Episode 30 - Dr. Ritchie Shoemaker's Response to Our CIRS Concerns

Dr. Ritchie Shoemaker  has devoted his career to unveiling the complexities of Chronic Inflammatory Response Syndrome—caused by exposure to damp buildings, cyanobacterial blooms, dinoflagellates, spirochetes, apicomplexans, and recluse spiders: among others.

Dr. Shoemaker began the first biotoxin illness practice in the US in 2002, and has treated over 10,000 patients with CIRS illnesses. His non-profit research group, the Center for Research on Biotoxin Associated Illnesses, has raised over $2,000,000 for private funding of academic research. As a medical expert, Dr. Shoemaker has testified in over 200 cases.

Shoemaker’s research has led to the publication of 11 books, several book chapters, and over forty peer-reviewed publications. His discovery of the role of VCS, HLA, MMP9, C4a, C3a, VEGF, TGF beta-1, NeuroQuant and several other biomarkers are widely used by healthcare practitioners across the country. Dr. Shoemaker has been training and certifying other healthcare providers since his medical retirement in 2012, and his lecture series now extends to Proficiency Partners through a 27-module training course and exam.  Dr. Shoemaker has been instrumental in bringing the academic research basis for CIRS illnesses to the public via their website www.survivingmold.com.

In this anticipated episode, listeners learn about the new data and methods of measuring Chronic Inflammatory Response Syndrome (CIRS),  what illnesses CIRS entails, what this means for mold experts, and the importance of the original evidence of mold at ground zero for CFS. Added to the episode is a post interview Q&A with our audience members.

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Transcript

Alicia Swamy: 0:06

Welcome everyone to our podcast where I, Alicia Swamy, Kealy Severson, and Erik Johnson are exposing mold. Today we have the founder of biotoxin illness, CIRS, Dr. Ritchie Shoemaker. Dr. Ritchie Shoemaker is a 1973 of Duke University and a 1977 graduate of Duke medical school completing a family practice residency at Williamsport Hospital in 1980. Dr. Shoemaker began his rural primary care family practice in Pocomoke, Maryland in 1980, where he lives today. Beginning with the outbreak of Pfisteria human illness syndrome in 1996. Dr. Shoemaker has devoted his career to unveiling the complexities of chronic inflammatory response syndrome caused by exposure to damp buildings, cyanobacterial blooms, dinoflagellates, spirochetes, and apicomplexans, and recluse spiders among others. Dr. Shoemaker began the first biotoxin illness practice in the US in 2002, and has treated over 10,000 patients with serious illnesses. His nonprofit research group, the Center for Research on biotoxin associated illnesses has raised over $2 million private funding of academic research. As a medical expert Dr. Shoemaker has testified in over 200 cases. Shoemaker's research has led to the publication of 11 books, several book chapters, and over 40 peer reviewed publications. His discovery of a role of VCS, HLA, MMP9, C4a, C3a, VEGF, TGF beta-1, NeuroQuant and several other biomarkers are widely used by healthcare practitioners across the country. Dr. Shoemaker has been training and certifying other healthcare providers since his medical retirement in 2012. And his lecture series now extends to proficiency partners through a 27 module training course and exam. In collaboration with Dr. James Ryan, Shoemaker is applying the once arcane field of differential gene activation to the primary care of CIRS patients. Dr. Ryan's discovery of the role of hypometabolism and CIRS was a hallmark finding that underlies other chronic fatigue illnesses including CFS, fibromyalgia, and post Lyme syndrome. Dr. Shoemaker has been recognized by Who's Who in America for their distinguished career Achievement Award in 2018, and was additionally awarded Maryland's family physician of the year for 2001. Together with Paul Taylor and Debbie Waidner, Dr. Shoemaker has been instrumental in bringing the academic research basis for certain illnesses to the public via their website, survivingmold.com.

Kealy Severson: 2:35

Hi Dr. Shoemaker.

Dr. Ritchie Shoemaker: 2:37

Well, good afternoon.

Kealy Severson: 2:38

I know you don't know me, but my name is Kealy Severson.

Dr. Ritchie Shoemaker: 2:42

Well, I'm pleased to meet you.

Kealy Severson: 2:43

Thank you. You know, I just started this page exposing mold kind of on a whim over a year ago in February because I had been mold sick, I didn't really know that much about it. I'm an acupuncturist and herbalist by trade, but we did not learn anything about mold illness or injury in school at all. So when I started to suspect it was causing symptoms, my first thought was, I'm being paranoid. And then I just had this nagging voice in my head that said, exposing mold, exposing mold, exposing mold, so I just went ahead and registered the domain website and started a Facebook page and wouldn't you know, Dr. Shoemaker, 30 days after I did that, I actually exposed mold hidden again in another rental. So I started talking about that quite a bit publicly. That's how I encountered Erik, just from talking about mold publicly. And so I'm really honored that you agreed to speak with us and I'm thankful because I know that you have a special place in Erik's story and Erik's history. Thank you so much for being here today. Dr. Shoemaker, you were the first person to look at the original evidence of chronic fatigue syndrome from a biotoxin perspective. Other researchers who revisited chronic fatigue syndrome only looked at viral causes. We know that rules of science, science 101 say we always go back to the beginning. And it seems that some people either do not know the rules of science, or deliberately break rules of science. So we thank you for being the first doctor to look at the historical evidence and acknowledge Stachybotrys at ground zero for chronic fatigue syndrome. You were the first person to validate Erik's story of Stachybotrys at ground zero for chronic fatigue syndrome and Erik's story is in your books and also mold is in all of your books. We appreciate that you've been the only doctor to adhere to the basic rules of science because we do not want to see things of the past depressed. Nor do we want to see doctors and researchers fighting to keep these things unsolved. This is why we value and appreciate that you were the only person to acknowledge Stachybotrys at ground zero for chronic fatigue syndrome in your books. Historically, we see power struggles in science when a doctor takes over a definition morphs it into whatever they want, and then attempt to take that definition and press it upon the original. Chronic fatigue syndrome was and is a research instrument created by Gary Holmes in 1988. And interestingly enough, the signs and symptoms, in fact, were lifted out of Erik's own medical chart. On one hand, Erik is known for mold avoidance and there are active opponents who criticize this and say it's not based on data. And technically, since we haven't gotten some research that we need, this could be true, but we know that many people use mold avoidance, we see people giving advice on moving tents away from houses. We know that when you were seeing patients, you had to use a fan to blow the air away so that it didn't bother you. And on the other hand, one listener actually shared with me, their hopes for our talk would be to prove that there are numerous bio contaminants in water damaged spaces that are capable of contributing to CIRS, which sometimes manifests as chronic fatigue syndrome. Research on one does not negate research on the others. This conclusion confuses me because we know that CIRS is not the same as CFS. Erik did not get bit by a spiderm nor have chronic inflammation from Accutane medication, nor stress. It was specifically Stachybotrys that was found. This seems to me CFS is still its own syndrome, with its own original data set to still be solved. To sat the opposite, that CFS which came, first is now a subset of CIRS seems like reverse logic. My questions to you are, what data is being used to rule out mycotoxin exposure in gene activation now that CIRS research is leading to gene activation via actinomyces and does this invalidate the original evidence of mold at ground zero for chronic fatigue syndrome?

Dr. Ritchie Shoemaker: 6:56

Well, thank you. I listened carefully to your question. And I think we can set that answer up as a goal. I did want to start with some some definitions just to be sure. Alicia very kindly told me we simply want to address the new sister science, we looking forward to hearing your views and learn what this new evidence means for people with a CIRS diagnosis. The question from Kealy is well stated and deserves ample time to flesh out the complexity of the answer. Specifically, I want to start with a case definition for CIRS because some people are defining CIRS one way and some another and the definition will show a limiting perspective on answers to just fungi is no longer something that we can really do. Now the evidence is here, basically CIRS as a chronic multi system multi symptom illness is characterized by exposure to the interior environment of a water damage building that WDB with resident toxigenic and flamagenic microbes, including but not limited to filamentous fungi and this is where Stachy comes in, gram negative bacteria, that's where endotoxins come in, and actinobacteria they used to be called actinomycetes, as well as inflammagens, including non limited to hemolysins, mannans, and beta glucans. As far as I could find, among others. And in fact, if you look at the consensus statement from the CIRS Academy apart of surviving mold, there are 32 different entities that are listed as causing inflammatory responses following exposure. The difficulty is that we rely on observations and we rely on biomarkers. So that's a lot of blood tests. It's a lot of echocardiograms, there's a lot of NeuroQuants, it's a lot of transcriptomics. And we have about 25 biomarkers. My friends in the chronic fatigue world have none. So I don't consider a CIRS, chronic fatigue be a subset of CIRS. I'm not sure what Chronic Fatigue is. I hear it called SCID, I hear it called CFS/ME and when we have disparities in definition, and we're going to have disparities in thinking, disparities in logic, and disparities and treatment. So those are the differences that I see is first, first glance, what's the real issue is that I'm going to try and make the point today that the data that I rely on is about 45 papers, 14 books, and of those 12 papers have been published since 2015, and 10, since 2018. So this is a mother lode of assortment of information that, quite frankly, could be a tsunami of drinking through a firehose, so to speak, if someone tried to digest all this once. We have three books, including a textbook that was published last year, so that one's not available for free. I think it's $24. But if you wanted to access a textbook, Dr. Andy Heyman and Scott McMahon who is a physician in Roswell and I have written that book, we also have a book on an eight transcriptomics primer and then there's frequently asked questions as well. So there's, there's a bunch of material out there to be looked at. But a lot of the upheaval, and I call it turning over the applecart in the mold world that I see and I'm not part of your Facebook group. So I'm seeing a bias point and point of view is that I am not saying that mold is not a problem. Mold certainly is. But when I wrote Mold Warriors, and there was a picture of Erik on top of Mount Whitney, still, I've got that in my office, he looked younger than I have not aged a bit, just the gray hair that's all. But it was was mold, it's all we knew. We knew Stachy and a few other things, if you instill it in the trachea of a mouse and a rat, bad things happen. We could find these things, through tape lifts, we could do culture, and variety of things. But the cultural methods were not giving us the right answer as to what kinds of fungi are present in a water damaged building. That had to wait until we have next generation sequencing. Now we can see it's not just five species of toxigenic fungi, it's 500. And Stachy doesn't get all the attention as it used to, because there are other things that we now know are bad as well. Actinomycetes and actinobacteria are not new to this case definition. I read it to you. That was my base case definition in 2003. First paper on actinobacteria was in 2001. And people knew these things were there. But they didn't have the mechanisms and the technology to identify presence of actinos. We didn't have the methods and the ability to identify bacteria making endotoxins We barely could identify endotoxins. But now we can identify all these things, we are able to suffice the answer of what is specific causation. Now that we've got specific causation, we don't have 32 different elements swirling around in an amorphus vortex inside the teachers lounge. So there Truckee high school that Erik observed, I think his observations were correct. I think there's more to it, whether there was cyanobacteria in Lake Tahoe or not, I don't know. But in the sense that we if you find fungi, you're gonna find actinos, and if the AWS activity water is over 0.9, you'll find bacteria making endotoxins as well. The difficulty in having marveled at how Erik is able to figure out how to make himself feel better and avoid a lot of the terrible things he went through. The book, the chapter he wrote for Surviving Mold was good. I still like the one he wrote for the Mold Warriors better myself, but I was just my own thoughts. But basically, he figured out a way to avoid exposure, but then something would go wrong with his pickup truck in the back, was it a deacon module or something he called it, I forgotten.

