah. And I mean, there's a very subjective component to your symptoms. And that's one thing that I found very interesting is that you're trying to relate your symptoms to someone else. And we can measure all these molecules and things in the body, but how does that translate to this very subjective experience of your pain or your fatigue or, yeah, your experience of the illness?
Haylie Pomroy: And one of the things that we've been talking about a lot with some of our other team members is how to express yourself in a way that can help you get care. And I think one thing that, when we look at the research piece of it, is it helps validate—for a long time, a lot of the neuroinflammatory disorders were thought to be all in your head. And I know you study the brain, which dwells in the head, but literally some sort of psychosomatic type of expression. And now, with science and research, thank goodness, although we have people in the community that still, as Dr. Harris was talking about, it takes the average person 10 physicians in 10 years to get an adequate diagnosis. One thing that is fascinating, I'm kind of looking at it from the patient perspective, that I always think is interesting about the work that you do is that you're able to model what potentially could help or hurt a patient before it's administered to the patient. It's almost like, and it is, outside of the body, an expression of treatment. Am I seeing that correctly?
Dr. Travis Craddock: Yeah, I mean, we're dealing in a realm of theory and possibilities. It's applying these theories of this is how we believe that the brain works. And if this is the way that it works, then this should happen if you do X, Y, and Z. And then we try and test that over and over again to say, OK, this is the best way to do X, Y, and Z. And so if we want to transition someone from a state of illness to a state of health, we can run millions, hundreds of millions of simulations to try and predict what is the best way to do that.
Haylie Pomroy: Do the simulations include like a drug intervention, a supplement intervention?
Dr. Travis Craddock: Any sort of intervention.
Haylie Pomroy: Give me some examples.
Dr. Travis Craddock: We've looked at drugs. FDA-approved drugs. We've run those. We've run nutraceuticals. Those are molecular interventions. When you get into herbs and stuff like that, it's a little bit different because you have a cocktail. But we've done multi-drug interventions, different changes in order and dosage and timing. We've looked at things even beyond that, such like how would a magnetic field or an electric field affect this region of the brain, depending on what system we're looking at.
Haylie Pomroy: At the Institute, we have, and I hate to kind of silo this, but we have research, we have lab, right, which is both in a research setting, but also in clinical setting. We have clinic, and then we have education. Do you think that with your work, your body of work, that the clinician experience with the patient is driving some of the what-ifs in modeling, or is some of the what-ifs in modeling, driving, the treatment protocol for patients?
Hi, it's Haylie Pomroy, your host. I've written six New York Times bestselling books on metabolic pathways. And my latest book, Toxic Overload, tells you exactly what to do when your body's overburdened. If you go to hayliepomroy.com/book, for a limited time, you can download a digital copy of this book completely free. That's hayliepomroy.com/book. Grab your free copy while supplies last. Now back to our show.
Dr. Travis Craddock: I think it's both. For example, we're dealing with something right now in conversations with Dr. Nancy Klimas. There's this literature in chronic fatigue syndrome involving Epstein-Barr virus.
Haylie Pomroy: Yes, yes.
Dr. Travis Craddock: And so we're looking at potential ways of how EBV viral reactivation might work in models in the brain.
Haylie Pomroy: I'm going to stop you just for one second. Just so everybody's clear. And I think some of this also came up with, I think, a little bit more urgency or maybe more resources because of COVID and long-haulers and potentially the correlation. But what you were talking about specifically is with individuals with ME/CFS, potentially having a viral reactivation specifically of which virus?
Dr. Travis Craddock: Epstein-Barr virus. Or the human herpes viruses. Epstein-Barr virus. And we're also looking at HHV-6, which is another human virus, herpes virus.
Haylie Pomroy: I want to make sure that you promise me that you'll come back, and I want to do an entire pod. Thank you. Let's see how this all ends up. Let's see how this works out. Specifically on EBV. Because so many people are talking about it right now, which is amazing and great. And I just listened to a lecture that you did in our faculty meeting the other day. And you were talking about lytic and latent when it's reactivated. I want to do a whole podcast on that because I think people will be fascinated with the body of research that you've done around that and also some of the cutting edge and the hope that we have with that going forward. I interrupted you, though. You were talking about with this particular chronic fatigue and EBV.
Dr. Travis Craddock: It was kind of I'd heard about it. I hadn't really looked into it. And then we had some interesting results with Dr. Lubov Nathanson with our 23andMe project, where we looked at the genotype of ME-CFS individuals. And we found a potential where there's these mucus proteins that are dysfunctional. And then, again, within conversation, again, getting from Nancy from the clinic, is that individuals with ME-CFS have, a lot of them have this thing called the crimson crescent, which is like this red throat.
Haylie Pomroy: Crimson crescent. I have not, yeah, I love it. Okay.
Dr. Travis Craddock: You get these ideas, and then you toy around with them. Like, are these things related? And I started talking with Jim Baraniuk, and he does stuff with chronic rhinitis and dry eye. And that's in your nose, where these mucus layers take place. And of course, obviously, when you're getting infected with something like EBV, that's in the nose and throat. And if you're having a mucus protective barrier problem, being exposed to a virus, it may be giving rise to these increased ability of the virus to get into the system, to initially infect or to—
Haylie Pomroy: It's kind of like your barrier to entry. And that's impacted.
Dr. Travis Craddock: Exactly. Okay. We take these ideas, and we bat them around. We're like, how could this all work? We throw it together. We come up with some crazy hairball idea. And then we put it into a model which follows rules. And we say, is this feasible? Would that work? It's like, oh, it does. And then you can recapitulate some signatures of ME/CFS that you would see. It's like, oh, okay. It works in theory. That's great. Then we use that. We use it to predict a potential treatment course, which we're still in the midst of. But then once you have that, you can make predictions, and then you go to the lab and say, okay, based on this model and this idea, we predict that this would occur or that you'd be able to measure this. Then people in the lab can start to measure. And if they find congruence with the model.
Haylie Pomroy: And they're measuring like B-cells and T-cells.
Dr. Travis Craddock: B-cells and T-cells and cytokines and hormones.
Haylie Pomroy: Very cool.
Dr. Travis Craddock: Yeah, molecular signatures across the board. And if they all line up, you keep going down the road. Okay, well, if that's the case, then this treatment should work. You start trying it out in cells and so forth. And eventually you may get down the road to Dr. Klimas is like, oh, that's reasonable. Let's try that treatment course out. Or it's like, that won't fly whatsoever. That's not what we're finding. And in that case, the findings from the lab come back to the theory group. And we're like, well, why, why not? The theory says that this should be the way it is. You have to try and either alternate, figure out what the theory is, what's wrong with the theory, what's wrong with the interpretation. And so that informs theory, which goes to the lab. And eventually gets down to the patient. It's always moving around.
