415. 80% of Homes are Fostering Chronic Illness | Dr. Scott McMahon & Dr. Ritchie Shoemaker

[0] Hello everyone.

[1] I'm talking today to Dr. Ritchie Shoemaker and Dr. Scott McMahon, and they are cardinal investigators into a problem known as Chronic inflammatory response syndrome.

[2] And you probably haven't heard that before.

[3] 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.

[4] 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.

[5] So the basic theory is something like this, a substantial number of buildings, especially those built with drywall using antifungal paints, have water damage.

[6] That water damage produces biotoxins of various sorts.

[7] For a substantial proportion of the population, about 25%, exposure to those biotoxins, produces an immunological response that has all sorts of neurological and behavioral negative consequences.

[8] And so I found out about this through my daughter, who's been wrestling with health disorders of various sorts for her whole life.

[9] She's convinced me that it was at least worth a, it was worth some investigation, and that's what I'm doing.

[10] And so I decided to, I read some of these gentlemen's research papers, and they struck me as highly credible.

[11] And so I'm talking to them today to find out just what there is to this.

[12] 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 damaged buildings.

[13] 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.

[14] And the government, by the way, seems to agree with that assessment, even though not enough has been done about that so far.

[15] So anyways, come along for the ride.

[16] That's what we're talking about today.

[17] Dr. Shoemaker, Dr. McMahon, welcome to the program.

[18] I'm very interested in talking to you guys today.

[19] My daughter has alerted me to your work, and I've been looking into it for the last four or five months.

[20] 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.

[21] 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.

[22] 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.

[23] And so we could all hope that you're not correct so that it isn't a catastrophe.

[24] But I know you've accumulated a substantial amount of evidence.

[25] And so maybe we'll start with you, Dr. Shoemaker.

[26] 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?

[27] Most people have a sense of what inflammation is.

[28] Our body is looking at environmental stressors that must be dealt with.

[29] And the inflammatory process is a general rule is part of the environmental response to the trauma.

[30] or stress, inflammation can be of two kinds.

[31] 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.

[32] So there's things will be experienced once, and then the twice as the next time is very quick.

[33] 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.

[34] Inolation is certainly the big way I worry about, but it could be elsewhere.

[35] 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 a hystocopatic locusa molecule on the antigen and packaging it in the antigen presenting cells to a naive lymphocyte, just waiting for something to happen.

[36] And when the naive lymphocyte sees this tasty little morsel package with HLA and an antigen on it, it should turn on a kind of C -cell, or a B -cell, excuse me, to make an antibody.

[37] 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 at a reduced fashion, if at all.

[38] When we look at now, what control do we have on inflammation if the stimulus is not stopped?

[39] And it doesn't have to be ongoing exposure.

[40] It is now in this world of antigen interaction with antigen presenting cells and T. lymphocytes that has gone awry.

[41] And the illnesses that we see become chronic because the antibody formation does not occur.

[42] Now, over the years, we knew about problems with antigen 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, metabolism.

[43] So if we look at metabolic problems combined with inflammation, we have molecular hypometabolism, which is a fancy way of saying that 95 % of patients with chronic fatigue have a specific abnormality and inflammation and metabolism that we can show with genetic makeup.

[44] 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 you correct gene suppression when it's not supposed to be suppressed.

[45] So what we're looking at is the transcriptomic or gene representative theory of illness causation and illness correction.

[46] Our last paper, and I hope you had a chance to take a look at it, but it's in your inbox.

[47] If you know, the next question is now when I'm looking at, to me, the Holy Grail, and that's correction of die -back central nervous system degeneration.

[48] You may hear it called Alzheimer's.

[49] You may hear it called Parkinson's.

[50] You may hear that same called for atrophic, myotrophic lateral sclerosis, or ALS.

[51] But we are there.

[52] We're there with gene activation and correction with our therapies that have been developed over the last 27 years.

[53] Okay, so you're going after a host of the immunological diseases.

[54] including extraordinarily widespread conditions like Alzheimer's.

[55] Dr. McMahon, do you want to explain to everybody what this has to do with where they live?

[56] So there are a number of potential triggers that can cause the innate immune system to activate.

[57] And as Dr. Shoemaker 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.

[58] So the innate immune system is then basically left to handle this by itself without the antibody cavalry coming in and reducing the burden.

[59] 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.

[60] And it's not just, for instance, say, mold spores.

[61] It can be old, dead mold spores that have lost their integrity, their cell wall was broken apart into hundreds of fragments.

[62] 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.

[63] as response to that, the innate immune system will overproduce cytokines in the same way that you would overproduce cytokines if you got the flu or if you got COVID or some other kind of viral infection and these fragments trigger the innate immune 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., etc. Okay, so let me get the whole sequence of this straight.

[64] So what you guys have been studying is sometimes just, and stop me, you know, at any point if I get any of this wrong, sometimes people refer to this as sick building syndrome.

