The Jordan B. Peterson Podcast - 415. 80% of Homes are Fostering Chronic Illness | Dr. Scott McMahon & Dr. Ritchie Shoemaker

Episode Date: January 18, 2024

Dr. Jordan B. Peterson speaks with Dr. Scott McMahon and Dr. Ritchie Shoemaker. They discuss their potentially groundbreaking research into CIRS, or Chronic Inflammatory Response Syndrome. Backed by research, these two doctors believe that many other illnesses and syndromes such as fibromyalgia, obesity, and even depression might actually be caused by mutations in common mold as a response to our own efforts to live in a hypoallergenic world. Scott W. McMahon, MD, founder of Whole World Healthcare has been practicing pediatrics in Roswell, New Mexico, for 26 years. His interest in Chronic Inflammatory Response Syndrome (CIRS) began in 2009. Dr. McMahon first learned about CIRS after being approached by a businessman whose daughter became ill while attending a local school. The search for this child’s healing led him to Dr. Richie Shoemaker, the global expert on mold illnesses. McMahon visited Dr. Shoemaker’s practice to learn about the treatment for CIRS and saw the tremendous need for more physicians prepared to treat CIRS. He immediately opened a practice in Roswell specifically to diagnose and treat patients with CIRS, starting with 15 patients from the local school. His CIRS practice has now grown and he has seen thousands of adults and children to date. - Links - For Dr. McMahon and Dr. Shoemaker: Surviving Mold (website) https://www.survivingmold.com/legal-resources/physician-referral-information/dr-scott-w-mcmahon-bio CIRC Diagnoses https://scottmcmahon.doctor/ Boot Camp: A Beginners Guide to Spiritual Warfarehttps://www.amazon.com/Boot-Camp-Beginners-Spiritual-Warfare-ebook/dp/B09QBKMP9Y/ref=sr_1_1?qid=1703614821&refinements=p_27%3ADr.+Scott+W.+McMahon&s=books&sr=1-1&text=Dr.+Scott+W.+McMahon The Art and Science of CIRS Medicine https://www.survivingmold.com/store/books/art-and-science-of-cirs

Hello everyone. I'm talking today to Dr. Richie Schumacher and Dr. Scott McMahon, and they are cardinal investigators into a problem known as chronic inflammatory response syndrome, and you probably haven't heard that before. But you may have heard about conditions like sick building syndrome or fibromyalgia or chronic fatigue syndrome, and you've certainly heard of conditions like Alzheimer's and other degenerative neurological conditions.

Doctors, shoemaker and McMahon think that they have discovered with the help of other people, obviously, at least one potential pathway to such conditions. And that has to do with toxins in buildings. So the basic theory is something like this, a substantial number of buildings, especially those built with drywall using anti-fungal paints, have water damage, that water damage produces biotoxins of various sorts, for a substantial proportion of the population, about 25 percent exposure to those biotoxins produces an immunological response that has all sorts of neurological and behavioral negative consequences. And so I found out about this through my daughter who's been wrestling with health disorders

of various sorts for her whole life. She's convinced me that it was at least worth a, it was worth some investigation, and that's what I'm doing. And so I decided to, I read some of these gentlemen's research papers, and they struck me as highly credible, and so I'm talking them to them today to find out just what there is to this. If they're right, about 20% of the population

is suffering from all sorts of conditions, often diagnosed as other illnesses, depression included, and that's actually a consequence of exposure to biotoxins in water damage buildings. And this also seems to be a particular problem, by the way, among the military, low grade military housing, much of it water damaged and mold infested. And the government, by the way, seems to agree with that assessment, even though not enough has been done about that so far.

So anyways, come along for the ride. That's what we're talking about today. Dr. Shoemaker, Dr. McMahon, welcome to the program. I'm very interested in talking to you guys today. My daughter has alerted me to your work and I've been looking into it for the last four or five months. You guys have been studying something called chronic inflammatory response syndrome and the more I've looked into this, the deeper the rabbit hole goes, I suppose you could say that. And I thought the best way to educate myself and potentially everyone else who's listening and watching would be to have you guys on this podcast,

so I could ask you all sorts of questions. And so I'm going to take a friendly skeptical approach if you don't mind because what you're studying is of such magnitude that if you're correct, it's a catastrophe. And so we could all hope that you're not correct so that it isn't a catastrophe. But I know you've accumulated a substantial amount of evidence and so maybe we'll start with you doctor Shoemaker do you want to just tell everybody what it is you've been studying and Why you started studying it and how widespread you think the problem is? Most people have a sense of what inflammation is our body is looking at environmental stressors that must be dealt

with in the inflammatory process as a general rule is part of the environmental response to the trauma or stress. Inflammation can be of two kinds. One is acquired or allergy or kind of the adaptive way that the body will learn how to make antibodies and respond to stressors with memory. So there's things we'll be experienced once and then the twice as the next time this is very quick. But we're looking at a different form, the left hand, if you will, compared to the right hand, of innate immune responses in which the response to an antigen or a foreign particle that's introduced in the body in many different ways, inhalation is certainly the big way I worry about, but it could be elsewhere. But specifically, once there is antigen detection by the innate immune response system, there should be processing

of an antigen and putting on a HLA molecule or hystacropatic, we will look at say molecule on the antigen and packaging it in the antigen presenting cells to a naive lymphocyte, just waiting for something to happen. And when the naive lymphocyte sees this tasty little morsel package with HLA and an energy on it, it should turn on a kind of C cell or B cell, to make an antibody. The problem with the illness that we have is that over 95% of the patients do not have antigen processing correctly so that antibodies are made in a reduced fashion if at all. When we look at now, what control do we have on inflammation if the stimulus is not stopped? And it doesn't have to be ongoing exposure, it is now in this world of

energy and interaction with energy presenting cells and telephysites that has gone awry and the illnesses that we see become chronic because the antibody formation does not occur. Now over the years, we knew about problems with the energy presentation, but now we know the gene mechanisms behind defective antigen presentation and the gene mechanisms to not only include inflammation in our venues, but also abnormalities in metabolism. So, if we look at metabolic problems combined with inflammation, we have molecular hypometabolism, which is an advanced way of saying that 95% of patients with chronic fatigue have a specific abnormality and inflammation in metabolism, though we can show with genetic makeup, and then with Scott's work and my work,

we've been able to show that we can correct the gene activation when it's not supposed to be activated and do correct gene suppression when it's not supposed to be suppressed. So what we're looking at is the transcriptomic or gene representative theory of illness causation and illness correction. Our last paper, and I hope you had a chance to take a look at it, but it's in your inbox,

if you've done, the next question is now when you're looking at, to me, the Holy Grail, and that's correction of dieback central nervous system to generation, you may hear it called Alzheimer's, you may hear it called Parkinson's, And that's correction of die-back central nervous system degeneration. You may hear it called Alzheimer's, you may hear it called Parkinson's. You may hear that same called for havedrophic monotrophic lateral sclerosis or ALS. But we are there. We're there with gene activation and correction with our therapies that have been developed

over the last 27 years. Okay, so you're going after a host of the immunological diseases, including extraordinarily widespread conditions like Alzheimer's, Dr. McMahon, do you want to explain to everybody what this has to do with where they live? So, there are a number of potential triggers that can cause the innate immune system to activate. And as Dr. Schumacher pointed out, these people, or at least around 90% of them, don't have adequate or effective antibody production to help mitigate when there is chronic exposure. So the innate immune system is then basically left to handle this by itself without the antibody calvery coming in and reducing the burden. And if you are living or working or going to school

in a water damage building where there is increased dampness or increased microbial growth from molds or bacteria or actinobacteria or all of the above. When you inhale those, your body recognizes those as being foreign antigens. And it's not just for instance say mold spores. It can be old dead mold spores that have lost their integrity, their cell walls broken apart into hundreds of fragments. And in fact, those fragments, when you inhale them, go even deeper down your respiratory tract into your lung. And again, trigger the innate immune system. As a response to that, the innate immune system will overproduce cytokines.

In the same way that you would overprodu produce cytokines if you got the flu or if you got COVID or some other kind of viral infection. And these fragments trigger the anatomy and system and the overproduction of the cytokines and then the cytokines cause the symptoms that we commonly relate to with the flu which could include headaches, muscle aches, joint pains, fatigue, malaise, difficulty sleeping, coughing, other respiratory issues, brain fog, etc. Okay, so let me get the whole sequence of this straight. So what you guys have been studying is sometimes just, and stop me at any point if I get any

of this wrong, sometimes people refer to this as sick building syndrome. You've brought in conditions like Alzheimer's and other immunological diseases, chronic fatigue syndrome. I know you've concentrated to some degree too on fibromyalgia. So the idea is that there are many buildings and we'll talk about how many, but there are many buildings that harbor airborne pathogens, mold being first and foremost among them, perhaps, that's much more likely in buildings that have been water damaged and not properly remediated.

The consequence of that is that if people are in those buildings, living in them or working in them, that they're chronically exposed to pathogens that can trigger an immune response. And some people, when that immune response is triggered, they're not producing antibodies in a proper manner. And there are genetic reasons for that, and possibly metabolic reasons as well. And then, is it the combination of the pathogens that are in the local environment, plus the genetic weakness or the metabolic problems that produce this cytokine storm

that you associated with flu-like symptoms and pain and chronic inflammation? And have I got all that right? Is that the way this lays itself out? You're doing great. Keep on. That is excellent. Okay, good. So, let's go through that one by one.