Haylie Pomroy: You're touching base on what's actually my next question, which is what kind of sets us apart? And I will tell you, coming in from other universities or institutes or research facilities, the thing that was really kind of mind-blowing, and I know you guys are all in the thick of it, but for me was how short the gap is between, maybe, research, translational research, and patient application, but also how holistic it is. I mean, we have our Friday clinicals, which is mind-blowing every Friday. We have our faculty, where everybody like I said, where you presented last time. But everybody, to your point, is sitting there and talking and pondering on behalf of these really complex illnesses that, outside of our institute, and with the layperson going out and trying to seek care, all of that data is not housed in many places. It's really remarkable. I have two questions, two-part questions. I'm going to let you, I just told you what I thought was spectacular. But what do you think it sets us apart?
Dr. Travis Craddock: I think it sets us apart. I mean, yes, the closeness of the group and a lot of the interplay. What I would say sets us apart is kind of the theory modeling aspect. Yes, there's a lot of bench-to-bedside groups, a lot of translational groups. And primarily when, if you talk to someone who's in the field of computational biology, they're doing what I call the data side of it. They're getting data from the labs, and they're analyzing data to find patterns within the data to identify a point that you want to hit or a point that it can be used as some sort of diagnostic to identify the disease. And it's very data-driven. And where I think we differ is we have this very, we have that, we still have that. I'm not saying we don't have that. But we also have this strong theory-driven side where it's, in theory, this is what, just very basic, this is how the inflammation system is supposed to work. It's not specific to any illness. It's not specific to anything. This is just how it's supposed to work. And if that's the case, then this is how it would work in this illness when you account for X, Y, and Z that we know about the illness. And so from that point, we're driving it by a lot of the theoretical knowledge is out there in the very basic science. And there are very, very few groups that do that.
Haylie Pomroy: And it's crazy because there's like this strong drive to get the patient better. There's this strong desire for knowledge to understand the disease. But there's this huge appreciation for the body as a whole. And everybody that we've been talking to in this podcast really talks about the complexity of the body and embracing that and understanding that.
Dr. Travis Craddock: I think one of the things that makes us so rapid as well is, I mean, we're focusing on approved drugs, nutraceuticals, things that don't require, hey, here's a new molecule and we got to see if it works in cells and if it works in animals. There's a very long drug discovery process. We can move fairly rapidly once we discover something, as long as it's safe, and that's determined by the clinical team; we can move rapidly right into phase one clinical trials and try these things out. The other thing is, is that we take these things, and we're not just, with the complexity you were mentioning. When we build these models, they're not a straight line. They're not linear. It's not that these things happen in an order. And if you just fix the thing right in the middle.
Haylie Pomroy: If they got eight hours of sleep, you'd be fine. If you drink a little more water, you'd be fine. If you took this medication.
Dr. Travis Craddock: Everything's tied together.
Haylie Pomroy: You just said everything's—say that again.
Dr. Travis Craddock: Interconnected.
Haylie Pomroy: Everything's interconnected. Yeah. I think that people need to hear that. And I think that people need to be empowered to talk to their practitioners, to their family, to get the appropriate support for them to be on their health and wellness journey is to understand that everything's interconnected. Everything means something. Every symptom means something. Every feeling means something. Every verbiage that you say or tell yourself every day means something. And it has an impact. To have individuals like you guys that are on our team that have this incredible wealth of knowledge and experience, validate that for someone that's going through chronic illness is really huge.
It's going to be really big for our community to understand that they have all these people that are thought leaders and research leaders, not in just this space, but in a broader space in the immune system. And that's why I say we believe you. We know this is going on. We see it every day. We see it all day. And we're working tirelessly to make an impact in it from a positive perspective. That's going to be huge for people that are hearing this, because a lot of people are out there struggling with chronic disease, especially neuroinflammatory disorders, because of the very part of the body that it affects, that feel hopeless. And I think that this is an important conversation to have because we want to instill that there's hope and that we're working really hard to get them help. We're working very hard.
To that point, this is my next question. If there were no bottlenecks, barrier to entry, money, dollars, time, 10 years from now, where do you see the field of neuroimmunology, of medicine? I mean, we got a huge—what would we call it, everything was sped up because of the pandemic. I mean, from a research perspective, from trying to figure this out perspective, from the inflammatory response that's going on with this perspective, I do think that was a ginormous catalyst. Let's take that. Let's harness it 10 years from now. Money's not an issue. Where do you see this field of medicine?
Hi, it's Haylie Pomroy, your host. When I was going through my health crisis, the worst part of it was feeling lost and alone, and I decided that I didn't want anybody else to feel as desperate as I did. That's why we set up a private membership group where you can come in, ask questions, get support, be connected with people that can actually help you on your health journey. If you go to hayliepomroy.com/member, you can join me for 30 days for free. I'll see you there. We can jump in and we can start to organize the path for your wellness. That's hayliepomroy.com/member. I will see you there. Now, back to our show.
Dr. Travis Craddock: Okay. Again, I'm going to be a little biased here because.
Haylie Pomroy: Please do.
Dr. Travis Craddock: The way I view it, this is the pipeline that we've tried to build where we are.
Haylie Pomroy: And you mean here at the Institute?
Dr. Travis Craddock: Here at the Institute, yeah. We have data comes in. There's so much data now. It's really a matter of trying to organize it and understand what's different between an illness group or a control group in these large reams of data. The process starts off with omics-level data. Measuring the whole expression of genomics, proteomics, lipidomics, metabolomics. There are all these different layers of measures.
Haylie Pomroy: Basically, how the body processes everything. How genes are expressed, how lipids are metabolized. Even complex carbohydrates. I mean, even for the macrogen strands.
Dr. Travis Craddock: What they do now is when you take a blood sample or saliva sample, whatever sample it is, when they analyze it, they're measuring everything that's in there. And so the idea then is you take that level of data, it comes in, and you would have some sort of AI process which would go through and either comb through the data, try and cluster it to pick out this is what's different in the illness group versus what's different in the control group using whatever algorithms are available. Once you identify that, the bottleneck that we have right now is transforming that, this is what we see is different, into an actual model. How does a B cell talk to a T cell with a given inflammatory mediator, a given cytokine signal, and so forth? What happens when a given cytokine like TNF-α interacts with a T cell, and what does the T cell do? And there are reams and reams of literature that's out there. What we want to do is take that data that what we found that's different in the illness group, from the control group, from the omics, feed that into another system that can comb literature, and naturally look for, in the language, look for connections and draw us out a map that says, here's the directionality of how it all works. And then we would apply a framework over top of that, either some sort of modeling equations that can then simulate the system. And so it would rapidly move from blood draws and everything through the AI system to build a model, then simulate it to produce both the illness and the healthy signature, and then optimize a treatment course to move illness back to health. And then we give back to Dr. Klimas: this is what we think you should do.
