EPISODE 235

[INTRODUCTION]

[0:00:01] ANNOUNCER: Welcome to the BetterHealthGuy podcast, where we take a deep dive into complex chronic conditions and explore ways to build resilience, improve vitality, and achieve better health. To stay updated on Scott's work, you can sign up for his newsletter in the show notes, where you'll also find ways to support the show and help make more episodes like this one possible. If you find the podcast valuable, please subscribe, rate, or leave a review, as it helps the show reach additional listeners exploring similar questions.

The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing discussed on this podcast should be considered medical advice. As always, please discuss any health-related decisions with your own personal medical authority. And now, here's Scott, your BetterHealthGuy.

[0:00:56] SCOTT: Welcome to episode 235 of the BetterHealthGuy podcast. If you are seeking new ways to create better health, I might just be your guy.

Today, we explore inside CIRS Lab and the Evolving Science of Biotoxin Illness with my guest, Dr. Christian Navarro-Torres. He is a cognitive neuroscientist with formal training in cognitive psychology, neuroscience, language science, and applied data analysis. He earned his PhD in language science from the University of California, Irvine after completing a Master's in Cognitive Psychology at Penn State and a Bachelor's in Philosophy from the University of Puerto Rico.

His research career has included post-doctoral fellowships at Princeton University and at Georgetown University where his work focused on the intersection between experience dependent neuroplasticity and clinical assessment in patients with brain damage affecting language and cognition. He is the co-founder of CIRS Lab, the Scientific Director of the CIRS Research Foundation, and a Research Consultant for the Einstein Mission which investigates erythromelalgia and CIRS. His recent scientific work extends into environmental health and immune dysregulation, including publications and presentations on biotoxin illness, its multi-system and multi-symptom pathology, and treatment outcomes with a particular interest in how CIRS-related brain changes may contribute to processes of neurodegeneration.

Equally important, his mission is grounded in lived experience. He is a complex, hypersensitive patient who's endured serious microbial colonizations, an underappreciated and often overlooked issue in the mainstream mold illness community, alongside tick-borne and protozoal coinfections. These overlapping comorbidities created a perplexing clinical profile that demanded self-advocacy where his scientific background became essential to navigating conflicting medical advice and fragmented care. Drawing from both his expertise and his personal recovery journey, he now provides training for physicians and clinicians on how to identify, understand, and treat those with complex multi-layered presentations.

And now, my interview with Dr. Christian Navarro-Torres.

[INTERVIEW]

[0:03:25] SCOTT: I've had the opportunity to talk with Dr. Navarro-Torres on several occasions and really was drawn to the way that he blends science with curiosity with his personal health journey and experience, and the work that he does to help people who are approaching their own recovery from chronic illness through CIRS Lab. He provides consulting services and offers his skills to bring new insights, interpretations, and actionable frameworks that can then be implemented by the patient working with their own practitioner. It's a great honor to have him today. Thanks so much for being here.

[0:04:01] DR. NAVARRO-TORRES: Thank you so much, Scott. I'm truly honored to be here. I'm very excited for this conversation.

[0:04:05] SCOTT: Me, too. I'm going to learn some new things from you today.

So, let's start by talking a little bit about your own health journey. What drives your passion for the work that you do today? Was it your own health challenge that was the catalyst for what you do in the work that you're doing with others?

[0:04:22] DR. NAVARRO-TORRES: Pretty much. Yes, maybe I'll walk you a little bit through my background because my background as a professional, as a researcher, it has everything to do with my involvement in the chronic illness community. Before I got sick with CIRS, I was studying as a PhD student, an intersection of cognitive psychology, cognitive neuroscience, language science. I was really interested in the brain from a different perspective. Specifically, around the idea of speaking more than one language, bilingualism and the potential neuroprotective or influences on brain function and brain structure. That was, yeah, my area of "expertise" as a scientist.

And there was already important ideas that I was exploring there because, with bilingualism, one of the things that we had, we were finding. And this goes back to researchers prior to me who had really found these results or findings is that bilingualism was consistently associated with a delay with the onset of Alzheimer's symptoms and dementia symptoms by about 5 years of a delay relative to, let's say, monolingual speakers.

Now that became a fascinating area of research. It also became an area of a lot of debate, let's, say in the scientific community about what does that mean. And some people were bringing in some potential questioning around are these results real? Just to say this really quickly, those effects did withstand the test of time. There are still studies that are showing these kinds of effects. Again, it's not that it prevented the illness itself. It's just that it pushed the onset of the manifestation of the illness.

Anyway, I was really into that idea. And of course, eventually, as I keep talking about this, we'll have a deep connection with my connection to chronic illness aside from a patient. I had a relatively functional, normal life throughout most of my life up until the early 30s where I started to experience more and more inexplicable symptoms, mostly digestive in nature, but other things were happening.

And in 2019, I had a really bad flare of unexplained GI symptoms paired with neuropathy-like activity and neuropathy pain or nerve pain. Also, all kinds of weird symptoms like tearing at night for no reason. Things like that. And I went to a lot of specialist doctors, as many patients do, and nobody can figure out what's going on.

I work with a gastroenterologist that was able to identify one little problem, which was I had what's called pancreatic enzyme insufficiency as measured by low levels of elastase, which is an enzyme that can show up in your stool. And it's usually an indicator of fat malabsorption. I had clinically observable insufficiency. And I started enzyme replacement therapy.

And so this would be something like prescribed enzyme medication like Creon where you take with your meals. And that somehow snapped me out of this crazy ordeal that I was dealing with which lasted for about 1 to 2 months where I just had major digestive issues. I couldn't tolerate foods. Even water would trigger just very severe abdominal issues. And I lost a lot of weight.

I snapped out of it. I thought this was just, "Okay, this is a quirk. I have this weird insufficiency." Nobody can figure out why because usually pancreatic enzyme insufficiency is associated with the structural problem in the pancreas. Meaning there's some kind of tumor or there's some kind of inflammatory process that you can actually see visually. And I had none of those after doing abdominal imaging, CT scans and abdominal MRIs. They couldn't figure it out. But I was happy that I had. In fact, I felt amazing. I had so much energy. I thought, "Man, this is great. Life is good."

That was 2019. In 2020, March actually, one week, I was in college at UC Irvine finishing my PhD. I was in the last year or so of my PhD working on my dissertation. First week of March, which I believe was one week before the COVID pandemic was announced, something happened that I started experiencing all kinds of inexplicable symptoms. And the only way I can describe it is I started feeling like death, to be honest. It was a very strange feeling. And I started to experience digestive issues again. They came back. I tried multiple diets. I started to experience severe anxiety. And it was incrementally getting worse and worse.

And I was trying different things. I was working with functional doctors. I was doing different modalities, mindfulness. Nothing was working. I would wake up at night with panic attacks at 2:00 in the morning, running out of the house because I had these crazy panic attacks and heart palpitations. I was experiencing depression. And then I started experiencing cognitive dysfunction, which for a PhD like me, it was like, "What is going on here?". Memory difficulties, word retrieval difficulties. These things were not part of my everyday vocabulary as a PhD researcher. All of that transpired in 2020.

Fast forward 2021, I'm working a lot with functional doctor. We're doing a lot of gut stuff. And the pattern was the same. It was like, "Oh, I feel a little bit better." And then a couple days, I'm back to where I was. Everything we're throwing at my body was just this loop. And at one point, we decided to try activated charcoal as a binder. And for the first time, I felt something moved that was very different. I'm like, "What is going on?" My vision got really sharp.

But then a week or two into that treatment, and I was also doing chlorella as well with activated charcoal. I remember that. I started experiencing the most insane, I think, moment of this illness in terms of the explosiveness. I started having frequent urination, 20 to 30 times a day, non-stop. It didn't matter how much water I drank. It was very scary. And it got to a point where I couldn't even get out of bed because I just couldn't put weight on my feet.

I was in a wheelchair for a couple months after that because I just couldn't put any weight. It was very humiliating for me for someone who was actually very active, not only intellectually but also physically. Someone that did strength training and a lot of physical activity since I was a kid to suddenly find myself in this situation of wheelchair at age 32 or 33.

Around that time, my functional doctor told me, "You know, you kind of look like someone that's suffering from this illness called Chronic Inflammatory Response Syndrome, or CIRS". He's like, "I don't know much about it, but maybe you should look into it. You're a scientist." He and I had amazing conversations during that time around research. And so he was very collaborative with me.

And then I started doing my research. And I ran into the work by Dr. Shoemaker and colleagues on CIRS, biotoxin illness. And I started reading all the work. I dissected all of that. I dissected all the lectures. And honestly, that became a coping mechanism for keeping me alive for what came afterwards. Because after that, I became incredibly hypersensitive as a patient to the point where I couldn't wear clothing. Clothing would trigger neurological symptoms. Touching surfaces would trigger neurological symptoms. Different parts of different rooms would trigger different kinds of signals. And I thought I was going crazy basically.

And at that point, I was weighing about 95 to 98 lbs. I had dropped about 50 lbs. I couldn't tolerate anything. It was pretty intense. And in that same timeline, I was getting ready to – and I had moved to Princeton, New Jersey to start my postdoc at Princeton, which was a dream come true. In the normal, non-CIRS service world, that was a dream come true for me. But I happened to have moved to a moldy apartment unfortunately during the post-doc.

Eventually during the post-doc, I was forced to take a medical leave, a short-term medical leave. I was trying to make it work. I eventually realized I need to move out of here. I tried another post-doc at Georgetown University in the D.C. area. And that was my last attempt to stay in academia. And during that time, I had started part of the Shoemaker protocol with binding. And I started learning a lot about my own reality as a patient. What does it take for someone like me to start moving forward even just a little bit?

So, with Welchol or colesevelam, which is a cholesterol sequester medication, that's what I started, that was the first time I started noticing something shifting in a way that kept moving me forward in some capacity. I was able to pass the VCS test. And I know we might talk a little bit about that later. A couple months of doing that.

There were some good things happening. But really, I hit a wall pretty fast. I would say I got maybe like 20% better, which was amazing at that time, but that was it. And I had tried to treat the nose with some MARCoNS stuff even though I had tested negative for MARCoNS in the sinuses. I still knew there was something going on in my sinuses. I couldn't figure it out for another 3 to 4 years. And we'll get back to that later because all of this connects.

But eventually, basically, I was at the post-doc at Georgetown. D.C. was horrible. I could not even tolerate being outside in the D.C., Virginia area. It was just a nightmare as a patient. I was forced to basically terminate my post-doc prematurely at the end of the first year, and basically say I have to give up my academic career. That was very demoralizing. I didn't know what I was going to be doing.

Thankfully, I had the opportunity to start my own business in a very humble manner, CIRS Lab. It really started just as Instagram content making short reels, trying to capture some of the nuances about this illness that I felt were not being talked about even in the proper CIRS communities, the Shoemaker communities. There were things that I was starting to pick up. It's like, "Wait. Wait a second. There's more to this illness than just get out of exposure, take Welchol, treat MARCoNS." I was dealing with this on a day-to-day basis. And basically, for 3 or 4 years I just spend my time running hundreds if not thousands of experiments to try to understand this inner relationship with what was going on with my body and how was the environment impacting that or influencing that.

And so, I started to just gradually do CIRS Lab and content, and eventually I got connected to the medical community. And as with my background in research, lo and behold, people were very interested in working with me in different capacities. And I was very interested in participating in the research enterprise creating, let's say, a new generation of research around biotoxin illness to really help move it into a more mainstream circle in terms of science, which I think it's one of the things that's currently lacking. And we can talk more about that later.

But I just gradually made my way. And along the way, I've been treating myself. I've been working with different practitioners both as a patient but also as a collaborator. And now we do CIRS Lab. I'm doing a lot of research. I'm part of this CIRS Research Foundation as a Scientific Director. I'm doing all these amazing things that I'm very blessed to have.

And just to put it in short terms, I had an opportunity to reinvent my life through CIRS. CIRS kind of took a lot away from me. And it also gave me an opportunity to do something that I don't think I would have ever been able to do in my traditional academic route. That's a little bit of my background there.