Then the first issue is then what percentage of buildings in North America and elsewhere in the world do you think are suffering from this problem? And if it's a large number of buildings, that's obviously a catastrophe. So what's the evidence for this and why did you guys become convinced of this? What we have seen is a similarity of the syndrome of acute exposure, followed by chronic exposure, wherever the person might live. It's not confined to Florida or why or why could be in Nepal or could be in in in in in Stuttgart. This worldwide exposure to an environment that pretty much has 62 to 78 degrees year-round. No winds, no rain, no change of the seasons indoors. In the mark of every one of these indoor places is water intrusion. So if we look to see if have a role, but we also know that endotoxins

from bacteria are second on the list and first is actenobacteria. And when you look at every building that's water damage that has these ecological parameters, you find the same symptoms, the same laboratory findings, and now that we have access to gene evaluation, the same gene activation and the likelihood that this would be due to something else becomes a statistical problem. In some of Scott's work, he's published that the likelihood is that you've got a p value of less than p is less than one to the minus 50th power. So it could be the same in suit guard if the most will the same, but actually statistically the idea that it's not the same is so remote to be impossible.

Okay, so what proportion of modern buildings, first of all, isn't modern buildings that are particularly affected? And if not, or if so, what proportion of buildings in general are we talking about? And are there specific kinds of buildings that appear more susceptible? I read in some of the work of yours that I reviewed, for example, that drywall seems to be a particular problem. So what kind of, how widespread is this problem, do you suppose?

And what buildings are particularly affected? Well, the EPA has published the United States Environmental Protection Agency has published that at least 50% of the buildings and up to 85% of the buildings in the United States are historically water damage. Buildings that are involved are not due to one year of construction or another, with modern structures put up quickly, contractors investing money, wants to turn over the house, sail quickly, so you may not wait for a master plumber to put in the bathroom, and a plumbing leak can develop. Instructions and defects for new homes are real bugaboo.

But even when we were in Scotland of the castles from the 1200s and before, we saw the same kinds of problems, but in the older buildings where they had not been paint used with fungicides in them, for example, we didn't find the same organisms making toxins the way we do in the newer buildings. In about a 1970 when the population got all set with the oil and bargones and houses were made to be tighter, we thought that that was the reason for the problem. It was actually not because what we were using were paints and sealants to keep down mold growth. What we did was create natural selection to kill off moles,

it could kill. And if the moles that survived, became toxin formers were before they didn't. So before 1970, it usually was a painting, a building that was retrofitted or retrofitted, retrograde, corrected or modern construction. The safest buildings, even their water damage are the old buildings with no paint. Okay, so there's no specific form of building that can be, that's a menable per se to water damage and the intrusion of toxins in in consequence, but you talk about buildings after 1970. You said your first hypothesis was these buildings were arguably more dangerous because they were more airtight as a consequence of panic over declining fossil fuel availability. And I remember when people started talking about sick building syndrome, I guess this went back

as far in my knowledge as far back as the 80s. They were concerned about these hypersealed buildings. But you said that your further investigations revealed that it wasn't the ceiling of the buildings per se, so much as the use of modern paints and sealants that had anti-fungal chemicals embedded in them. Now, hypothetically, the reason they put those anti-fungals and anti-mold chemicals in the paints was to keep the fungus and mold down. But you said, or you're implying, I think you said directly, that the consequence of that, the unintended consequence of that, was that we produced molds and other toxins that were more toxic rather than less as a consequence of natural selection. So, why did natural selection, which was obviously selecting molds and other biohazards

that could tolerate the exposure to this poison. Why did they become more toxic? And what's your evidence for that? Bunch, I also have response to environmental hazards. And the environmental hazards of being killed will cause abnormal activation of genes in fungal species such that they'll make toxins where beforehand they didn't. With the main role of a microtoxid, for example, has nothing to do with defense. It has everything to do with predation. So the fungus wants to be eating a plant and the plant doesn't want to be eaten. So it'll release things like a peroxidase and the fungi may compounds who eliminate the

fungi. They eliminate the peroxidase, therefore eliminate the plant defenses. But it's predation of fungi on its prey. That's foremost for all this goes on. Meanwhile, actinobacteria, love, and alkaline environment molds like an acid environment. And the alkaline environment from actinone is created by manufacturer substances that will kill off fungi and change the pH of the drywall. So that as you see an initial building, the initial colonization will be with fungi, it will be replaced by actinone bacteria as time goes on. But meanwhile, if there's a flood or a hurricane event or a natural disaster, the water saturation

or AW is the people should say, activity of water will initially lead in organisms that like very saturated conditions or AW.9 to its maximum of 1.0 or 100%. So we see one group of fungi of water damage that's acute, one different species of will be grouping of water damage that's less acute, and in the end, then we'll see of sources that have very dry buildings with where the moisture has changed the ecosystem. Now, actinobacteria, our famous for creating mus smell. And interestingly, the musty smell or musty odor that we've long associated with fungal

certain colonization is coming from actinus. From jiosmin. There are also architectural design features that make it building more likely to become water damage than others flat roofs or more likely to leak than then Pish troughs are basements and crawl spaces are more likely to have water intrusions than you would see in Homes that are built on a slab You know that drywall is more likely to have problems than plaster on the lathe. So there are a number of different materials and architectural styles that can make a house or a commercial building more vulnerable or less.

Right. Well, you could imagine, you know, when I'm thinking my paranoid thoughts, I know here's an example. So one of the reasons that the Roman Empire fell was because the Romans used lead to seal their wine emphora and lead is a known neurotoxin. And when we introduced lead into gasoline to stop the gas from our internal combustion engines

from knocking, we lowered the IQ of people around the world by a substantial margin. It was really quite a catastrophe. And that was, it was also the case that in relatively low, let's see, in older houses that had used a plethora of lead paint, where the paint was allowed to deteriorate and young children were therefore ingesting lead paint powder. They were also impaired in terms of their intelligence and also much more likely to be anti-social and criminal. And so the reason I'm bringing this up

is because it's possible for a society to introduce something into their myths that's then distributed in an extraordinarily widespread fashion. Experimental vaccines come to mind, by the way. And all of a sudden, all sorts of things that we didn't, that weren't understood about that thing that's being introduced, make themselves manifest. And it sounds like that's a case that you're making for drywall,

is that it's extraordinarily light, easy to work with, cheap building substance. But it isn't, we don't have a lot of historical experience with it. It was introduced in a very widespread manner in the latter half of the 20th century. And so, and then you're saying that in combination with the fungicides and so forth, that was put in the paint that we put ourselves in a situation where we've contaminated something approximating 50 to 80% of buildings. So that's really quite the bloody catastrophe.

So now, let's take that apart a little bit. If it's 50 to 80% of buildings, how many of them in your estimation are contaminated to the point where that actually constitutes a serious health problem? Like, you know, I know that that's a threshold issue, but there's lots of threats that people have to contend with, obviously. And if your house is contaminated with mold and water damage, that's a big deal. It's a really difficult thing to fix or it can be. And so, under what condition should people be prioritizing this as an actionable risk factor? And how widespread do you think this problem is, and it's more serious forms?

Yes, study after study has looked at individuals' susceptibility, which underlies who gets sick and who doesn't. The individuals' susceptibility of the immune response in Spanachromosum-Sexley, GLADR, was shown to be present in just about every person who has serves, and the percentage of not having serves HLA, but having an illness is less than 5% of the total. So 95% were broken down into six separate haplotypes, around there are 54 available, and out of those six is 24% of the population. We look at this 24% we put them

in exposure and followed them prospectively. We can show that the initial responses once a primal event has taken place is essentially 100% in those individuals of ability. We're seeing this exactly the same way with COVID, COVID creates an inflammatory response that turns on an 8-immune responses, which turns on gene-based susceptibility. So long COVID has the same genetic makeup and we've published a paper on this in June of last year as well that creates a new illness, a new target where once was before.

And we looked at people who had, we're living in a building and find, got COVID, got better from COVID, but then that turned on the innate immune response system that didn't stop and lowered the whole a month later, two months later, three months later. They had long COVID syndrome, but actually what they had was a chronic inflammatory and metabolic response syndrome. It was just a different initiator. It could be a whole of a horrid of of yellow that and jacket stinging people in the picnic creating a inflammatory response or it could be an illness. In this case, COVID feels available. COVID fails to develop. Okay, okay. So you could imagine that there's a manner of conceptualization that allows

for two kinds of disease processes. There's disease processes that are associated with pathogens per se, and then there are disease processes associated with an anti-disease response or an immunological response gone astray. So if I'm following you correctly, we have a situation where, let's say, 75% of our buildings are contaminated. And so three quarters of the population is exposed to the pathogens that could produce an immune hyper response.

But 25% of the population in those buildings is particularly susceptible to that because they have a genetic predisposition to immune overreaction in response to the specific kinds of pathogens we're describing or is that a more general susceptibility to immune overreaction you seem to be implying that in relationship to the COVID issue So so it's 25% of 75% essentially is the number of people who are hypothetically affected. So that's about 25%. That's about 20% of people. All things considered might be experiencing this as a serious problem. So have I got all that right?

If yes, you do. And you picked it up very quickly. I thank you for that. One of the reasons that it's so important. It's that we look at illnesses that are at serves, they actually are serves and add up who has chronic fatigue syndrome, who has fiber of my answer, who has depression, who's just getting older because they're cognitive. Children not doing well in school is it the lead paint that they swallowed? Is it the lead in the applesauce that they've been taking in? Are there environmental factors that are creating this overall systemic illness of which the brain is the injury I worry most about in adults. Scott sees children more than I did so we can let him speak about children with cognitive issues. But the issues are then when we look carefully at chronic fatigue syndrome, we find serres.

And I'd like you to serve, if you could, to identify one significant biomarker that distinguishes fibromyalgia from not. We have 30 biomarkers for serres and 0 for fibromyalgia. Why does fibromyalgia have such a proponderous of people? And how many people with adults have fibromyalgia. Why does fibromyalgia have such a proponderous of people? And how many people are adults have fibromyalgia? 10% and 3% for chronic fatigue syndrome, how about post-line syndrome, how about depression? Boy, we've got 25% all of a sudden and we must start looking at those details. We can stratify sick versus not sick, cases versus controls,

treat them, and show that cases equal to controls, and they become controls after treatment as we go curt. Okay, so one of the things that the non-medical listeners and watchers of this podcast might not know is that there's a lot of overlap in symptoms between different hypothetically different illnesses. And so let's take depression as a case in point. And when I was assessing my clients for depression, the first thing I always tried to figure out was, are they just ill?