[65] you've brought in conditions like Alzheimer's and other immunological diseases, chronic fatigue syndrome.

[66] I know you've concentrated to some degree to on fibromyalgia.

[67] 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.

[68] That's much more likely in buildings that have been water damaged and not properly remediated.

[69] 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.

[70] And some people, when that immune response is triggered, they're not producing antibodies in a proper manner.

[71] And there are genetic reasons for that and possibly metabolic reasons as well.

[72] And then is it the combination of the pathogens that or 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?

[73] And have I got all that right?

[74] Is that the way this lays itself out?

[75] You're doing, Greg.

[76] Keep on.

[77] That is excellent.

[78] Okay, okay, good.

[79] So let's go through that one by one then.

[80] 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?

[81] And if it's a large number of buildings, that's obviously a catastrophe.

[82] So what's the evidence for this and why did you guys become convinced of this?

[83] What we have seen is a similarity of the syndrome of acute exposure, followed by chronic exposure, wherever the person might live.

[84] It's not confined to Florida or Hawaii, could be in Nepal, or could be in Institute Guard.

[85] This worldwide exposure to an environment that pretty much is 62 to 78 degrees year -round.

[86] No wind, no rain, no change of the seasons indoors.

[87] And the mark of every one of these indoor places is water intrusion.

[88] So if we look to see, is there a water damage?

[89] building, we should be able to find an ecosystem of organisms.

[90] You mentioned fungi, and I've written books surviving mold and mold warriors out of the best evidence at the time, and that was wrong.

[91] We know that fungi have a role, but we also know that endotoxins from bacteria are second on the list, and first is actinobacteria.

[92] And when you look at every building that's water damage that has these ecological parameters, you find the same symptoms, the same in 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.

[93] In some of Scott's work, he's published that the likelihood is you've got a P value of less than, P is less than than one to the minus 50th power.

[94] So it could be the same in Suitgard if the Lewis was the same, but actually statistically, the idea that it's not the same is so remote to be impossible.

[95] Okay, so what, Scott, 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?

[96] And are there specific kinds of buildings, that appear more susceptible.

[97] I read in some of the work of yours that I reviewed, for example, that drywall seems to be a particular problem.

[98] So what kind of, how widespread is this problem, do you suppose?

[99] And what buildings are particularly affected?

[100] 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 damaged.

[101] The buildings that are involved are not due to one era of construction or another with modern structures put up quickly.

[102] Contractors investing money wants to turn over the house, sale quickly.

[103] So he may not wait for a master plumber to put in the bathroom and a plumbing leak can develop.

[104] Construction defects for new homes are a real bugaboo.

[105] But even when we were in Sky Island of the castles from the 1200s and before, we saw the same kinds of problems.

[106] but in the older buildings where they had not been paints used with fungicides in them, for example, we didn't find the same organisms making toxins the way we do in the newer buildings.

[107] In about in 1970, when the population got all upset with the oil embargoes and houses were made to be tighter, we thought that that was the reason for the problem.

[108] 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 molds that could be killed, and if the molds that survived became toxin formers were before they didn't.

[109] So before 1970, it usually was a building that was retrofitted or retrograde corrected or modern construction.

[110] The safest buildings, even though they're water damaged, are the old buildings with no paint.

[111] Okay, so there's no specific form of buildings.

[112] that's amenable, per se, to water damage and the intrusion of toxins in consequence.

[113] But you talk about buildings after 1970.

[114] 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.

[115] And I remember when people started talking about sick building syndrome, I guess this is, this went back as far, in my knowledge, as far back as the 80s.

[116] they were concerned about these hyper -sealed buildings.

[117] But you said that your further investigations revealed that it wasn't the sealing of the buildings per se, so much as the use of modern paints and sealants that had antifungal chemicals embedded in them.

[118] Now, hypothetically, the reason they put those antifungals and anti -mold chemicals in the paints was to keep the fungus and mold down.

[119] 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.

[120] 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?

[121] And what's your evidence for that?

[122] Sponjai also had a response to environmental hazards.

[123] And the environmental hazards of being killed will cause normal activation of gains in fungal species such that they'll make toxins where beforehand they didn't.

[124] The main role of a mycotoxin, for example, has nothing to do with defense.

[125] It has everything to do with predation.

[126] 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 make compounds to eliminate the fungi.

[127] They eliminate the peroxidates, therefore eliminate the plant defenses.

[128] But it's predation of fungi on its prey, that's foremost where all this goes on.

[129] Meanwhile, actinobacteria love an 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.

[130] So that as you see an initial building, the initial colonization will be with fungi, but it'll be replaced by actinobacteria, as time goes on.

[131] But meanwhile, if there's a flood or a hurricane event or a natural disaster, the water saturation, or AW, as people should say, the activity of water, will initially let in organisms that like very saturated conditions, or AW.

[132] you a 0 .9 to its maximum of 1 .0 or 100%.