Haylie Pomroy: That's amazing.
Dr. Travis Craddock: That's the idea is that give us your omics, and we'll give you a treatment course.
Haylie Pomroy: That's very cool. I think that what's amazing is there was no patient testing.
Dr. Travis Craddock: Well, there was at the beginning to get that.
Haylie Pomroy: Absolutely. But then you can take that data, and you can run with it and not shorten, like maybe you would need something to be administered to a patient for 90 days before you could get data. You're getting data, masses, amounts of data processed very quickly. And also, like we talk about how important it is that we all come together and collaborate. That concept now takes the world of knowledge, right, of all scientists and resources, and collaborates that data and funnels that into findings. That's kind of mind-blowing and very, very exciting. On the research side of things, you're seeing kind of a mass amount of population, more than a practitioner can see one-on-one or a clinician can see one-on-one.
Dr. Travis Craddock: Sorry, what do you mean by that?
Haylie Pomroy: Like, if an individual comes into the clinic, they get data on one person, and in our clinic, every one to three hours, right, because we have extended visits with our patients. In computational biology and in your research lab, you get the data of many; you can process the data of many individuals.
Dr. Travis Craddock: Yeah, that's it.
Haylie Pomroy: It's not one patient per hour, one patient every three hours. But if you were to say, for those of us that are out here that are working towards wellness, we want to be on our own personal journey to health, maybe even our own personal quest to reverse disease. What are things that you could say as a whole impress upon you that make a positive impact in individual's health? And then even specifically an individual's health with neuroinflammatory disorders?
Dr. Travis Craddock: I think I'm lost.
Haylie Pomroy: I love that. That's perfect. Good. I finally did it today. No, so basically what I'm saying is like, so we see, and I've been in clinical setting, it'll be 30 years, May. And there are things that I see where I say, okay, people definitely need sleep. And I know that we conceptually can all say, but you're studying the brain, and you're studying what happens in the brain. And it's so hard sometimes; medically, we can use drugs or even nutraceuticals to hit the body, but we can't make an impact in the brain. And so I guess what I'm thinking or what I'm wondering, is what kinds of things can we do that can make a positive impact in the brain? What have you seen that seem to make a positive impact on the health of the brain?
Dr. Travis Craddock: Well, I mean, you brought up sleep. I've done some work with Dr. Jamie Tartar here at NSU on sleep. And one thing that we found was that throwing off your sleep cycles definitely affects your immunity. It definitely affects your hormone system, at least the stress steroid system. Yes, sleep, not just—
Haylie Pomroy: Do you have an eight-hour rule?
Dr. Travis Craddock: Yeah, so this is a complete tangent here, but...
Haylie Pomroy: I love the number eight, so I'll go with it. I'd like some science behind it.
Dr. Travis Craddock: This was in college age kid population, but we looked at a cohort of individuals and we found that those individuals that slept at least eight hours a night, or sorry, at least seven hours, I think seven was the cutoff, and went to bed before midnight had lower levels of inflammatory markers and stress markers compared to those who were getting eight hours of sleep a night, but going to bed after midnight.
Haylie Pomroy: Oh, wow.
Dr. Travis Craddock: And then an additional group was those that were going to bed after midnight and not getting eight hours, or sorry, seven, not eight, seven, but getting less than seven, going to bed after midnight versus going to bed after midnight, getting less than seven and seven hours. It's not just how much sleep you're getting, but when you're going to sleep. Trying to stay in line, that has to do with your circadian rhythm and so forth, your natural rhythms of the body. Trying to get that adequate amount of rest at a reasonable time. Some of the other things that we've dealt with is gastric health; we're looking right now a lot at how gut-brain axis is your stomach is talking to your brain, your brain is talking to your stomach. The stomach has a lot of neurotransmitter receptors in it; I think more neurotransmitters than the actual brain itself. So, making sure you take care of your gut health, that's something that we, that we see a lot. I'll turn it around though. One of the things that, that helps us is if we hear from someone something that works. Even for one individual, they're like, oh, I did this, and it worked. Then that's something that can spur these theories and ideas of, oh, let's see if there's anything behind that. A lot of people have said, getting sleep, watching what I eat, those types of things have helped manage a lot of their symptoms. Being away from certain environmental triggers, molds, chemicals and things like that, that helps. Why? We may not know yet, but that's something we can look at. So, things like molds and toxins, that's something that we're currently looking along with this this viral, viral theory. Metals, that's another area that's something else that we're looking at is ions. Metals are ions or metals in the brain, and how, if you throw off the balance of those, especially things like iron, zinc, and copper. These are the ones; if you see these go off, you'll find a lot of these neuroinflammatory illnesses and neurodegenerative diseases is that there's an imbalance of those. Why? Not 100% known, but it's something to consider.
Haylie Pomroy: It's interesting and fascinating. Do you see the possibility of the future in medicine for us being where you could have a sample from one person, from an individual, and do modeling and propose a customized care program for that individual?
Dr. Travis Craddock: At some point. I mean, that's way down the road.
Haylie Pomroy: Like the next couple months or?
Dr. Travis Craddock: Next week.
Haylie Pomroy: I remember I said finances, there's no problem. We have all the funding we need.
Dr. Travis Craddock: So like I said, with the models that we have with the brain right now is that it's just the base theory of how it works, and then we'll tune it to the illness. Whether it's Parkinson's or ME/CFS or so forth. The next step down the road is we tune it to your Parkinson's or your ME/CFS.
Haylie Pomroy: That's exactly where we're going.
Dr. Travis Craddock: And the next step may not be personal individually, but clustering people.
Haylie Pomroy: Male, maybe.
Dr. Travis Craddock: By gender is like the very first one. That's one we already do. If you look at someone with ME/CFS, there's distinct clusters. Someone who has more brain fog and musculoskeletal pain versus.
Haylie Pomroy: It's kind of manifesting in a certain.