Because there's all sorts of evidence associating depression particularly with immunological dysfunction and so I would inquire into their sleep habits and their eating habits and also their associated health conditions to find out if we could because my sense was before we diagnosed something as psychological we should take a look and see if there's actually something causing it and depression is a relatively non-specific cluster of syndromes. Now, you're pointing to a whole set of syndromes that have relatively non-specific symptoms. Some of them even more difficult to diagnose. And easier to be skeptical about in relationship even to their existence,

as safe fibromyalgia and chronic fatigue syndrome, right? That's hard to dissociate from general depression and anxiety and a kind of global neuroticism or even a hypokondriosis. Now, you're saying, you know, your first claim is that 20% of the population is likely to be experiencing these symptoms, but we don't see that, that, we don't see this serious chronic inflammatory response syndrome in 20% of people, because essentially we're placing them in the wrong bins. Now, and so how much of, so let's walk through, let's walk through what the symptom constellation is for chronic inflammatory response syndrome, that's Sirs, and how you think we should go about distinguishing that

from safe fibromyalgia, which is poorly understood or chronic fatigue syndrome, which is poorly understood or depression. And why do you think that your category system, which put places all these people in the box of chronic inflammatory response syndrome, why do you think that that's preferable to the approach that's being used by physicians now? Because you're making a lot of radical claims here,

and I'm certainly not in a position to dispute them, but you know what they say, radical claims require radical evidence. And you're saying, well, first of all, that 80% of our buildings are in serious trouble, that 20% of the population is suffering dreadfully as a consequence and that there are genetic predispositions to this, and that many, many people with many other disorders are fundamentally misdiagnosed,

and that this is actually the root cause of their symptoms, like including absolutely devastating diseases like Alzheimer's. So, what is it? Let's go through. First of all, what are the symptoms that point to serves as far as you're concerned? And then what do you use to prove that that's the condition? As Dr. Schumacher said, we have roughly 30 biomarkers.

These are tests which can distinguish ill people or what we call cases from healthy people with all controls. We have roughly 30 of them and all of them have been validated to show that they separate cases from controls. When we look at the diagnosis of serres, you have to have objective evidence that shows that you have several of these biomarkers. You know, I mean, at least four, or maybe five or more before you can actually even make the diagnosis, the statistical likelihood

of finding a healthy person who had five abnormal biomarkers out of the five we draw or the 10 that we obtain, it is so small, I mean, it's in the one to a million. Then when you start looking at a larger group of people, maybe several people in the same hall, or in the same office building, or in the same school, when you start looking at that, and each person's probability of having those

abnormal biomarkers multiplies by the next person, and then multiplies by the next person. By the time you get to 10 people, you have such astronomically low probability that we see some free gaxidate that it can't be dismissed. I think what the main problem is, and why this hasn't been seen before in chronic fatigue patients or irritable bowel patients or fibromyalgia patients is because most physicians or many physicians don't run the tests that we do. We are looking specifically at the innate immune system as a possible root cause for these different symptoms. And if they'd ran the tests that we do, they would see the same kind of data that we found.

My data is very similar to Dr. Schumacher's. I've seen roughly 2,000 patients, 2,000 that I've evaluated this. For him, it's much more because he's been doing a much longer than I have. And our data is very similar. Okay, so your argument basically is, and I just wanna walk through this very carefully

so that everyone listening understands, is that you've identified a number of biomarkers. You said 30 overall, but apparently you concentrate on something like 5 to 10. Now, there's a probability that any given test is going to produce a result that's positive falsely. So someone will be diagnosed as abnormal on that evaluated dimension, but in truth not be abnormal. But that probability declines as a function of the number of tests administered. So maybe there's a one in 20 chance that any given test will show that you have the condition. But there's a one in 400 chance that two tests would show that,

and a one in 8,000 chance that three tests would show that. And so your case basically is that as you accumulate evidence of the biomarkers, you decrease the probability of a false diagnosis. And there aren't biomarkers as far as I know, there certainly aren't biomarkers for depression. So that's not specific, what would you say, physical or chemical biomarkers.

You know, there's sometimes there's elevated cortisol or decreased cortisol, but it's very known, the markers are very non-specific. So if you're correct and there are specific biomarkers for SERS, that implies that it can be more accurately diagnosed than the other conditions with which it might be confused. And so what are the prime biomarkers that you guys use to make the diagnosis? And why did you pick those and how valid do you think they are and why? We need to start with a case definition. The case definition in 2003 that our group came up with was modified in 2008 by the U.S. Government Accountability Office. When they looked at the potential for exposure, this is what CDC used with Fiskeria back in 1997-1996.

He didn't get sick from a microalgo bloom unless you're exposed to it. So the potential for exposure is number one. Number two is symptoms the same were similar to those seen in published peer reviewed literature. The third element is laboratory findings the same or similar to those seen in published literature. And then the fourth is objective response of biomarkers to treatment. So if we then say what biomarkers have stood the test of time, back in 2000, it was trial and error. By finding HLA was the explanation of why did some people get sick and other people didn't? Was there risk factor like cigarette smoking or alcohol use or age or under kind of the illness with diabetes? No, no, no, no. It was based on genetic markers.

So, individually, immune responses became our first biomarker. Actually, the first biomarker came from the EPA with Kenna now, been studying the neurotoxicology features of visual contrast sensitivity, which is a mechanism to see an abnormal neurologic function of vision. Contrast is one that's been stabilized over time and is adversely affected as velocity of flow of red cells and red and a neural rim of the optic nerve head increases. So VCS was our first HLA was our next in that group. There was a regulatory neuralptide, melanocytes stimulating hormone, which is essentially a negative in all cases and normal in all controls.

And then with treatment, we saw as improvement in MSH, not as much as what we wanted. And that was the impetus to keep on. Scott mentioned cytokines. In 1986, 1985 was the first publication of a paper on cytokines. And here we are in 1996 postulating that this cytokine effect could be huge. And now if we fast forward to COVID, it's a cytokine storm and everyone that drugs toward knows what a cytokine storm is, they're buying COVID tests. They're looking for mechanisms that we have been studying and cytokine storms can are part of an 8-immune response so you'll have it in COVID, but you have it in

service to and COVID doesn't have the same HLA that we know of yet. We'll probably finally doesn't have the same PCS and it's a sorting process. So we took them inflammatory markers, TGF beta one, no lab was running that, so I hired a lab to prove that there was such a marker, and then we showed it with the abnormal and

showed it in its, in its height, with some of the worst illnesses of all. And then we treated it with medications that were available over the counter or with with, with, uh, with the in informed consent. And then every time we had re-exposure, here we came to the prospective acquisition of illness. Proof of causation. We took people that could have been sick for one building, fixed them all the

Atlanta, Alabama, Ohio, and Michael's were the same. And then with informed consent, they stopped all medicines and stayed away the suspect building. Three days, nothing. Put them back in the day, in the building on day one. At the end of day one, laboratory findings changed day two, laboratory changes, findings can change again. Day three, we had the exact syndrome of labs, BCS, and symptoms prospectively proven upon re-exposure only. No other choices could have been affected.

It wasn't depression in three days. It was serves in three days. Okay, so let me elaborate on the story now. So the biomarkers that you described, the first one, which is a very odd one, I've taken this test by the way and failed it, and quite dramatically. And so there's an online test, which is a visual contrast sensitivity test, and basically what you're doing, and stop me if I get this wrong, because it's been a while, is you're

testing people's sensitivity to what visual acuity in relationship to closely spaced lines on a diagram, essentially. And the hypothesis that you're putting forward is that in the presence of these inflammatory syndromes, retinal acuity is compromised, and I don't understand the mechanism there, but that's basically the issue, right? So you have a, there is an online test, visual contrast sensitivity that people can take. See, it's a strange test because it seems like it's so far removed from the symptom set that people would be experiencing. It's very difficult for someone like myself.

I'm scientifically trained. And all of this stuff that I've encountered as a consequence, all of the findings I've encountered as a consequence of going through the findings I've encountered as a consequence of going through your material have really come as a shock to me. This visual contrast sensitivity test being one of them because it's so far removed from the symptoms that it's hard to believe that there could be a relationship. It almost seems like voodoo. Now you said that the reason that this visual contrast sensitivity test works is because the retinal, the retinate self is compromised as a consequence of immunological malfunction. And so, have I got that right? We have a objective parameter and that's velocity of flow of red blood cells

in the red blood vessels and the capillary beds as well as the neural and the optic nerve head. We can measure objectively the high-alburetino flow meter how fast red blood cells move, and they move more slowly if the inflammatory response promotes production of what are called adhesions, which is one mechanism to decrease flow in the area of hyper inflammation and treatment will be shown to improve flow as the environmental stimulus is fixed and is corrected with treatment. So sick patients, you have reduced flow, healed patients, have restored the normal flow to equal controls, but re-exposure, here we go, prospective exposure again. This is how we determine risk in all of medicine and science,

prospectively in our association, but both prospectively re-expose people get the same findings back again. We fix them, we get them back to the same mechanism they were when they are healed to equal to controls. This in and out, in and out, and constant answers to the critics. How could this possibly be true? Well, here are the data. And if people want to argue with me, they can argue with my data. Okay, so let me elaborate on not a little bit before I return to the biomarkers per se. So I know that the closest tissue

that's deeply analogous to the brain itself is retinal tissue. And so I don't know if that's relevant in this regard, but it seems to me that if what you're measuring with the visual, what does it mean? You're with the visual acuity test, visual sensitivity, visual contrast sensitivity test, you're measuring retinal dysfunction.