Erik Johnson: 12:46

Mobile environmental control unit.

Dr. Ritchie Shoemaker: 12:48

I knew you'd be there. But basically, there were times that you knew that you were now being sickened by the safe environment and you thought there was mold present, I thought it was mold present, I didn't know any better. Now I'm looking more at the likelihood that human habitat derived actinos were seeded through your skin or somebody else's skin as well and created an environment in your mobile decon unit or whatever I'm supposed to call it. But that's speculative because we haven't done testing to know that.

Erik Johnson: 13:18

When my MECU, my mobile environmental control unit went bad, because that wound up in Surviving Mold, how Erik is facing some current health problems. So you know, it's, his most avoidance is not perfect, even though I tried so hard by building this custom built camper. Well, after the book came out, actually, within months, actually, I found out that the problem was in my refrigerator. The RV refrigerators are built with foam injected into a cardboard former and that served as a great substrate for guess what? Black mold. So it wasn't, it didn't look to me like actinomycetes, it looked like black mold. And I was able to remediate it, I found it, I isolated it, I got it out, and I fixed my my camper. So there again, my problem was not with some kind of soil bacteria, it was with black mold.

Dr. Ritchie Shoemaker: 14:14

Specifically, if we look at and here's the quote, this is from a paper in National Resource Archives inn February of 2021, scientific disciplines depended on accurate and analytics invariably evolved, that's where we are, due to advances in technical aspects of measurement, okay, and disciplines in which adequate measurement is not available for applications to public health policy. That's where we were. The impact of new paradigms, that's where we are, and measurement can extend far beyond scientific thought. Both of these concepts apply to the effects of exposure to water damaged buildings on human health. What causes the putative illness and what governments should do to make building safe to use have been impacted by development of molecular methods particularly next generation sequencing, or NGS, and transcriptomics. The impact of human exposure to actinobacteria for example, and identification of immune reactivity specific to these bacteria, are now revolutionising one, both detection and quantitation of newly recognized pathogenic organisms and two, the approach to the genomic basis for diagnosis and treatment is manifested by differential gene activation. When I was in Tahoe in 2009, in Reno with a chronic fatigue meetings, I met Erik, had a great time at a casino, didn't gamble, I didn't lose any money, but it was fun. But what we were there was talking about the state of the art which is transcriptomics, in my dreams. We talked about symptoms, visual contrast, and proteomics. That's all we had. And people saw the researchers from Florida ran away when we came across them and tried to hide because they couldn't they couldn't get away Erik and let him go. But basically, where we are now is differential gene activation, and we are making more advances by the day. Next generation sequencing permits quantitation of exposure and confirmation of risk, ah, prospective word risk associated with threshold of exposure. Ah, we now can determine threshold of exposure using defined human health biomarkers that in turn led to the advances in metabolic. Here's the big deal, Erik and I know in 2000, the metabolic complications are ones we published last year, in September, they are real. That was what brought the attention to actinos to my mind, but basically the metabolic and inflammatory issues and water damage building cancers, both from molecular hypo metabolism and nobody heard about molecular hypo metabolism until Jimmy Ryan published that in 2015. We brought forward discussion of ciguatera, another one of the uncommon CIRS, by the very virtue of the we thought would make people less worried and less argumentative and less concern about controversy if we talked about ciguatera. So ciguatera was our first. But then what came were mold problems, and treatment with VIP at the end of the treatment protocol in 2016. So those were the foreunners that led to us to transcriptomics. Now in preparation for today's talk, I looked to see yesterday afternoon, how many people we have that are untreated, who have CIRS, it's over 1000, and of those 48% showed positive for the specific biomarkers for actinomycetes. That's a little higher than what I've reported before 32%, where we're looking at at endotoxins. Right around 10%, now, we're good a little better than 7%, our simple mold. Now these were derived for people that have positive tests for actinos and negative they can test for bacteria and negative tests for mold. That is where the actino number comes from. Conversely, if we have HERTSMI-2 positive and negative actinos, and negative endos. That's where the mold stuff comes from. But the diversity of findings of what we thought we would find in the literature for fungi has not been held out to be true. Part of the reason for that is this paper from medical research archives, which has about 25 references, looking at what people have done to try to remediate homes and ask the question, why is remediation largely not work? Why is it largely not work? And the answer is fungi are overrated as being contaminants. Mycotoxins are overrated. when Michael Sawyer from Vienna Austria can identify 500 mycotoxins in a water damaged room. Why are we content to think that five or six are just playing Stachy alone is not. Erik started the ball rolling down the hill, and he identified Stachy. To his credit, what we have now are the descendants of that early observation. And the descendants are based on scientific disciplines that are dependent on accurate analytics. So our summary for this abstract is a current recommendations for assessment of exposure reactivity to fungi. We didn't have assessment or reactivity to fungi in 2009, or 2000, year one, or 1999 when I got started in mold. We didn't have methods remediation based on fungi alone that work, we still don't. And those methods based on fungi alone, do not support continued use now that endotoxins and actinobacteria have had a major causes of human illness from exposure to water damaged buildings. Now there are some names I want you to know thinking about data and what are the science says. Rachel Adams, from Cal Berkeley has written more than anybody else with modern analytic methods. So if you just do a Google search or Pubmed search of Rachel Adams, she's the one that first identified for example, that he was human habitat derived actinos, deep in the the bowels of a building, the inner sanctum of bedrooms and bathrooms. That's where you'll find those seated. You can find these in buildings that are water damaged and buildings that are not water damaged. You will find Martin tavole tea is something as pronounced wrong to UB from Finland, just leading the path saying that our perception of what to do with remediation is wrong, if it doesn't include everything. And then Michael solio because he's expert in mycotoxins, he's written 250 papers, and I urge you to look at that. The key issue in the new revolution of what is the science of water damaged buildings comes from Jimmy Ryan, who's a transcriptomics and he identified by simple observation of differential gene activation of molecular hypo metabolism. He saw suppression of RNA production that will lead to manufacture of ATPasis, he saw a reduction of cytocycle oxygenation in the electron transport chain, he saw reduction in translocases. Well translocase sound like something's moving from one location to another. That's exactly right and in our bodies, we use glycolysis to break down glucose to make three carbon fragments called pyruvate, that should be transported through the outer membrane of mitochondria into the inner workings of the matrix of the mitochondria provide fuel for ATP production. If the translocases that do this job, are not present if they're suppressed, will pyruvate get into mitochondria? No. Will mitochondria be functionally giving us energy? No, what will happen to that pyruvate? Pyruvate vaguely metabolized and broken down into lactic acid and lactic acid can be secreted against the gradient and exported outside the cell; lactic acid is an intracellular poison. So what we look at is this difficulty with suppression, through ribotoxins through small molecular weight biomarkers, together with some of the other things we're talking about with actinos that prevent normal metabolism. This is normal metabolism, once it's it's led astray leads to abnormalities and complications of metabolism that affect essentially everyone with CIRS. Now it's not everyone, it's only 85% will be full blown to have proliferative physiology, about 10% do not have proliferated physiology. But this is all derivative of the Warburg effect. So if you're using pyruvate to make lactic acid, you'll get a couple ATP. But that's about it, you won't get 36. So the search for what are we looking for Erik started and in 2016, we looked at the gene makeup of coagulation abnormalities and cytokine abnormalities, things we thought we knew we didn't know about. Erik, you and I didn't know about coag problems. We saw people with clots and we worried about sed rates. Why were sed rates always so low? You know, we didn't think about viscosity but other people did, and they had looked at it. And sure enough, that's the answer to your question one time, late one night, oh, how come this viscosity correction? How come we have problems with low set rates and not high in this illness? Long comes new treatments. My treatment protocol was established by 2003. It lead to a rare case definition. By 2008, we had the VIP, the VIP became a miracle worker for some people. It did not answer the question of how do we remove everybody from exposure. But by establishing case control data sets that we collect to this day over 40 building investigations and population investigations. We know that some of the complications we dreamed about that were there we found out in 2017 were abnormalities of gray matter nuclei. And we could identify mechanisms of atrophy of people's nuclei in their brain, we can show it definitively and reproducibly. And in an MRI facility from place to place throughout the country throughout the world that gave a reproducible diagnostic pattern of finding enlargement or edema forebrain or white matter, edema form of cortical gray or gray matter and then suppression of occipital nuclei. Those three together conformed to now what we see and you can recognize it takes 10 seconds Erik for you and I to refute those experts that said cognitive issues was just depression, cognitive issues with just anxiety. Yeah, cognitive issue was structural abnormalities of the brain that respond to treatment, that response to VIP and correcting the illness. Yeah, that's depression, all right.

Kealy Severson: 25:07

Can I just ask you a question? I'm sorry for interrupting you. But I just got a little confused with something that you said it sounded like you said that you and Erik started at mold but didn't see CIRS start with Pfisteria and not mold?