Dr. Travis Craddock: In a certain way. And that's something we're trying to do more as well when we're analyzing individuals is we're not, we don't want to take everybody and lump them all together because not everybody's the same. We try, and instead of having this very heterogeneous population, we try and make it a little bit more homogeneous. Everyone in group A has similar symptoms and similar onsets and similar triggers. Whereas group B looks a little bit different. And so we analyze those, and that's something we just did with Gulf War Illness and looking at one segregating by gender. And the other was those that have meet the diagnosis for PTSD or have a high degree of PTSD symptoms versus not. And so one, we found that there was a very distinct signature for those with Gulf War Illness that did not meet the criteria for PTSD, which we were not seeing in the other group. And that signature looked an awful lot like what you would see in ME/CFS.
Haylie Pomroy: Wow. That's fascinating. I'm very excited for the world at large, the community, to see the crazy things that we all sit around and ponder.
Dr. Travis Craddock: Crazy as they may be.
Haylie Pomroy: Yeah. It's crazy, but it's exciting, and it's inspiring. And I just want to thank you so much for being here.
Dr. Travis Craddock: Oh, thank you for having me.
Haylie Pomroy: Promise me you'll come back.
Dr. Travis Craddock: Yes.
Haylie Pomroy: Okay. I want to just talk about EBV. I want to talk about naltrexone. I want to talk about—there's so much. I have obviously a huge passion in the autoimmune space, but this is great. And I just want to share with our community that there's hope. We're holding that out for each and every one of you out here. And we're here to provide help with education and knowledge and just kind of, I would say, pulling the curtain back a little bit on the things that all of our scientists and clinicians and just the whole team think about on a daily basis. Thank you so much. I really appreciate it. And we will talk again soon.
Dr. Travis Craddock: Excellent. Okay. Thank you.
In this episode, Haylie Pomroy is joined by Dr. Travis Craddock, PhD, Associate Professor at Nova Southeastern University, to explore how computational biology and computer modeling of the brain are changing the way researchers understand and treat neuroinflammatory disease.
Dr. Craddock explains how his lab builds virtual models of the brain's immune system, simulates disease states before ever treating a real patient, and applies this theory-driven approach to conditions like myalgic encephalomyelitis, chronic fatigue syndrome, Gulf War illness, and Parkinson's disease.
Together, they discuss the ongoing investigation into Epstein-Barr virus reactivation in chronic fatigue syndrome, why the body cannot be understood as a simple cause-and-effect system, and practical findings on sleep timing, gut health, and mineral balance that support brain health.
Discover how theory-driven modeling is shortening the distance between research and real-world treatment, and why understanding the brain as part of one interconnected system may be key to reversing chronic illness, here on Fast Metabolism Matters.
If your body feels like it's running on empty, overburdened, or just not responding the way it used to, Haylie's latest book, Toxic Overload, tells you exactly what to do. Download your free digital copy today and start understanding what your body is trying to tell you.
Free Download: Get Your Copy of Toxic Overload 👉 https://hayliepomroy.com/pages/toxic-overload?utm_source=podcast&utm_medium=podcast&utm_campaign=travis_craddock
You don't have to figure this out alone. Inside Haylie's private membership community, you get personalized guidance and support, member discounts on supplements and shakes, and the ability to ask questions directly to podcast guests like Dr. Systrom. Join free for 30 days and take the next step on your health journey.
Join the Fast Metabolism Membership — First 30 Days Free 👉 https://hayliepomroy.com/pages/fast-metabolism-membership?utm_source=podcast&utm_medium=podcast&utm_campaign=travis_craddock
Dr. Travis Craddock is an Associate Professor in the Departments of Psychology & Neuroscience, Computer Science, and Clinical Immunology at Nova Southeastern University. His lab builds computational models of the brain's immune system to study neuroinflammatory conditions, including myalgic encephalomyelitis/chronic fatigue syndrome, Gulf War illness, and Parkinson's disease. By simulating disease states in a virtual brain before testing any intervention on a real patient, his theory-driven approach helps identify viable treatment paths more rapidly, bridging basic science, clinical research, and patient care at the Institute for Neuro-immune Medicine.
LinkedIn: https://ca.linkedin.com/in/travis-craddock-30918978
Haylie Pomroy, Founder and CEO of The Haylie Pomroy Group, is a leading health strategist specializing in metabolism, weight loss, and integrative wellness. With over 25 years of experience, she has worked with top medical institutions and high-profile clients, developing targeted programs and supplements rooted in the "Food is Medicine" philosophy. Inspired by her own autoimmune journey, she combines expertise in nutrition, biochemistry, and patient advocacy to help others reclaim their health. She is a New York Times bestselling author of The Fast Metabolism Diet.
Learn more about Haylie Pomroy's approach to wellness through her website: https://hayliepomroy.com
Instagram: https://www.instagram.com/hayliepomroy
Facebook: https://www.facebook.com/hayliepomroy
YouTube: https://www.youtube.com/@hayliepomroy/videos
LinkedIn: https://www.linkedin.com/in/hayliepomroy/
Edited Transcript:
Dr. Travis Craddock: If we want to transition someone from a state of illness to a state of health, we can run millions, hundreds of millions of simulations to try and predict what is the best way to do that. We've looked at FDA-approved drugs, we've run those; we've run nutraceuticals; we've done multi-drug interventions, different changes in order, dosage, and timing. We've looked at things even beyond that, such as how would a magnetic field or an electric field affect this region of the brain, depending on what system we're looking at.
Haylie Pomroy: Hi, I'm Haylie Pomroy. I'm the Assistant Director of the Integrative Medicine Program at the Institute for Neuro-Immune Medicine. And I'd like to welcome you to our podcast, Hope and Help for Fatigue and Chronic Illness. Today, I have an incredible guest, Dr. Travis Craddock. He is a physicist, get this, who builds computer models of the brain to find new treatments for neuroinflammatory illness. Dr. Craddock, thank you so much for being here today. I really appreciate it.
Dr. Travis Craddock: Thank you for having me, Haylie.
Haylie Pomroy: Absolutely. I'm going to start with, what does that mean? Help me understand what you mean when you say builds computer models of the brain.
Dr. Travis Craddock: Okay, so there's a lot of work in understanding how the brain functions, various things about how the immune system in the brain works. And there are a lot of theories out there. And so in order to understand how these things work, we have to put it into a computer and use equations of math and computer algorithms to describe how the brain functions and to simulate actually what it does.
Haylie Pomroy: You've been with us for 10 years.
Dr. Travis Craddock: 10 years, yeah.
Haylie Pomroy: Congratulations. Happy anniversary. A term that floats around that I learned actually coming here from you, which is computational biology. Is that the essence of what we just talked about?
Dr. Travis Craddock: It is. Computational biology is a very, very large term. Using computers to study biology in any way, whether that's analyzing large sets of data, such as in genomics, like with Dr. Nathanson, or building models of how a biological system works, from ant colonies and viruses to brains and humans and so forth.