[0:16:07] SCOTT: I think we'll talk about some things CIRS and other things maybe that are not really discussed in the CIRS arena today. But I think both of us definitely appreciate and have a lot of gratitude for Dr. Richie Shoemaker and his work, and bringing a lot of this to light. Certainly, my journey was many years before your journey. But the whole mold and mycotoxin piece of the conversation was a big part of my journey as well. Even though we may kind of go beyond some of the CIRS protocol, I think we both absolutely have a lot of gratitude for Dr. Shoemaker.

My other mentor is Dr. Neil Nathan. And he talks a lot about sensitive patients. I'm curious, as you were going through this, did you find yourself someone who could really tolerate any treatment? Were you reactive to things that logically should have helped you? What were maybe some of the approaches or hacks that you took to move your health forward as a more sensitive patient?

[0:17:01] DR. NAVARRO-TORRES: Amazing questions. So, I'll start with the first set of questions around my journey. And keep in mind, I'm talking in a timeline at about 4 years in the making of trying to figure out all of this. But I'll go back to when I started taking Welchol. At that point, supplements that should have been helping me were making me more reactive, like histamine supplements, for example.

And this is going to sound crazy, but just to give people a sense of sensitivity that I had. When I got the bottle for Welchol for the first time, I remember opening the bottle and just opening it triggered a reaction in my body. I was like, "What is going on here?" And I knew this was going to be an intense introduction for this particular supplement, but I wanted to.

I did a lot of microdosing. Microdosing everything. Very gentle exposures. Even touching the supplement. Little steps like that. That's how I made my way into trying new things and figuring out is this a signal that seems to me that's conducive towards moving forward. Or is it a signal that's just going to make me worse and no resolution? That was always kind of the assessment that I was trying to make based on my symptom pattern. And with Welchol, I could tell I could tell there was something unique about the way I reacted by just opening the bottle. It's like, "Ooh, there's something really profound, but it's going to be intense."

What I did is I crushed the tablet. I put it in a water bottle. It diluted. And I literally just had the tiniest sip you can ever imagine of water. And I felt like the whole world was falling apart instantly within like 10 seconds. I was like, "What is going on here?" I almost felt like I was about to black out. It was really intense. A really intense experience, nothing I've ever experienced before.

Short description of that. It took me about 8 weeks to get to one tablet. And for those who don't know, the typical max dose for Welchol tablets and biotoxin illness is six tablets. Either two tablets three times a day or three tablets twice a day. So, it took me about eight, maybe a little bit more, to get up to one tablet. And it was just incremental.

The first time I tried it, I only tried it that one time and I waited like 2 weeks or something like that just to see what was my reaction afterwards. Because my body completely shifted after that microdose. Things change, sleep patterns change, bowel movement started changing, blood flow dynamics. I would start noticing that weight standing up. And then suddenly, I started developing some intolerances to supplements I was tolerating. Curcumin was a really good example. It was making me pass out, and I would get bruised. Eventually, I realized, "Oh my god. I might be thinning my blood, and I might have some coagulation issues going on," which are very characteristic of CIRS patients. It could be in the form of microclotting or microbleeding, or fluctuations that are very subtle.

But I started experiencing all these shifts in my body. And so I had to basically just be very patient microdosing and paying careful attention to my signals in my bodies. I learned to discern which signals were more likely to give me this is going to give me some kind of resolution. It's going to be a desirable difficulty. Initially, I'll have some intensification of some kind. But I can tell this is going to eventually translate into something good.

So, I was trying to hone in into which supplements would give me that signal versus which supplements, which give me the kinds of flares that I'm like, "I just don't resolve. I feel worse." I actually feel like something really bad can happen. I'm having like a really, really bad histamine reaction afterwards. And it took me like 3 days to recover, and I'm still not quite well. Trying to discern those processes. Overlaid on that.

I had about eight purifiers in a one-bedroom apartment. This was the apartment that had mold. I was doing insane amounts of cleaning like a crazy person at that point. Just a disclaimer, I don't do these things anymore. And maybe we'll talk about that that I don't live my life like this anymore. I'm going to a past that's no longer who I am. But I had eight purifiers. I learned through that process that the iAdaptAirs were the purifiers of choice by far for someone like me. And I learned to understand them better. What was it that they were doing for us in the environment?

Initially, I actually reacted negatively to iAdaptAirs. So I freaked out. And then I realized that that was actually – not that it was a desirable thing, but it was a necessary step because of the decontamination process that was taking place with the bipolar ionization. Anyway, a lot of cleaning, a lot of purification, and a lot of microdosing the kind of basic ingredients to work my way through that whole sequence for the first year of starting, let's say, the Shoemaker treatment or the CIRS treatment that's more traditionally known. That's in terms of how I went about that.

[0:22:03] SCOTT: And then where from your lens do things like nervous system regulation, and limbic system retraining, and vagal tonification come into that sensitive patient conversation? And then lastly, building on that, how often do you find that trauma is involved and needs to be explored in this patient population?

[0:22:23] DR. NAVARRO-TORRES: The first thing I want to say is I think those modalities are incredibly important. They have a role in chronic illnesses like CIRS and biotoxin illness. But in my experience, I mean, I was already doing a lot of mindfulness prior to that time as I was getting worse in 2020, 2021. I was doing mindfulness. I was doing chiropractic. I talked to therapists. I did EMDR, CBT. In fact, even the person who was doing EMDR looked at me after like the third session and said, "You kind of look like you have a PTSD-like thing, but you don't quite have it. You look like something else." She was like, "I don't know if we need to do this right now because I just don't see – there's an experience tied to this stress response that you're experiencing." And I felt like that. I felt like these things were just not working at that time.

For me, those kinds of modalities became more and more relevant maybe initially a little bit just to quell things down, but it wasn't preventing what was happening, the cascade that was taking place. It's like my body had taken over, and it said, "I'm taking over here. I'm going to be dictating what is going to happen until you figure out how to fix me." That's how my body felt.

But initially, there was a little bit of relief from some of the mindfulness and things like that. But then once I got proper into CIRS and I started treating, and these last three, four, five years, none of that really worked for me. It wasn't until I started working more on endogenous components of my body, meaning potential chronic infection burden, potential colonization burden in the body. And in my case, we have a strong – we've always – with the practitioners I've worked, there's been a strong suspicion. I say that because we have a lot of indirect markers that point into these, but not getting the typical traditional test confirmations.

Bartonella and parasites, both of these have always been – not always. But they became more and more readily. Like, "I think you have a very, very severe case of burden around these entities, and maybe something like fungal issues," because I did have a lot of fungal rashes initially. And then eventually Actinobacteria became a huge part of this. And we'll talk more about that. But all of this pointing into there's a lot of burden in my body that's independent from the environment.

Once I started doing that, especially once I started working with parasite treatments, I felt like I was able to start going back into modalities. Anything from therapy, anything from relaxation practices and body practices. And now I feel like I have opening into exploring those modalities. That was my personal journey.

In terms of your last question, trauma, how does trauma play a role? Well, there are some practitioners in the CIRS space that actually have questionnaires to assess early childhood trauma. And one of the things that stands out from that, just clinical observations, this is not like published work in the context of biotoxin illness or CIRS, but trauma severity as measured by these questionnaires tends to look like it's very predictive of severity of CIRS. Including things like hypersensitivity.

And I wholeheartedly believe, that is one of different potential big contributors that will influence how severe of an illness are you going to develop when that time comes, or if it ever comes. I don't think it's the only one. But early childhood trauma is probably one of those big things that if you were to run a large data set, and it was longitudinal, and you had these questionnaires, and then you had some kind of severity of biotoxin illness, it would probably come out if I had to throw a prediction as one of the significant contributors of predicting those kinds of outcomes.

[0:26:21] SCOTT: So let's talk about where you see HLA-DR fitting today. And whether or not someone's HLA-DR type correlates to either the propensity for the development of CIRS or potentially the difficulty in recovering from it. And my understanding is that HLA-DR, if we're talking about mold or multi-susceptible, that that's a predisposition to mold. It is not a predisposition to mycotoxins. The mold exposure can drive that inflammatory response in CIRS. But then we have the mycotoxin aspect as well, which as I understand is not directly tied to HLA. So I wanted to see if that's your understanding as well.

And then when we think about the newer things that potentially are causative, Actinobacteria, endotoxins, beta-glucans, mold and mycotoxins are less of a focus now. We'll talk a little more about that. But do we have any insights or correlations in terms of which HLA-DR types seem to be more predisposed to Actino, endotoxin, or beta-glucans as drivers or causative factors in the development of CIRS?

[0:27:31] DR. NAVARRO-TORRES: Yeah. So, I have somewhat slightly different take on HLAs. I mean it is very much founded in some of the clinical insights that Dr. Shoemaker and his team have made over the years. I don't think we necessarily have the ability to say with a lot of confidence, "Okay, there's a mold-specific HLA." I think of it at a much more general level, meaning at the level of just inefficiencies in antigen presentation and antigen processing. And there might be groups of organisms of microbial organisms where, depending on the conditions of the immune system, might be less likely to be properly introduced into the communication between the innate and adaptive immune system.

I mean, just to give you an example. And you asked about Actinobacteria and endotoxins. My HLA, it would be 17-2-52B, which is tagged as mold susceptible. And I actually have some ideas about mold. But I mean I've had massive Actinobacteria burden. I have all these elements that almost look like a multi-susceptible HLA person. And I've seen a lot of people like this that don't necessarily ascribe in terms of the illness severity. I don't think HLA's really specify anything about illness severity. It's just a potential opening; it's a risk factor essentially. To me, it's a risk factor. I think there needs to be other conditions in place for those risk factors to play out.

In terms of the mycotoxin component, yes. I mean, when we talk about HLA and antigen recognition, we're talking about DNA fragments. And that could be from whatever microbial organism we're dealing with that the immune system is having a hard time fully processing or integrating. I think in that sense, mycotoxins are metabolites. These are compounds that are excreted from molds, but they're not necessarily really the thing that the HLAs would be paying attention to in order to create an appropriate immune response. I think, yeah, that's my sense on it.

In terms of Actinobacteria and endotoxins, the one thing I'll say very quickly, Scott, is I think of Actinobacteria more as a late-stage problematic organism. I don't necessarily think of it as a priming event. So I think the distinction between what are priming events and what are components of the illness that drive persistence in the illness once you've already triggered the illness, those are two separate things.

To me, Actinobacteria falls in the second category. It tends to creep in once the immune system is so exhausted and dysregulated. You're metabolically a mess. Your brain might start to show signs of atrophy. You've lost a lot of resilience by then. If you've turned on CIRS, and it's been at least a couple years, maybe many years before, Actinobacteria really starts showing its face. And it's all the byproduct of downstream dysbiosis to me in the system.

In that sense, I think of mold more as likely to be a primer, a priming event. Fall in the category of priming event. And I think this speaks a little bit to the tension that currently there is in the functional medical community about what role is mold playing in the illness. I think it plays potentially a massive role as a priming event.

In fact, I think there's a beautiful mechanistic story here which is ribotoxins. Fungal ribotoxins are uniquely one of the very few things in mother nature that can disrupt RNA sequencing and these like ancient loops in our RNA activity, like the sarcin-ricin loop, which is something Dr. Shoemaker have talked about. And people don't really think about that. How that sets the stage for everything else, including HLA susceptibility. I actually think that is a precursor of CIRS before anything happens. It's about the ribotoxins perhaps.

[0:31:30] SCOTT: So there tends to be a lot of focus on the mycotoxin detoxification aspect of CIRS. We're using binders. We're saying that that does not appear to be associated to HLA. So why do those people who are mold HLA susceptible, if that is even playing a role in the propensity to develop these conditions, why are they also unable to excrete efficiently the mycotoxins? Is that coming back more into what Dr. Chris Shade talks about, where when there's more inflammation, that we have less detoxification. And when inflammation is down, then we upregulate our ability to detoxify. What is the connection there? If it's not a genetic predisposition, why do most people that have CIRS also have an inability to detoxify the biotoxin?