Dr. Ritchie Shoemaker: 25:21

We didn't know CIRS till 2010. We didn't know that other the lab abnormalities Pfisteria had until it could run the essays. The tests weren't invented in 1996, 1997 was diagnosing Pfisteria. Pfisteria diagnosis was the best we could do with what we had. What we had was observation of where the kills were looking at confounders and ruling out differential diagnosis and symptoms. Along came visual contrast sensitivity in 1998 nd it wasn't until 1999, We found that VCS worked for cyanobacteria, and other dinoflagellates in addition to Pfisteria, but it also worked for mold. And we never knew that there were actinomycetes involved and never knew that they gave a deficit to VCS as well. Your question is an excellent one. We had all kinds of names and in litigation in deposition, I got hammered a lot. Well, how what's this chronic biotoxin associated illness doctor? You call it CIRS now, why couldn't you come up with one name? Well, things evolve in science based on new information. The fact that Erik recognized things and I recognized things, I think is to our credit. I'll say good things about him and then maybe he'll say good things about me early on. But we've come a long way. We see way much more. Does that answer your question? That was convincing. So what are these complications from metabolism? If you have consumption of pyruvate to make lactic acid and use secret it against the gradient, you will have a problem. I was all ready for today. Here it is. You will have a discrepancy between untreated patients and treated patients and stage one is untreated. Stage two is after my protocol including VIP. Stage three is after VIP and stage four is off VIP. If we look at people who have molecular hypometabolism shortage of all of those ribosomal and ATP translocases that I talked about, and they have positive virus two as the insulin receptor substrate two that opens the door that lets glucose enter the cell. Why is that important? Glucose entering the cell will feed glycolysis creating more pyruvate creating more problem with lactic acidosis, proliferative physiology. If we fin out of six now, and people who had molecular hypometabolism IRS2, add a six a trophic nuclei, who's got a six nuclei of 4.1 or a trophic 4.1. This is all on treating people all comers. If you look at people who have a hyper metabolism, but don't have IRS2, so they don't have prolific physiology, it's down to 3.0. So reduction of brain injury, if you're not relying on proliferative physiology. If you have MHN negative IRS2 negative, you're down to 2.8. About the same as is stage two stage one and with MHN positive. But how about you have MHN negative and IRS2 positive? Sounds like something better than than the everything else 1.2 on the mean. And that starts to get less than what's predicted for greymatter nuclear atrophy. How about superior lateral ventricle that is a fluid filled container near the just above the fourth ventricle spear lateral ventricle buses the cortical gray and if you have cortical gray atrophy, guess what happens to this ballon likes spiral ventricle, it gets bigger. So in stage 16.1% are MHN positive IRS2 positive. That's the worst one. We go down to 7.6, 6.1 and zero. If Kealy if you had your brain injured, you would not want to have MHN positive IRS2 positive, you would want to MHN negative IRS2 positive. You can't get that any other way other than transcriptomics. It's the only way to get there. And it for that reason alone, identify without question, the mechanism of brain injury that's that's that's enough. That won lawsuits, $3 billion in the cases we had at Norfolk Island in Norfolk, Virginia, with people in the military, you know that they try to separate one case for another is bloody warfare of everybody including me that was in it but was where NeuroQuant made its way, and $3 billion was the final total or so I'm told. All right, how about some easy way? Erik, he knows I'm probably gonna bring this up. If you want to know, inexpensively without NeuroQuant without doing transcriptomics? How can you look to see who's got lactic acidosis? If we look at people who have a widened anion gap, that why anion gap in CIRS patients is due to excessive lactic acid in capillary beds. Now Kealy, I'm going to pick on you today, what he is and I and gap is the son of sodium plus potassium. So potassium may be 4.5 and sodium may be 139, or 144 just for sake of argument. From that we subtract the sum of chloride at 104, co2 at 124. That's 124, 145 minus 124 it was a normal anion gap, we'll have a number about 12 or 13. But I just gave you a CIRS patient is 24. We can follow sequential anion gaps look to see who gets better. It's reproducibly reliable. But the big deal. Why does so many people with CIRS has shortness of breath? Now the EPA tried to tell us they all had asthma, 21% was the number. They didn't even do PFTs, they said you got to ask what was no PFT markers, come on, give me a break. But if you look at what they really had, which is pulmonary hypertension, that develops in 80% of people who's got anion gap widening, with nuclear atrophy of 4.1. With this injury to the superior lateral ventricle, all of these entities go together. And that is published and that is peer reviewed in 2019. I urge you to look at this paper in medical research archives 24 number seven. This is a very difficult paper to read, because it's full of terms of metabolism. But you have to read it once you're gonna read it twice or three times. The jargon that goes along with CIRS makes it impenetrable. Erik, it was a lot easier when you identified Stachy as being the problem in the teachers lounge. There was more to it back then. But it's a cinch that when we look now, we've got to know about not just gray matter nuclei atrophy, we need to know about superior lateral ventricles and cortical gray as well, because the longer people stay sick, the longer they stay exposed, the longer they have lagged translocase abnormalities, the more likely they are to have brain injury. So that when we look at people with premature onset of Alzheimer's like syndromes in CIRS patients, and I know you know plenty of them, those are largely correctable. You can profile with NeuroQuant, it takes 10 seconds to read NeuroQuant For God's sake. Paper from the from the correction of gray matter nuclear atrophy is also an internal medicine review, April 2017. This was done with VIP after they'd been on the protocol by itself. Theoretically, CIRS has application to here's a question anion gap widening is due to excessive presence of lactic acid in capillary beds in circulation. What we're seeing now is the chronic fatigue illness is more than just CIRS more than just Pfisteria, more than just ciguatera, more than cyanobacteria, we are noticing now that what's called TA17, Treg imbalance is intimately tied to the transcriptomics in our new Genie 2, the second version, we can show the link from what was CIRS only, to acute coronary syndromes, acute resection of products, huge section of a descending thoracic aorta. We also can show that deficits of T regulatory cells that are part and parcel of the metabolic complications are present. If you've got t reg cells, will there be normal resolution of tissue based inflammation? What do you think Kealy? Do you think you can fix tissue inflammation without t reg cells? I'll give you a clue. No. So this illness that started with Stachy, started to get added with other things is now going on way beyond just mold problems, way beyond ciguatera probelms, way beyond just actino problems. We're looking at. What about diabetes? IRS2 let's sodium in, let's let's glucose in? What else does it do? It'll turn AKT 1, 2 & 3. It turns on MTor it turns on OGT to create insulin resistance for God's sake. I kept on marveling how many people had insulin resistance by type four Fredriksen lipoprotein phenotype, they were everywhere. Why, because OGT was turned on as a mechanism to alternative delivery, a biosynthetic pathway when you've got too much pyruvate, and it's turned on and glucosamine to make these other proteins now modified. OGA is suppressed, OGA takes that, and acetyl glucosamine off, it fixes the problems we have with insulin resistance. But insulin resistance is led to the inflammatory in metabolic abnormalities in this common illness. So that paper was written by Shoemaker Heyman and James Ryan. That's from 2017. 2018, this book got the worst review I've ever had. This is a GENIE primmer for healthcare providers, the genomics of CIRS and associated molecular pathways, interpreting the transcriptomic results. Well, why is this the worst book I ever wrote, because nobody could understand it. And I didn't understand much of what I wrote either. I talked about how to interpret transcriptomics, we were looking at 50,000 genes, Holy cats, who couldn't do that, nobody. So what Jenny and I did Jenny mostly, was widdle down are 50,000 genes. But basically, we went on down to 2000 genes, they gave the most signal to noise ratio. That said, this is CIRS and not something else. And then we cut it down to 187. These are the cream of the crop. And now without an 87, that's whatour GENIE is looking at now. So when we look at all of this information about GENIE, 187 genes, that means when I'm looking at everything, it means there's other things that aren't there, I urge you to look at the consensus statement for the diagnostic process or chronic inflammatory response syndrome. The report of the consensus committee of surviving mold, we now call ourselves the CIRS Academy sounds a little highfalutin to me, but it's basically people that want to have an academic basis for this illness that keeps on enlarging every day. This was published in May of 18. It's a free download, and all these are free downloads from the survival website. Unfortunately, the gene primmer is not as sort of a free download. You don't want to read that anyways, the jargon is just ridiculous. Okay, so now we're getting closer when we look at I'm not going to talk about any mycotoxins unless I have to. It's a sense that the paper I wrote on mycotoxins in 2019 looked at 45 studies from around the world, looking at mycotoxins found in urine in control patients who were perfectly healthy. The metabolism paper I mentioned to you, that was in 2020, in September. But what really made the difference was finding out that actinomycetes are huge players in metabolism. If I want to disrupt pyruvate delivery to to into mitochondria, I can use translocases. And that's one thing that's happens with a small molecular weight compounds. They're called ribotoxins, ribosomal inhibitory proteins, there's a whole bunch of them. Mycotoxins do that to a certain extent, actinos way more than bacteria that are a little less extent. But then if we want to really do bad things, we can focus on what's called the voltage dependent and ion channel the vdac. This is the channel a pore about 20 nanometers. Now, Erik, somebody told me you were looking at nanometers structures, is that right? Yeah. Boy, do I have things to talk to you about man because the nanometers from what we're going to talk about it with an extracellular vesicles, Boy is that exciting things. And you may love it, right? If I didn't use the word, I didn't use the word, but boy is this fantastic. Nanometers stuff that deliver packets of biochemical inflammation and metabolism abnormalities from cell to cell biochemical communication, and that's the next paper that's coming out next month, if I hurry up and write it. But basically the VDAC is another way to disrupt pyruvate distribution into mitochondria. It's a pore in the outer mitochondrial membrane. It lets him ions soluse pyruvate, it lets out ATP, while we let in ADP, and ATP is made an ATP, whereas ATP go, it comes out through this, this pore. It also lets out reactive oxygen species, which is part of toxicity that we can have here. So it's not all a good thing. But it has a dual role with translocases. Also in the brain, tthe hexokinase enzyme, it's bound to vdac blocks outflow of ATP. So that's a fairly complicated thing. But basically, what we're looking at is that polymyxin, here's one of the compounds made by actinos. That shuts down and shuts off VDAC. So if translocases shut off VDAC and porins. What about actinos? Yes. Here's where the big deal comes from. There are two papers, a researcher from Hopkins named Head who's published wonderful papers looking at the effect of Itraconazole on vdac. Closes it right down. Now other antifungals are not quite so bad. But Itraconazole is one of the most widely used antifungals and one of the words to create proliferative physiology. Now in discussions with people like Eric Gordon, he says, but people feel better when they're taking antifungals. That's right. When you're proliferative, you're making new cells, people do feel better. But meanwhile, silently, quietly, you are causing problems with brain injury, you're creating difficulty with T reg cells, you're creating pulmonary hypertension, that's not a fair trade if you ask me. Always good questions on that one. But the papers are Now, the other issue is that actinos make compounds that disrupt the electron transport chain directly, piericidin a knocks out electron transport complex one, and oligomycin probably heard all the ways and, and knocks out electron transport chain three, that is a permanent change. So this actino effect, that knocks out vdac, is also knocking out mitochondrial function. I mentioned in passing Martin Tabal and just to tell you that the CIRS Academy led by Michael Schrantz, has written a consensus panel statement, the surviving mold, indoor environmental professional panel consensus, we're in microbial remediation 2020 he came out last year in September, I urge you to get it's a free download. The writing is not obstructive to normal thought processes. It's clear, it's well written, it's a good piece of paper to read. But he does start to talk about actinos and endotoxins, together with with fungi, and filamentous fungi, or where we're after against. One spin off of all this work looking at actinos had to do with COVID because it was interesting that the symptoms of COVID and some of the findings of COVID the the hypometabolism, proliferative physiology that post COVID patients had were typical what CIRS patients had, it was fascinating to look at people who were proven to be healthy before COVID, had a test that showed they did have COVID, and then had tests to show they didn't have COVID, and a month later, they started getting sick again. So they were healthy, sick, healthy, sick. And the idea was that was there something about COVID that could create the same thing that CIRS and inflammatory basis, and sure enough 56% of people had evidence of the specific causation for specific immunoreactivity have a positive isolate for actinos MAP kinase positivity and TGF beta receptor positive as well as the triple header. They had all three and those were turning on TGF beta one signaling, which is what we see in CIRS patients, which is where the fibrosis comes in with epithelial to mesenchymal transformation that is going on in kidney is going on in heart. It's going on in liver. Where do you think all this cirrhosis is coming from? For people that don't drink it's coming from fibrosis from TGF beta one certainly. It's coming in lung as well. So when people say that's asthma, and you do a diffusion capacity, you'll find a large number of people have got these problems from fibrosis. I maintain that the COVID can act as a CIRS. There's so much noise about what people say about COVID. I want to run away from that. That's for sure. The last biomarker we're reporting, Scott McMahon is the lead author. I'm sure everybody's heard of PANDAS and PANS, and children pediatric acute onset neuropsychiatric syndrome. We had done a multi sites trial four years ago, looking at it, what did we find every one of our 33, PANDAS and PANS patients all met the case definition from the Stanford consensus statement from a few years ago, they all they were they were fine. Everything that Sandra said, Yep, we got them. Except they all had mold. They all had problems. We didn't assess them for actinos, I'm sure we'll find them. We found mold for every one of them and when we treated them with cholestyramine first few steps the protocol and remediated the environment. They got better their, pain just went away, their psychiatric symptoms went away. Okay. I've been trying to raise the issue of what data and what science is there. I've given you 12 papers in two books. It's your turn, I'll try to answer questions.