[133] So we see one group of fungi of water damage that's acute or different species.

[134] We'll be grouping of water damage that's less acute.

[135] And in the end, then we'll see sources that have very dry buildings, but it's where the moisture has changed the ecosystem.

[136] Now, actinobacteria are famous for creating most smell.

[137] And interestingly, the musty smell or musty smell.

[138] musty odor, we've long associated with fungal colonization, is coming from Actinous.

[139] G. Osmond.

[140] There are also architectural design features that make a building more likely to become water damage than others.

[141] Flat roofs are more likely to leak than pitched roofs are.

[142] Basements and crawl spaces are more likely to have water intrusions than you would see in homes that are built on a slab.

[143] We know that drywall is more likely to have problems than plaster onlaid.

[144] And so there are a number of different materials and architectural styles that can make a house or a commercial building more vulnerable or less home.

[145] Right.

[146] Well, you can imagine, you know, when I'm thinking my paranoid thoughts, I know here's an example.

[147] So one of the reasons that the Roman Emmer, empire fell was because the Romans used lead to seal their wine amphora.

[148] And lead is a known neurotoxin.

[149] 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.

[150] It was really quite a catastrophe.

[151] And that 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 antisocial and criminal.

[152] And so the reason I'm bringing this up is because it's possible for a society to introduce something into their midst that's then distributed in an extraordinarily widespread fashion.

[153] You know, experimental vaccines come to mind, by the way.

[154] 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.

[155] And it sounds like that's a case that you're making for drywall is that it's an extraordinarily light, easy to work with, cheap building substance, but it isn't, we don't have a lot of historical experience with it.

[156] It was introduced in a very widespread manner in the latter half of the 20th century.

[157] 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 percent of buildings.

[158] So that's really quite the bloody catastrophe.

[159] So now let's take that apart a little bit.

[160] If it's 50 to 80 percent of buildings, how many of them, in your estimation, are contaminated to the point where that actually constitutes a serious health problem?

[161] Like, you know, I know that that's a threshold issue, but there's lots of threats that people have to contend with, obviously.

[162] And if your house is contaminated with mold and water damage, that's a big deal.

[163] It's a really difficult thing to fix, or it can be.

[164] And so, under what condition should people be prioritizing this as a actionable risk factor?

[165] And how widespread do you think this problem is in its more serious forms?

[166] Study after study is look at individual susceptibility, which underlies who gets sick and who doesn't.

[167] The individual susceptibility of the immune response genes found in chromosome 6, HLA, DR, was shown to be present in just about every person who had SERS, and the percentage of not having SERS HLA but having an illness is less than 5 % of the total.

[168] So 95 % were broken out into six separate haplotypes.

[169] There are 54 available, and out of those six, it's 24 % of the population.

[170] When we look at this 24%, we put them in exposure and follow them prospectively, we can show that the initial responses, once the priming event has taken place, is essentially 100 % in those individuals susceptibility.

[171] We're seeing this exactly with the same way.

[172] With COVID, COVID creates an inflammatory response.

[173] it turns on innate immune responses, which turns on gene -based susceptibility.

[174] So long COVID has the same genetic makeup, and we've published a paper on this in June of last year as well, that it creates a new illness, a new target where once it wasn't before.

[175] And we looked at people who were 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, lo and behold, a month later, two months later, three months later, they had long COVID syndrome when actually what they had was a chronic inflammatory and metabolic response syndrome.

[176] It was just a different initiator.

[177] It could be a horde of yellow jacket, stinging people at a picnic, creating an inflammatory response, or it could be an illness.

[178] In this case, COVID fills the bill.

[179] Okay, okay.

[180] So you could imagine that there's a manner of conceptualization that allows for two kinds of disease processes.

[181] There's disease processes that are associated with pathogens per se.

[182] And then there are disease processes associated with an anti -disease response or an immunological response gone astray.

[183] So if I'm following you correctly, we have a situation where, let's say, 75 % of our buildings are contaminated.

[184] And so three -quarters of the population is exposed to the pathogens that could pretty an immune hyper response.

[185] 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.

[186] Or is that a more general susceptibility to immune overreaction?

[187] You seem to be implying that in relationship to the COVID issue.

[188] So it's 25 % of 75%, essentially, is the number of people who are hypothetically affected.

[189] So that's about 25%.

[190] That's about 20 % of people, all things considered, might be experiencing this as a serious problem.

[191] So have I got all that right?

[192] Yes, you do, and you picked it up very quickly.

[193] I thank you for that.

[194] One of the reasons that is so important is that we look at illnesses that are at SERS, that actually are SERS, and who has chronic fatigue syndrome?

[195] Who has fibromyalto?

[196] Who has depression?

[197] Who's just getting older because their cognitive effects are really important?

[198] Are children not doing well in school?

[199] Is it the lead paint that they swallowed?

[200] Is it the lead in the applesauce that they've been taking in?