[0:32:22] DR. NAVARRO-TORRES: I mean, at one level, we're dealing with poor antigen presentation, meaning there's a breakdown in the ability to create antibodies to tag the fragments or the microbe itself if necessary. I mean when you're talking at that level, that includes compounds that can come from the organism that are supposed to be eliminated. Now that's one piece.

The other thing is once you've turn on chronic innate immune activation, like you see in CIRS and biotoxin illness, over time that's going to have all kinds of downstream effects. It's going to impact your ability to release bile from the liver. Bile becomes severely dysfunctional. And detoxification deeply, deeply depends on proper signaling from bio-sequestration.

Inflammation in of itself, once it reaches a certain level and it pushes the body into a certain threshold, it's going to have all these downstream effects that will impact detoxification for different reasons. And I'm just giving you one there with bile, but also at the mitochondrial level. All the things that are shifting at the cellular level in terms of energy production, cells are shifting into this more defensive state and less into harboring energy and being very cooperative state.

And in that state, sometimes cells may on purpose shift some of these pathways that are so important for detoxification in order to be protective. Maybe even like holding on to heavy metals because that could be thought of as a protective mechanism against a potential microbial threat that's lurking in the background. There could be all these kinds of different downstream effects.

[0:34:00] SCOTT: So let's talk then a little bit about how GENIE, the transcriptomics testing, might reveal a fingerprint of what is the causation or someone's trigger for the CIRS condition that they're experiencing. So, do you find that GENIE consistently points you in the direction of what that person should focus on? Does it tend to match up to other data points when you're evaluating someone's case? Have you seen GENIE reveal a Lyme pattern in someone with chronic Lyme? And then how do you navigate the scenario where a client is diagnosed with CIRS, but none of the more common causal patterns seem to express in their GENIE results? How is GENIE informing you in the consulting work that you do with your clients?

[0:34:48] DR. NAVARRO-TORRES: I see GENIE as pretty much every other test in terms of it's a tool. It's part of a bigger inventory of toolkits that you can use. I'm a big fan of bringing in multiple sources of evidence to figure out, to paint a picture of what could be possibly going on.

GENIE in on itself, it can sometimes be helpful to generate certain inferences about what could be connected in terms of biotoxin exposure and metabolically what's going on. I personally find it a little bit tricky to really think about what this means, what GENIE means deeply without bringing in other tests. That may include NeuroQuant. It may include blood work. It may include symptom history, VCS patterns in the person, the person's living situation. You have to bring all of this. That's the first thing I wanted to say.

That said, when I put it in that context, yes, GENIE does often show patterns that more or less correspond with a lot of the Dr. Shoemaker maker insights with MAP kinases upregulated. And if you see that with TGF beta 1 receptors upregulated, you tend to see a correlation with Actinobacteria burden. I mean the toll receptors which are traditionally thought of more as endotoxin connected, those are tricky. Because toll receptor 2, for example, very, very triggered by Cutibacterium acne, or P. acne. Formerly known as P. acne. That is well established in the literature, that P. acne or C. acnes is a very strong stimulator of toll receptor 2. You have to be very careful there.

But if you see something like CD14, you're thinking maybe endotoxins. At least initially someone is early in treatments. And then there's the metabolic stuff that you see all the time, I think, with a lot of patients. And it's very telling. I think the GENIE is a useful tool. I don't think of it as a diagnostic tool. I think you need other pieces. It can tell you about potential connections with environmental exposures. But you got to be careful because those patterns of gene expression, as the patient moves forward with treatment, can start reflecting things that could be perhaps more endogenous, not necessarily so environmental.

There's no reason to say that MAP kinases or toll receptors are uniquely about the environment, right? So you have to be very careful to discern when are these patterns really most likely connected to environmental issues versus something that's going on endogenously. Sometimes endotoxin activity could. We don't have data for certain in terms of the CIRS context. But this is something that has been looked at outside the CIRS world. When you see upregulated toll receptors, there could be something like endotoxemia, which could just be your gut is very leaky. And some endotoxin activity is leaking from the gut into the bloodstream, and there is innate immune activation triggering that kind of stuff.

[0:37:37] SCOTT: Okay, we're going to come back to that endotoxins, and whether endogenously created endotoxins could also be a trigger, because I think that's another debate in the CIRS community. But I'm going to hold off on that one for now.

Let's talk about some of the more traditional biotoxin illness markers. So VCS, you mentioned. We've talked about things for many years like C4A, TGF beta 1, MSH, MMP9. Are those still helpful? And particularly thinking about C4A, where, for many people, it's become very difficult to get it to National Jewish Hospital in Denver. And there's questions about whether or not doing it through other labs is really reliable. There's also the question about TGF beta 1 given that it seems that most people now in the COVID era have much higher levels. The methodology for the testing also changed over the pandemic period of time. Are these still helpful markers? And when there's an elevation in something like TGF beta 1, C4A, MMP9, a low MSH, do we then know that it is potentially mold? Or are these factors that are not pointing us in any specific causation?

[0:38:51] DR. NAVARRO-TORRES: Yeah. On their own, again, they don't necessarily point to specific causation. You kind of have to look at the pattern in the context of the patient. Very often in the context of CIRS patients, if they're treatment naive, and they've been sick for years, and you're getting those elevated markers, it likely means it's chronically elevated or chronically abnormal. And in that context, if you're a practitioner, you're doing the process of the diagnosis. Likely, this is indicative to chronic innate immune activation tied to exposure to biotoxins, right?

With C4A, I think you said it. Right now, I don't see it really being very informative these days, unfortunately, unless you're doing something like National Jewish. There's methodological issues there with C4A. Unfortunately, hopefully that can be sorted out soon. TGF beta 1, you're right about the skew of the effects since the pandemic because of presumably how people were being sampled in order to contribute to the bell curve of what's considered a normal distribution of values. And probably COVID shifted that distribution.

But what I will say is, for TGF beta 1, one thing that's very reasonably established in the scientific literature is when you see numbers above 10,000, that's usually flagged that something is unusually off in terms of inflammatory activity. That is a consensus observation that has emerged from scientific literature. That is something that I keep in the back of my head whenever I'm looking at TGF beta 1s. And I try to perhaps not think so much. Again, not as a medical doctor. Just if someone is consulting and looking for my thoughts, I have that in the background. Are we dealing with a TGF beta 1 that's 5,000? Or is it above 10,000? Because, then, that really is harder to rule out as it's just noise for any given person.

And MSH, I think, is a very underappreciated hormone to the point where we recently published a paper because we think we need to go back to that to really unpack what does it mean to have an MSH deficiency. What does it mean to recover in a patient suffering from biotoxin illness?

[0:40:59] SCOTT: And I think if we look at the diagram, the biotoxin illness pathway that Dr. Shoemaker created many years ago, we see that MSH is really in the center of that. And a lot of the downstream effects all kind of tie back to MSH. So, we're going to talk more about that study shortly.

I want to touch on NeuroQuant. Talk through the process that someone would go through to order a NeuroQuant. How do they find the type of MRI equipment that's necessary? How do those results then get to CoreTechs Labs to produce that NeuroQuant report? Is that something that you all offer as a service at CIRS Lab? And then which reports are you looking at? Is it more what we used to call the TBAR, the Triage Brain Atrophy Report? Is there still an issue where we have to do some conversion because the older format is required versus the newer format? And then how difficult is it for practitioners to learn the NeuroQuant interpretation, those patterns to be able to effectively interpret them for their patients?

[0:42:03] DR. NAVARRO-TORRES: Yes. The first thing I'll say is we, CIRS Lab, have a NeuroQuant license. One of the things that we do is provide services for generating reports, NeuroQuant reports. One of the things that we do in addition to generating NeuroQuant reports is we provide consultations with clients and practitioners as well to help them brainstorm what could this NeuroQuant be telling us, right? Yes, we do offer those services.

In terms of how to get a NeuroQuant, there's basically two options. One option is you go to an MRI facility. Essentially, just about any modern MRI facility. The critical thing is that the MRI facility needs to have access to the settings for the scanner that will be applicable in order for someone to generate a NeuroQuant report.

What we do on our end is that if a client is interested in getting a NeuroQuant, we will send them instructions, document with the scanner settings. They can then send them to the MRI facility. And we've had reasonable success and good success in getting MRI facilities to basically include the scanner settings. And then we receive afterwards the raw DICOM files. And those can be sent to us in a CD. Or they could be sent through a cloud-based program. And then we can generate the NeuroQuant reports. That would be one way to get a NeuroQuant.

Another way is you just get a regular MRI order from a physician and you go to an MRI facility that already has a NeuroQuant in place. And so you get the NeuroQuant reports automatically alongside with your MRI images. The problem with that in the context of CIRS is, as you were pointing to, Scott, we have an issue with different software versions of NeuroQuant. Because a lot of the work that was done on the brain and NeuroQuant with CIRS and biotoxin illness patients was done with earlier software versions that use very specific segmentation methods that were more conventional.

More recently, Cortechs AI have versions of NeuroQuant that are using AI in order to inform the segmentation procedures for segmenting different brain parts, essentially. And that's essentially now like doing an apples to orange comparison. Those are very different criteria. What counts as a designated brain region in one version can be significantly different in the other version.

What we've had to do is acquire a license that is compatible with the work that Dr. Shoemaker has done using his criteria. And this is specifically in the context of morphometry report, which is used to create the surviving mold NeuroQuant analysis report. For that report, you want to have that version. Those are the two ways to potentially get a NeuroQuant report.

In terms of what I use, I do pay a lot of attention to the Triage Brain Atrophy Report. What I love about that report is you have a very high-resolution breakdown of about 47 brain regions or so. And these are ranked ordered relative to healthy people of your age and gender. There's a matching there. And it's completely blind of something like CIRS or biotoxin.

If you see abnormalities that are consistent with Dr. Shoemaker's criteria, let's say on the morphometry report, and then you see converging evidence and the Triage Brain Atrophy Report, that to me really elevates the confidence. And this is not a fluke. These abnormalities are not subtle. These abnormalities, we need to pay attention into them. And they're likely indicating something that is serious here for the patient.

[0:45:39] SCOTT: For your clients, can you order the MRI? Or do they still need to do that through their practitioner?

[0:45:45] DR. NAVARRO-TORRES: They still need to do that through a practitioner. We would not be able to do that as of now.

[0:45:50] SCOTT: What insights do you glean from a NeuroQuant? What are the key patterns? Things like mold, or Alzheimer's, or other neurodegenerative conditions, or maybe traumatic brain injuries, for example. My understanding, and correct me if I'm wrong, but my understanding was the original Lyme algorithm that we talked about in the realm of NeuroQuant was really more for acute Lyme, not so much for chronic Lyme. Is there a distinct pattern that you see in people with chronic Lyme? Talk to us a little bit about the patterns. And then how you might also see atrophy and hypertrophy, which is potentially more of a concern. And what might that tell us?

[0:46:31] DR. NAVARRO-TORRES: Yes. I use the NeuroQuant for all of those things that you mentioned. I'm looking for patterns that could be potentially correlated with exposure to water-damaged building. And there are some fingerprints that, I mean, Dr. Shoemaker has published, and also Dr. McMahon. There's two publications documenting brain abnormalities in CIRS patients connected to water damage exposure.

And I'm also currently doing some very initial but promising research with Dr. Andrea Jordheim, where we're looking at fingerprints of CIRS potentially looking at the Triage Brain Atrophy Report. And we're seeing some converging evidence between what Dr. Shoemaker had initially discovered and what's emerging in this data set. It's very preliminary. But one of the things that I see very often in CIRS patients, especially if they're in earlier stages of the illness, and I like to call that CIRS brain on fire. It's kind of like phase one. One of the things that you tend to see a lot is enlargement or elevations of the white matter tracts. It's a very, very common feature.