Erik Johnson: 45:20

Well, I'm glad to see that my evidence for moldy ground zero for chronic fatigue syndrome still stands. A lot of people have been telling me that, with this new evidence that no longer matters, and the entity moved on since then. Now, if you look on page 439, of your book, Mold Warriors, when I explained to Dr. Cheney that I wanted to look into mold. I said, there's probably bacterial involvement as well.

Dr. Ritchie Shoemaker: 45:48

Good for you.

Erik Johnson: 45:49

But this is no reason to fail to discover the toxic mold that was in the teachers lounge, which was the actual cluster, that Dr. Cheney called the Center for Disease Control to come investigate. Now, I was amazed that all these researchers crowded around a bunch of sick teachers, in a sick room, and it somehow failed to occur to them that they ought to look in the room for a common denominator that was making them all sick. And the reason I stick with Stachybotrys, of course, is because after the CDC gave up, after Dr. Gary Holmes gave up, after Dr. Cheney stopped looking, the school authorities did look into the room and behold, they found toxic mold. Which is what these researchers would have found they would have been the first to discover Stachybotrys and they only acted like scientists looked. So when I saw the confusion of the chronic fatigue syndrome world, growing up in all different directions, studying viruses, mycoplasma, sometimes Lyme disease, never knowing what they were looking for. I thought about the process involved, how to do science. Now, if the Center for Disease Control is called for something very specific, like a cluster of teachers, at the very least out to continue the investigation. So remember when you and I were at the 2009 conference in Reno, and I approached Dr. Paul Cheney, and identified myself to him. What an unusual reaction he had. You think that somebody with my level of evidence he would be eager to talk to, and yet, this was not the case. He turned around and ran. Well, it seems to me that this seems to be the common psychological element of academics, doctors in general, is to suppress evidence by running away from it. And this is what they did at the origin of chronic fatigue syndrome. They came, they saw what they didn't want to find, and they turn around and ran. And you were the first doctor after 20 years, the very first, to come and look to even talk about the evidence that actually started chronic fatigue syndrome. I mean, the actual thing that Dr. Cheney, Dr. Peterson, called the CDC for help with. And this is just amazing to me, that so many researchers, the world over seem to have forgotten to due processes of science, and I thought when my story was published in your book, the title alone, mold at ground zero for chronic fatigue syndrome would make it clear that there was overlooked evidence, other researchers would respond. And here it is 15 years later, not a single one has. Not a chronic fatigue syndrome researcher, not a mold researcher, not the Australian parliamentary inquiry, which is looking at both biotoxins and chronic fatigue syndrome. Nobody. So I'm wondering, where did they forget how to do science? And what right do they have to even talk about chronic fatigue syndrome, if they've never been looked into evidence that started it? Stachybotrys is a symbol of the most utter malfeasance of the academic world, the medical profession that has probably ever happened in the history of science. 100% of chronic fatigue syndrome, researchers failed to do the simplest thing and ask how the syndrome began. So to me, that's why I obsess about it. That's why I stick to it, because it's a symbol. There's other evidence they overlooked as well. But this is the main one. Now when the indoor air quality profession started to get involved in 1994. And in the proceedings manual, they were speculating about this. Jeremy recently coined chronic fatigue syndrome. They asked in several chapters even dedicated one chapter specifically to the question of whether chronic fatigue syndrome was associated with Stachybotrys. Now to me this meant they want an answer. It's really they want a prototype for the syndrome. Somebody was there who could walk up and possibly give them some documents, showing that, indeed, this is the case. So I was very surprised to contact these researchers and learned that they didn't want an answer at all. That was the last thing they wanted. So to me, this is a complete breach of science, and a betrayal of the Hippocratic Oath of logic and common sense to actually refuse to look into the very thing that you said you wanted an answer to. When you flew me out to the mold Congress in 2019, I thought we were finally going to settle this matter for good. I told my story, Dr. Chin Yang and other esteemed mycologists were there. In fact, two other people led intimate association with the event that chronic fatigue syndrome of the original Holmes 1988 chronic fatigue syndrome was coined for, were there. And we could have settled this matter pretty much within minutes. But after this January 2019, Mold Congress, there was no further interest by any of the mold Congress, the matter was dropped. And here the opportunity to resettle this one subset, a very important one, because it did start a syndrome, slipped away, and appears to be funneling into oblivion. So that's why I was trying to resurrect that by criticizing other people in the Mold Congress, and doctors and researchers in general, for lack of a systems approach to do their basic science. When they get into confusion. They don't know where to go, start at the beginning, go back to the origin of chronic fatigue syndrome. And this is described in your books, anybody could read it, they know where to go to find out about chronic fatigue syndrome and there is nothing stopping them except their own unwillingness and their apparent desire to bias the scientific method by manipulation, deliberate omission of evidence. So I'm using Stachybotrys as a symbol and glad to see that you're continue to validate my story, there's nothing wrong with it. It may be just a subset, but it's an important one. And I believe that we can still proceed with that and as more people are getting interested in chronic fatigue syndrome, and more researchers want to know if COVID is connected with chronic fatigue syndrome, they will read this in your books, and they will come back and we can sell this matter.

Dr. Ritchie Shoemaker: 52:35

You know, in the ahab mentality of searching for the great white whale. I think there should be another book written. It'd be Erik Johnson's voyage and when you get your big leg or something, man, because you you stuck, you stuck to it. But you know, the the idea of the approach that could have been taken, let me assume that what you say is true. It raises certain questions. How can we answer these? We didn't have the technology you didn't know the technology back then. We have it now. And its risk of, of over emphasizing things like COVID, we are looking at it in a world that is now increasingly affected by climate change and I have no idea what's going to happen to the next microbial growth. One of your buddies talks about the sands blowing off the Sahara desert and being blown over to Florida. Well, we've known forever that when the sands come when they came yesterday to Florida, that's where we get blooms of dinoflagellates, red tide, but the environmental factors that are torturing Florida from from microcystis, because the whole state of Florida is is one mass phosphate mine. And he started going to place after place after place after place and you know, the houses being burned down on the last one, are they gonna burn them build their houses back with, build the soil? Well, yeah, sure and then if you start building houses with soil, will you be bringing soil based microbes in? So the questions are mounting exponentially and I think part of those new the informed researcher is to remember where you started. Never forget history, but then keeping an eye on the prize, which is what does tomorrow bring? Are there any other questions?

Erik Johnson: 54:20

I just like to say that science starts with observation. And the first observation in chronic fatigue syndrome was extremely well documented and validated. So if anybody wants to find out more about chronic fatigue syndrome, they can go right back to the source. And at the very least, we can settle the matter of whether Stachybotrys is associated with the syndrome.

Dr. Ritchie Shoemaker: 54:41

Let me spend five minutes because that's all I got left on the new actinomycetes index. I'm skipping because this is going to the next paper. On July 7 of this year, Envirobiomics put forth the actinomycetes index. I had been interested in that in one of the markers from the building is a musty smell. And then you say we ask the experts, what is the musty smell from? It's from well, geosmin, is made by soil base actinomycetes organism actinobacteria. So here one of the three ways to say you got a moldy building is to find actinos. So it's a little crazy.

Alicia Swamy: 55:20

I'd like to just interrupt that statement really quickly, I just spoke with Dr. Joan Bennett, who's a fungal geneticist and she does understand that in buildings there are microbial VOCs but in her research, she has found that primarily 1-octen-3 -ol, which comes from a fungus, is what causes the smell, the moldy mildew smell. So it's interesting to see the conflicting science of what you're what you're talking about, and what a fungal geneticist has uncovered.