[201] Are there environmental factors that are creating this overall systemic illness of which the brain is the injury I worry most about in adults?

[202] Scott sees children more than I did so we can let him speak about children with cognitive issues.

[203] But the issues are that when we look carefully at chronic fatigue syndrome, we find SERS.

[204] And I'd like you, sir, if you could, to identify one significant biomarker that distinguishes fibromyalgia from not.

[205] We have 30 biomarkers for SERS and zero for fibromyalgia.

[206] Why does fibromyalgia have such a preponderance of people?

[207] And how many people, adults have fibromyalgia?

[208] 10 % and 3 % for chronic fatigue syndrome, how about post -line syndrome, how about depression?

[209] Boy, we've got 25 % all of a sudden, and when we start looking at those details, we can stratify sick versus non -sick, cases versus controls, treat them and show that cases equal to controls and they become controls after treatment has occurred.

[210] 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.

[211] And so let's take depression as a case in point.

[212] When I was assessing my clients for depression, the first thing I always tried to figure out was, are they just ill?

[213] Because there's all sorts of evidence associating depression, particularly, 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.

[214] And depression is a relatively non -specific cluster of syndromes.

[215] Now, you're pointing to a whole set of syndromes that have relatively non -specific symptoms.

[216] Some of them, even more difficult to diagnose and easier to be skeptical about in relationship even to their existence as, say, fibromyalgia and chronic fatigue syndrome.

[217] That's hard to dissociate from general depression and anxiety and a kind of global neuroticism or even a hypochondriasis.

[218] Now, you're saying, your first claim is that 20 % of the population is likely to be experiencing these symptoms, but we don't see this Sears chronic inflammatory response syndrome in 20 % of people because essentially we're placing them in the wrong bins.

[219] Now, and so how much of...

[220] So let's walk through what the symptom constellation is for chronic inflammatory response syndrome, that serves, and how you think we should go about distinguishing that from, say, fibromyalgia, which is poorly understood, or chronic fatigue syndrome, which is poorly understood, or depression?

[221] And why do you think that your category, 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?

[222] Because, I mean, you're making a lot of radical claims here, and I'm certainly not in a position to dispute them.

[223] But you know what they say?

[224] Radical claims, require radical evidence.

[225] 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.

[226] So what is it?

[227] Let's go through.

[228] of all, what are the symptoms that point to SERS as far as you're concerned?

[229] And then what do you use to prove that that's the condition?

[230] As Dr. Schumacher said, we have roughly 30 biomarkers.

[231] These are tests which can distinguish ill people or what we call cases from healthy people with all controls.

[232] We have roughly 30 of them, and all of them have been validated to show that they separate cases from controls.

[233] When we look at the diagnosis of serves, you have to have objective evidence that shows that you have several of these biomarkers.

[234] I mean, at least four or maybe five or more before you can actually even make the diagnosis.

[235] 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 is so small.

[236] I mean, it's in the one to a million.

[237] 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 bile markers multiplies by the next persons and then multiplies by the next persons.

[238] By the time you get to 10 people, you have such astronomically low probability that this is a freak accident, that it can't be dismissed.

[239] 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.

[240] We are looking specifically at the innate immune system as a possible root cause for these different symptoms.

[241] And if they ran the tests that we do, they would see the same kind of data that we have.

[242] My data is very similar to Dr. Shoemakers.

[243] I've seen roughly 2 ,000 patients, 2 ,000 that I've evaluated this.

[244] For him, it's much more because he's been doing it much longer than I have.

[245] And our data is very similar.

[246] Okay, so your argument basically is, and I just want to walk through this very carefully so that everyone listening understands, is that you've identified a number of biomarkers.

[247] You said 30 overall, but apparently you concentrate, on something like 5 to 10.

[248] Now, there's a probability that any given test is going to produce a result that's positive falsely.

[249] So someone will be diagnosed as abnormal on that evaluated dimension, but in truth, not be abnormal.

[250] But that probability declines as a function of the number of tests administered.

[251] So maybe there's a 1 in 20 chance that any given test will show that you have the condition.

[252] 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.

[253] And so your case basically is that as you accumulate evidence of the biomarkers, you decrease the probability of a false diagnosis.

[254] And there aren't biomarkers, as far as I know, there certainly aren't biomarkers for depression.

[255] So that's not specific, what would you say, physical or chemical biomarkers.

[256] You know, sometimes there's elevated cortisol or decreased cortisol, but it's very nice.

[257] The markers are very nonspecific.

[258] 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.

[259] And so what are the prime biomarkers that you guys use to make the diagnosis?

[260] And why did you pick those and how valid do you think they are and why?

[261] We need to start with a case definition.

[262] The case definition in 2003 that our group came up with was modified in 2008 by the U .S. Government Accountability Office.

[263] When they looked at the potential for exposure, this is what CDC used with fiscaria back in 1997, 1996.