And we can speculate about what that means. One very plausible hypothesis is that that's connected to microglia activation. Microglia are innate immune cells in the brain, essentially, right? And so we think about CIRS as a chronic innate immune activation profile. We can easily make that connection.

Elevation of white matter tracts is a big one that I see very often. I sometimes, not as often, but quite a bit, will see atrophy of the pallidum. And what's really interesting about that is that the pallidum is an incredibly metabolically sensitive brain structure. If there's something wrong metabolically in your body, the pallidum is probably the first region to start giving you a signal that something's wrong metabolically.

When I see that, I'm thinking what Dr. Shoemaker has called molecular hypometabolism. I start thinking about Actinobacteria. To me, Actinobacteria and metabolic disturbances in that category, especially when they're persistent, when you've started treating and you're still having those issues, I start thinking about Actinobacteria potentially being an issue.

There's the CIRS component there. And then there's later stages of CIRS where you just start seeing widespread atrophy of cortical gray matter sometimes. You'll see the pallidum as well. You might see some of the limbic structures start shrinking as well. And that can be more later stage once – again, the body is more depleted. The brain is running out of resources and things like that.

In addition to CIRS, I will look for patterns, especially using the Triage Brain Atrophy Report to see is there any evidence of a potential traumatic brain injury history. And very often, we will find that with CIRS patients. And when you start asking them, yep, they have the profile. They've had something, even when they were like 5 years old. I had a head injury when I was 10 years old. And I did my first NeuroQuant when I was 35 years old. And when I looked at that, I realized I had a fingerprint that was very much likely connected to that head injury that I had when I was 10 years old. We will look for that.

I will also look for any potential patterns connected to chronic infection. Those are more speculative. I would say that is not a necessarily a very established scientific. There's not a strong consensus about how the brain is impacted by things like chronic infections, chronic Lyme, and things like that.

But I do see some patterns. And one of them is atrophy of the white matter tracts. I tend to think Bartonella if I've been able to rule out other potential explanations. Because white matter tracts are one of the first brain structures to go away or to suffer when there's poor blood flow, or blood flow issues, or vascular issues in the body. And we know Bartonella particularly puts a lot of stress in the vascular system, endothelial stress, and that kind of thing.

[0:50:30] SCOTT: What are some of the more effective treatment interventions when you see someone having issues with their NeuroQuant? We talk about VIP. There's also more recent conversations potentially about the plasmalogen precursors from Dr. Dayan Goodenowe's work. Maybe other lipid replacements. What are you seeing is helping people the most when they have either atrophy, or shrinkage, or hypertrophy, or swelling, or inflammation when you're doing a follow-up NeuroQuant? How long after an initial baseline would someone potentially repeat that? And are there any scenarios where it might be unrealistic to see significant improvements? What some people have called the sea of red? Or can most people improve the health of their brain using NeuroQuant as the lens to identify what might be impacting it?

[0:51:24] DR. NAVARRO-TORRES: Yes. In terms of how often to do something like NeuroQuant, I would say reasonably every 6 months or so are good timelines if you're in treatment and you want to capture potential meaningful sustained changes in NeuroQuant. And some people will do it every 6 to 12 months. Some kind of interval between there, right? Those are interests.

But sometimes you'll see changes as soon as three to four months. It all really depends on are you doing meaningful interventions that are geared towards helping restore brain volumes and normalizing them, right? I would say if you want to be just on the safe side, every 6 months is a good interval for a NeuroQuant.

In terms of what I have personally seen to work the most in the context of normalizing brain volumes as measured by NeuroQuant, the two things that stand out to me are vasoactive intestinal peptide, VIP, high dosages, and ProdromeGLIA, right? From Prodrome Sciences company from Dr. Goodenowe. That combination, I've seen actually quite a few miracles. Let's put it that way. Cases where it's not just atrophy in the assessments by Dr. Shoemaker. It's also widespread, very bad atrophy in the Triage Brain Atrophy Report, which again would be an independent assessment. And some of these patients, neurologically very limited in their ability to function. And within an 18-month period or so, turn that around into normalizing looking at those percentiles. And you can't really even tell if this is a patient or if this is a healthy person.

I've seen quite a few of those now. And those are two of the things that I see work best, especially if there is white matter abnormalities or deviations, especially if there's white matter atrophy, something like ProdromeGLIA is an amazing tool to have. Now, there might be other things that will help promote neuroplasticity, but I think those would be the two foundational things if you're thinking about restoring brain volumes.

[0:53:35] SCOTT: I am a huge fan of ProdromeGLIA, as you know, because we've talked about that before. Is there a role here for any other lipids like phosphatidylcholine? And if so, are you more inclined to use soy-derived, sunflower-derived, egg-yolk-derived, or maybe lipids? I know Dr. Patricia Kaine many years ago talked about caviar as a source of lipids. Do any of those stand out?

[0:54:00] DR. NAVARRO-TORRES: Yeah, for me, animal-based choline and phosphatidylcholine is one of those things that would be at the top. But I tend to see, and this is myself, a lot of intolerance to those kinds of interventions if someone is really sick and still dealing with a lot of infection burden.

I tend to see that playing better out once patients are in later stages of healing from CIRS or biotoxin illness. And there might be different reasons for that. I particularly see – and this is very observational. I'm not making any absolute scientific claims. The animal formulations work better. I think the plant-based formulations, which I think are also great, in my experience, tend to seem to work better for things like detoxification, supporting liver functioning, and those kinds of peripheral organs. But when it comes to the brain, it's animal-based that seems to be the most impactful. Yeah.

[0:55:00] SCOTT: And by animal-based, are you then including both egg yolk and caviar as sources for animal-based lipids?

[0:55:07] DR. NAVARRO-TORRES: That would be right. And caviar particularly would be – sometimes people can't afford, let's say, the Prodrome PC+, which is the version that has animal choline from egg yolk. It's an expensive product. And so, when that is not available, some people will try just caviar regularly, and that is a very high concentrated dose of animal-based choline.

[0:55:31] SCOTT: So since we're talking about Dr. Dayan Goodenowe's work, are you also using the ProdromeScan or the BioScan? And how do those inform you in addition to all of the other tests that you might be exploring for a given client?

[0:55:45] DR. NAVARRO-TORRES: Yes, I certainly use them quite a bit, not all the time. Again, as part of a bigger – I love to bring in the ProdromeScan with GENIE and NeuroQuant. That to me is like a holy trinity, especially if you're trying to optimize. If you're at a stage where you're trying to optim – the two contexts where I think ProdromeScan can add a lot of value for me is if someone is in later stages and you're trying to optimize things, and see what's left over. And sometimes you will see, "Hey, your plasmalogen pool, maybe it's not deficient," but it looks like your body is trying to steal plasmalogens from where it should – it's trying to make plasmalogens without really having the resources to do it. It's trying to compensate. You want to try to work on that. That's one scenario. The other scenario is where if you're working with someone where there's either confirm or suspicion that this person is at high risk of neurodegeneration, right? Those kinds of profiles, you want to look into that.

[0:56:43] SCOTT: Are there any other tests that come to the top of your list? And just to get a little controversial, any thoughts on urine mycotoxin testing or mycotoxin antibody testing in the blood? Do you also use organic acids? What other things are helping you to paint the picture of the person in front of you?

[0:57:02] DR. NAVARRO-TORRES: Those are not generally tests that I will have. I will work with the kinds of clients that come to me or with practitioners. And it's not a knock on them. In my particular context with the kinds of questions and problems that I am trying to help solve, those are not necessarily the most useful tests for me.

Now, again, that doesn't mean that those tests wouldn't have utility. I can certainly see value, for example, for mycotoxin urine testing in the context of understanding an exposure component and correlating that to exposure. And it could be an environmental exposure. And maybe there is also a correlation with activity or fluctuations in detoxification, and these systems either coming back online or shutting down. I can see a lot of value in that context. But yeah, for me, those are not my go-to tests.

[0:57:52] SCOTT: Talking then about the external environment, what are some of your go-tos for clients exploring that? Are you generally using an ERMI? Are you also having them do the expanded test that includes the Actinobacteria and the endotoxins from the dust sample? Are you using any mold plate testing? Do you think people should go directly to an IEP and do a professional inspection? And how important is proper testing and remediation in improving the health of the people that you're working with? What tips can you provide us for improving the external environment in support of improving the internal environment?

[0:58:28] DR. NAVARRO-TORRES: Yes, I'll answer the last part first. I absolutely think that remediation, proper remediation is incredibly important. It's foundational. With the current landscape of how we build and how we construct, I think that is a critical piece. The other thing I will say that I think it's important, especially for hypersensitive patients, you want to think about the ecosystem more generally, not just the house. What is the environment in which that house is placed?

And I had to learn that the hard way as a hypersensitive patient. Your body is supposed to tolerate when it's healthy to tolerate certain kinds or certain degrees of exposure. But there are thresholds that your body will say this is enough. And sometimes that can come from outdoor sources that are nearby, like a water treatment plant where there is very high amounts of endotoxins. You want to have a lot of conscious thinking, informed decision thinking, not just in terms of the house but also in the vicinity nearby. What are the things? Do you have like a lake that has high cyanobacteria? Do you have a water treatment plant? Is this like a place that's prone to a lot of flooding, historic flooding, and things like that. I think those things are all very important.

In terms of testing, a lot of clients will bring in their own environmental tests. I do work a lot with environmental tests, understanding that they're not absolutes or absolute answers to a potential underlying problem. They're more like proxies to start getting a sense of what could be a potential issue.

I think in general, I find it useful to always have a HERTSMI-2 available just because it will kind of start giving you a sense of, "Well, if these numbers are not good, chances are there's a lot of correlated issues with this house." If you have a HERTSMI-2 or 14, 15, 16, or even in the gray zone area 12, 13. And then you start looking at the species, you start generating some questions. What's going on here? Is there active water intrusion? Is it something residual?

Now, when I'm working with clients who have a profile where Actinobacteria seems to be a big problem, and there are symptoms, there are patterns that I'm going to be looking for that tend to show up in that context, then I will start talking about the possibility or maybe you should consider doing Actinobacteria testing. And there's different kinds of tests that you could do there. Obviously, environmental. There's skin, there's also sinus, which I think we'll talk about in just a moment, which we are feeling that in some ways might be more important to look at in some clients.

[1:01:05] SCOTT: I think just to underscore the importance of what you just said about thinking outside of your building, I had recently done an ERMI. The HERTSMI-2 was a four, but there were two spore equivalents of Chaetomium, which kind of for me was like, "Ugh. Where's that coming from?" I did a HERTSMI sample outside on the gutter downspouts after having fairly recently remulched around my house, and the outdoor Chaetomium was 23 spore equivalents. That was an interesting find that I've heard John Banta and others talk about Stachybotrys, and cardboard, and all that kind of stuff outside. But I don't know that I had thought about it as much as I do now. Totally agree with you there.

Would you say that CIRS is more about immune compromise or about immune dysregulation? Do we need to boost the immune system? Do we need to modulate the immune response? How do we modulate, or soften, or balance, or create more tolerance with that innate immune system while also supporting the adaptive system? Is it that the immune system is weak, or is it that it's confused and maybe not discerning enough? And then what's the crossover between immune dysregulation that we see in CIRS and autoimmune conditions? Does the immune system eventually become so focused on the environment outside of us that then it's less focused on the environment inside of us and potentially then leading to the increase of these microbial burdens.

[1:02:37] DR. NAVARRO-TORRES: I think of CIRS primarily as an immune dysregulation problem. And one way I like to talk about that as an analogy is your attention system and how your attention system works for you. Attention is all about selectivity. It's about paying attention, prioritizing one thing at any given point and doing it in a way that's relevant to the situation at hand. Your immune system works very much like this. It should know what to pay attention to, when to pay attention to, and how to go about that. Right?

To me, CIRS is fundamentally a breakdown of the attention system within the immune system where you have the chronic elevated innate immune activation. Adaptive immunity at least initially might be a little bit underwhelming in terms of being a little bit too silent more than what it should be, right? And part of that is presumably because of the handoff.