What are the implications of that measured retinal dysfunction for a broader central nervous system dysfunction or brain dysfunction? Does that lead us logically into a discussion of degenerative neurological conditions like Alzheimer's. It does. The same mechanism of cytokine response in capillary beds is the same whether it started with a fungus, whether it started with the actinobacteria, whether it started with the flu. But this innate immune response is not specific in how it responds, but it will respond. And we can measure its tendency to recur regardless of where it happens.

It'll happen in kidneys. It happens in lung, it happens in liver. And it happens in the neural rim of the optic nerve head, which is the first part of the central nervous system. We've added countless additions to that, but that was the beginning. That was 1998. After studying this for one and a half years, we finally had our first biomarker that showed the way to cytokines. We could separate with treatment. But by having treatment,

we had the way around the skeptics. Because I can say, all right, you use your due to the medicine for a week. And I'll use my due to the medicine for a week, and I'll use my due to medicine for a week. We'll see who's going to work harder. When yours doesn't, in mine does, but I'm going to say I win the battle. Right. Well, that's particularly powerful as you pointed out in combination with evidence that you can re-instantiate the illness once treated with re-exposure. Because then you have direct causality, right?

Instead of the weak sort of correlations that often go to hypothetically prove the existence of a given condition. Okay, so let me get this straight again. So you have the vision test, you have HLA, maybe you can tell us again what that is. Melatonin stimulating hormone and cytokine detection. So that's four, those are the four primary biomarkers. Vision, we also saw, you mentioned cortisol in depression. Yeah, we measured simultaneous

ACTH in cortisol because low and behold, there was dysregulation of ACTH, which is made by the same set of environmental and metabolic pathways in the brain. They're all melanocortins, MSH and ACTH are melanocortins. So if we have disruption of MSH, we're gonna have disruption of ACTH, and cortisol can either follow in step, which it often will, or have create in its own marker. So dysregulation of ACTH and cortisol is one.

We found antiidiuretic hormone doing the same thing. People walk around with chronic headaches and said they had migrating and constantly, but we find out they were, they're all functionally dehydrated with elevated osmolality and reduced ADHD. That was another measurement. We looked at pulmonary hypertension as a very common cardiac conditions mistaken for cardiovascular disease. People are short of breath and you have chest pain with exertion. We think that it's from doing the coronary disease. When in fact, we measure the velocity of flow coming in the force of the flow coming from the right ventricle to the lung, that's

reduced if the pulmonary pressure is increased. When we measure that, we find that over 60% of our cases have pulmonary hypertension that's eluded the cardiologist because they didn't do the echocardiogram to show it. And it hits just one after another. When we get to genomics, and I hope we don't have time for today, I if not, we should do this tomorrow or another day. The gene mechanisms are the real gold line for the researcher and for the clinician alike. Okay, well, I'll return to the genomics issue and don't let me forget that if we don't get there.

I wanna, okay, so we basically walk through, we've done a reasonable overview of the biomarker space. So let's do this now. Let's let's talk about behavioral and cognitive behavioral emotional and cognitive symptoms. Like what are people, what are people who have serves going to experience in their day-to-day life that they might confuse with chronic fatigue syndrome or depression or fibromyalgia, for example, or you said pulmonary hypertension as well. So what are the fundamental symptoms that people should be alert to?

And do they differ in adults and children? Well, as we were talking about decreased red blood cell flow to the optic disc, you have to understand that there's decreased red blood flow to different places in the body, not just to the optic disc, you have to understand that there's decreased red blood flow to different places in the body, not just to the optic disc. So for instance, you know, peripherally, as you look at the hands and feet, we'll see that there's reduced red cell flow there too. Our patients will often have cold hands or cold feet or both. They can have cramping in their hands, they can have pains in their hands,

even sometimes discoloration, you know, that looks like cyanosis. And we see that that goes away with treatment. Dr. Schumacher was talking about the lungs, we also need to talk about the brain. The brain will also have a decrease blood flow. And Dr. Schumacher actually demonstrated that in unpublished data back in the late 2000s when he was doing MR spectroscopy and showed that there was an increasing lactic acid in certain areas of the brain and there was abnormality in the glutamine ratio, both of which suggested that there was hypoprofusion or a reduction of that red blood cell flow. So why is that important? Well, the blood carries the oxygen and the sugar,

the glucose that's necessary for production of energy at a cellular level. It will be chronically reduce the amount of oxygen that is getting to any cell. It will stop making energy as well. and then we get into genomics findings. But what we know is when you're not making enough energy, then you have to ration the energy that you have, and the cell will underperform in different areas. And so that will lead into brain fog and potentially into cellular death, which can then lead into things like, you know,

die-back regeneration and the neurologic illnesses. Now, you also... how do you directly evaluate brain state and brain function? If I remember correctly, I mean, I've been investigating this with my daughter and my wife for some time and some of the details are unclear to me. We've also had brain scans specifically done to look for neurological damage that might be associated with this exposure and sensitivity. And so for everyone who's watching and listening, I might as well tell you why I'm particularly interested in this. I mean, there's a longstanding history of depression in my family, and my suspicions are strong that it has a physiological basis, because first of all, it has a seasonal component, and

that indicates something physiological right off the bat. But it's also associated with a lot of immunological trouble, which seemed to culminate in this case of my daughter, who had endless numbers of immunological problems. And she's treated a lot of those successfully with a very restricted diet as have my wife and I, but she's become convinced more recently that the cause of the food sensitivity that's driving her immunological conditions might be

associated, might be attributed to sensitivity to these biotoxins that Dr. Schumacher and McMahon are talking about. And so, well, that's what we're trying to track down at the moment because this has been a multi-generational catastrophe in my family. And I would like to get to the bottom of it. And so, we did some of these neurological tests that did indicate some neurological damage hypothetically as a consequence of toxin exposure.

And so can you can you walk everybody through those tests and what they indicate and then maybe we can talk a little bit about treatment before turning to genomics. We skipped over symptoms. You asked a couple of them. Yes, right. Yes, all right. Let's pick up that loose end before we hit end is neurocon and all that. The focus on reporting that I did when I had visual contrast is my only biomarker was compulsive logging down of what symptoms the people have. The symptoms is that

I listed in an interview wasn't a self-former question here. The patient would fill out. It's the process of doing a medical history that we're all trained to do in the four years of medical school or longer if we specialize, but specifically fatigue and weakness or not specific, it didn't have two with the others. Aking and cramping, unusual cramping of the legs when you'd get spasms the nighttime and get a Charlie horse or on the hands

and it was hard to extend fingers because the muscles were in spasms at night time, you'd get a Charlie horse or in the hands, and it was hard to extend fingers because the muscles were in spasms. Basically, that was the end of circulation. The fingers and the toes were the end. That's where the accumulation of lactic acid was greater. So that's where the muscle spasms was. Respiratory issues, cough, shortness of breath, sinus congestion, there was chronic,

not related to seasons necessarily. I findings we have red eyes, blurred vision, tearing, sensitivity of bright light, with cough and shortness of breath and difficulty with exertion we had lung involvement. Didn't have a lot of speed and production, and the biomarker was restrictive lung disease, not, not obstructive. It wasn't asthma, was called asthma by some, but it's not, not obstructive. It was an asthma. It was called asthma by some, but it's not. It's restrictive. Abdominal pain, secretory diarrhea, vomiting, nausea, also present, joint problems, soreness, stiffness, first thing in the morning and throughout

after sitting in a chair for two hours. The cognitive issues were there, difficulty with memory, difficulty with assimilation of new knowledge, difficulty with concentration, difficulty with disorientation. The executive cognitive functions are six. Hypothelamic system, we had change in appetite, change in weight suddenly, and weight gained out of the blue, change in sweats and night sweats, especially, change in bio-intempage regulation. Those are all the MSH-related things. So let me ask you a technical question about that.

So when you're going through that as a psychologist, so what I would think would be helpful in relationship to that diagnosis would be to make a list, like a questionnaire of all you listed off about 40 symptoms. I think that's about how many you covered. So you can imagine that you have people fill out a questionnaire and then you could associate each questionnaire item with the biomarkers and you could find out

which of the symptoms were cardinal with a factor analysis. Have you guys done any questionnaire development that's oriented towards symptom identification? Yes, every person that takes their visual contrast test will undergo a symptom analysis and a symptom discussion. And we look to see if there's cluster analysis to test a function of saying yes or no based on visual contrast and symptoms alone without any of the other biomarkers. Yeah, just statistically we can tell you 98.5% likelihood of serrs just on VCS and symptom clusters. It's incredible. No one believes it until they take it and they say my god, my symptom cluster has gone from eight down to six down to four, you're halfway there. We want you down to one.

Have you done a factor analysis of the symptoms by any chance? Yes, it was published in 2006. Okay, okay, all right, all right. So we've covered symptoms now. There's about 40 of them. We covered biomarkers. What, and we talked a little bit about illnesses that are hypothetically attributable to that, but let's go through that in some more detail. What common illnesses, now I don't remember if it's you guys or not, but I read a paper here recently while I was doing background research that showed that there's a much higher risk than in most countries in Finland for the development of of Alzheimer's. And that that was

associated in this paper with a particularity of if I remember correctly, a Finnish architectural design that made their houses more susceptible to these biotoxes that you describe. And that's produced a statistically significant increase in the rate of Alzheimer's in Finland. Was that your work? I got no right. I'm familiar with that work. All I want to do to finish people to show is that treatment will correct the abnormalities and then create the, correct the Alzheimer's.

By the time it gets to the Alzheimer's, we're 20 years late. We can pick up the difficulties of TAB and A4A and TUBB1 and ALS. On a congenital basis, we can identify that. It's very young ages. Certainly, from the time we've got people when grandma is getting trouble with her cognition, we think it's old age. Her problems got started when she was 30 and 40. It's recognizable then and all the other. Scott, I've been manipulating talking to you, your turn. If you guys never tried a verbal fluency test by any chance, because verbal

fluency seems quite susceptible to disruption by certain forms of neurological degeneration that interfere with verbal fluency quite dramatically. And it might be a good marker for cognitive interference. They're very easy to administer. Lindgren and Publi from University of Maryland published on Fisteria, the neurocognitive abnormalities. Verbal processing was one of the panel they had. It was published in the Lancet in 1998. We were taking a look at.