Haylie Pomroy: But that's what we use, right?
Dr. Travis Craddock: Yes, correct. 100%.
Haylie Pomroy: How is your computational biology lab very specific? I'm going to take that big, long sentence that I just gave. How does it work to study neuroinflammatory disease, neuroinflammation?
Dr. Travis Craddock: Like I said, we focus specifically on the brain and how the immune system works in the brain. We look at how individual cells talk to one another and how they initiate inflammatory processes. And then when we build a model, it follows some sort of algorithms and rules. And when we put those into the system, into the computer model, it follows those rules, and we compare that against various experimental data to make sure that we're recapitulating or reproducing what we see in experiment. And then we know we have a viable model, a model that actually can do what we see in actual experiments. Once we have that, we can then play around with it, and we can do things that you wouldn't normally be able to do to somebody.
Haylie Pomroy: So like? Give me an example.
Dr. Travis Craddock: Like, so if we have a model of the brain or the neuroinflammatory process and we can tweak it to either look like a healthy person or an ill person, if we make it look like an ill person, we can start basically simulating ways to treat them. We can throw a host of different drugs at them in different combinations.
Haylie Pomroy: But when you say them, you're talking about a pseudo-human being.
Dr. Travis Craddock: I'm talking about a virtual.
Haylie Pomroy: This is like AI in medicine.
Dr. Travis Craddock: Kind of, yeah. Larger scale.
Haylie Pomroy: Yes.
Dr. Travis Craddock: But when I say the simulation, I'm not saying it's a person. It's just this brain compartment that we're looking at.
Haylie Pomroy: Got it.
Dr. Travis Craddock: As we build up, we add different things. And hopefully one day in the far future, people will be able to simulate the whole human body.Right now, small bits.
Haylie Pomroy: Okay. I have like 80 questions flooding my brain right now, but I'm going to try and land the plane here for a second. What types of diseases fall under that category? When we talk about neuroinflammation, we talk about setting inflammation in the brain. What do we see it manifest in the patient?
Dr. Travis Craddock: Any disease of the brain has neuroinflammation. Depending on what aspects we add into the model determines what kind of disease that we're looking at. For example, I primarily do research in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), Gulf War illness, Parkinson's disease. And each of those has, they all are based on the same brain, obviously, and the same inflammatory system. But there are key aspects that you'd want to focus on. For instance, in Gulf War illness, we believe it's associated with something that's gone wrong in the cholinergic system, the acetylcholine system.
Haylie Pomroy: Okay, say that again. With Gulf War illness, we believe that something's gone wrong, and I'm just going to—because it's probably going to be 15 different podcasts, which I love, but I want to make sure that we walk away with that. Is that a part of the brain?
Dr. Travis Craddock: Gulf War illness, 1990-1991, Gulf War, troops came back, about a third of them had this unexplained illness. And one of the leading theories is that it was due to overexposure to these chemicals that altered the cholinergic system, which is to deal with acetylcholine. That's a brain signaling molecule. It's in certain parts of the brain. Overexposure to these organophosphates or—
Haylie Pomroy: Like pesticides.
Dr. Travis Craddock: Pesticides and nerve agents.
Haylie Pomroy: Metals and chemicals
Dr. Travis Craddock: Yeah, I think it messed up that cholinergic system. We believe that it sets up these problems in the brain. That, when we're doing a Gulf War project, is something we want to make sure that we have in the system. We want to make sure that we're dealing with acetylcholine and how that signals in the brain. Whereas for something like Parkinson's disease, Parkinson's has been tied to molecules like alpha-synuclein, which is a misfolded protein in the brain.
we want to make sure that we include that within our models. And so that way we take that general neuroinflammatory system and then tie it into specific things that are disease-specific.
Haylie Pomroy: People don't just land in this field for no reason. Overarching theme in the Institute is we believe you. We're in your corner. We have empathy for what you're going through. But what I'd like to know is: what drives you? What's your passion? How did you get into this? Because you work tirelessly, all of us watch. And with such a drive, where is this coming from?
Dr. Travis Craddock: Originally, I started out in a field completely different than this. My first master's, which I didn't complete because I thought I didn't want to go down that road, was in subatomic physics. I was looking at radioactive beta decay and how electrons are shot at a nuclei or whatever. I was like, that's not for me.
I started getting interested in the brain and how the brain works. And in specific, how does the brain, from a physics standpoint, produce something like subjective experience and consciousness? And so I started looking into modeling things like proteins in the brain and how it contributes to overall brain function in order to try and understand this very, very large concept. Consciousness, okay.
In that process, once I got into the area of trying to find funding. A lot of people don't want to fund basic consciousness research. Research into illnesses is where a lot of the funding goes. I moved from consciousness to memory and started looking into things like Alzheimer's disease. That kind of went from Alzheimer's disease to neurodegenerative diseases in general, Alzheimer's and Parkinson's. And then because of the tie-in with neuroinflammation, that's how I got into neuroinflammation. And then eventually I came down here.
Haylie Pomroy: Do you feel like it's a little bit full circle because consciousness is such a significant part in getting well in chronic disease?
Dr. Travis Craddock: Of course. Yeah. And I mean, there's a very subjective component to your symptoms. And that's one thing that I found very interesting is that you're trying to relate your symptoms to someone else. And we can measure all these molecules and things in the body, but how does that translate to this very subjective experience of your pain or your fatigue or, yeah, your experience of the illness?
Haylie Pomroy: And one of the things that we've been talking about a lot with some of our other team members is how to express yourself in a way that can help you get care. And I think one thing that, when we look at the research piece of it, is it helps validate—for a long time, a lot of the neuroinflammatory disorders were thought to be all in your head. And I know you study the brain, which dwells in the head, but literally some sort of psychosomatic type of expression. And now, with science and research, thank goodness, although we have people in the community that still, as Dr. Harris was talking about, it takes the average person 10 physicians in 10 years to get an adequate diagnosis. One thing that is fascinating, I'm kind of looking at it from the patient perspective, that I always think is interesting about the work that you do is that you're able to model what potentially could help or hurt a patient before it's administered to the patient. It's almost like, and it is, outside of the body, an expression of treatment. Am I seeing that correctly?
Dr. Travis Craddock: Yeah, I mean, we're dealing in a realm of theory and possibilities. It's applying these theories of this is how we believe that the brain works. And if this is the way that it works, then this should happen if you do X, Y, and Z. And then we try and test that over and over again to say, OK, this is the best way to do X, Y, and Z. And so if we want to transition someone from a state of illness to a state of health, we can run millions, hundreds of millions of simulations to try and predict what is the best way to do that.