[264] You didn't get sick from a microalgo bloom unless you're exposed to it.

[265] So the potential for exposure is number one.

[266] Number two is symptoms the same were similar to those seen in published peer reviews.

[267] literature.

[268] The third element is laboratory findings the same or similar to those in published literature.

[269] And then the fourth is objective response of biomarkers to treatment.

[270] 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.

[271] Was there a risk factor like cigarette smoking or alcohol use or age or undercutting illness with diabetes.

[272] No, no, no, no. It was based on genetic markers.

[273] So individually immune responses became our first biomarker.

[274] Actually, the first biomarker came from the EPA with Ken Hudnell, been studying the neurotoxychology features of visual contrast sensitivity, which is a mechanism to see an abnormal neurological function of vision.

[275] Contrast is one that's been stabilized over time and is adversely affected as velocity of flow of red cells and retina and neural rim, the optic nerve head, increases.

[276] So VCS was our first, HLA was our next.

[277] In that group, there was a regulatory neuropeptide, melanocytes stimulating hormone, which is essentially negative in all cases and normal in all controls.

[278] 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.

[279] Scott mentioned cytokines.

[280] In 1986, 1985 was the first publication of a paper on cytokines.

[281] And here we are in 1996, postulating that this cytokine effect could be huge.

[282] And now if we fast forward to COVID, it's a cytokine storm, and everyone in the drugstore knows what a cytokine storm is.

[283] They're buying COVID tests.

[284] They're looking for mechanisms that we have been studying.

[285] And cytokine storms are part of innate immune response, so you'll have it in COVID, but you have it in SARS too.

[286] And COVID doesn't have the same HLA that we know of yet, but we'll probably find it doesn't have the same VCS.

[287] And it's a sorting process.

[288] So we took then inflammatory markers, TGF Beta 1, no lab was running that.

[289] 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 height.

[290] with some of the worst illnesses of all.

[291] And then we treated it with medications that were available over the counter or with informed consent.

[292] And then every time we had re -exposure, here we came to the prospective acquisition of illness.

[293] Proof of causation.

[294] We took people that could have been sick from one building, fixed them all the lab biomobiromachers were the same.

[295] And then with informed consent, they stopped all medicines and stayed away the suspect building.

[296] Three days, nothing.

[297] Put them back in the building on day one.

[298] At the end of day one, laboratory findings changed.

[299] Day two, laboratory changes finding changed again.

[300] Day three, we had the exact syndrome of labs, VCS, and symptoms prospectively, proven upon re -exposure only.

[301] No other choices could have been affected.

[302] It wasn't depression in three days.

[303] It was SERS in three days.

[304] Okay, so let me elaborate on the story now.

[305] 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.

[306] 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.

[307] 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?

[308] So there is an online test, visual contrast sensitivity that people can take.

[309] See, it's a strange test because it seems like it's so far removed from the symptom set that people would be experiencing.

[310] saying, it's very difficult for someone like myself, I'm scientifically trained, you know, and all of the stuff that I've encountered as a consequence, all of 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.

[311] It almost seems like voodoo.

[312] Now, you said that the reason that this visual contrast sensitivity test works is because the retinal, the retina itself is compromised as a consequence of immunological malfunction.

[313] And so, have I got that right?

[314] We have a objective parameter, and that's velocity of flow of red blood cells in the retina blood vessels and the capillary beds, as well as the neurorembiopic nerve head.

[315] We can measure objectively with a Heidelberg retinal flow meter, how fast red blood cells move.

[316] and they move more slowly if the inflammatory response promotes production of what are called adhesions, which is one mechanism to decrease flow in an area of hyper -inflammation and treatment will be shown to improve flow as the environmental stimulus is fixed and is corrected with treatment.

[317] So sick patients, you have reduced flow, healed patients have restored to normal flow to equal controls, But re -exposure, here we go, prospective exposure again.

[318] This is how we determine risk in all of medicine and science prospectively, not an association, but with prospectively re -exposed people, get the same findings back again.

[319] We fix them, we get them back to the same mechanism they were when they are healed to equal to controls.

[320] This in and out, in and out, in and constant answers to the critics, how could this possibly be true?

[321] Well, here are the data.

[322] And if people want to argue with me, they can argue with my data.

[323] Okay, so let me elaborate on that a little bit before I return to the biomarkers per se.

[324] So I know that the closest tissue that's deeply analogous to the brain itself is retinal tissue.

[325] 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 retinal 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 broader central nervous system dysfunction or brain dysfunction and 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 actinobacteria, whether it started with the flu.

[326] But this innate immune response is non -specific in how its response, but it will respond.

[327] And we can measure its tendency to recur regardless of where it happens.

[328] It'll happen in kidneys.

[329] It happens in lung.

[330] It happens in liver.

[331] and it happens in the neural rim of the optic nerve head, which is the first part of the central nervous system.

[332] We've added countless additions to that.