Dr. Ritchie Shoemaker: 55:50

Geosmin is an actinomycetes, I'm sure she'll agree with that. What we're after, is looking to see are soil base actinos going to be the same threat that human base skin base actinos? The answer is that soil base but by and large are not likely to fill it and the ones from human skin are likely to fill it, so that certainly washing with soap and water rarely will clear skin breakdown by actinomycetes, or getting out of the bottom of the pits where the sebaceous cysts are. But basically the idea is that what we want to do is compare what species is dominant and that's the ratio of number of different species of human habitat is 33 that are more than 10% listed on the pathogenic bacteria actinos made by Envirobiomics, and then 13 are leftover to be looking at are soil based. So you divide x over 33, divide that by y over 13. Get a number that's the dominance index, the more important is the prevalence index and we take the five most common species of human habitat organisms, and then take the mean of their bacterial equivalents per milligram, and then divide that by the mean of the soil based habits and you get a number gives you the prevalence index and that number is over 2.0, you're going to have adverse effects from actinomycetes. If that's the case, right now, unfortunately, the technology is only through transcriptomics, you'll need to ask, say, for map kinases are six or more years. They are not specific on their own right. They're part of a lot of different pathways. They're not related to IRS2, not related at all, even though the books say they are. But basically, if we have a map kinases and TGF beta one receptor, there's three of them, one, two, and three. It's more complicated than that as we go further, but that will give you specific causation, specific immune reactivity. So that gives us two that gives us endotoxin, cd 14, and 204. And then we've got map kinases, and then we have tgfb are looking for actinos. What we're looking for and working very hard, I think I mentioned to you yesterday on the phone, that stat one, one of the cytokine genes is looking pretty good. It may be a biomarker for filamentous fungi. Numbers are small right now. But there's bound to be one that will be a specific biomarker for fungi and that's gonna make our world a lot easier, not worrying about amoebas not worrying about, you know, protozoa, this and that. But it's an exciting time to be involved in research. And basically, as far as I know, Mycometrics does an essay for streptomyces griseus. But they don't do the full panel, I think, can't say certainly will do that sooner or later. Maybe you check with with Dr. Laddies and he should do a speaker for you as well, asking you How come he's not doing that in human?

Erik Johnson: 58:52

Okay, and how do all these new findings affect the people who have an existing CIRS diagnosis that was based on the idea that it was probable mold illness?

Dr. Ritchie Shoemaker: 59:01

If a mold illness is confirmed by HERTSMI-2 there's no real difference at all. It's where you get combinations of the other two factors become involved. And that really is the new era and we have not had, we have not had a publication yet. We were next month for the first one, bringing the the actinos to forbear to look to see what role they have versus mold and something else, is what we had before was more than something else here.

Erik Johnson: 59:30

Well, all these people that had mycotoxin summits and mold summits have to change their name?

Dr. Ritchie Shoemaker: 59:36

I think so. I think they were never were someone to begin with.

Alicia Swamy: 59:40

I just want to point something out really quickly on your paper that you said "New molecular methods bring new insights into human and building health risk assessments." With Heyman, McMahon and you wrote specifically here "current recommendations for assessment of exposure reactivity to fungi and methods of remediation based on fungi alone do not support continue use. Now the endotoxins and actino bacteria are found to be the major causes of human illness from exposure to water damaged buildings." Now, I have an issue with this because there is so much data on mold showing issues and everything that you list beautifully and scientifically, thank you for that presentation, you can go back to the literature and you can see that it also can happen in someone who's exposed to mold and mycotoxins. So for me, when I read that statement from your paper, it's almost throwing the baby out with the bathwater, to say, actinos and endotoxins are now what you need to be concerned about Oh, and mold, forget it. That's not a problem. Which I don't think is exactly correct and now everyone has their remediation companies on mold, mold doctors, like Erik said, mold summit's and everything that's going around, Campbell has an explosive amount of research on mold, and he's constantly pumping out papers. And so it's hard for me to just sit here and pretend like mold isn't a major issue. When we have so much studies, I have collected all the studies that show almost same of the mechanisms that you present in your papers for actinos and endotoxins. To show that more than mycotoxins do about the same thing to the body, including the pulmonary hypertension, it actually Stachybotrys is connected to pulmonary arterial remodeling, which is very concerning. And you also said yourself, there's over 500 molds and fungus and everything that's out there, when it makes sense to actually put more time into looking into the mold?

Dr. Ritchie Shoemaker: 1:01:42

Until we had transcriptomics, nobody knew the extent to which endotoxins add specific reactivity and nobody knew that there were specific reactivity for actinos, we now know that, we can ballpark A, B, or C symptoms will not separate the three symptoms will not separate the other 29. And if we say symptoms for Stachy, no, symptoms won't separate Stachy from Walemia, for example. And here's where the duty comes. Erik is right that science has dropped the ball because there's no funding for it. If there's no money, and you got to pay the bills, and you are a scientist you want to look at something either grant for or not. You get people like me, it's all private. We've raised over $2 million privately, we will continue to try to raise money to be provided live long enough to do that and with that work. Your point is well taken. What is the tip off, that you've got a fungus, a filamentous fungi versus an actino? Well, you start with isolation. And that can be done now inexpensively. Then you proceed with biomarkers, biomarkers have been validated. You and looking at at NeuroQuant and looking at GENIE and now GENIE 2 because as soon as we started extending GENIE 2 to diabetes, someone like you shaking your head is gonna say, well, don't you think we ought to be looking at A1C hemoglobin for diabetes? We should be looking at the mechanisms that are in addition to what's known. It's like going to the North Pole, you know where it is magnetically everything, everything here is south but you don't know the chasms and the capacitors that you got to go through. So it's a new exploration and that's my message, is we now know, there's more things to look at, beyond fungi. There's a lot of work done on fungi, I take pride in what I've done. But I also know it was inadequate now with newer methods.

Alicia Swamy: 1:03:39

Transcriptomics also has its own limitations as well for testing. So we cannot forget that, we can't say that this is a fully advanced foolproof way of testing and go forward and not point out the limitations as well. So I think that's just my issue because a lot of Heyman's patients, a lot of your patients come to us, and they ask about, I have this GENIE test, no one knows how to treat me. I don't know what to do. So there's a concern.

Dr. Ritchie Shoemaker: 1:04:09

Sorry. I'm sorry. You're at the end, because I would like to talk to you again. I do and so let's do this again, sometime.

Kealy Severson: 1:04:16

Thank you for your time today, Dr. Shoemaker, maybe we can schedule you for a part two and continue this conversation at a time that works better for you. Thank you so much.

Dr. Ritchie Shoemaker: 1:04:24

That's good short notice, bye

Erik Johnson: 1:04:27

And my final message is that nobody has the right to talk about chronic fatigue syndrome until they look into the evidence that started this syndrome.

Alicia Swamy: 1:04:36

If you guys wanted to ask some questions, feel free while you have us here. We'll say about another 5, 10 minutes if you're interested.

Kealy Severson: 1:04:44

Yeah, that's actually a good idea. If anyone wants to ask Erik a question now it'd be a great time. You guys can do that in the chat or just unmute yourselves.

Unknown: 1:04:52

Hi, William. Hi. Sorry. I'm very dark here. Oh, that's okay. There. Did you feel that that answered some of the questions that you had?

Erik Johnson: 1:05:02

Yeah, the main thing I wanted to find out is whether Dr. Shoemaker still considers my story in his books to be valid or not. And he does.

Unknown: 1:05:10

Do you feel that he's just dismissing the Stachybotrys ties to some degree?

Erik Johnson: 1:05:17

Absolutely, because if he considered this to be important, I would still be working on trying to connect this evidence to the origin of the syndrome. You know chronic fatigue syndrome is a specific research document authored by Dr. Gary Holmes, and officially adopted by the Center for Disease Control for the purpose of solving a mystery. That mystery still hanging in space, though it was it comes right down to this cluster of teachers had reactivated epstein barr virus, all got sick in the same room, no apparent reason. At the very least, we can go ahead and clear up this matter and find out if this situation in place to other clusters, especially Dr. Chin Yang presented evidence of a 2019 Mold Congress. It makes Stachybotrys more of a buttkicker than ever before, it shows that certain strains, the evil twin, if you will, is actually more dangerous than Stachybotrys chartarum because it shuts down cell division. It's a powerful protein synthesis inhibitor, but without the overt neurotoxic effects. And Dr. Yang was speculating that a lot of the times they thought Stachybotrys might not actually be that harmful. It's because this evil twin didn't give you the warning you needed to get out of the situation.

Unknown: 1:06:38

It feels like as well because of the CDC's lack of acknowledgement towards the effects of Stachybotrys as a neurotoxin may be affecting Dr. Shoemaker's decision.

Erik Johnson: 1:06:49

Unfortunately, we didn't get into this. I mean, there's always there's never enough time. But when Dr. Cheney, Dr. Peterson, Dr. Komoraff and other researchers converged on Incline Village back in 1985. They generated so much good evidence that it scared the heck out of people it made it appear that incline village was ground zero for a deadly new disease. If you look at the Holmes committee, they had many good names under consideration for the new syndrome. Mild to conceptual model itis was one post viral fatigue syndrome, epidemic neuroesthenia, chronic mononucleosis, like syndrome, and a lot of different serious sounding names. And they chose the dumbest one of all and the reason for that is they wanted to trivialize the outbreak, to diffuse this scare to bring the tourists back to Lake Tahoe they could conduct research quietly without the fear factor that was going on. And we hoped that researchers would come back and take a look at how this syndrome began and consider this evidence to be what chronic fatigue syndrome was for. But instead it took off and talked about it like it was a chronic fatiguing illness. And all the CDC ever knew about was tired people, just ridiculous. a cursory reading of the outbreak of the history how this started, you can see that there was something really scary going on. And it was a lot more than just tired people. The complaining with chronic fatiguing illness, that's right there shows a mistake in methodology.

Alicia Swamy: 1:08:28

The toxic mold issue and the mogan buildings and housing exploded ten fold - Google right now and google mold in the US there are so many news articles. It's not actinomycetes, it's not endotoxins. I understand its a new technology, I understand it is something new, but I think it's too premature to connect causation with actinomycetes and endotoxins to illness and then throwing out mycotoxins that Oh, that's not really a big deal. So I think that's that's my issue that I have with that. And I would love to talk about that even more with Shoemaker, it's hard because you can see that it's very science, science, science, but no one is really understanding what is being said. And so we need to bring it down to a more understandable level so that we can all understand what the hell is going on, because everyone is sick, and no one knows what to do. And we want to know that data over to make it sensible for the people that these doctors are treating, because we don't talk like that, scientists don't even understand that.

Erik Johnson: 1:09:36

I think we need an investigation into the sociological aspect of this because how on earth did every researcher on the planet every single one, claiming they wanted to solve chronic fatigue syndrome either fail or refuse to look into the evidence that started in the Lake Tahoe outbreak? We a couple of us in incline village discovered that by going up to the nearby desert, we experienced a recovery that was so startling. The doctors actually lost interest in this, because they couldn't believe it. That was my strategy. That's what I did, I went out to the desert. And over time, my sensitivity became more acute, I became more aware of what it was back in town that I was reacting to. And I finally narrowed it down to toxic black mold, that if I stay away from that treat it like plutonium. It was the worst, toxic, horrible substance on the planet. My recovery was absolutely beyond belief. So naturally, I wanted to see if I could reproduce this and others, like Jennifer Brea, and Julie Rehmeyer. I told him about the toxic mold. I told him what the benefits were of conducting this style of avoidance and they became mold avoidance.