I don't have your skills, but she did, and those abnormalities were found. When you neuro psychological testing of patients, the two most common abnormalities that I see are deficits in working and memory. Emory deficits in processing speed overall. And one of the complaints that we very commonly see is that people are still able to do the functions of their job. It just takes them much longer than it used to.

So what they used to be able to wrap up in power now, three or four hours, which I look at way unproductive and eventually they end up on disability. See, that's why verbal fluency might be a real useful marker because it's a time test, right? How many words can you write down that begin with the letter S in three minutes? And so it's because it's a speeded test, it might exactly pinpoint that interference with ongoing processing, say rather than long-term memory or crystallized intelligence.

So that's really widespread. Well, that's why it's spring to mind what's also an unbelievably easy test to administer. And there's wide individual variability and it'd be very interesting to see if that was associated with the genomic markers that you described. And maybe we could turn to those now. And then I want to delve a bit more into, you know, we brushed over this very quickly, the idea that the symptoms that culminate in Alzheimer's decades later can be detected decades. Previously, I know, for example, by the way, this is another reason the verbal fluency test popped into mind.

I know there was a study of nuns. They looked at their writing samples from when they were in their 20s, and they could tell by an analysis of verbal fluency, which nuns were most likely to develop Alzheimer's in old age. It's the longest long-hunger to study the eye, exactly. So, another reason for verbal fluency might be an interesting marker. So, okay, now, and we just, so I wanted to go in two directions. One direction was, okay, what is the panoply of neurological degenerative,

neurological conditions that you think are likely to be associated with SIRS? We didn't have a assumption-based discussion about symptoms and neurological abnormalities that we thought were for SIRS. We had recorded executive cognitive function, we recorded tremors, we recorded metallic case, dizziness, vertigo, tremors, but we didn't have any way of assessing what was going on with the brain.

We couldn't measure abnormalities in brain and long in 2007 comes Neurokwan. And Neurokwan with one MRI image can look at 11 different volumes that we then could start to correlate with parameters and by 2015, Scott and I made both published papers looking to them, they were reproducible abnormalities in Neurokwan, in serospatients, and then with treatment we can fix those. But the beauty in 2017 was we could actually fix multi-nuclear atrophy. So our treatment was non-specific, non-degenerative, but instead of just fixing the hippocampus,

we were fixing hippocampus of megalo and quadate. We were fixing palad, we were fixing of the mean number of the abnormalities was 3.4 out of 6. And we could fix those to equal to controls to 0.9 abnormalities, in case of equal controls. So Neuroquant early on became of interest, but the final change was neuroquant associated with genomics. And before we go there, I should just mention that there's a pattern of damage that we see in the brains of people that have chronic inflammatory response syndrome. In fact, there's more than one. If you develop your chronic inflammatory response syndrome, the result of water damage buildings,

we tend to see that the forebrain perencoma will be swollen. We see that or enlarged, I should say. We'll see that the critical brain matter will be enlarged and that the cate nucleus will be a trophic, will be smaller. If you develop chronic and functor response intervals, the result of Lyme disease and post-treatment Lyme disease syndrome, we see a completely

different pattern and that pattern is that the right thout is enlarged and that the putamen is smaller and atrophic. And we showed that on two different studies and then in the third study that Dr. Schumacher and I published together looked at different treatment. And when we used Dr. Schumacher's treatment protocol up to the next to the last step, we saw that the forebrain perancamam that had previously been in large and the cortical gray that had previously been in large came back to control values. But we didn't see it proven in the multi-nuclear atrophy. The next paper, though, did, and that was with use of VIP, Basel Actimatesch Halle peptide,

which is a substance that your body makes. And it's an anti-inflammatory peptide. It's a neuroregulatory peptide that brings your activated immune system back down to normal when it's appropriate to do that. And so with VIP therapy, which Dr. Schumacher by hand, we have seen Codate nucleus and multi-nickr atrophy either stopping

or reverting back toward normal. Have you guys used that same treatment protocol for conditions like Alzheimer's or other degenerative neurological diseases? Obviously, there's an overlap there, which we've discussed or hypothetically, there's an overlap there with CERS has anybody been looking at the application of this particular treatment protocol to these degenerative neurological diseases? Yes, we published one study just a few weeks ago.

But what we didn't have was looking at people that were untreated or stage one patients compared to stage two, which is treated with the first part of the protocol, stage three, treatment with the IP, with stage four. That's where we had the off VIP and then doing well. We had a reduction of the basic mechanism of dieback CNS to generation,

looking at changes into UBA for a 44% reduction in three months. That's not been published yet, but it's high on our list. Yeah, I bet it's high on your list. Yeah. It's like we've got to get going on this one. There are other things that other people are doing or where this is a complex field and no one in the illness parameter will fit everybody. But if you've got the micro tubular dysfunction, that we add a Lutitilathe UBA4A and TBB1, you have that as a marker and you have cognitive issues and you're using your respond to VIP, the reduction is 44%. And that's just in three months of work. Okay, so I would like to take this in two directions now and we've got about half an hour left in this segment

although we can run a little longer if that seems appropriate. I wanna know about what people should do, what constitutes treatment. And so that would be building testing, building remediation and then the interventions that you described. But I would also like to talk about, I know Dr. Shoemaker that you and Dr. McMahon have brought this problem to the attention of government officials. And I believe,

particularly in relationship to military housing, but not only that. So let's start with everybody who's listening to this is going to be thinking, well, I know people who have this cluster of symptoms, you know, what in the world should I do about it? So let's talk. We had our houses mold tested, and you know, the results were rather dismal. And I'm not exactly sure what to do about that because I have properties now that appear to be quite mold saturated.

And you know, the step after that's not exactly clear. One of them was just remodeled and I'm not that inclined to bloody well do the whole thing again, you know, but that's partly why I'm investigating this to the degree that I am. But what is it? What are the steps that people should take in order to determine, first of all, that they have this problem and then and then in order to do, first of all, that they have this problem and then, and then in order to do something about it. We first need to make sure the patient satisfies the case definition. If they don't satisfy the case definition and the serves, this doesn't apply.

But if you satisfy the case definition, then we want to define the ecological parameters within the building. If the building is water damaged and you should have fungi, but it doesn't, and you don't test for actinobacteria, you've made a mistake. But if you don't have fungi, is that because you never had them? Or is it because it's overrun with with actinobacteria that making the drywall surface alkaline and, fungicide, only very well? And then if that's not the case, what about the water saturation with endotoxins? Because of the three things that cause the greatest amount of damage to the brain endotoxins lead to list, specifically for every abnormality that we find in the gene that shows us a specific causation.

That's the building contractors' words. Specific causation for endotoxins. We've identified in Neurocon. We've also identified in combination with the genetesting or genomic testing. So the two go together. But then we wanna know, do you have endoshoctions? Do you have bacterial bacteria? Do you have fungi?

And you can do that on one dust sample, collected at home by someone who can put a glove on one hand and wipe the swiffer cloth in one direction, over 10 to 30 surfaces that are horizontal above the floor, and send that off to a lab that's reputable to this license. It's not a fly-by-night insurance organization, but there are those that are out there.

They really are. But specifically, if we've got a reputable lab that shows us the abnormalities, you've defined the illness parameters, you divide the environmental parameters, now we define the treatment. Do you want to go for treatment? Scott?

First part of treatment is taking care of the exposure. So if you're living in a home that's water damage or it's your workplace or maybe school that you're attending, you need to either fix that or mediate that or leave that. The most important step of any kind of treatment for any kind of immunologic illness is getting away from exposure. That is the most important step. It's probably the most difficult step

for many people always. Great. Spensive and it's mind bending. And as there is a certain variation in knowledge of this illness amongst physicians, there is also a variation in knowledge of this illness amongst mold testers and mold remediers too.

So you want to make sure that you were working with somebody that has stood the test of time and actually knows to some degree about the cellness. But that is the most important step. The second step that we initiate for almost all patients is the use of a binder. And there are different kinds of binders. Dr. Schumacher pioneered the use of colostyramine and colost several also known as well-called.

They are very effective. And typically, we will see improvements within two to three months if you can get that first step taken care of. There are a host of other people that will use other, what I would consider less effective binders, like charcoal and oak repepsin and different kinds of clays and things like that.

I find in my experience that those work, but they take much longer. Most people would like to get better faster. So we use the more aggressive therapy. After you go through those two steps and we see that you're improving, usually your VCS test that was previously negative is now positive or is normal. We usually draw some blood work to look at the tests that you had previously that were abnormal. And based on which one's continued to be abnormal, the rest of the therapy is follows back to she made the experiment. And we just go up the pyramid. And when we've gone

through all of those steps and corrected or attempted to correct the various different systems of inflammation that we're still causing abnormalities in the lab test. After that, we'll contemplate whether usage of intranasal VIP is useful. For most patients, it is. Certainly, in my experience, if you have not recovered at least 70% of your energy, 70% in your cognitive ability, 70% of your exercise tolerance. If you haven't recovered those from the rest of the therapy, then it's time for VIP. You said, if you have or haven't, if you have not. So I'm anticipating every one of my patients will recover at least 70 and up to 90%

will recover at least 70 and up to 90% of their previous capability. If they can follow the protocol as I just outlined. Okay, so I've been trying this call a styrene. So what I've found with it, and this is still tentative conclusion on my part, but to begin with, it seemed to make my symptoms quite a bit worse, even at a relatively low dose. And then I moved the dose up and down for a while, and I seemed to find a dose that wasn't disturbing me. So what it was doing to me was producing symptoms of psychomotor slowing. So it was harder for me to do things. I was thinking more slowly. I had more pain, especially in the morning. More depressive malaise, none of which, as you obviously know, is particularly pleasant.