And so what we think or what I think happens over time is you're priming that imbalance between the innate immune system and the adaptive immune system. And over time, that attention span starts shifting away from the body and you start paying – or the immune system or parts of the immune system start paying more attention, prioritizing what's going on out there disregarding what's happening in your own body to some extent.

And I wouldn't say it's strictly speaking immunocompromised in the traditional sense. We're not talking about an HIV patient or someone who's undergoing chemotherapy where these people, they're in imminent danger. Like, they can die imminently if they're not protected properly. But there is an element of immune compromise especially for long-term CIRS patients where there's depletion of resources. Again, you start seeing more metabolic issues. You might start seeing more brain atrophy. You might start seeing plasmalogen deficiencies creep in. You might start seeing a lot of infection burden or colonizations taking over. And you may become very permeable, not just in the gut, but systemic permeability.

And once those things are compromised, there is a fatiguing element of the immune system, where you start seeing like the immune system is just kind of giving up a little bit. At least parts of it. And so from that sense, I do think there can be an element of immunocompromised in CIRS, but it's not in the traditional sense.

[1:04:57] SCOTT: And would you say it's reasonable then that that lack of immune discernment, that immune confusion, maybe the increase of microbes within us because of the focus on the external environment could also then be a reason why we see autoimmunity that is then kind of diagnosed in people. But really, it's more the immune system responding to that increase of microbial burden.

[1:05:20] DR. NAVARRO-TORRES: Yes. I mean, you can certainly potentially think of autoimmunity, right? It's on the adaptive immune side. That's an inflammatory response from the adaptive immune system. And there's going to be genetic susceptibility to that. There are some people who are more likely to have autoimmune at the forefront of their chronic illness. And there is a subtype of CIRS patients that are CIRS autoimmunity dominant in some patients. I'm not particularly in that category. I've had things like Hashimoto markers elevated, but it's never been at the forefront of my illness profile.

For those people, yes, one possible hypothesis that I think could be substantiated is that what could be happening here is the adaptive immune system is trying to take matters into its own hands because things are not proper. Maybe there's been a breach of colonizers and chronic infections in specific tissues where the immune system is able to see something that's wrong, or at least the adaptive immune system is able to see that something's wrong. And then participate in the attack even it means attacking our own tissues.

[1:06:29] SCOTT: Can we say then that addressing the environmental factors allows the body to better respond, more appropriately respond to the microbial overgrowths? And that addressing the microbial overgrowths also takes some of the burden off of the immune system. So maybe doing a combination of both, working on the external environment while reducing the internal microbial burden is the optimal approach. But when in the recovery timeline would you focus on the external environment compared to the internal environment? Can we start to work on those microbial burdens in parallel with mitigating the external environment?

[1:07:06] DR. NAVARRO-TORRES: Great question. It's a bit of a yes. In my personal experience, starting with the environment is the place to start. With the types of clients that I work with and with myself, my version of this illness, what I tend to see is you will throw all kinds of treatments for suspected infections. And it's almost, again, this endless loop. They keep coming back.

And it's only until you start disrupting the right layers that start with the environment, you start bringing – it's not about having a perfect environment. It's just lowering signals from the environment to start allowing the immune system to shift its attention inwards, right? By that logic that I just laid out, what we want is to compel the immune system to start shifting away from what's going out there to what's going inside you.

From that perspective, treating the environment first. Then this is where something like Actinobacteria can come in as a middle step, not as a final destination. If you're someone that has very high Actinobacteria burden in the body, and there's different ways again to test for that, that in my experience seems to be a critical step at lowering the burden, not eradicating. Lowering the burden to then set the stage for the deeper problematic organisms that tend to be tick-borne infections and parasites.

[1:08:23] SCOTT: You recently published a paper in Frontiers in Endocrinology with Dr. Peg DiTulio. Congratulations on that. The paper was titled 'Clearance of multiple antibiotic-resistant coagulase-negative staphylococci is selectively associated with higher circulating α-melanocyte stimulating hormone in patients evaluated for chronic inflammatory response syndrome'. I'm glad you guys picked a simple title.

Let's talk there about what that paper showed. Was there an association with MSH levels in someone that had or did not have MARCoNS in that study? Was everybody in the study MARCoNS positive at the onset? What was the protocol that was used? It looks like those that were MARCoNS positive on follow-up still also had an increase in MSH but not as significant as those who are negative. Why would we potentially see that?

What was the percentage difference of MSH in those two groups or two time points? Did any other markers of biotoxin illness show improvement? And do you feel that the paper supports the statement that “clearing MARCoNS dramatically restores MSH” or not?

[1:09:35] DR. NAVARRO-TORRES: Starting with the last question, no, I don't think the paper makes a definitive support of that claim because this is a correlational analysis. Strictly speaking from a scientific perspective, what we're doing in this study is documenting a correlation that it's statistically very robust. it survived scrutiny from our end. And that has clinical utility as well. But that's as far as this paper goes in terms of making strong claims about causation. I want to lead with that, because it is a limitation of the study. Every study has its own strengths and limitations.

In terms of the study, yes, we looked at 188 CIRS patients working with Dr. Margaret DiTulio, also known as Peg DiTulio at her clinic. And these were all cases of people who had tested positive for MARCoNS at a baseline time point. And around that baseline time point, different assessments were made, including assessments of MSH, MMP-9, and VIP levels in the blood.

And so what was looked at is a follow-up assessments of those exact same markers after undergoing an intervention of MARCoNS treatment for at least six weeks. In terms of treatment duration, that varied from patient to patient. And that's something we couldn't control for because this is an observational study. This is how things just happen incidentally. And we're trying to take a snapshot of that.

And in terms of the specifics of the treatment, it varied also. There were variations of silver, EDTA, xylitol. It depended on the profile of the patient. And then Dr. Peg DiTulio would make decisions as to which combinations to use. That's another potential limitation of the study that we did. It's not a study about an intervention per se. It's all about documenting associations between the markers, specific biomarkers.

And what we found was that number one, as you alluded to, we saw, let's say, improvements, or we saw significant changes in MMP-9, VIP and MSH regardless of whether patients had cleared MARCoNS at the follow-up assessment or not. That's really important because that's speaking to a more general idea that treatment around CIRS, there's something to it. We're seeing these markers normalized.

The one that I was most shocked was the MMP-9. The average was about 800, and it went down to 350, or something like that on average. That's not like an individ – that's a trend over almost 200 cases. That's a remarkable drop. It speaks to treating CIRS. The treatment around CIRS as a real legitimate thing that people should be thinking about very seriously in the scientific world and in the medical world.

Now the additional result that we found, and this was the highlight of the study, is that only for MSH did we see an interaction between presence or absence of MARCoNS and MSH recovery. Meaning, people who had cleared MARCoNS at the follow-up assessment were showing higher levels of MSH compared to those who still had MARCoNS after that intervention.

What this paper is providing when it comes to that particular result is that we should be paying attention very closely as to what does this mean that MSH can fluctuate correlated with microbial activity in the sinuses. Now for us, this might look like a trivial. Finding in the mainstream world of science, this is actually a very novel connection to be made. That things that are happening in the sinuses could very closely correlate with modulations of neuroendocrine activity in the pituitary hypothalamic region.

And the last thing I want to say is, as you pointed out it, is the case that we saw increases in MSH for everybody regardless of the intervention. Now that's important because what that's telling us is there's likely more to this story than just MARCoNS, or at least as to how we're measuring MARCoNS. And we now know, or we strongly suspect that there is more to the sinuses that accounts or that could potentially account for recovery of MSH levels in a clinical setting.

[1:13:52] SCOTT: So Dr. Shoemaker has suggested that the people that may need to treat their MARCoNS are those where MARCoNS are creating polycyclic ether toxins. To my knowledge, the only way we can glean information about that today is from the GENIE. Did the study consider whether or not the subjects fell into the group that had MARCoNS that were maybe producing these polycyclic ether toxins versus not? Might that have shed some additional light on the potential value of treating their MARCoNS or not? And do you think that the existing MARCoNS tests that are available will at some point be able to differentiate those people that should treat versus those that should not treat? My hesitation is so many people get their MARCoNS test. But we don't know whether the MARCoNS is actually a contributor to their condition. And then they're spending months or years doing all kinds of things when it may or may not be significant.

[1:14:52] DR. NAVARRO-TORRES: Yes. And I agree with you. And this is one of the reasons we published this paper, because what we had prior to that was clinical observations that were coming from documented in conference proceedings, not published research or published papers.

Really, the literature correlating MARCoNS and something like MSH, or just symptom severity, symptom persistent is non-existent in terms of published work. It is existent in terms of clinical observations and what some practitioners are seeing. But I think we need that literature to really understand what's going on here.

In terms of MARCoNS, being able to know when it could be potentially contributing and what not. I agree with you that there might be more about staph bacteria that we're not able to measure. And one of the limitations in this study was we didn't really consider things like the patterns of antibiotic resistance. We didn't really consider any other metrics other than you either tested positive or negative based on a sort of strict criteria cutoff. You have two or more patterns of antibiotic resistance in this test. That was a distinction. But there's all kinds of things that we could factor into that to understand. There's also like biofilm activity is one thing, right? And then, of course, there's the big elephant in the room, which is what other potential organisms could be present in those ecosystems.

[1:16:21] SCOTT: Let's broaden the lens then. Since you mentioned that it was correlation not causation, let's consider that the interventions used might have had effects on other organisms beyond MARCoNS. Talk to us a little bit about the MicroGenDX SinusKEY. What are the patterns that you've seen from that testing? Are you seeing any Actinobacteria in the sinuses? Do you see any fungi in the sinuses? Are there potentially a broader list of contributors that will lead to other therapeutic interventions? And how are you addressing the many microbial overgrowths that potentially are found in the sinuses? How do we maintain the sinubiome?

[1:17:05] DR. NAVARRO-TORRES: Yes. And this is this is work in collaboration with different practitioners. I'm going to mention them because I would like them to be acknowledged. Dr. Andrea Jordheim, Dr. Lacey Venanzi, and Dr. Lauren Sparks. These are CIRS practitioners that have all participated in some form or another looking into this and trying to figure out. Because they all knew, there's something more to the sinuses that what we've been picking up on.

The SinusKEY test is a DNA-based test that allows us to quantify the relative abundance of organisms. And it speciates the nasal biome more generally. It's not just looking for staph. We can see anything from fungal stuff, to gram-positive bacteria, to gram-negative bacteria. And so once we started looking into that – by the way, this started with me as a self-experiment. A sample size of one. When I looked into SinusKEY my own results, what I saw was three species of Actinobacteria. Starting at the top with C. acnes or P. acnes as the dominant species. Way too much dominance. Corynebacterium tuberculostearicum is second. And then an unusual – I think it was a Cutibacterium species that's very rare, but was there in low levels. And then staph epidermidis, which is a staph bacteria that could be MARCoNS, but could be just a commensal. That was my entry point. It's like, "Wait a minute. There's more to this."

We started putting together pieces of what if we start doing trying intervention modalities that cater more to Actinobacteria? Because these people still have low MSH. They still have fatiguing metabolic issues. They've been doing treatments. And they just don't move forward, right? And so that's the initiative here. It's not just do you have something like Actinobacteria? It's what's the profile presentation? Are these people stalled? Are they not responding to any of the other treatments? This is what warrants in our heads to start looking more carefully into this.

Actinobacteria emerged as a very primary suspect here as potential problematic organisms when they're too high in the sinus biome, where they're too abundant. Specifically, C. acnes and C. tuberculostearicum. There could be more Actinobacteria participating. We don't know for sure. We're currently doing data. We're looking at different data sets to try to understand those things. But that's what we started seeing with Actinobacteria as a very common organism present in the sinuses of a lot these patients were stalling.

Now, in terms of clients that I work with, I do see sometimes fungal DNA traces. And sometimes it tends to look more like from the environment. Maybe there's some spores. And then they can get cleared out with like rinsing protocols or things like that. But sometimes you do see something that kind of looks like a potential colonization issue.