Unknown: 1:10:49

How did she recover, is she okay? I watched her documentary on PBS, Unrest, I think it's called, is very, very interesting. I don't know was it mold that quotes or problems?

Erik Johnson: 1:11:02

Yes. In fact, if you read the blogs about written by Jen Brea, she talks about she now believes that the neurological dysfunction was triggered, it was originally set in motion by exposure to toxic black mold.

Unknown: 1:11:17

Now, this isn't a chronic, inherited illness, my sister lived in the house that we were born in for most of her life, and she died in December of last year, where the mold I'm sure, ate away at her body like battery acid. I mean, you don't want to know the horrible way she went.

Erik Johnson: 1:11:41

The clusters at the way certain schools all got sick at the same time, the same place. The likelihood of people with some kind of rare genetic susceptibility, all congregating at the same place at the same time is astronomically unlikely. I believe that just forget about the genetics. Let's look at the mold, it kicks ass. And the more we look at Stachybotrys in particular, the more we learn mechanisms, where it's fully capable of doing exactly what we say it is.

Unknown: 1:12:12

We both lived in that house for many, I lived in a house for 30 years, she lived in that that same house and you know, when we were children, the basement used to flood not totally flood, but the sewer would would back up.

Erik Johnson: 1:12:28

Now look at the look at the original cluster. If you've read Osler's Web, or read about the Truckee teachers, let's look at them. They didn't get sick at home, they got sick at school. Their exposure just at the school and in particular, one room was enough to trigger something so that from then on, they could not recover. Now, the position of all the doctors at the time was that this is like an allergy, if you get away from something, that's it, it's over. But if you read my chapter in mold warriors, I realized that foods was comparable to a peanut allergy. Where something had sensitized us so badly, that microscopic amounts of this was capable of up regulating our immune system and just like with my commanding officer with the peanut allergy that I almost killed when I breathed peanut molecules in this face. I go what would happen if you got hit with a few molecules of peanut every single day, not enough to kill you, but just enough to really beat you up. What if you got that every day, and I believe that its a probable situation with mold illness. We were hyper sensitized, nd from that moment on, what we have to avoid is microscopic amounts, we have to avoid the immune damaging immune upregulation, which keeps us from recovering. Those of us who go to the desert, we achieved a level of pristinity in our environment, it was so good, so mold free, that recovery came naturally. But then you see the same people, they go back into town, they fall apart again. Now, this is not an easy illness. But I believe that we have a better chance of treating it if we would study it. Rather than keep making excuses and avoiding the evidence.

Alicia Swamy: 1:14:15

Yeah, and looking into other things, making that more of a priority since selling$1,000 tests and making a whole other, it's almost like a distraction for me. I'm just going to be real with you guys. It's a distraction, really, towards what is the actual issue. Like we need to look at the issue and we understand why the issue is not looked into, because it's such a big issue, if that makes sense, for insurance companies and whatever. I mean, imagine having to overhaul an entire infrastructure, like that would never happen. So you know, let's blame a bacteria on your skin. Let's blame the bacteria on the dirt and that solves the mold problem. We know that's not a problem anymore. So I mean, it's just, it's a really touchy subject, I'm calling bullshit on it, nd I'm not afraid to, because I have looked at the literature that he's putting out compared to the mold literature. And I've seen similarity so to say causation through actinobacteria and endotoxin. That's not enough for me, you have to really show some more data on that, because it's so premature.

Erik Johnson: 1:15:26

Either mold or chronic fatigue syndrome, to refuse I mean, flat out refuse to look at the very clued that starts chronic Fatigue Syndrome. That is such an outrageous breach of science, that I believe we need to examine researchers and find out what the heck is wrong with their heads. Science starts with observation. This is an important one, look into it.

Unknown: 1:15:48

What's up with the vaccine, my biotoxin Dr. Brunning said that he is not advising his CIRS patients to get the vaccine, but the walls are closing in. I can't remain in my bedroom for the rest of my life. Until this goes away. I'm scared to death to go into public. I have breathing problems as it is. I'm so horribly sick, that I can't get out of bed to take shower. So how am I going to go into the grocery store without getting affected? I'm so weakened my whole system is just, I don't know how to avoid getting COVID I can't get the J&J vaccine. It's not available anymore. My regular doctor is like, Great, yeah, go get the vaccine. But she doesn't understand biotoxin illness. So you know, what do you advise people to do?

Kealy Severson: 1:16:47

Unfortunately, I'm the only health care provider here and vaccine recommendations are not under my scope. So our podcast cannot advise you on whether or not you personally should get a vaccine. That's a really, really individualized choice, that every person's immune system and medical history has to take into account for themselves. But I think you bring up some other really good points and that is you're sick, and you're confused about what your diagnosis means and how to get better. And that's really what and that's really what we're after here, is to fight that fight with you. Because we know that there's a lot of people like you in that same confusion and it does seem a little confusing to take the words, fatiguing illnesses, or chronically fatiguing illnesses and then make it sound like it's the same thing as chronic fatigue syndrome and then say chronic fatigue and illnesses are a big part of a, b, and c where people can't even then look at chronic fatigue syndrome and trace back just what that is to just to just rule whatever that was out. Erik, I you know, there was so much science that got tossed out, there is data sets on chronic fatigue syndrome patients, there were findings. So did I miss here? Dr. Shoemaker say there was no data set for chronic fatigue syndrome? Or did he say there was no data set?

Erik Johnson: 1:18:13

He keeps repeating that he keeps saying that the chronic fatigue syndrome people have nothing, no evidence, no data. And that is completely false. If you just read Osler's Web, you find out that the reason why the Center for Disease Control was so scared and why they came up with the stupid name is to disguise just how scary the evidence was. I mean, we had cell flow cytometry, we had the low sed rate, we had red cell abnormalities, elevated viral titers, aberrant results on an EBV serology test, which is a standard test, which any doctor can do. So there were tons of evidence. So when anybody says there was no evidence of chronic fatigue and illness, they're not talking about chronic fatigue syndrome, which is a bit of a conflation here that should not occur. In order to overcome that. Some people are trying to say, Well, this is ME/CFS. And you stick them together, and then you have to take into account all the evidence that's associated with myalgic encephalomyelitis.

Kealy Severson: 1:19:15

Well, let's just talk about that for one second for context, because I know when chronic fatigue syndrome, when the term was coined, there were actually three researchers that were myalgic encephalomyelitis researchers that thought hey, this looks like ME, maybe we should name it that and that didn't happen. You know, I have to ask the question like it's what was just chronic fatigue syndrome name switch, confusing.

Erik Johnson: 1:19:43

It's worse than that. The Center for Disease Control actually fully embraced the idea that the Lake Tahoe outbreak was indeed myalgic encephalomyelitis, and this was written into Gary Holmes official documents with Dr. Carlos Lopez who convened the Holmes committee. When he came out to this meeting to announce the creation of a new syndrome, he described that the purpose of the new chronic fatigue syndrome was to compare the evidence to find out if it was congruent with myalgic encephalomyelitis. And somehow doctors managed to dumb this down into chronic fatigue syndrome is depression and it's fatigue. I mean, this is literally the worst failure of the medical system, as far as I can tell, in the entire history of medicine.

Alicia Swamy: 1:20:31

Well, it started with neurasthenia, right? That was a the first name that they given it that is similar.

Kealy Severson: 1:20:37

Would you just go through the progression of how you seen the mold related illnesses progress into different names, because most people haven't heard that from anyone.

Erik Johnson: 1:20:48

Chronic fatigue syndrome was actually based on an outbreak, its primary goal was to determine what contagious organism had passed through Lake Tahoe and left people permanently disabled. And this was very similar to the Royal Free myalgic encephalomyelitis outbreak in 1955. In fact, as far as they could tell, to all outward appearances, including the low sed rate, it was identical. But we had new viruses involved, so we really didn't know. But thanks to the CDC stupid name, and the gullibility of doctors, in falling into the trap of thinking that this was just chronic fatigue, they never looked at the evidence. So I thought, well, even though they've made a total mess of this thing, I can get them to look into the mold factor, which is apparently unknown to the medical profession because nobody who was examining these clusters back in 1985, came up with the idea that mold has anything more than an allergy. They insisted it was it was, if there was mold, it was only a weakness that came out because of the virus. Now well, if you look at the clusters, you'll find that it was the prior mold exposure that set the stage for the chronic illness. So at the very least, I can use chronic fatigue syndrome as a vehicle to get researchers when they come back and look at the first clusters to get some good out of the deal. At least we can study what's going on with this toxic mold. And over time, this mold effect went from completely unknown, so rare, so unfamiliar that nobody was able to recognize it, to millions of people have a mold story today. That is an extremely dramatic paradigm shift in a very short period of time.

Kealy Severson: 1:22:38

Well, in what were the words that you said that started chronic fatigue syndrome?

Erik Johnson: 1:22:43

Well, I was the first prototype, selected by Dr. Paul Cheney used my own signs and symptoms right out of my medical chart for the Holmes committee to create this new syndrome. And I initially refused, because I thought, well, if the CDC finds out that mold is involved, this might give them an excuse to not look, they'll just consider it an allergy. And go, it's not worth worth looking into because, you know, you're just confusing, chronic allergies. And I talked about it with Dr. Cheney and he said, no researchers will come they will look into all aspects of this. So your mold complaints won't be a hindrance. And I said, Fine, I'll agree to do it. And then I warned Dr. Cheney, because I felt that the first words to be spoken over the inauguration of the new syndrome would be significant. I said, I have an inexorably increasing reactivity to mold, that progresses, gets worse no matter where I live, or how well I take care of myself, and whatever is going on here. If it continues, there will be millions of people like me reactive to mold. You should look into the mold before there are millions of us. Here we are. So yes, the mold is fascinating. But we also need to ask how it is that not a single researcher, no one ever looked into it. If you look at the mold experts these days, if you time there's a sick building somewhere. They say, Oh yeah, that's more that's probably toxic mold. They identify with these. How is it that they can read about the clusters of chronic fatigue syndrome, all documented? These are on videos, these are in millions of blogs, they're in books. How is it that not a single one can read about these clusters and go, gosh, I wonder if that might be mold?

Kealy Severson: 1:24:38

Well, the bottom line here is you thought when you started chronic fatigue syndrome, that mold could be behaving in a new way and it could be becoming more aggressive and so could other microbes. And the bottom line here is if you're right, if you are right, it means the research that's been done on CIRS is more harmful than it is helpful.