And if I decreased the dose enough, that went away a week ago, I increased the dose again, and then those symptoms came back. And so why, why, I know that that's not uncommon, that return of symptom, and that that means that the dose should be decreased, but that obviously makes treating this even more complicated because when you first start using the binder, it can make what's wrong with you worse. So, why does the binder do, and why might it be the case that it would make symptoms worse, and who would be susceptible particularly to that worsening of symptoms? When we have intensification, which is the word that I use for people who got worse when they

took a colostiomy, we found that pretreatment, usually with compounds that were reduced inflammatory responses, reduced cytokines, pretreatment was, say, five to to seven days and then restarting cholesterol staramine at red low dose for another five to seven days. You increase the dose five or seven days. And at the end of the month, you get up to the full dose of cholesterol staramine and you go off the the extra medications. Omega three fatty acids are widely used for this. They work very nicely. Actose was a beautiful drug. It's got an FDA black box on it for another reason, but that's still available, and that's for people that are worse. Now, most commonly, when people intensify, there are either two problems pre-existing that we would know

we need if we had done the evaluation. If you have a multiple antibiotic resistant, coagulose negative staff colonizing your nose, not infecting your nose, not creating symptoms, but colonizing your nose and you treat with binders, there can be intensification because this organism makes the toxin, a polycystic ether toxin, a lot of all the cyclic etherin, that is released when it's disturbed in a psychosystem. And there's a binding coefficient looking at other toxins that are bound to a receptor. And when the start pulling the toxin off with colostiramine binding it and the gut, there will be a response of the receptor to suddenly release all cytokines that are bound. So you frequently will create a cytokine storm.

Now the paradigm illness for this is post-lime syndrome. Post-lime syndrome, if you've got Lyme disease and the diagnosis is difficult to prove, but specifically you pre-treat with omega-3s for five days, start low-dose colostiramine and way ago. Now, for other people who don't have marcones and don't have Lyme disease, we found that paradoxically, the last step of VIP can be used in low doses, microdoses, as the first step.

This is from a textbook that Scott and I wrote on the art and sciences service medicine. It's called the low VIDs, the protocol. And we can start people on that, get through the intensification, decrease the VIP, increase the cholesterol, and people sail on. But they've got to be willing to take things slowly and defeat the intensification monster because it is horrible. It is absolutely horrible having experienced it myself. So what does it mean for people, so when I'm contemplating this and contemplating doing

something about it, I'm wondering, well, what's the implication here for travel, for visiting other people? So how's this? I mean, I already almost eat nothing, which makes me, you know, an annoying guest in many ways. And now, you know, if I'm sensitive to these sorts of toxins, that also means that in principle, it's going to be more difficult for me to travel and to visit people. And if you recover, if you're in a clean environment, and you recover,

and you use the treatment protocol that you describe, what does that do in terms of people's, you know, relative long-term resistance, assuming they're not living in an absolutely mold saturated house? If MSH levels don't rise, which is the most common situation, the susceptibility is not changed because your HLA is not changed. It was low in a SH if you get it real, go somewhere to a hotel or an airplane and you reacquire marcons because they're ubiquitous in the environment. And then a marcon starts to grow, you will relapse and re-create us with your assumptions within

three days. Folks who travel extensively, like I used to, will be on medications on a prophylactic basis and take them on a regular basis. I have a room sanitizer that I use when I travel. And I would go to the hotel room and plug that in, you clean out the hotel room, because whether they're kind of heating devices, they might have in the corner underneath the window that has some humidity coming out. We try to keep up with heat or the cool air cooling system, but hotels are doing torsely with carpets and next to bathrooms and kids playing the bathroom.

Oh, let's play hockey and saturate the rug. And you don't know it was there saturated a week ago. And you walk into the little spline, but you are basically re-exposing yourself. It means that you need to manipulate your environment as best you can, yes, your first guess. But then you need to take medication on a regular basis. Fortunately, the side effects of low dose VIP

are essentially zero. So that's a way you can live as far as the carnivore diet as you reduce the inflammatory result of using veggies and other things that are not carnivore food, you will find that VIP is your good friend and it is will be something helpful unless you expand your diet. Once you have reduced the maximum medical improvement from the carnivore diet. Do you think this is a slight sideways move and I won't pursue it for long, but do you think that there's any association between SERS and the obesity epidemic? Oh my goodness, you're describing leftptin-resistance. Leptin is made by a GP-130 cytokine receptor in the brain, right in the hypothalamus where MSH is involved. And leptin must bind to

its receptor, send off a stat-1 residual to turn on production of POMC, pro-OPO melanocortin, to make MSH. So if you're left and resistant because of weight problems, you don't turn on MSH and so that by itself will turn on fatigue, pain, and then now obesity. And what a try-and, and a good day, a good month, a good month, where left in resistance patient, not dimension, an insulin resistance patient, and when in MSH division, is half a pound per month. That's not a good thing. Wow.

Wow. Well, okay. So, so, so what do you think about this? Okay. Well, you know, I've been reviewing the statistics lately, not only with regard to the prevalence of obesity, let's say in the United States, but also two, it's a rate of increase. And the last projection I read was something like 40% of Americans will be grossly obese, morbidly obese by the year 2030.

40%. And that's, well, it's impossible to overstate what a catastrophe that is. That's half of the search patience. If you look at someone who weighs 300 pounds, we're not going to use pedantic terms like morbidly obese. Yes, yeah, yeah. Specifically, when weights are problem, what's left to what are adipocytocides doing, what's insulin doing, and more importantly, what's molecular hypometabolism doing?

Because we've got a prescription. Now we've been using it. They'll defeat the mechanisms. The physiologic mechanism for weight storage and fat storage. We looked at the adipocyte of kinds and brown fat. We wanted to turn on brown fat on a coupling protein. One, two, and three were found. It used to be just one, but I'm coupling one, two, and three are found. We can convert base fat to brown fat and have increased metabolic consumption

of energy by turning on brown fat activation. This is one of the advantages from Finland again. Here we heat you up and have a nice sauna and then we always tend to let you go out and jump into a snow bank without Without making shivering, that turns on brown fat physiology. That turns out energy production like crazy is wasting heat, non-shivering thermogenesis is what that is. Okay. How many papers have you two published between you that are related specifically to this topic, approximately. Over 30. 60. Okay, okay, so we did two of us together, we're 60.

Okay, okay, so 60 papers, all right, so you've brought your findings to the attention of various government bureaus. What has been, what have you delivered in terms of reports? What has been the consequence of that? Hold on, nothing. Well, I had the privilege of speaking before, Adjuncts of the House, the Senate, our services committee in December of 2019,

and then they made a report in the full Congress. And 16 days later, they appropriated $300 million to look into military housing, particularly as it pertained to troop readiness and suicide in the military. And you probably didn't hear about that because the next day, the impeached President Trump for the first time. And when that news cycle was over, we had this little thing called COVID. And then after that, it's like everybody seems to have forgotten. Yeah, well, I read big chunks of that report. And my conclusion was that the people to whom you presented this report regarded your findings as credible.

And three, like I can't imagine how you could spend $300 million testing military housing. I mean, that's an insane amount of money. But it does indicate, regardless of that, it does indicate that they took what you were pointing out seriously. What did you find in relationship to military housing and what do you think the consequences of that are for, let's say, military readiness and for the mental and physical health of the servicemen? The people that I was meeting with had visited a number of military bases

and had seen the military housing. So they were already aware of the rad and infestations and the mold growing on the walls and whatnot. I mean, they'd seen it with their own eyes. What I presented was that this was definitely causing problems with troop readiness. Even when the GI is living there and going and being deployed, just being aware that your family is living in that, and that your family is getting sick and chronically

fatigued and your children are having cognitive issues and chronic headaches and chronic stomach pains that local pediatricians will usually say are psychological symptoms because they don't know what biomarkers to check for it. They did, they find that somewhere between 80 and 90% of those children, both with chronic headaches and chronic stomach problems that they really have serves and it's treatable on it can be reversed very quickly. Yeah, well, it's not uncommon for the patient psychological problems to be a direct consequence of the fact that they've

been misdiagnosed by a physician. You know, like I was always extremely loathed in my practice to attribute any serious physiological alterations to psychological condition, you know, because it just strikes me as highly unlikely. And so it's very easy to assume that if you don't know how to diagnose something, it's a consequence of the male, male functioning psyche, psyche of your, of your patient or your client, and that's an easy thing to fall into. I don't want to be cynical about this. That's an easy thing to fall into if it's also associated with, let's say, depression and anxiety, because those are pretty non-specific symptoms of most psychological conditions, right? And depression, which is essentially a pain-like condition and anxiety, are very easy to attribute to psychological factors, even though they have a profound underlying psychophysiological

substrate. So, you know, I can, I can, I have some sympathy for the physicians, but, but it's all too easy to attribute an illness to someone's male functioning psychological processes. This might be particularly relevant with kids. I understand, Dr. McMahon, you've spent a fair time looking into the problem of sears with children, so maybe we could just touch on that briefly. Yeah, at this point I've seen about a thousand children for that. For 28 years I had my own prior practice, or I worked with a nurse practitioner. In the last 10 years I evaluated the children there that had chronic illnesses for serums also and found that again, the majority of children that had chronic headaches.

And we're talking 10 million children in the United States alone. The majority of those, the large majority, they had serves when I evaluated them for that. And when I treated them for that, their headaches would either go pale or they would become much less severe, much less frequent. It's the same with chronic abdominal pains. I was taught in residency and I went to a fantastic residency, but I was taught that that stomach pains that were

recurrent in children, maybe 10% of the time you could make a diagnosis of your an attract infections or constipation or maybe there's some visceral problem with their liver or some other organ in their abdomen. But that the majority of times that the children were actually seeking either primary or secondary gain and that was psychological. But what I saw in my patients when I started evaluating them for serves is that about 90% outside of that 10%, so we're talking closer to 80, 81% of these patients had four or more biomarkers for surge.