What's really interesting about that is you do tend to see, or I do tend to see – when I see the profile of fungal colonization, you also tend to see high Actinobacteria activity in the SinusKEY. There's an interesting correlation between those two.

And then the last thing I'll say is there's all kinds of interventions that we're trying to develop around addressing this. We are seeing some results, myself included, again. A sample size where, for the first time, started working around Actinobacteria and lowering those numbers. For the first time, my MSH went from less than 8 to 21. It's also correlated with significant symptom improvement in certain areas. And so there's been all these really good things that happened for me. There's other cases where this has been the case as well, but it's still very early. We're still learning about this.

[1:20:39] SCOTT: So let's talk now a little more about Actinobacteria and endotoxins, which now are said to be 42% and 28% of CIRS causation based on GENIE testing. We've already talked about the fact that even though GENIE now suggests that mold and mycotoxins is only 7%, that you do still see that as more primary. We touched on the fact that you tend to see Actinobacteria as something that happens later in the process in someone who's maybe more compromised.

But once it's impacting a person, how important is it to address the Actinobacteria in order to restore their health? Do we need to focus first on the tigers, and then what some might see more as the secondary contributors will sort themselves out? Does treating Actinobacteria really symptomatically move the needle, or is it more of a prerequisite to then get to later addressing the tigers?

[1:21:34] DR. NAVARRO-TORRES: Great questions. I think it's a little bit of both. In my experience for some cases, it is a necessary prerequisite in order to move forward to doing work like treating chronic infections and parasites, and benefiting from something like VIP. I do think that is on the table for some people.

And also, the thing about Actinobacteria, it's such, I think, a misunderstood organism in general. I'm not just talking about our communities. And I understand why. And I think Actinobacteria, at least human Actinobacteria like C. acnes, they're commensals in our skin. But again, when there's been so much breach with permeability, immune dysregulation, these are organisms that are very opportunistic. And they happen to go for parts in our bodies that are very immune tolerant. That is one thing that's really important to understand. They don't like to trigger the immune system that much. They like to hide and try to get away with as much as possible without causing a lot of trouble, at least obviously.

And one of the things that again I alluded to this earlier that you tend to see with people with very high Actinobacteria burden is a lot of metabolic issues. A lot of what I call the dreaded zombification symptoms. Very low energy, fatiguing. It could be cognitive fatigue, it could be physical fatigue, it could be this zombie-like frozen brain, frozen body. Those kinds of symptoms when they persist and you've been doing CIRS treatment, it usually indicates that there is an Actinobacteria component.

In my experience, the only way I found those things to improve is by working on Actinobacteria, whether it's in the sinuses, in the skin, or a combination environment, skin, sinuses. Maybe even in the gut. And that's something that Dr. Lacey Venanzi and I have been exploring and talking a lot about.

And in that sense, I think of Actinobacteria as the prime candidate for creating that ADHD immune confusion or immune dysregulation profile. It's not necessarily triggering insane inflammatory activity like endotoxins that can trigger sepsis or even fungal exposure. Fungal exposures can be very inflammatory. Actinobacteria to me is much more on the metabolic side.

[1:23:51] SCOTT: Yeah. One of the challenges I think we tend to kind of vilify Actinobacteria and, at the same time, Bifidobacteria is an Actinobacteria, right? We don't necessarily want to be trying to get rid of every Actinobacteria. And a lot of times, when we're using antimicrobials because we think there's something that's more in the pathobiome, we could also maybe negatively impact the microbes that we actually want to be there.

I want to talk a little bit about pH and how the acid alkaline balance comes into the Actinobacteria discussion. Are there certain pHs that create an environment that Actinobacteria is more likely to thrive in? Does shifting the pH of either the body or the skin, does that become another aspect of treating Actinobacteria? Do we want a more acid gut microbiome but a more alkaline blood pH? How do you test for and shift pH in a more health-supporting direction?

[1:24:52] DR. NAVARRO-TORRES: Yes. And I think you're tackling or tapping into something really important about Actinobacteria that's very misunderstood. And we're talking about a specific class of Actinobacteria that are these opportunistic human Actinobacteria, C. acnes and Corynebacterium species. Thanks for clarifying that. But what you're tapping into here is it's less about killing them. It's much more about shifting ecosystems that disrupt their ability to stay opportunistic and to just get away with whatever they want basically.

And so, one of those axes is pH. You mentioned that. And mucosal tissues, including the skin barrier and in the sinuses, the gut, vaginal area. And one of the things that you often see with CIRS is people where there's high Actinobacteria. But also, you'll see other things. You might see fungal issues in the gut. You might see a lot of parasites. It's a lot of alkalinity in the mucosa.

Now, that's different from blood pH. We tend to see the opposite in CIRS. In the blood, you tend to see acidification. And that is one of the potential contributors of the fatiguing issues, and the metabolic issues, and all those things. But in the mucosal tissues, you tend to see the opposite. A shift from more acidity, which is usually these tissues like to have some acidity to excessive alkalinity. And that is a very favorable environment for a lot of these organisms, including some of these Actinobacteria species to just thrive and get away with everything.

The one thing that I want to add to the pH in combination, because this is about ecosystems now, is lipophilic activity. Meaning, organisms like Actinobacteria, specifically C. acnes or P. acnes, they thrive in these lipid-rich ecosystems under the skin, under the epithelium. And that's where they hide.

And so, what we've been learning is that it's more about disrupting those ecosystems and less about is going to kill them. In fact, some practitioners have tried antibiotics that are supposed to get rid of C. acnes, and they don't. Because, again, it's not about infection. It's just about an ecosystem issue that needs to be restored or brought back to balance. And one of the things that we need to do there is the pH rebalancing.

There are all kinds of things that can help depending on the tissue that you're working with. And some of these also have lipophilic activity. The number one thing that I'm going to mention here is Horopito, which is a New Zealand herb that's touted as an antifungal herb. Very ironically, again, fungus and Actinobacteria seem to correlate again. That one of the things that it does is it disrupts these lipid-rich ecosystems. It kind of dissolves, help dissolves these, so that the organism is exposed to the immune system.

The other thing it can help do is acidify the skin. There's a topical version of Horopito that you can apply in the skin and can help acidify at the same time. There are other products like Lume Body Wash. And there's other products that will say they're acidic or pH, low pH. And all of those are supposed to help. They, on their own, may not be enough to move the needle. You may have to do a little bit of additional work. You may have to do a little bit of killing depending on how severe or aggressive the burden is for a given person. For other people, it might just be like just do like pH rebalance, a little bit of lipophilic disruption, and then you're good to go.

[1:28:36] SCOTT: The Horopito conversation was an interesting one that we had before. I actually came to be excited about that through muscle testing using Dr. Klinghardt's system of ART several years ago. I then had a colleague, Dr. Marie Matheson, who mentioned it, who also was very excited. You also mentioned it. I've had some people that have used it particularly that were dealing with high levels, like 27 million Actinobacteria on the skin, and had very good results with it. I personally take the soft gel to kind of balance maybe some potential fungal bacterial things as well. I'm very excited.

And I know people are going to ask. So I think the product that we're talking about is from the company called Kolorex. K-O-L-O-R-E-X, if I remember right. Kolorex.com for people that are interested. I think your recommendation was similar to my observation. More the soft gel rather than the capsule. Am I remembering correctly?

[1:29:32] DR. NAVARRO-TORRES: Oh yeah. The soft gel for – Yes. Soft gel. Yes.

[1:29:37] SCOTT: Endotoxins come from gram-negative bacteria. They can also be a contributor to CIRS. Would you say that when they're present, that those are more primary than opportunistic? What are the common sources that you see in your clients? I know in the lab testing we're generally raising some concern when the levels are 100 or above.

And then coming back to what we talked about earlier, do you think that all endotoxins that could be contributors to CIRS must come from the external environment? Or can they be endogenously created in our own microbiomes and still be a trigger for CIRS? And then while someone is aware of the fact that they have an endotoxin issue but they're still trying to identify the source, would you also then consider an endotoxin binder like cholestyramine or colesevelam?

[1:30:27] DR. NAVARRO-TORRES: Yes. In terms of what role do endotoxins play, I think the jury is still out how to think about endotoxins. But if my educated guess is that endotoxins might also be a little bit more on the side of they become a real, real big problem once you prime CIRS.

I'm not so sure about thinking of endotoxins as priming events again. However, if you have an environment with a lot of fungal burden, and there's a lot of ribotoxin injury, and you have something like endotoxins, they can become a significant amplifier. That's how I think about them. I don't necessarily think in terms of, "Oh, this is a priming event in of itself."

In terms of whether can they play a role endogenously and not just externally, absolutely. I mean, there is again an entire literature on neurodegeneration documenting endotoxemia in Alzheimer's patients and Parkinson's patients. I mean, whether it's coming from the environment or from bacteria, well, it's still the same problem if you're permeable enough in your body.

The problem with endotoxins is more about permeability. If you're permeable, what starts happening is this start crossing into the bloodstream. Our innate immune system evolved to trigger an insanely aggressive innate immune response that can kill us. And that's called sepsis. And it's very specific to endotoxins. This is really about immune overactivation, and then making sure that those toxins remain in the gastrointestinal tract.

The digestive tract is actually meant to hold on to quite a bit of endotoxin activity. And there's studies that show that if you just inject tiny, tiny, tiny amounts into the bloodstream of healthy people, you're going to get things like cognitive dysfunction. You're going to get things like depression, mood dysregulation, and things like that. And that can linger for hours.

I think for me, when it comes to endotoxins, it's more about how permeable is the person. Because if a person is very well in terms of barrier strengths in the skin, in the gut, in all these tissues, they're going to be much more resilient to something like endotoxins. But to answer your question, it can come from both. There's nothing that would say that it's only from the environment. If someone has a compromised digestive tract in terms of permeability, activity from gram-negative bacteria in the gut can be contributors.

[1:32:54] SCOTT: And it's very interesting because you're the first CIRS expert that I've spoken to who has given that some acknowledgement. It's always been a question in my mind. How would the body know the difference? I know there's many different kinds of endotoxins based on what they're coming from, which bacteria. But I've always had that question. And so I'm happy to hear that you think that it's possible that we need to be thinking about those endogenous production of lipopolysaccharides or endotoxins as well.

And then let's go into a little more on the binder piece. And then you can tell me whether you also think that there's a role for cholestyramine, or colesevelam, or charcoal in the endotoxin binder space. But what are your thoughts about natural binders in CIRS?

For the most part, we talk about cholestyramine and colesevelam, or Welchol, that they have a positive charge, where natural binders tend to be more negatively charged. Is charge the only property of a binder that leads to it being able to bind and help remove a toxin from the body? Do you see a role for natural binders in CIRS? And if so, what are some of your favorites?

[1:33:57] DR. NAVARRO-TORRES: Yes, I do see a role for natural binders. I mean, I've done them. I do think the order is very important to pay attention to the order of when you use them. In my personal experience, when I started with charcoal and chlorella, unfortunately that sort of opened a cascade of problems. And I took that as an interpretation that my body was not ready to engage with those kinds of natural binders. That in my case, I needed to start with something like colesevelam, which was more selective for bile sequestration. And not like heavy metals, and chemicals, and everything at the same time, right?

I'm not going to go into a whole lot of details for the sake of time. When it comes to binding agents, it's not just about the polarity. That is one component that defines its ability to pull things out. It's also what's the level of analysis that it's operating at. Meaning, are you actually doing a one-to-one correspondence with the toxin directly and binding that, or are you doing something like cholestyramine and colesevelam, which is more at the level of bile acid. The molecule, the bile molecule is what's being bound.

And within those bile molecules, you're going to have certain kinds of toxins and fragments of microbes that are going to stay or stick there very nice and tight. And then colesevelam and cholestyramine are very good at pulling those kinds of toxins, right?

And in that sense, I mean there's studies that have shown that bentonite clay will bind to things like lipopolysaccharides, right? I think they're operating at different levels in that sense. It's a little bit misleading to equate these as they're all in the same layer. They're doing different things. And from that perspective, to me, they're much more complimentary than anything. And it's all about knowing when to use them and for what purpose?