Haylie Pomroy: Do the simulations include like a drug intervention, a supplement intervention?
Dr. Travis Craddock: Any sort of intervention.
Haylie Pomroy: Give me some examples.
Dr. Travis Craddock: We've looked at drugs. FDA-approved drugs. We've run those. We've run nutraceuticals. Those are molecular interventions. When you get into herbs and stuff like that, it's a little bit different because you have a cocktail. But we've done multi-drug interventions, different changes in order and dosage and timing. We've looked at things even beyond that, such like how would a magnetic field or an electric field affect this region of the brain, depending on what system we're looking at.
Haylie Pomroy: At the Institute, we have, and I hate to kind of silo this, but we have research, we have lab, right, which is both in a research setting, but also in clinical setting. We have clinic, and then we have education. Do you think that with your work, your body of work, that the clinician experience with the patient is driving some of the what-ifs in modeling, or is some of the what-ifs in modeling, driving, the treatment protocol for patients?
Hi, it's Haylie Pomroy, your host. I've written six New York Times bestselling books on metabolic pathways. And my latest book, Toxic Overload, tells you exactly what to do when your body's overburdened. If you go to hayliepomroy.com/book, for a limited time, you can download a digital copy of this book completely free. That's hayliepomroy.com/book. Grab your free copy while supplies last. Now back to our show.
Dr. Travis Craddock: I think it's both. For example, we're dealing with something right now in conversations with Dr. Nancy Klimas. There's this literature in chronic fatigue syndrome involving Epstein-Barr virus.
Haylie Pomroy: Yes, yes.
Dr. Travis Craddock: And so we're looking at potential ways of how EBV viral reactivation might work in models in the brain.
Haylie Pomroy: I'm going to stop you just for one second. Just so everybody's clear. And I think some of this also came up with, I think, a little bit more urgency or maybe more resources because of COVID and long-haulers and potentially the correlation. But what you were talking about specifically is with individuals with ME/CFS, potentially having a viral reactivation specifically of which virus?
Dr. Travis Craddock: Epstein-Barr virus. Or the human herpes viruses. Epstein-Barr virus. And we're also looking at HHV-6, which is another human virus, herpes virus.
Haylie Pomroy: I want to make sure that you promise me that you'll come back, and I want to do an entire pod. Thank you. Let's see how this all ends up. Let's see how this works out. Specifically on EBV. Because so many people are talking about it right now, which is amazing and great. And I just listened to a lecture that you did in our faculty meeting the other day. And you were talking about lytic and latent when it's reactivated. I want to do a whole podcast on that because I think people will be fascinated with the body of research that you've done around that and also some of the cutting edge and the hope that we have with that going forward. I interrupted you, though. You were talking about with this particular chronic fatigue and EBV.
Dr. Travis Craddock: It was kind of I'd heard about it. I hadn't really looked into it. And then we had some interesting results with Dr. Lubov Nathanson with our 23andMe project, where we looked at the genotype of ME-CFS individuals. And we found a potential where there's these mucus proteins that are dysfunctional. And then, again, within conversation, again, getting from Nancy from the clinic, is that individuals with ME-CFS have, a lot of them have this thing called the crimson crescent, which is like this red throat.
Haylie Pomroy: Crimson crescent. I have not, yeah, I love it. Okay.
Dr. Travis Craddock: You get these ideas, and then you toy around with them. Like, are these things related? And I started talking with Jim Baraniuk, and he does stuff with chronic rhinitis and dry eye. And that's in your nose, where these mucus layers take place. And of course, obviously, when you're getting infected with something like EBV, that's in the nose and throat. And if you're having a mucus protective barrier problem, being exposed to a virus, it may be giving rise to these increased ability of the virus to get into the system, to initially infect or to—
Haylie Pomroy: It's kind of like your barrier to entry. And that's impacted.
Dr. Travis Craddock: Exactly. Okay. We take these ideas, and we bat them around. We're like, how could this all work? We throw it together. We come up with some crazy hairball idea. And then we put it into a model which follows rules. And we say, is this feasible? Would that work? It's like, oh, it does. And then you can recapitulate some signatures of ME/CFS that you would see. It's like, oh, okay. It works in theory. That's great. Then we use that. We use it to predict a potential treatment course, which we're still in the midst of. But then once you have that, you can make predictions, and then you go to the lab and say, okay, based on this model and this idea, we predict that this would occur or that you'd be able to measure this. Then people in the lab can start to measure. And if they find congruence with the model.
Haylie Pomroy: And they're measuring like B-cells and T-cells.
Dr. Travis Craddock: B-cells and T-cells and cytokines and hormones.
Haylie Pomroy: Very cool.
Dr. Travis Craddock: Yeah, molecular signatures across the board. And if they all line up, you keep going down the road. Okay, well, if that's the case, then this treatment should work. You start trying it out in cells and so forth. And eventually you may get down the road to Dr. Klimas is like, oh, that's reasonable. Let's try that treatment course out. Or it's like, that won't fly whatsoever. That's not what we're finding. And in that case, the findings from the lab come back to the theory group. And we're like, well, why, why not? The theory says that this should be the way it is. You have to try and either alternate, figure out what the theory is, what's wrong with the theory, what's wrong with the interpretation. And so that informs theory, which goes to the lab. And eventually gets down to the patient. It's always moving around.
Haylie Pomroy: You're touching base on what's actually my next question, which is what kind of sets us apart? And I will tell you, coming in from other universities or institutes or research facilities, the thing that was really kind of mind-blowing, and I know you guys are all in the thick of it, but for me was how short the gap is between, maybe, research, translational research, and patient application, but also how holistic it is. I mean, we have our Friday clinicals, which is mind-blowing every Friday. We have our faculty, where everybody like I said, where you presented last time. But everybody, to your point, is sitting there and talking and pondering on behalf of these really complex illnesses that, outside of our institute, and with the layperson going out and trying to seek care, all of that data is not housed in many places. It's really remarkable. I have two questions, two-part questions. I'm going to let you, I just told you what I thought was spectacular. But what do you think it sets us apart?
Dr. Travis Craddock: I think it sets us apart. I mean, yes, the closeness of the group and a lot of the interplay. What I would say sets us apart is kind of the theory modeling aspect. Yes, there's a lot of bench-to-bedside groups, a lot of translational groups. And primarily when, if you talk to someone who's in the field of computational biology, they're doing what I call the data side of it. They're getting data from the labs, and they're analyzing data to find patterns within the data to identify a point that you want to hit or a point that it can be used as some sort of diagnostic to identify the disease. And it's very data-driven. And where I think we differ is we have this very, we have that, we still have that. I'm not saying we don't have that. But we also have this strong theory-driven side where it's, in theory, this is what, just very basic, this is how the inflammation system is supposed to work. It's not specific to any illness. It's not specific to anything. This is just how it's supposed to work. And if that's the case, then this is how it would work in this illness when you account for X, Y, and Z that we know about the illness. And so from that point, we're driving it by a lot of the theoretical knowledge is out there in the very basic science. And there are very, very few groups that do that.