Erik Johnson: 1:24:59

That's a distinct possibility, Yes.

Kealy Severson: 1:25:02

I'm going to remain hopeful because Dr. Shoemaker did say something interesting and it sounded like there was something about nanoparticles that it might be showing up on his side somewhere. And I know that I've heard you say that nanoparticles could be affecting actinomycetes, the same way that it's affecting fungi. So it could be the same effect on multiple microbes. So I'm really hoping that maybe there's still a window there where there could be meaningful research done because...

Alicia Swamy: 1:25:37

At the end of the day, that's the whole effect, right, is that the nanoparticles are increasing the virulence of these microbes, and they're acting like they've never acted before.

Erik Johnson: 1:25:49

Yeah, that's my theory. I presented on this at Dr. Shoemaker's 2015 CIRS symposium in Phoenix, Arizona, and amazingly enough, this did not inspire any researcher to ask a single question about it.

Unknown: 1:26:03

Do all of these illnesses fall under the biotoxin illness umbrella?

Erik Johnson: 1:26:08

Well, I guess they do. But unfortunately, Dr. Shoemaker has drawn in so many different pathogens, Pfisteria, Lyme disease, brown recluse spider bites, ciguatoxin. This is all confusing. It's very difficult to study. In science, if at all possible, you can narrow down the variable to one thing easy to study, you can make swift progress. So I don't really this is why I don't call my illness, CIRS, and why don't use the biotoxin rubric, because it's too vague and confusing. And I know that most people think that chronic fatigue syndrome is a confusing name, because it was deliberately contrived to be that way. But if you look at what that name represents, it is a cluster of teachers, right at its very core, you can trace back chronic fatigue syndrome to three teachers in a single room. And if you study it, scientifically, according to what happened to those teachers, how their illness progressed, then chronic fatigue syndrome is a specific type of mold illness is a certain type of damage, and this hypersensitivity syndrome, it's really a better thing to call it hypersensitivity than a disease. It's a lot easier to just narrow it down. So that like I say, That's why don't use the biotoxin name, or CIRS name, and I was hoping that Dr. Shoemaker was going to eventually move towards connecting up CIRS with chronic fatigue syndrome. But his focus on actinomycetes has been so complete, these kind of stepped away from that for the last year and a half. But by validating me here, perhaps we can get back on track, get some researchers to come back and look at how their Holmes chronic fatigue syndrome started and look at one variable and make some progress, just at least for this subset.

Unknown: 1:28:00

Erik, I have a question for you. So I'm in interior construction, I build commercial buildings. What are your thoughts on gypsum drywall as a control? That's one of the variables that I see most often is the substrate of gypsum with a paper backing of drywall tends to be in fantastic petri dish as it were for Stachybotrys mold. Do you think that that could be one of the reasons that the CDC stays away from it because every building in the United States has been built out of paper walls now?

Erik Johnson: 1:28:41

Yeah, and it's not just a fabulous substrate, but the spores of Stachybotrys and other moles are incorporated into the paper. They survived the drying process so they're just waiting for a water leak.

Unknown: 1:28:56

Or to be broken up where they'll spread their spores everywhere?

Erik Johnson: 1:29:00

Yeah. Yeah, 20 years ago, I just went around to various construction sites and gathered samples of sheetrock from widely dispersed area. So that whatever grew hopefully would be from within the paper, not from the local environment. And each and every one of them, you know, I just a little Ziploc bag with some water, and they all lit up with mold. And then we later found it. Yes, the Stachybotrys spores. When they first encounter water, they harden their shell, they don't try to grow right away. They actually form a really impenetrable capsule, which is easily capable of surviving the processes of making paper. So yes, one of the reasons they don't want to talk about the problems with the sheetrock is because we've created a huge problem. It is now waiting to light up with any water leak or condensation that comes along.

Unknown: 1:29:58

Which came from a lot of With the litigation that happened in the early 2000s, with the Texas lawsuits that happened with the builders, I forget the name of the lawsuit. But that's where all the disclaimers come from.

Erik Johnson: 1:30:15

When you look back at Melinda Ballard's, Dripping Springs incident, which really put toxic mold on the map. I mean, that was the first time it made national news, USA Today headlines, what people don't talk about is how angry the residents of Dripping Springs got with Melinda. Because when they started testing, she rock in the adjacent houses that whole area, they found that all of them had Stachybotrys. So their property value went down.

Unknown: 1:30:47

I lived in Austin at that time, I'm in Arizona now. But I remember that distinctly with the news, then it was a big deal. And it's still a big deal because it changed the way that they write the insurance policies for these houses and mold not being covered under our insurance policies.

Erik Johnson: 1:31:06

The early Yahoo groups that were emerging at that time, this was before Facebook, before Twitter, and Yahoo was just getting going, nd I joined doctor groups, I told them, watch out because the exclusions are on the way, soon you will be receiving a letter for change to your policy that's going to exclude anything to do with water damage or illness from mold. So they actually started getting these. Oh, my God, how did you know this was coming? Well, all you have to do is watch the insurance companies because unlike people waiting for science, which takes forever, when insurance companies see a problem, they act immediately.

Alicia Swamy: 1:31:45

You know what's really funny is, you know, the whole actinomycetes rap of the actinomycetes being on your skin, and then you're contaminating your house or the actinomycetes are outside on the dirt. Like, who can you go after that? If actinomycetes are the major problem, you can't go off to your landlord, nothing will get done and you'll remain sick. So you have to think about those things sometimes.

Erik Johnson: 1:32:11

I'm having a really tough time understanding Dr. Shoemaker's shift in focus. I mean, the toxic mold is so fascinating, so well documented, it's been reproduced so many times, but to move away from that, and look into a common soil bacteria. I mean, we'd have so many examples of people that got sick after the black mold grew. Why lose interest in that?

Kealy Severson: 1:32:34

You just made me realize if they're not focusing on mold than seeing it doesn't need to be prioritized for human health and just the pathogenic bacteria on the patient's skin. That's gonna lead to always blaming what the patient's own skin biome for their illness?

Alicia Swamy: 1:32:50

It's the same stuff with the genetics, like, Oh, you have bad genetics, that's why you're sick.

Kealy Severson: 1:32:56

Blaming your biome both take the focus away from the external environment.

Unknown: 1:33:04

I think he's looking at downstream effects. This is my intuition and kind of my understanding through personal experiences, that mold is really the primary cause, and he is it on the about toxin pathway where essentially causes all sorts of issues. One of the downstream issues that occurs is that the microbiome in your GI essentially diminishes both in the variability of the types of microbes in your GI, and the levels of them. That then with the lack of the diminished antimicrobial peptides, then causes a susceptibility to skin issues. I think it's not potentially but the mold is causing the primary issue, and so what Dr. Shoemaker seen is really the secondary pathology that's a follow on.

Erik Johnson: 1:33:57

If actinomycetes were the problem. Why is it teachers in buildings with Stachybotrys getting sick and not gardeners and ditch diggers?

Unknown: 1:34:05

Yeah, exactly. It is possible to get sick from from gardening. But everyone is essentially like you're saying it's in buildings. When you have water intrusion issues, there's biofilms being formed, and there's all sorts of things going on. As we know mold is kind of the primary you can. It's pretty obvious, it's visible. You can see it and it's dominant.

Erik Johnson: 1:34:32

Dr. Shoemaker is acting like we've got some kind of positive evidence when we don't. Stachybotrys was extremely well studied has been ever since the 1990s, and every study confirms that it's a real buttkicker.

Kealy Severson: 1:34:48

Yeah, thing that you just said is we actually found this in a study Erik just sent a study to Alicia and I and it was how trichothecenes and I don't remember what else was mentioned. But how it basically just disintegrates the gut microbiome through like destroying the mucosal layers in the GI tract and how that is like a primer for immune system failure, and that bacterial problems are coinfections are like an afterthought. And so it seems like there's already research published that's not the primary thing.

Alicia Swamy: 1:35:20

I mean, if you want to make a case for actinomycetes and endotoxins, that's great. But don't say that, that it's the main thing and the mold is very tiny.

Erik Johnson: 1:35:27

You can't just throw out evidence, especially when it's the very clue that starts a syndrome.

Kealy Severson: 1:35:32

Did he explain how he ruled out mold and mycotoxins for the brain injury and the inflammation that he was seeing because I heard a lot of like, how they're identifying like...

Erik Johnson: 1:35:46

He just said that it's statistically negligible on his GENIE test, less than 7% of the gene activation. Well, 7%, and you know, if you read his own books, he goes, one change in one gene can lead to downstream effects. So you cannot look at this from a statistical point of view, because one gene can make all the difference.

Unknown: 1:36:08

I've gone through pretty much the hells run of biofilm issues, and for me, I had mold issues long before biofilm issues I didn't. I was totally unfamiliar with biofilms. Now, you know, a major issue with the CDC release saying that there's 6 million miles of pipe contaminated making 7 million people a year are sick. And I think that's an underestimate, by far based on what I've experienced. And also, since we got kicked out of our home last year by the Saharan dust storm, we've stayed in hotels until now, and rented cars since my car broke down. Everything's been contaminated since the Saharan dust storm, all the cars we've rented the rental trucks. Every hotel, we've been in has had issues. Though, there's been a major ecological shift since the last our last year. It's impacted, you know, pet stuff you buy in the stores, it's pretty hard for me to find clothes that are not contaminated. We moved to Florida and it's like, I can go to a dozen stores and just about all the clothes are having issues. Usually it's not very easy to see you have to hold the clothes up to the light in a certain way in order to see the filaments going on. But it's everywhere. So there's been ended that's that's an that's a new shift, though. It's hasn't been around, you know.

Erik Johnson: 1:37:34

Have you seen the Strange Days on planet Earth, Nat Geo special?

Unknown: 1:37:40

I don't think I've seen that.

Erik Johnson: 1:37:42

Oh, you've got to watch that then because Oh, among other things, it talks about drought in Africa, Lake Chad, drying up and the dust storms off Lake Chad, going all the way across the Atlantic and hitting the Caribbean and causing asthma in schoolchildren and among other things. They traced the actual genome of a specific mold Aspergillus. It was originating in Lake Chad, they found it was the same thing. It was afflicting the coral was making the coral sick in the Caribbean.