[1:35:50] SCOTT: I totally agree. I tend to really like the combination of a natural binder with Welchol or colesevelam. And I think that's actually emerged as maybe the better tool, even better than cholestyramine. I know that tends to be a little bit more where the CIRS community is moving. We used to say that it was 20% as effective as cholestyramine. But I think clinically, practitioners in the CIRS community are seeing that colesevelam is actually really good and does move the needle but doesn't have the same level of side effect.

[1:36:21] DR. NAVARRO-TORRES: That's right. And that was my experience. I started and I've stuck with colesevelam. And it tends to have a much better tolerance profile.

[1:36:31] SCOTT: With Actinobacteria and endotoxins, and the clients you work with, how often do you find that they also have a water-damaged building component where they then need to remediate, versus a scenario where there is not a water damage component and maybe the solution to their Actinobacteria or endotoxin has a less invasive solution.

[1:36:52] DR. NAVARRO-TORRES: That is a great question. And I have not thought about that carefully. But I can tell you that I would say about 8 out of the 10 clients that I would see on any given point are dealing with – and there's selection biases here. Let's say that, right? With the kinds of people that are more likely to come talk to me are probably going to have these kinds of problems. This is by no stretch global estimation of any kind. But for me, roughly speaking, 8 out of 10 people that I see on any given moment will have an Actinobacteria component that to me seems clearly to be primarily in the body endogenous.

And so there are people that are definitely in some kind of exposure, and that is a concern. I would not say that applies to all of those eight cases, let's say. Maybe it's like half of that, where we have very clear water intrusion issues.

There is definitely a subgroup of people where – and I'm one of them. Again, I moved into clean environments, and then what would happen is a couple days into that place I start getting sick. And that is a very Actinobacteria fingerprint in terms of a correlated thing. The people who go into a place, it's clean, they're good the first day. 2, 3, 4, 5 days later, they start getting sick. That's a very common thing that you'll see with people with elevated Actinobacteria. You have to be careful and make sure is it really the environment? Is it that they have a lot of burden that includes Actinobacteria, like C. acnes, but could also include things like parasites and just a lot of infection burden that needs to be worked on.

[1:38:32] SCOTT: We know that Lyme and co-infections can be a trigger for CIRS. But I would say historically, Lyme has not been a big focus of the CIRS conversation. Interested in your thoughts on Borrelia, Bartonella, Babesia, other vector-borne infections. If someone has those, does addressing mold illness resolve their vector-borne infections or Lyme disease. Do we still need to address the Lyme components as well? Why do you think there isn't more of a focus on lime in the realm of CIRS? And is that changing?

We know Dr. Shoemaker recently did a presentation talking about his excitement about maybe using herbs for Lyme based on a publication from Dr. Jodie Dashore. Do you think we're going to see more about Lyme in the CIRS conversation? And what are some of your favorite tools for vector-borne infection remediation?

[1:39:24] DR. NAVARRO-TORRES: Yes. I think the main problem with chronic infections of the nature of Lyme, Bartonella, Babesia, and so on is testing. It all comes down to testing. the testing modalities that we currently have available are not great. And this is actually true, by the way, for parasites, too. This is another category that's very tricky to get a reliable testing result.

What I think is happening is there's actually more false negatives, meaning people often come back with negative results for these kinds of infections when in fact they do have something there. And hopefully, we'll figure this out in the next couple years in terms of thinking of better testing modalities.

But often, practitioners that do look at this are forced to rely on symptom patterns doing do no harm, interventions with botanicals, and see the response and the recovery pattern. I had to do this for myself because I'm one of those people. And I think that's the fundamental problem. And so there are practitioners that don't feel comfortable moving forward with a false-negative situation. And I don't blame them. This is not an easy situation to navigate. And other practitioners feel more comfortable.

That creates a situation where I think what's happening is the prevalence of chronic infection in that category, in the CIRS population, is probably much higher than what has been acknowledged. I'm hesitant to say specific numbers, but I wouldn't be surprised if half of the CIRS population was dealing with this, at least.

[1:40:59] SCOTT: I mean, I definitely feel like those people who have chronic Lyme and have treated for years and aren't making progress, that mold and mycotoxins is almost always a piece of the conversation. Sounds like the reverse is also potentially true. If they've been working on mold and mycotoxins, they're not getting better. Maybe exploring these different microbial burdens is important.

Some of us would argue that Bartonella is possibly the most significant of the three Bs, Borrelia, Bartonella, and Babesia. I'm seeing more conversation where some practitioners are maybe shifting to thinking that it's Babesia. I hear others still saying that Borrelia is the kingpin. What have you observed? And then have you seen that when one is present, there's a high probability that two or three are present? I know Dr. Bob Mozayeni recently has talked about the fact that when Bartonella is present, Babesia is almost always there. When Babesia is present, Bartonella is almost always there. What are your thoughts on that?

[1:41:56] DR. NAVARRO-TORRES: Yes, I agree. I think it's more likely that if you have any of those, there's a chance that at least there's a second player that's significantly contributing. In the context of CIRS, the CIRS population, the signal that tends to stand out the most as clinical observation is Bartonella. Bartonella.

For example, you will see cases with elevated VEGF instead of low VEGF as a blood marker for CIRS. And it's chronically elevated. I'm one of them. My VEGF was at one point over 400. I was a little bit worried, because I was thinking is there connected to cancer or something like that. And that started to go down when I started doing botanicals cater for Bartonella. And so these are one of my correlates that the group of practitioners I've been working with we've been using to track this correspondence.

But Bartonella is, to me, the one that stands out the most in this population. People who have a lot of the more Lymey presentation tend to have more like chronic pain in the body, moving pain. And maybe they feel more flu-like. The Bartonella patients tend to present with more neuropsychiatric issues. Babesia patients as well. That combination of Bartonella, Babesia. I see it quite a bit when I work with people.

[1:43:19] SCOTT: Yeah, definitely agree. I think Bartonella is the more significant of the three. But for some people, Babesia as well can be very significant triggering hypercoagulation and other things that we see as well. How do you view the chronic virus conversation in terms of their role as a contributor in complex chronic illnesses? Are they more opportunistic and reactivate under certain conditions? Are they more drivers? Things like Epstein-Barr virus, Cytomegalovirus, Varicella, other herpetic viruses, are those primary or secondary contributors to illness? And do you see a need to support the body in mitigating some of those viral contributors specifically?

[1:43:59] DR. NAVARRO-TORRES: I think before experiencing CIRS, they could absolutely serve as a priming event. I don't see why not. It couldn't be a component of adding stress or amplifying the priming event signal in combination with something else like water damage exposure. I think that's absolutely possible.

And I think once you had CIRS, in my experience, I don't tend to see a lot of viral reactivity issues that seem to clearly say if you don't work around that, you're not going to get better. In some cases, those things seem to self-correct with other treatments, like treating things like chronic infections, like the ones we just discussed, or any of the other entities that we've discussed.

In other cases though, there are people that have had very aggressive viral activation to the point where there is structural issues in the spine or the discs, in the spine connected to that viral reactivity. And so there's cases like that, but it's not the most frequent profile that I see. I think they can contribute to burden. I think of them more as secondary once, something like CIRS, has been turned on.

[1:45:19] SCOTT: Parasites are another area that you've mentioned already. Some people think that everything is explained by a parasites. Others don't believe parasites play any role in chronic illness in the United States particularly. They think of it more as something you have to travel to acquire. Where do you stand on the potential contribution of parasitic infections to either CIRS? Or maybe not to CIRS, but to the more complex chronic illness landscape? Is it that the parasites are shifting the immune balance in a direction that allows other organisms to become more entrenched, meaning shifting us more towards Th2 dominance? And if you do find parasites to be part of that landscape, what are some of the tools that you're using both in terms of testing and treatment?

[1:46:04] DR. NAVARRO-TORRES: This might be a bit of a hot take or controversial take at least in some circles. I think when you're looking at a very hypersensitive patient with CIRS, you're looking at a patient with massive parasitical burden. This is a hypothesis. I'm happy to just put it as a hypothesis and to be proven wrong. But I start thinking about that because that's what I've had to go through.

I think parasites are probably the big enablers. Meaning, once they start taking over, other things come downstream. We could even put Actinobacteria potentially there. Again this is more of a hypothesis observation. I'm not basing this on published research. I am basing it on mechanisms, plausible mechanisms. I know what parasites can do to the immune system. And they can very much actually influence things like the GENIE. Some of these markers in the GENIE could be influenced by certain kinds of parasites.

In terms of testing, again, testing is notoriously bad. And Scott, you might have some suggestions of your own. One that I've worked with quite a bit, and Dr. Lacey Venanzi often uses, is from parasitetesting.com, this CSA test. It's a culture-based test. And it will culture parasites, and it will culture things like fungal issues and Actinobacteria. I've actually seen some Actinobacteria in there.

[1:47:32] SCOTT: I think that's Dr. Omar Amin's lab. Is that right?

[1:47:34] DR. NAVARRO-TORRES: Yeah, that's right. That's right. That is one test. And I think someone like Dr. Venanzi, what she would do to use that test is to do a first collection maybe 2 days prior to the full moon. Then wait about one day after the full moon to do the second collection. That is a testing method. It's not bulletproof. You still run into what I think are false negatives.

In my experience, what I've seen work a lot for myself included, tinctures in the category of black walnut, wormwood, and clove. Very amazing combination At some point, I think if the burden is too much, I think for CIRS patients, they should consider talking to their doctor about doing a rounds of ivermectin and one of the albendazole or mebendazole. Probably albendazole. And consider doing cycles of that. I've seen people, like myself, where once we started doing that in the right order, "Oh my goodness," big healing moments start happening.

[1:48:32] SCOTT: Yeah. I think probably my favorite is Dr. Raphael D'Angelo with ParaWellness Research is another tool. But I think the one that you mentioned is great as well.

Talk a little more broadly about the gut in terms of these complex chronic conditions. How does it impact immune regulation? What role does the microbiome play? Do you have any favorite tools for looking at the pathobiome or microbiome? Is it fairly common to see that CIRS patients also have SIBO? And what are some of the things that you're reaching for in exploring the gut and its contribution to complex chronic illness?

[1:49:07] DR. NAVARRO-TORRES: Yes. Gut issues, very, very prominent in CIRS at large, especially in the kinds of clients that I see that are the hypersensitive, high Actinobacteria. If you're seeing something like high Actinobacteria, C. acnes, or Corynebacterium burden with low MSH in the sinuses, chances are there's a lot of work to be done in the gut. These people tend to have the most – and then parasites. A lot of food intolerances, a lot of histamine issues connected to perhaps mast cell activity in the mucosal tissues.

Just to share a little quick story, when I started doing nasal spray called Beekeeper's Max, the Max formula that has eucalyptus and propolis in it, it was meant to start catering more to the Actinobacteria burden that I had in the sinuses. Within two weeks of just doing that, my histamine gut issues went away about 60%.

The one thing I want to say, I'm trying to allude to with that, is these ecosystems and systems, the gut and the sinuses, very interconnected. They influence each other. And then there's the brain component also, the neuroendocrine signaling. And once you've had those systems breached, you have to work on them. In my experience, let's look at the sinuses. Let's try to address that and then work downwards, right? That is kind of the order of operations that I tend to see work well for people like me, essentially.

In terms of testing, DNA testing, that's either Shotgun or 16S. And these are different methods. DNA-based methods. This would be things like Ombres stool testing, or Tiny Health, or NirvanaBiome. And this is all coming from, again, Dr. Venanzi, who's really the person here that works in the gut. These kinds of tests are really equipped to be more sensitive to the distribution, the biome distribution that's going on in the gut. With some of the other tests, the signal and the sensitivity is a little bit more overplaced because of the methods that they're using.