Haylie Pomroy: And it's crazy because there's like this strong drive to get the patient better. There's this strong desire for knowledge to understand the disease. But there's this huge appreciation for the body as a whole. And everybody that we've been talking to in this podcast really talks about the complexity of the body and embracing that and understanding that.
Dr. Travis Craddock: I think one of the things that makes us so rapid as well is, I mean, we're focusing on approved drugs, nutraceuticals, things that don't require, hey, here's a new molecule and we got to see if it works in cells and if it works in animals. There's a very long drug discovery process. We can move fairly rapidly once we discover something, as long as it's safe, and that's determined by the clinical team; we can move rapidly right into phase one clinical trials and try these things out. The other thing is, is that we take these things, and we're not just, with the complexity you were mentioning. When we build these models, they're not a straight line. They're not linear. It's not that these things happen in an order. And if you just fix the thing right in the middle.
Haylie Pomroy: If they got eight hours of sleep, you'd be fine. If you drink a little more water, you'd be fine. If you took this medication.
Dr. Travis Craddock: Everything's tied together.
Haylie Pomroy: You just said everything's—say that again.
Dr. Travis Craddock: Interconnected.
Haylie Pomroy: Everything's interconnected. Yeah. I think that people need to hear that. And I think that people need to be empowered to talk to their practitioners, to their family, to get the appropriate support for them to be on their health and wellness journey is to understand that everything's interconnected. Everything means something. Every symptom means something. Every feeling means something. Every verbiage that you say or tell yourself every day means something. And it has an impact. To have individuals like you guys that are on our team that have this incredible wealth of knowledge and experience, validate that for someone that's going through chronic illness is really huge.
It's going to be really big for our community to understand that they have all these people that are thought leaders and research leaders, not in just this space, but in a broader space in the immune system. And that's why I say we believe you. We know this is going on. We see it every day. We see it all day. And we're working tirelessly to make an impact in it from a positive perspective. That's going to be huge for people that are hearing this, because a lot of people are out there struggling with chronic disease, especially neuroinflammatory disorders, because of the very part of the body that it affects, that feel hopeless. And I think that this is an important conversation to have because we want to instill that there's hope and that we're working really hard to get them help. We're working very hard.
To that point, this is my next question. If there were no bottlenecks, barrier to entry, money, dollars, time, 10 years from now, where do you see the field of neuroimmunology, of medicine? I mean, we got a huge—what would we call it, everything was sped up because of the pandemic. I mean, from a research perspective, from trying to figure this out perspective, from the inflammatory response that's going on with this perspective, I do think that was a ginormous catalyst. Let's take that. Let's harness it 10 years from now. Money's not an issue. Where do you see this field of medicine?
Hi, it's Haylie Pomroy, your host. When I was going through my health crisis, the worst part of it was feeling lost and alone, and I decided that I didn't want anybody else to feel as desperate as I did. That's why we set up a private membership group where you can come in, ask questions, get support, be connected with people that can actually help you on your health journey. If you go to hayliepomroy.com/member, you can join me for 30 days for free. I'll see you there. We can jump in and we can start to organize the path for your wellness. That's hayliepomroy.com/member. I will see you there. Now, back to our show.
Dr. Travis Craddock: Okay. Again, I'm going to be a little biased here because.
Haylie Pomroy: Please do.
Dr. Travis Craddock: The way I view it, this is the pipeline that we've tried to build where we are.
Haylie Pomroy: And you mean here at the Institute?
Dr. Travis Craddock: Here at the Institute, yeah. We have data comes in. There's so much data now. It's really a matter of trying to organize it and understand what's different between an illness group or a control group in these large reams of data. The process starts off with omics-level data. Measuring the whole expression of genomics, proteomics, lipidomics, metabolomics. There are all these different layers of measures.
Haylie Pomroy: Basically, how the body processes everything. How genes are expressed, how lipids are metabolized. Even complex carbohydrates. I mean, even for the macrogen strands.
Dr. Travis Craddock: What they do now is when you take a blood sample or saliva sample, whatever sample it is, when they analyze it, they're measuring everything that's in there. And so the idea then is you take that level of data, it comes in, and you would have some sort of AI process which would go through and either comb through the data, try and cluster it to pick out this is what's different in the illness group versus what's different in the control group using whatever algorithms are available. Once you identify that, the bottleneck that we have right now is transforming that, this is what we see is different, into an actual model. How does a B cell talk to a T cell with a given inflammatory mediator, a given cytokine signal, and so forth? What happens when a given cytokine like TNF-α interacts with a T cell, and what does the T cell do? And there are reams and reams of literature that's out there. What we want to do is take that data that what we found that's different in the illness group, from the control group, from the omics, feed that into another system that can comb literature, and naturally look for, in the language, look for connections and draw us out a map that says, here's the directionality of how it all works. And then we would apply a framework over top of that, either some sort of modeling equations that can then simulate the system. And so it would rapidly move from blood draws and everything through the AI system to build a model, then simulate it to produce both the illness and the healthy signature, and then optimize a treatment course to move illness back to health. And then we give back to Dr. Klimas: this is what we think you should do.
Haylie Pomroy: That's amazing.
Dr. Travis Craddock: That's the idea is that give us your omics, and we'll give you a treatment course.
Haylie Pomroy: That's very cool. I think that what's amazing is there was no patient testing.
Dr. Travis Craddock: Well, there was at the beginning to get that.
Haylie Pomroy: Absolutely. But then you can take that data, and you can run with it and not shorten, like maybe you would need something to be administered to a patient for 90 days before you could get data. You're getting data, masses, amounts of data processed very quickly. And also, like we talk about how important it is that we all come together and collaborate. That concept now takes the world of knowledge, right, of all scientists and resources, and collaborates that data and funnels that into findings. That's kind of mind-blowing and very, very exciting. On the research side of things, you're seeing kind of a mass amount of population, more than a practitioner can see one-on-one or a clinician can see one-on-one.
Dr. Travis Craddock: Sorry, what do you mean by that?
Haylie Pomroy: Like, if an individual comes into the clinic, they get data on one person, and in our clinic, every one to three hours, right, because we have extended visits with our patients. In computational biology and in your research lab, you get the data of many; you can process the data of many individuals.