Unknown: 1:38:17

Oh, wow. Yeah. There's a black band disease. So in the coral, in my experience that one of the main pathogens is called Beggiatoa. It's easy to identify, the second largest bacteria and, you know, don't just walk down to the beach right now and see it on all the seaweed there. Essentially, since 2015, the equivalent of 7 million elephants washing onto the shores of the Caribbean, Mexico, and here in Florida, it's an immense shift in the ecosystem. And when the stuff on the seaweed, which usually seaweed is related to the floor of the sea, the seaweed is free floating and so NASA can actually track it pretty easily, and it washes onto the shores, and it washes onto the shore. Essentially, if you want to remove it, you have a very short period of time to be able to do it without making workers affected to the health issues because once it starts rotting, it creates a toxic gas called hydrogen sulfide. Hydrogen sulfide can kill you if it's not very high concentrations, and then hydrogen sulfide is the favorite food for Beggiatoa. I can go to the beach and take photos of all the seaweed there. It's all covered with Beggiatoa, and it's usually it's transparent, so it's not very easy to see if it's in your environment, like in a home or on your clothes. But it glows in the dark under blacklights it'll glow blue the filaments do. It turns white, if it has access, access to sulfur. And I went to these doctors in Atlanta, we had issues in the house, and the last thing I expected him to say is that the biofilm issues that were happening happening, again, our skin felt like with burning on fire. I didn't expect you it's been say it's essentially CIRS and this was an allopathic infectious disease doctor, and I didn't expect him to be testing. So he demand the CIRS profiles, the lab, the basic ones, and said, his conclusion is, you have massive exposure to biotoxins. Our house was pretty messed up. Anyway, I didn't realize it was affecting my skin. So I connected with one of the Facebook groups and then realized that I had telltale signs, I think this is all downstream from really was being caused originally for me from a mold from a house which had mold problems, it caused my immune system, my immune system to go wack, and then like I said, cause the GI issues where the microbiome is not healthy. And then the microbiome in your, in your intestines, and in fact your entire body.

Erik Johnson: 1:41:17

We're seeing a lot of things going wrong. I mean, the trees are dying of mold, frogs, snakes, bats, we've seen a fungal diseases take off like nobody's ever, they couldn't have existed before, because now we've got species going extinct from it. So something major is happening but what to research? You know, the problems getting funding, getting research, getting attention to something specific. Well, I thought, at least by starting this chronic fatigue syndrome, which has turned into a really big deal, at least we can get research into one thing, we can get some serious funding going, some research going. And yet every chronic fatigue syndrome researcher, every aspiring ambitious advocate, or researcher all wants to look at their own pet theory, and by doing this, they don't cooperate, they form a competition. So nobody gets any attention.

Alicia Swamy: 1:42:11

You go nowhere with that, you know, at least if we looked into the mold, maybe that could have went down a path of maybe looking at even more external issues.

Erik Johnson: 1:42:21

My offer to the Mold Congress, to Dr. Shoemaker was by connecting up your entity with this famous syndrome, then this will leverage research, they'll have to respond because it's something I mean, like 20 million people have a chronic fatigue syndrome diagnosis.

Unknown: 1:42:40

Yeah, but that benefits the insurance companies. There's like Dr. Schoonmaker just said there's no money to study it.

Erik Johnson: 1:42:50

He could get it if you were to admit, if you were to connect CIRS with chronic fatigue syndrome and I think that would open up some doors.

Unknown: 1:42:58

I think, you know, like he said, He's running on private funds. He can do it, I think, if wanted to.

Erik Johnson: 1:43:08

Why would a researcher turn down the opportunity to to get that kind of leverage?

Unknown: 1:43:14

Yep. So you know, I've worked in universities for years and there's all sorts of politics that go on. If you're a scientific research in a university, there's things you can't touch.

Erik Johnson: 1:43:26

Right? Why would a researcher do reverse politics? Why would he engage in behaviors that undermine his own ability to get power, influence, and research?

Unknown: 1:43:37

Are you talking about Dr. Shoemaker in particular?

Erik Johnson: 1:43:41

Yeah, but all of them are done that

Unknown: 1:43:43

All of them yeah. So if you can't publish something, you're not going to study it. If the editors of the major journals don't find it attractive, you're not going to get it published. It's an entire system of really control that's causing us to be marginalized. One reason is because there's no blockbuster drug that will take care of it. It's a systemic issue. If insurance firms actually had to cover replacing your homes, to the extent of medical necessity, it's going to cost. You know, it'll put them out of business, essentially. You know, getting treated like you did going to the desert. They do that in Russian, actually, they'll send you away to retreat to get to get it well. But in the US, there's no system like where they'll send you away. Unless you're intoxifying yourself with heroin or something, then they'll send you to a retreat.

Erik Johnson: 1:44:44

My focus was not on getting everybody to go to the desert. I said, this is a clue. This is an insight into the etiology of this process. We can study it. So one of the reasons One of the ways that they're working to defeat my efforts to get research is they do this constantly, Erik wants everybody to live in the desert. I don't care if anybody goes to the desert. This is a clue.

Unknown: 1:45:09

It's like a bathtub. If your bathtubs overflowing, you'd have to get to a place where less water is going in and more water is going out.

Erik Johnson: 1:45:17

I am extremely against this toxic soup, toxic overload concept. That has been the most destructive interference to science because anytime you try to look at any one thing, they go, Well, you can't do that because there's something else. You look at this, you might not discover, everything goes into the toxic soup trash bin, and if research has not fallen into that trap, been the discoverers of toxic mold, within a few minutes.

Unknown: 1:45:45

Everybody has toxic loads from modern living.

Erik Johnson: 1:45:48

Remember, Lake Tahoe is the most pristine, beautiful mountain community. It's the place where people go to get healthy. So there was something specific that happened. If it were toxic overload, everybody in Mexico City or Sacramento would be dead before anybody got sick in Lake Tahoe. So why did we have cluster upgrades at Lake Tahoe? We've got such a beautiful, pristine environment. If you look at for a toxic agent, it's capable of doing this and forget about the toxic load. Wow, it turns out that there are a couple things that showed up in the environment that are capable of doing exactly what we said they were doing.

Unknown: 1:46:28

Yeah, the toxic load on it becomes an issue after you get exposed to the mold stuff. It's there. It's in the background. It's causing diabetes and all sorts of things.

Alicia Swamy: 1:46:37

Erik called it chemically induced AIDS. Right, Eric?

Erik Johnson: 1:46:42

Yes, I did.

Alicia Swamy: 1:46:43

As scary as that sounds, but it's acting like a chemically induced AIDS, it's completely suppressing your immune system. And then whatever is happening in your environment, you're going to get sick from that virus or that fungus or whatever. And so it's just like.

Erik Johnson: 1:46:58

It blows me away, as Dr. Chin Yang, explained this at the World Congress, and I thought, Oh, my God, all these mold experts, they're going to go into shock. They're going to go wow, there is a specific mold that's capable of shutting off your immune system. So this fits the facts. Not a single one of them did. Not one. They didn't even tell anybody about it.

Alicia Swamy: 1:47:23

How do you hear that information and then you completely don't say anything about it ever again?

Kealy Severson: 1:47:28

They all went to Erik's groups and started attacking him. Like he's a complete piece of garbage and that none of his evidence mattered.

Unknown: 1:47:37

I just wanted to just stop in and say that I hope it went well because, you know, my, my concern is always that the advocates try to stay on as much of the same page as possible because we've got bad guys to fight, who are influencing the policies with naysaying. Like, we don't exist, we're not real, we're making it up and so it always concerns me when I see conflicts among those who know that we're sick and there is something to it, I like to see those get smoothed out.

Kealy Severson: 1:48:10

For us to have mold policies, we all need to acknowledge mold as part of the problem, and so we're not going to fight any bad guys on any mold policies with this being not mold. So I agree with you, 100%.

Unknown: 1:48:25

I mean, you know, that's the thing. Some of some of our proponents are more fighting mold, some are more fighting mold, toxins, some are more trying to fight all the toxins. So it's hard to keep everybody on the same group. I like to try and encourage people to say, Well, I don't agree with Dr. However, I think he's a fine physician, and sometimes that's really hard to do it. So anyway, I'm glad Dr. Shoemaker came on. I hope it encouraged, you know that we're all fighting to get treatments together on this and I just like to deal with knocking out the bad guys. So I don't know what you stand what you all do.

Erik Johnson: 1:49:11

Something that you missed was we asked Dr. Shoemaker if he felt that the new findings with actinomycetes would force the CIRS community and the people who were doing all these mold and mycotoxins summits to change their name, because mold is no longer the main focus. And he said yes, so he's really moved away from mold in a big way.

Unknown: 1:49:30

Has he moved away from it or is he trying to include another aspect of the toxins of the water damage building?

Erik Johnson: 1:49:40

His action speak different.

Kealy Severson: 1:49:41

Well, Erik asked him if some of like the mold businesses are going to need to change their name to actinomycets businesses, and Dr. Shoemaker said yes, probably.

Unknown: 1:49:53

Well, that could be true, but that doesn't mean that mold is completely out of the picture or mycotoxins are completely out of the picture. It just means that Dr. Shoemaker is focusing his efforts more in that area, is how I interpret that.

Erik Johnson: 1:50:11

The people from his own organization, he got in my group and started criticizing me, you can see that they clearly took this to mean that we have moved on from mold. We've gone from chronic fatigue syndrome, and Dr. Shoemaker's new science, new research is th only direction to go

Unknown: 1:50:27

That's their opinion, Erik, you and I've been doing this for so long. We know here's not going to be, everybody's not going to agree on everything. You just have to keep going in your area.

Alicia Swamy: 1:50:39

Well, I think that s about it you guys, we've been n here for a while since noon Thank you for joining us today. It was a very interesting conver ation. I just really want some a swers and I want us all to g t the help that we need, and I eally want people to look into rik's evidence, the original ev dence so we can finally get e es on mold and Stachybotrys beca se it seems like it's a lost ca se with everyone, for some reas n, with the people that re important that need to be looking into this. So we re really just trying to conti ue on with what we're doing, nd continue on bringing on peo le who are experts in the field ho do validate mold, but we do a so talk about other things, in terms of healthy living, heal hy housing, and all that g od stuff. So thank you, again or joining us and we will have a new podcast for you Monday a keep an eye on that. It's a really good one, he really go s in depth into the mental heal h and suicide aspect of being si k of mold illness. It's a ver, very hard conversation to hav, but it needs to be had becaus this really and as we all know devastates our life, even to th point where we feel like w don't want to live anymore. S check out that episode and chec out all the other episodes, w do have some cool stuff o Patreon coming up, we do allo early access to all of ou episodes on Patreon. So if yo can't wait and you want to hea it when I release it before, g ahead and become a Patreo donor. We have some really coo Q&A's coming up in the future, and actually a book that talks about Erik's situation but also includes the effect and information on that. So we are working on all these projects and different things and we can't wait to share it with you o thanks again everyone. Take are