[333] But that was the beginning.

[334] That was 1998 after studying this for one and a half years.

[335] We finally had our first biomarker that showed led the weight of cytokines where we could separate with treatment.

[336] But by having treatment, we had the way around the skeptics because I can say, all right, you use your voodoo medicine for a week, and I'll use my voodoo medicine for a week.

[337] We'll see who's going to do it works better.

[338] When yours does and mine does, then I'm going to say, I win the battle.

[339] Right.

[340] Well, that's particularly powerful, as you pointed out, in combination with evidence that you can reinstantiate the illness once treated with re -exposure.

[341] Because then you have direct causality, right?

[342] Instead of the weak sort of correlations that often go to hypothetically prove the existence of a given condition.

[343] Okay, so let me get this straight again.

[344] So you have the vision test, you have HLA, maybe you can tell us again what that is.

[345] Was it melatonin stimulating hormone and cytokine detection?

[346] So that's four, are those the four primary biomarkers?

[347] Vision.

[348] We also saw, you mentioned cortisol and depression.

[349] Yeah.

[350] We measured simultaneous ACT -TH and cortisol because, lo and behold, there was dysregulation of ACTH, which is made by the same set of environmental and metabolic pathways in the brain.

[351] They're all melanocortans.

[352] M .S .H and A .T .H. And M .C .T .H. So if we have disruption of MSH, we're going to have disruption of A .C .T .H. And cortisol can either follow in step, which it often will, or can create its own marker.

[353] So dysregulation of A .C .T .H. and cortisol is one.

[354] We found anti -diaretic hormone doing the same thing.

[355] People walked around with chronic headaches.

[356] They said they had migraine constantly.

[357] But we find out that they were all functionally dehydrated with elevated osmolality and reduced ADHD.

[358] That was another measurement.

[359] We looked at pulmonary hypertension as a very common cardiac conditions mistaken for cardiovascular disease.

[360] People are short of breath and have chest pain with exertion.

[361] 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.

[362] 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.

[363] And it hits just one after another.

[364] Well, we get to genomics, and I hope we'll have time for today.

[365] If not, we should do this tomorrow or another day.

[366] the gene mechanisms are the real gold line for the researcher and for the clinician alike.

[367] Okay, well, I'll return to the genomics issue, and don't let me forget that if we don't get there.

[368] I want to, okay, so we've basically walked through, we've done a reasonable overview of the biomarker space.

[369] So let's do this now.

[370] Let's talk about behavioral and cognitive, behavioral, emotional, and cognitive symptoms.

[371] Like, what are people who have CS 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?

[372] So what are the fundamental symptoms that people should be alert to?

[373] And do they differ in adults and children?

[374] 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.

[375] blood flow to different places in the body, not just to the optic disc.

[376] 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.

[377] Our patients will often have cold hands or cold feet or both.

[378] They can have cramping in their hands.

[379] They can have pains in their hands, even sometimes discoloration, you know, that looks like cyanosis.

[380] And we see that that goes away with treatment.

[381] Dr. Schumacher was talking about the lungs, we also need to talk about the brain.

[382] The brain will also have a decreased blood flow.

[383] And Dr. Shoemaker 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.

[384] And there was the abnormality in the glutamate glutamine ratio, both of which suggested that there was hypoprefusion or a reduction of that red blood cell.

[385] flow.

[386] So why is that important?

[387] Well, the blood carries the oxygen and the sugar, the glucose that's necessary for production of energy at a cellular level.

[388] It chronically reduced the amount of oxygen that is getting to any cell.

[389] It will stop making energy as well, and then we get into genomics findings.

[390] 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.

[391] And so that will lead into brain fog and potentially into cellular death, which can then lead into things like die back regeneration and the neurologic illnesses.

[392] Now, you also, how do you directly evaluate brain state and brain function?

[393] If I remember correctly, I mean, I've been investigating.

[394] 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.

[395] And so for everyone who's watching and listening, I mean, I might as well tell you why I'm particularly interested in this.

[396] 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.

[397] 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.

[398] 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, it might be attributed to sensitivity to these biotoxins that Dr. Shoemaker and McMahon are talking about.

[399] 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.

[400] And I would like to get to the bottom of it.

[401] And so we did some of these neurological tests that did indicate some neurological damage hypothetically as a consequence of toxin exposure.

[402] And so can you walk everybody through those tests and what they indicate?

[403] Then maybe we could talk a little bit about treatment before turning to genomics.

[404] We skipped over symptoms.

[405] You asked a couple.

[406] Yes, right.

[407] Let's pick up that loose end before we hit in the neuroquin and all that.

[408] The symptom reporting that I did when I had visual contrast is my only biomarker was compulsive logging down of what symptoms the people have.

[409] Maybe symptoms that I listed in an interview, it wasn't a self -form or questioning the patient would fill out.

[410] It's the process of doing a medical history that we're all trained to do in their four years of medical school or longer if we specialize.