[1:51:14] SCOTT: Let's talk about another controversial topic, which is the potential for fungal colonization. The potential for yeast and mold to be thriving in the body. Some say the person can become the moldy building, become colonized in the sinuses and the gut, become a mycotoxin-production factory. I'm wondering what you've seen in terms of fungal colonization. Have you seen value in using antifungals in some people? And have you also found that some antifungals may impact organisms beyond fungi?

[1:51:47] DR. NAVARRO-TORRES: Yes, there are cases, documented cases of CIRS patients feeling amazing with antifungal medications, at least on the subjective front. There's documented cases of that. And I know that there are concerns in the CIRS world around the use of antifungals, rightfully so. There are some metabolic concerns. There are concerns of if you have already pre-existing atrophy and all of these issues. Whether that can worsen it. And there are good mechanisms to explain that concern in addition to other things. Those are all founded. But we still need to reconcile the discrepancy with what we're seeing with some cases, right? Why are some people getting better?

And I think the idea that I would like to introduce here for people to think about for practitioners is that antifungals are not just tackling fungi in the body. Now, in some cases, that might mean, yes, there is a fungal overgrowth or overload in the body, and that is tackling that. But in other cases, it might be doing other things. And one of the things that at least some antifungals can do pretty well is disruption of these lipid-rich ecosystems, where something like P. acnes loves to thrive and hide.

Disruption of these systems is one of the things that antifungals can be doing. And you want to be thinking or considering the possibility that these antifungals may sometimes be working at a level of systems and not at the level of kingdom. I think it's an important thing that practitioners should just think about when they're tackling a patient under their care. So, yeah.

And I'm not particularly against or for; I do think there are cases of people. I mean, I had a lot of fungal issues at the beginning from the outside. And they have gone away over time with different treatments. Some of it seemed downstream to me, like just taking binders. A lot of these fungal rashes would start to go away. I'm not sure how to think about that personally. I'm very agnostic and open about how to think about the fungal piece. There are people who clearly have some kind of fungal issue going on. We see it sometimes in the nose. Sometimes you'll see evidence in the gut. But whether the treatment is exclusively targeting that or not, I think that's something that we need to keep talking about.

[1:54:06] SCOTT: I think it's also important to separate the conversation about potential concerns around itraconazole, and whether or not fungal colonization can exist, and maybe then warrants treatment but with something else. Just because we have concerns about fluoroquinolone antibiotics maybe having more risk than reward, and maybe we don't use them as much in Bartonella treatment anymore, it doesn't mean that we don't consider Bartonella as a potential contributor to complex chronic illness.

[1:54:39] DR. NAVARRO-TORRES: Right.

[1:54:39] SCOTT: Right?

[1:54:40] DR. NAVARRO-TORRES: Yes, I agree.

[1:54:41] SCOTT: Just curious as we start wrapping up, what have you seen that's changed since the pandemic, SARS-CoV-2, spike proteins? Do you think that these conditions are more driven by the persistence of SARS-CoV-2 by spike protein as a toxin by the unmasking that happens of things like EBV, Bartonella, Mycoplasma because of the immune dysregulation that happens? What are you seeing in the population of long-COVID?

[1:55:10] DR. NAVARRO-TORRES: I think for me right now, there's a lot we don't know or understand about COVID. I know there was an initial idea in the CIRS community about COVID being some kind of biotoxin. I think COVID to me, based on what I've read in the literature, seems to be more likely to act mostly as a priming event.

We go back to my story at the beginning. I mean, I never tested positive for COVID. I never had the classic COVID symptoms. And I was testing for a whole year while I was in isolation. But I still think I came into contact with COVID on campus. And that was enough to set or prime my immune system and be like the last straw where my body said, "Enough. I can't deal with this anymore."

I think in the context of CIRS, to me it's more likely to act as a priming event and creating a lot of dysregulation. And then suddenly, people start becoming sensitive to things that they were not sensitive before. And I think a lot of people talk about vaccine shedding. And there's something physiological experiential about that. But it could be something like Actinobacteria shedding, and that the system is getting out of balance. And now, suddenly, everything is becoming very dysbiotic, and now you're very sensitive to that. Again, these are just speculations. But I think COVID is more likely to operate in that in terms of a dysregulator of systems, including the immune system.

[1:56:38] SCOTT: Does that dysregulation of the immune system allow for more latent Bartonella infections or EBV infections to become activated?

[1:56:47] DR. NAVARRO-TORRES: I think so. I think so. It opens the door for all kinds of imbalances.

[1:56:52] SCOTT: One of my bigger areas of interest for many years has been the coagulation topic, hypercoagulation, fibrin accumulation. We know that Dr. Shoemaker talks about coagulation. And there's a section on the GENIE as well. What role do you see coagulation having in CIRS, in complex chronic conditions? Are you looking at anything like prothrombin fragment 1 and 2, thrombin/antithrombin complexes, any of those? How important is exploring coagulation as a potential symptom driver where we're getting less nutrient and oxygen delivery to the cells, we're getting impaired waste removal? Is that a big player or a little player from your lens?

[1:57:31] DR. NAVARRO-TORRES: It is a big player in terms of severity of the illness and burden, symptom burden. And I'm one that has had to deal with that. It's pretty scary. You see your arms, and they're all bruised up for no reason after walking into a grocery store or something like that.

It is I think a very serious issue that needs to be on the radar for everybody, because part of it is long-term. If you're in the side of microclotting, that can start creating increased risk for clotting-related or vascular disease. And that could include some forms of dementia or neurodegeneration. Or that could include strokes. There are cases or people that I've worked with that they've had history of strokes. Yeah, it is something that you want to – if there's presentation, you want to look into more carefully, because it is one of the main systems that become disrupted in CIRS. The clotting sequence, or the clotting cascade becomes massively disrupted.

In terms of, yeah, testing, you mentioned all these different tests that I think you should look at. Von Willebrand's panel is another one. Cardiolipin. And all these different things. And GENIE can sometimes give you a lot of information around that. Now, the next question you should be asking is, "Well, if the CIRS treatment, the basic CIRS treatment is not addressing that, what's driving that?" And it could be something like a Bartonella component or Babesia, because they put massive stress on the endothelial system, right? There's all these questions that you have to start asking.

[1:59:06] SCOTT: Yeah. And I see heavy metals as a trigger for coagulation as well, another player. One of the other topics that we maybe don't talk about much in the CIRS landscape is mast cell activation syndrome, histamine intolerance. Do you think that's playing a role as well? Do you find that some people need to reduce their histamine, let's say dietarily, then stabilize the mast cells? And potentially then work on the triggers like the mold, or the parasites, or the EMFs, or the Bartonella? How often does that play into the people that you're consulting with?

[1:59:38] DR. NAVARRO-TORRES: And I'll speak for myself because I think I'm just the best example for this. I went to the ER several times due to anaphylactic-like reactions from foods, from things in the environment. What I realized, for me, it was less about the food in of itself. More about what environment am I eating or consuming this food in. Or from what place is this coming from? I started realizing that that was a big antecedent for my histamine flares. And if I ate that same food in a environment that felt much cleaner, maybe I had a little bit of a histamine response, but it wasn't anywhere near as it would be if I was eating that in this other location. For me, histamine support was absolutely necessary. And yeah, there are a lot of patients that deal with that.

And I would say MSH and MMP-9 are two markers that are correlated with modulations of histamine response. We actually have some data from, again, Dr. Peg DiTulio's data set. Not published. But we presented it at a conference, CIRSx. What we find, we see these interesting correlations with people who are very aggressively treated for histamine over the years. And their ability to recover MSH, their ability to see lower MMP-9 levels and things like that. I think it's absolutely important. And ultimately, in my experience, if getting out of exposure doesn't correct it, you're again thinking of maybe some kind of infection or colonization burden.

[2:01:10] SCOTT: The MMP-9 correlation to mass cell and histamine issues was discussed by Dr. Raj Patel and Dr. Talia Hale clinically many, many years ago. I'm excited to hear that that's now from more research and more clinical observation appears to be a real correlation. And that that's something that we're looking more at.

With the broad community of people with CIRS that you've consulted with, how often do you find that you have to expand the exploration beyond the 12-step CIRS protocol to achieve a full recovery? And when you have someone that doesn't fully recover and they've gone through those steps, what were the top items that you later identified where they needed some additional treatment to help them achieve a more complete and more durable recovery?

[2:01:58] DR. NAVARRO-TORRES: Yes. I would say almost everyone that I work with falls in that category. It does not mean that CIRS treatment or the protocol by Dr. Shoemaker does not work. It does. I think we just want to think about what it actually is meant to do. It is an entry point foundational framework that helps you understand steps that are really critical following a sequencing of steps.

Now, in the kinds of clients that I work with, they have a lot of hyper sensitivity. They're very complex people. And those people often – yeah, those 12 steps. Bare bones are not going to be sufficient. Again, there's going to be probably a lot of work around infection and colonization burden. And the three things that I tend to see stand out is high Actinobacteria burden, a chronic infection, most often Bartonella, and then parasitical stuff. And parasites tend to be at the end of the tunnel for a lot of these people in terms of more later stage. And they start to feel, myself included, where actually things are working.

And in that scenario, to me, the critical thing is to make sure you're addressing that third step of the Shoemaker protocol. I think of it more as addressing the sinuses. Whether it's MARCoNS, whether it's Actinobacteria, whether it is something else that's contributing to MSH, I think the sinuses are the most privileged and important body part in a CIRS patient because that's what starts creating all the activity in these parts of the brain that then generate all these multi-system problems for a patient.

If you win that battle, you start regaining control over everything else, and then you can start working on everything else. That's the sequence that I've seen play out best most of the time. And then sometime after that, I think bringing in something like VIP makes a lot of sense. Engage much more in repair and healing once you've done some of that work.

[2:04:03] SCOTT: My last question is the same for every guest, and that is what are some of the key things that you do on a daily basis in support of your own health?

[2:04:10] DR. NAVARRO-TORRES: In support of my own health? Well, I certainly try to live a very CIRS-conscious life while still allowing for normal life to take place. I have my own routines for cleaning once a week that are kind of catered towards the things that have worked well.

I travel with an iAdaptAir whenever I do traveling. Little things like that. I have an air tamer that's a little ionizer device that I travel whenever I go to public places. And I'm not going into these places out of fear. It's just more informed decision making of understanding what are the things that will keep my body working optimally.

And I'm still in treatment. So there's work to be done. I'm still doing parasite treatments. I still do some binding. And, yeah, I'm still working in the gut and things like that. I will say this is going to come from a bit of a curveball. I think as you start moving forward, what's really important is really be very intentional about reintegration in your life. It's a super important component. You do all this work for the physiology, which is absolutely necessary.

Along the way, you have to introduce a lot of corrective experiences back into your life. As you're lowering these signals, whether it's parasites, or whatever colonizer infection, and you're out of exposure, you have to do that for the healing cycle to really have resolution in its entirety. I am trying currently to live a life where I'm practicing those things in all kinds of different ways. I have my own ways of doing that.

[2:05:48] SCOTT: Amazing. We'll put a number of links in the show notes to CIRS Lab, also the CIRS Research Foundation. You recently launched a podcast called the Coherent Health Podcast as well. So we'll make sure people have access to that. This was such an amazing conversation. I think you're doing amazing work. I love that you're open-minded. And maybe another way to say that is curious and continuing to look for all of these connections.

I think you're very heart-centered and highly intentioned, and really wanting to make a difference in helping people. I honor you for all the work that you do. And just really appreciate that you're a resource for people, and just loved connecting with you. Thank you so much.

[2:06:29] DR. NAVARRO-TORRES: Thank you, Scott. I appreciate it.

[2:06:32] ANNOUNCER: Thank you for listening to today's episode of the BetterHealthGuy podcast. You can learn more about today's guest, including relevant links and resources in the show notes. This podcast may provide community discounts and occasionally share links from affiliate partners. You can find this and other episodes on YouTube, Spotify, Apple Podcasts, Amazon Music, iHeart, and more. To learn more about Scott's personal journey to better health, visit BetterHealthGuy.com. Join us next time on the BetterHealthGuy Podcast.

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