And then when we treated them, there are abdominal pains either went away completely or became much less frequent and much less severe. So it's a really fundamental game changer. These are two of the most common visits for pediatricians, is children with chronic headaches, children with chronic abdominal pains. There's another 10 million who have a chronic abdominal pain. And then you can also expand that to adults. This is the number one reason in my reading

for a visit to your primary care physician is chronic stomach pains, which are considered functional in most adults. They actually have a tumor, functional abdominal pain syndrome. And again, if you were doing the correct testing, looking at the innate immune system, again, my experience is about 90% of those people

with this functional pain will have the biomarkers consistent with the diagnosis of sers. And then treatment, you know, just follows it all. Um, Dr. Schumacher, you, you insisted earlier in the discussion that we returned to the issue of genomics and, and genetic susceptibility. And so I don't feel that we've covered that inadequate depth. So do you want to expound on that for a moment or two?

And so for everyone watching and listening, so the causal pathway is an affected building. That's a building affected by water damage. That's increased. The probability that that will be problematic is increased. If it's drywalled and the drywall is also sealed or painted with an anti-fungal chemical. And then that isn't sufficient altogether to produce the syndrome. You also need a person who's susceptible, and that's about 25% of people, and they're susceptible for a variety of physiological and genetic reasons. And so we're going to delve into the genetic markers for a moment. And the genomics aspect of that.

So Dr. Schumacher, you want to take that away? When we look at the role of metabolism in this illness, it's been under, understudied for years, but now it's risen to the head of the cream of the crop. The structure that makes proteins, and there's a million of these in every cell, it's called a ribosome. And if you remember your high school biology, ribosomes make proteins in and mitochondria make energy.

But the mechanism of protein production comes from RNA, copy in Bophledine, and traveling from the nucleus into the cytoplasm of the cell. And that messenger RNA gives a signal to the ribosome to assemble one ameto acid at a time, and given protein, this code is for by the RNA. So DNA message transcribed to RNA, transcribed to RNA makes a protein. What happens in chronic fatigue illnesses is that the structure, you call the sarsin, rice, and loop, and this get little, little constant, little complicated here, is present in every living feature.

Every, every feature known to God has got a sarsin, rice, and loop in. And at the one point, the 15 nucleotide, where there's an adenosine moiety, a toxin can cause replacement or elimination of that wound plane adenosine moiety, a toxin can cause replacement or a elimination of that wound plane adenosine and the loop won't work. So suddenly a million ribosomes, losing half a million of its capability, won't make the protein needed for cell function and the cell stops functioning normally. Meanwhile, glucose is being driven into the cell by two transporters, and their glycolysis or breakdown of glucose to six carbon,

chain of circle or chain, and there's the circuiters compound, is broken into two, three carbon fragments in a chain called pyruvate. Pyruvate must be delivered across an outer membrane of the mitochondria to get into the middle membrane across the inner membrane to get to the cyclogeoxygenase pathway to make energy. So if you don't get pyruvate going into the nucleus, you don't make the 36 ATP or 38 ATP, the nucleus can break. So on a warberg study this in 1928 and 1955, he found it in a fast way, but he studied cancer. And he found that pyrovate was readily available, but it was not being metabolized in the binocondria. He was being broken down from pyrovate,

a three-carbon chain, into lactic acid, a three-carbon chain. Lactic acid was secreted outside of the gradient into the capillary bits, and lactic acidosis became common. We see this proliferative physiology, and lactic acidosis, in 85% of our surface patients. We have ribosomal attack on protein. We've got lack of proper energy metabolism going on, but at the same time, in addition to metabolic acidosis, will I have lack of a regulatory T cell population, thymus derived

T cells? Will I have the increased gray matter and nuclear atrophy? We'll get pulmonary hypertension. We'll get, here's your obesity. We'll get pulmonary hypertension. We'll get, here you're here's your obesity. We'll get insulin resistance. You get five complications of metabolism abnormality and 95% of the patients who've got molecular hypometabolism. That is prescription for your disaster.

So we start looking at insulin receptor substrate too. That will increase delivery of glucose regardless of what the diet has it involved. A lot of people will be on a diet called a keto diet. With keto diets, they want to make themselves burning fat. Well, if R.S.2 is increased, then that keto doesn't get into the to the cell. It'll be turning on uptake of glucose. So you wasted the keto function in FireS2 is elevated. So if you're going to get serious about a diet and the Carnivore diet also gives tremendous source of glucose. Remember, Aspartate and Glutamator broke down in glucose very quickly when your energy is low. And so that protein wasting goes along with the carnivore diet if IRS 2 is up and having done a

little bit of work with carnivore diet, I would just urge people to know what your IRS 2 is before you stop eating all the gall carbon ice rates. But secondarily, we start seeing disruptions of apoptosis. This is program cell death. Where cell should die normally, the fragments of cells be coated with membrane released into the circulation, but not causing inflammation. But here in this illness, apoptosis, we have defective apoptosis. Where the cell is laced without coating of the internal fragments that are antigens,

so we get now a surge of antigen load in bloodstream with apoptosis in someone who's got defective apoptosis genes. RIPK1, we can tell you that, and that will create an endogenous source for sears. And I realize again, it's a little technical, but look at coagulation factors. These genes are up-regulated like crazy, and they will bind to tall beta in the brain and then create a microclot which will lice, you know, microbleed, and that's where Alzheimer's gets its start.

But it begins with extra coagulation factors. cytokines, we mentioned the tremendous increase in cytokines. We also mentioned there's specific causations for endotoxins. There's there are three markers that we use in addition to environmental samples for actinobacteria. We use tgfbr1 and 2 that will turn on fibrosis. There's a way to tell about the bacteno-entry. And then we look at MAP kinase as it does its own bad things being turned on by a teno bacteria. Bungi will have apoptosis and then you'll have the kinase in the brain cells. So all of these kinase and there's more. Honestly, there's this,

it's been a two hour lecture. Yeah. Lessons from Genie available on free downloads from surviving one website. You just take a look. You don't have to pay a doctor and you can just get it read yourself. Let me ask you, let me ask you a question about the, is there an association between the genetic markers that interfere with cell optosis in the way you described and susceptibility to Alzheimer's? Does anyone know that? What we have shown is that the susceptibility is separate. The cytoskeleton or microtubule genes to UBA4A and to UBB1, that's the one associated with dieed loss. Remember, every neuron of every eukaryote has got a cell body connected to a series of tubes called an axon. The tubes convey ions and nutrients that must get

from the cell body down to the end of the row to the axon to the synapse. Energy demands like crazy. You've got to maintain a gradient of sodium potassium. That costs energy. But if the microtubules are disrupted, as there are in dieback neuropathy, what you will see is loss of this neuron, and then the next neuron, the next neuron, is going on. Meanwhile, graduation is going on,

and you're getting the vascular phenomenon that leads to cognitive impairment. They're both going at the same time and if you don't have blood supply bringing energy in to already damaged nervous system, it just piles up. It is a positive feedback loop of abnormalities and blood flow, abnormalities and energy flow, abnormalities can be identified in Genie. Now we were talking about the government, she's wanna remind you that 2004,

John Connors convened a special session of Congress, Sharon Kramer was the contact person, and she's been a real fighter on all these years for mold rights, for mold patients and all that. She's the one to first move the whistle on military housing problems around the North. I had an energy base, the three billion dollars later that those lawsuits have been settled. But along the way, Sharon also rent blue the whistle and Ted Kennedy's HEL

Committee Health Education and Labor Committee sent a group of physicians, including me, down to New Orleans, to look to see what happened. We could train in Rita. And there are most of New Orleans, this is in February 2006, was still underwater, and Smolius can be, and a female is to win things. But we had a ship. The Scotia Prince was our control group.

None of these people been involved with New Orleans in any way, but they were there, and taking controls for the group, and we had people being stashed on the boat. They were from firemen, they're from children, they're homeless people, people from St. Bernard Parish, and I had a case control study I did over the weekend. All we did was symptoms and visual contrast, 250 patients, and we showed to stink markers if you had more than five symptoms, you were a case with the incredible report was released to St. Bernard Parish on a Monday. He was taking down on Tuesday. That's the last I've heard of it. Well, it's not surprising as far as I'm concerned

because if this problem is as severe and as widespread as you describe, then it makes the asbestos problem look trivial by comparison. And you know, a long time to care if a asbestos mold just makes you feel like you want to die. Right, yes, right, right. Well, but it's so unbelievably prevalent. And it's so, I mean, you lay out very carefully what the treatment course is,

but it's certainly it's a complicated and life-altering process to undergo the diagnosis, the house remediation, which can be expensive. And then the lifestyle and other alterations that would be necessary to bring this under control. And if it's as widespread and severe as you claim, it's no wonder that there's tremendous resistance. Let's speak about that to maybe bring this to a close. You guys have been hard at this for quite a long time and you said some 60 papers published, which is quite a substantial.

That's for everyone watching and listening. That's about the equivalent of 20 PhD thesis, by the way. So you can get a PhD thesis essentially for three publications. It's a lot of work. And what sort of response have you had from the from the from the broad medical community? Like how is your how is your work being received? Do people know this or do they are you on the fringe and outer edges of what's regarded as

acceptable medicine? How have you been received? There is a drugatory term that is still widespread use. I have done a study about emergency infositions called a patient they would see with multiple symptoms called a goma. Yeah. Get out of my emergency room. Yeah. Because there's people take time. And when you have a healthcare system that gives you 10 or 15 minutes to see a patient in primary care facilities and you've got someone who needs two hours of time, who's going to lose? The two-hour patient or the 10-minute patient?

And who's going to go without care? So I think it's a systemic approach, not an individual approach. I think a healthcare system has some of the best positions in the world, but I'm biased because I've seen this in action for 40 years. But specifically when we look to see who's doing the carrying, it's the primary care doctors. The specialist, there is a hand in the waiting room. There's a hard in the, in the cath lab. But that's a person with a hand.