[411] But specifically, fatigue and weakness, or not specific, didn't have two with the others, aching and cramping, unusual cramping of the legs when you get spasms at nighttime and get a Charlie Horse or in the hands.

[412] And it was hard to extend fingers because the muscles were in spasm.

[413] 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 spasm was.

[414] Respiratory issues, cough, shortest of breath, sinus congestion, that was chronic, not related to seasons necessarily, eye findings, we'd 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 in production, and the biomarker was restrictive lung disease, not obstructive.

[415] It was an asthma.

[416] It was called asthma by some, but it's not, it's restrictive.

[417] 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.

[418] The cognitive issues were there.

[419] Difficulty with memory, difficulty with assimilation of new knowledge, difficulty with concentration, difficulty with disorientation, the executive cognitive cognitive function is six, hypothelamic system.

[420] We had change in appetite, change in weight suddenly, and weight gain out of the blue, change in sweats, and night sweats especially, change in temperature regulation.

[421] Those are all the MSH -related things.

[422] So let me ask you a technical question about that.

[423] So, I mean, when you're going through that as a psychologist.

[424] 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.

[425] I think that's about how many you covered.

[426] So you could imagine that you had 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.

[427] Have you guys done any questionnaire development that's oriented towards, symptom identification.

[428] Yes.

[429] Every person that takes their visual contrast test will undergo a symptom analysis and a symptom discussion.

[430] And we look to see if there's cluster analysis, a statistical function of saying yes or no based on visual contrast and symptoms alone without any of the other biomarkers.

[431] Yeah.

[432] Just statistically, we can tell you 98 .5 % likelihood of SARS just on VCS and symptom clusters.

[433] It's incredible.

[434] No one believes it until they take it.

[435] And they say, my God, my symptom cluster is gone from eight down to six, down to four.

[436] You're halfway there.

[437] We want you down to one.

[438] Have you done a factor analysis of the symptoms by any chance?

[439] Yes.

[440] It was published in 2006.

[441] Okay.

[442] Okay.

[443] Okay.

[444] All right.

[445] All right.

[446] So we've covered symptoms now.

[447] There's about 40 of them.

[448] We covered biomarkers.

[449] What?

[450] And we talked a little bit about illnesses that are hypothetically attributable to that.

[451] But let's go through that in some more detail.

[452] 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 Alzheimer's.

[453] And that that was associated in this paper with a particularity of, if I remember correctly, a Finnish architectural design.

[454] 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.

[455] Was that your work?

[456] I got that, right?

[457] I'm familiar with that work.

[458] All I want the Finnish people to show is that treatment will correct the abnormalities and then create the Alzheimer's.

[459] By the time it gets to be Alzheimer's, we're 20 years late.

[460] We can pick up the difficulties of 2BD and A4A and 2BBBB, in ALS, on a congenital basis, we can identify that.

[461] It's very young ages.

[462] Certainly by the time, we've got people when grandma's getting trouble with her cognition, we think it's old age, her problems got started when she was 30 and 40.

[463] Right, right.

[464] It was recognizable then and all the other.

[465] Scott, I've been manipulative talking too much.

[466] Your turn.

[467] Have you guys ever tried a verbal fluency test by any chance?

[468] Because verbal fluency seems quite susceptible to disruption by, well, there are certain forms of neurological degeneration that interfere with verbal fluency quite dramatically.

[469] And it might be a good marker for cognitive interference.

[470] They're very easy to administer.

[471] Lynn Gratton, from University of Maryland, published on Phisteria, the neurocognitive abnormalities.

[472] Verbal processing was one of the panel they had that was published in the Lancet in 1998.

[473] we're worth taking a look at.

[474] I don't have your skills, but she did, and those abnormalities were found.

[475] When you take neuropsychological testing of patients, the two most common abnormalities that I see are deficits in working and memory, and deficits in processing speed overall.

[476] And one of the complaints that we very commonly see is that people are still able to do the functions of their job.

[477] it just takes them much longer than it used to.

[478] So what they used to be able to wrap up in an hour now, three or four hours, which is pilotically unproductive and eventually they end up on disability.

[479] See, that's why verbal fluency might be a real useful marker because it's a time test, right?

[480] How many words can you write down that begin with the letter S in three minutes?

[481] And so because it's a speeded test, it might exactly pinpoint that interference with ongoing processing, say, rather than long -term memory or crystallized intelligence.

[482] So that's really why it's sprang.

[483] Well, that's why it sprang to mind.

[484] Well, it's also an unbelievably easy test to administer.

[485] And there's wide individual variability.

[486] And it'd be very interesting to see if that was associated with the genomic markers that you described.

[487] And maybe we could turn to those now.

[488] 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 death.

[489] decades later can be detected decades.

[490] Previously, I know, for example, by the way, this is another reason the verbal fluency test popped into mind.

[491] I know there was a study of nuns.