Dr. Travis Craddock: Yeah, that's it.
Haylie Pomroy: It's not one patient per hour, one patient every three hours. But if you were to say, for those of us that are out here that are working towards wellness, we want to be on our own personal journey to health, maybe even our own personal quest to reverse disease. What are things that you could say as a whole impress upon you that make a positive impact in individual's health? And then even specifically an individual's health with neuroinflammatory disorders?
Dr. Travis Craddock: I think I'm lost.
Haylie Pomroy: I love that. That's perfect. Good. I finally did it today. No, so basically what I'm saying is like, so we see, and I've been in clinical setting, it'll be 30 years, May. And there are things that I see where I say, okay, people definitely need sleep. And I know that we conceptually can all say, but you're studying the brain, and you're studying what happens in the brain. And it's so hard sometimes; medically, we can use drugs or even nutraceuticals to hit the body, but we can't make an impact in the brain. And so I guess what I'm thinking or what I'm wondering, is what kinds of things can we do that can make a positive impact in the brain? What have you seen that seem to make a positive impact on the health of the brain?
Dr. Travis Craddock: Well, I mean, you brought up sleep. I've done some work with Dr. Jamie Tartar here at NSU on sleep. And one thing that we found was that throwing off your sleep cycles definitely affects your immunity. It definitely affects your hormone system, at least the stress steroid system. Yes, sleep, not just—
Haylie Pomroy: Do you have an eight-hour rule?
Dr. Travis Craddock: Yeah, so this is a complete tangent here, but...
Haylie Pomroy: I love the number eight, so I'll go with it. I'd like some science behind it.
Dr. Travis Craddock: This was in college age kid population, but we looked at a cohort of individuals and we found that those individuals that slept at least eight hours a night, or sorry, at least seven hours, I think seven was the cutoff, and went to bed before midnight had lower levels of inflammatory markers and stress markers compared to those who were getting eight hours of sleep a night, but going to bed after midnight.
Haylie Pomroy: Oh, wow.
Dr. Travis Craddock: And then an additional group was those that were going to bed after midnight and not getting eight hours, or sorry, seven, not eight, seven, but getting less than seven, going to bed after midnight versus going to bed after midnight, getting less than seven and seven hours. It's not just how much sleep you're getting, but when you're going to sleep. Trying to stay in line, that has to do with your circadian rhythm and so forth, your natural rhythms of the body. Trying to get that adequate amount of rest at a reasonable time. Some of the other things that we've dealt with is gastric health; we're looking right now a lot at how gut-brain axis is your stomach is talking to your brain, your brain is talking to your stomach. The stomach has a lot of neurotransmitter receptors in it; I think more neurotransmitters than the actual brain itself. So, making sure you take care of your gut health, that's something that we, that we see a lot. I'll turn it around though. One of the things that, that helps us is if we hear from someone something that works. Even for one individual, they're like, oh, I did this, and it worked. Then that's something that can spur these theories and ideas of, oh, let's see if there's anything behind that. A lot of people have said, getting sleep, watching what I eat, those types of things have helped manage a lot of their symptoms. Being away from certain environmental triggers, molds, chemicals and things like that, that helps. Why? We may not know yet, but that's something we can look at. So, things like molds and toxins, that's something that we're currently looking along with this this viral, viral theory. Metals, that's another area that's something else that we're looking at is ions. Metals are ions or metals in the brain, and how, if you throw off the balance of those, especially things like iron, zinc, and copper. These are the ones; if you see these go off, you'll find a lot of these neuroinflammatory illnesses and neurodegenerative diseases is that there's an imbalance of those. Why? Not 100% known, but it's something to consider.
Haylie Pomroy: It's interesting and fascinating. Do you see the possibility of the future in medicine for us being where you could have a sample from one person, from an individual, and do modeling and propose a customized care program for that individual?
Dr. Travis Craddock: At some point. I mean, that's way down the road.
Haylie Pomroy: Like the next couple months or?
Dr. Travis Craddock: Next week.
Haylie Pomroy: I remember I said finances, there's no problem. We have all the funding we need.
Dr. Travis Craddock: So like I said, with the models that we have with the brain right now is that it's just the base theory of how it works, and then we'll tune it to the illness. Whether it's Parkinson's or ME/CFS or so forth. The next step down the road is we tune it to your Parkinson's or your ME/CFS.
Haylie Pomroy: That's exactly where we're going.
Dr. Travis Craddock: And the next step may not be personal individually, but clustering people.
Haylie Pomroy: Male, maybe.
Dr. Travis Craddock: By gender is like the very first one. That's one we already do. If you look at someone with ME/CFS, there's distinct clusters. Someone who has more brain fog and musculoskeletal pain versus.
Haylie Pomroy: It's kind of manifesting in a certain.
Dr. Travis Craddock: In a certain way. And that's something we're trying to do more as well when we're analyzing individuals is we're not, we don't want to take everybody and lump them all together because not everybody's the same. We try, and instead of having this very heterogeneous population, we try and make it a little bit more homogeneous. Everyone in group A has similar symptoms and similar onsets and similar triggers. Whereas group B looks a little bit different. And so we analyze those, and that's something we just did with Gulf War Illness and looking at one segregating by gender. And the other was those that have meet the diagnosis for PTSD or have a high degree of PTSD symptoms versus not. And so one, we found that there was a very distinct signature for those with Gulf War Illness that did not meet the criteria for PTSD, which we were not seeing in the other group. And that signature looked an awful lot like what you would see in ME/CFS.
Haylie Pomroy: Wow. That's fascinating. I'm very excited for the world at large, the community, to see the crazy things that we all sit around and ponder.
Dr. Travis Craddock: Crazy as they may be.
Haylie Pomroy: Yeah. It's crazy, but it's exciting, and it's inspiring. And I just want to thank you so much for being here.
Dr. Travis Craddock: Oh, thank you for having me.
Haylie Pomroy: Promise me you'll come back.
Dr. Travis Craddock: Yes.
Haylie Pomroy: Okay. I want to just talk about EBV. I want to talk about naltrexone. I want to talk about—there's so much. I have obviously a huge passion in the autoimmune space, but this is great. And I just want to share with our community that there's hope. We're holding that out for each and every one of you out here. And we're here to provide help with education and knowledge and just kind of, I would say, pulling the curtain back a little bit on the things that all of our scientists and clinicians and just the whole team think about on a daily basis. Thank you so much. I really appreciate it. And we will talk again soon.
Dr. Travis Craddock: Excellent. Okay. Thank you.