That's a person with a heart. That's a person with a brain. Let's look at what the fundamental unit of care has got to be. It's a person Scott and I spent all day long two hour of business and listen to people. I had one Rheumontologist give me a hard time at University of Washington in Seattle. My Center patient in from Corte-Line who needed to have a TGF beta one done, because he had June on room between arthritis was going blind. And TGF beta one was the cause of that. And he goes, well, I've never heard of a TGF beta one. This is years ago. And being a smart ass, I said,

there's only 75,000 papers published on TGF beta one. I would not admit that. You didn't know any of them in front of the public about were you. Well, right. Needless to say, he got the TGF beta one, the child can see now. But the point is, it's hard to read everything. We're asking you to be an expert in endocrinology,

an expert in metabolism, an expert in cardiology, an expert in pulmonology. We want you to be an expert in pre-renal vasotemia and pots and pans. We want you to do all of it all day long. Yeah, yeah. Well, when I was first introduced to this by my daughter, I thought, I started to read it and I thought, oh my God, you know, it's going to take me two years just to get on top

of this conceptually to figure out, well, first of all, if it's credible information and second of all to really understand how I would possibly reorganize my life to deal with it. So it's really a major. But on the other hand, a long-term prognosis of chronic depression and immunological trouble plus Alzheimer's sounds like a pretty dismal way to conduct life. So you always have to read. Right, well, right, well, right. And I've already discovered some things about how immunological systems work.

I mean, I've been struck to the core by how effective this carnivore diet has been for so many people. And I would have never believed that 20 years ago, that the probability that just the very idea that people could live on nothing but meat would have struck me as outright preposterous and that it was the actual, that food sensitivity was the cause of so much immunological suffering, or at least a cause also struck me as highly improbable, but you know, here we are. It does seem to be the case. And certainly the body of data that you guys have accumulated in the studies you've done, they're difficult to,

once you go through them, they're very difficult to just shunt away and ignore. And I really think that's too bad because I would have just as soon shunted them away and ignored them if I had my druthers. Is there anything that we haven't covered in this two-hour presentation? Now, I wanted to ask you, the textbook that you said, that was Art and Science of Sir's... Treatment? Medicine. Art and Science of Sir's treatment medicine. Art and Science of Sir's medicine. Okay, so that's where medical practitioners can learn about this. What's the best source for just general public people?

I know my daughter's put up a big website about Sir's related disorders and we'll put that in the links. But where should people go online to gather more information about this? Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher,

Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Dr. Schumacher, Well, trusted knowledge is the most literature, the most videos about this are either from Dr. Schumacher's www.survivingmold or sersexcirx.com. Then you go to those two places you can find just about anything you need, including a local provider who would know something about this, if you think that you have this illness. Okay. So those two places are fairly exhaustive and complimentary. Okay. Dr. Mann, McMahon, is there anything that you would like to bring

to the attention of people who are watching and listening before, as everybody watching and listening, knows we're going to do another half an hour with these two gentlemen behind the daily where our plus platform. But before we turn to that, Dr. McMahon, is there anything else that you would like to bring to the attention of the people who are watching and listening?

There's really just one other part of the pathophysiology that we didn't discuss, and that is the blood-brain barrier. Most people, including myself, when I was going to medical schools, thought of an artery that carries blood as being like a garden hose The blood enters one end and it comes out the other But it turns out that actually the cells that make up the lining of blood vessels is pretty porous and small Proteins and fluid can flow outside of the blood vessels and into the body where the cells are.

The cells do not seem to mind that. Maybe they get a little extra snack. And in addition, you've got the lymph system to clean that up. But the brain is much more sensitive tissue. And the brain doesn't want all those potential chemicals and possibly toxins oozing into it. So by five days of life, the brain has set cells to intercalate into those arteries that are feeding the brain and create what's called the blood brain barrier. The blood brain barrier is maintained by chemicals like VIP, maintained by chemicals like vascular endothiode growth factor.

And we see that the vast majority of our patients have low levels of VIP, and at least the third have low levels of vascular endothiode growth factor. So what is created is actual breaches or changes in permeability in that blood brain barrier. What other scientists have shown is if you have an excess of cytokines, doesn't matter what, could be from a TH1 process, a TH2 process, or a TH17 process. If you have additional cytokines in your body

and you have breaches in your blood brain barrier, then the cytokines will go into the meat, the perencoma of your brain, and will cause a low-level inflammatory process. And I'm saying that to some degree for the people that might be listening, but especially for you, Dr. Peterson, to understand that now you've got an infiltration of cytokine setting up low-level inflammatory processes. And not only that, but there are a couple of key areas in the hypothalamus that don't even have a blood-free bear because they're busy sampling, you know, cortisol or sampling

with the serimosmolality is. And so these areas have direct exposure, not it doesn't have to filter through. We can define similar processes in the gut and those processes are maintained primarily by MSH which is almost universally low in our patients and so they develop with great frequency, food sensitivities, true food allergies and whatnot, and they are often reversible. So, if we're going to sum all that up, we're those who are watching. Curses is a terrible disease, but it's diagnosable and it's treatable, and we usually see people recover 70 to 90% of their previous function if they can follow through Dr.

Schumacher's protocol. And then the last point that I would want to make is that I believe that the illness is basically preventable. And eventually what I'd like to see is screening of young children, primarily looking at either their HLA to see if they have a predisposition or perhaps their MSH which again is almost universally low so that you can determine who are the people most likely to develop this and then you also need a some sort of process to fix the buildings or build new buildings the schools many many of my, their exposures were in the public school. We're required by law to go to. We've had as many as four or five children and the teacher in the same room who had problems. And once they remediated the room, these children's headaches

went away. These teachers,ized syndromes went away. So that would be my messages, that awareness has to get out, doctors need to be trained, and policies need to be made to eradicate this illness. And I believe it's totally possible. Yeah, well, that's a pessimistic and an optimistic conclusion. I mean, the pessimistic conclusion is that this is very widespread and it's very serious and the optimistic conclusion is, yeah, that's true, but we know what it's what causes it and we know how to treat it. And so, the news could be a hell of a lot worse. Dr. Schumaker,

do you have anything to say in closing? My greatest concern is that for long or neurologic syndromes like Alzheimer's, like Parkinson's, we are stuck with the lack of a prospective study to prove causation of the physiologic abnormalities we've identified. We can find them and fix them, but how do we know we've prevented a disease that wouldn't show up for 25 years? Yes, we don't. So we have the ethical issue of letting people stay in a water damage building for 25 years and watching them develop Alzheimer's. I don't think that would be a very nice idea. I would not like to be treated that way. And so we could do it with short term exposure with sequential activation of an atom you know elements, but the the changes of environmental toxicology, it's not just biotoxins anymore, it's other inflammatory situations, plasticizers, who knows what they're doing. It's far greater, but the availability of the primary care physician to be the leader

of the pack, the leader of the cadre that does the work and does the patient-oriented research is limited by a current medical system that treasures academics and university appointed specialists and not the primary care who person who sees 15,000 people a year. All right, gentlemen. Well, that was a lot of information. I'm going to sum it up here just for the convenience of everybody watching and listening. So, we're in a situation hypothetically where 50 to 85% of buildings are affected by the invasion of toxic living creatures, molds, fungi, et cetera, bacteria, as a consequence of water damage. Some buildings are more susceptible than others to that, particularly those that are made of

drywall and drywall that's being painted with substances, hypothetically designed to stop those biological organisms from getting a foothold. It's had a paradoxical effect. That's affecting a lot of people. There is a subset of people, about 25% of people who are particularly susceptible to those effects. There are various ways of identifying them.

And there are array of biomarkers that are available to diagnose this illness. There is about 40 symptoms that are associated with it and there is a standardized treatment protocol that has been worked on and publicized by Dr. McMahon and Dr. Schumaker and you can find out about that at the URLs that we've put in the description of the website. And so that about sums it up.

It's complicated. And the implications are relatively horrifying. But the good news is that it's actually identifiable and treatable and that the causal sequence has been pretty well identified. So, well, we'll make of that what we can as we move forward. Everybody's going to have to evaluate this to some degree for themselves because it's a very complicated topic. We talked about this textbook for physicians that's the art and science of serves medicine and the websites for public consumption.

And so I'm going to talk to doctors, McManage, you maker for another half an hour on the daily wire plus side. And so you guys can join us there if you're inclined to. And thank you very much, gentlemen, for walking through all that information, for me and for everybody who's watching and listening today. Thank you.

You are the best interviewer I've had. So I thank you for your skill. Oh, my pleasure, man. Well, I want to understand what you guys are talking about. And I certainly feel like I'm more on top of it now. You know, the problem I had when this was all brought to my attention, my daughter started talking to me about it. You know, and there's a real difference between someone just telling you

something, even if it's extraordinarily vital and actually understanding it. It was quite frightening to me to encounter this information to begin with because I thought, oh my God, I'm gonna have to dive into, well, I'm gonna have to dive into this literature and try to understand it, just to even interpret, for example, why would I believe that the visual acuity test is a reasonable diagnostic marker?

That's not simple. I mean, you're logic, I think, is impeccable in relationship to that, but it's just another indication of how complicated it is to get on top of a potential disease process of this complexity. My experience is even though it's complicated, if you're speaking to a provider,

physician, nurse practitioner, whatever, who has an open mind and is willing to hear about it, it's not very difficult to convince them that this is a reality and it answers a lot of unanswered questions. There are always people that don't want to know and don't want to hear and obviously we don't have the same success with them, but in people that have an open mind, this is actually very enlightening for them. All right, well, I'm very glad to hear that. That's a good positive note to end on. Okay, so thanks again, gentlemen. And to everyone watching and listening,

your time and attention is always much appreciated to the daily wire plus people for making this possible. That's much appreciated as well. And so we'll see many of you on the next episode. Thanks again, gentlemen. Thank you. Thank you very much. Music