[492] 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.

[493] It's the longest long study.

[494] Yeah, exactly.

[495] So another reason verbal fluency might be an interesting marker.

[496] So, okay, now, and we just.

[497] So I wanted to go in two directions.

[498] One direction was, okay, yeah, what is the panoply of neurological, degenerative neurological conditions that you think are likely to be associated with SERS?

[499] We didn't have a assumption -based discussion about symptoms and neurological abnormalities that we thought were for SERS.

[500] We had recorded executive cognitive function, we recorded tremors, regardless of metallic taste, dizziness, vertigo, tremors.

[501] But we didn't have any way of assessing what was going on with the brain.

[502] We couldn't measure abnormalities in brain.

[503] And long in 2007 comes Neuroquant.

[504] And Neuroquant with one MRI image can look at 11 different volumes that we then could start to correlate with parameters.

[505] And by 2015, Scott and I have both published.

[506] papers looking to, there were reproducible abnormalities in neuroquant, in service patients, and with treatment, we can fix those.

[507] But the beauty in 2017 was we could actually fix multi -nuclear atrophy.

[508] So our treatment was non -specific, non -degenerative, but instead of just fixing the hippocampus, we were fixing hippocampus amygdala and caudate.

[509] We were fixing paladin.

[510] We were fixing of the mean number of abnormalities was 3 .4 out of 6, and we could fix those to equal to controls to 0 .9 abnormalities, the case is equal to controls.

[511] So neuroquant early on became of interest, but the final change was neuroquant associated with genomics.

[512] 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.

[513] In fact, there's more than one.

[514] If you developed your chronic inflammatory response syndrome as a result of water damage buildings, we tend to see that the forebrain parochema will be swollen.

[515] We see that, or enlarged, I should say.

[516] We'll see that the critical gray matter will be enlarged and that the caudate nucleus will be atrophic, will be smaller.

[517] If you develop chronic inflammatory response syndrome as a result of Lyme disease and post -treatment Lyme disease syndrome, we see a completely different pattern.

[518] And that pattern is that the right thalus is enlarged and that the putamen is smaller and atrophic.

[519] And we showed that on two different studies.

[520] And then in the third study that Dr. Schumacher and I published together looked at different treatment.

[521] And when we use Dr. Schumacher's treatment protocol up to the next to the last step, we saw that the four -brain parankima that had previously been enlarged and the cortical gray that had previously been in large came back to full values.

[522] But we didn't see improvement in the multi -nuclear atrophy.

[523] The next paper, though, did, and that was with use of VIP, basoactive intestinal polypeptide, which is a substance that your body makes, and is key for, it's an antinean inflammatory peptide.

[524] It's a neuroregulatory peptide that brings your activated immune system back down to normal when it's appropriate to do that.

[525] And so with VIP therapy, which Dr. Schumacher by hand, we have seen caudate nucleus and multi -nucoratrophy either stopping or reverting back toward normal.

[526] Have you guys used that same treatment protocol for conditions like Alzheimer's or other degenerative neurological diseases.

[527] Obviously, there's an overlap there, which we've discussed, or hypothetically, there's an overlap there with SERS.

[528] Has anybody been looking at the application of this particular treatment protocol to these degenerative neurological diseases?

[529] Yes.

[530] 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 VIP, with stage three, with stage for that's where we had the off VIP and in doing well we had a reduction of the basic mechanism of die back CNS to generation looking at changes in TUBA for a 44 percent reduction in three months that's not been published yet but it's high on our list but yeah i bet it's high on your list yeah it's it's like we we've we've got to get going on this one there are other things that other people are doing or aware this is a complex field and no no one illness parameter will fit and fit everybody but if you've got the microtubular dysfunction that we add alluded to a t ub a4a and tub b1 if you have that as a marker and you have cognitive issues and you use and you respond to VIP, the reduction is 44%.

[531] And that's just in three months of work.

[532] Okay, so I would like to take this in two directions now.

[533] And we've got about half an hour left in this segment, although we can run a little longer if, you know, if that seems appropriate.

[534] I want to know about, you know, what people should do, you know, what constitutes treatment.

[535] And so that would be building testing, building remediation, and then the interventions that you described.

[536] But I would also like to talk about, I know Dr. Shoemaker, that, you know, 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.

[537] So let's start with everybody who's listening to this is gonna be thinking, well, I know people who have this cluster of symptoms, you know, what in the world should I do about it?

[538] So let's talk, we had our houses mold tested, and 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 the step after that's not exactly clear.

[539] 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.

[540] But what are the steps that people should take in order to determine, first of all, that they have this problem and then in order to do something about it?

[541] We first need to make sure the patient satisfies the case definition.

[542] If they don't satisfy the case definition and then it serves, this doesn't apply.

[543] But if you satisfy the case definition, then we want to define the ecological parameters within the building.

[544] If the building is water damaged and you should have fungi but doesn't, and you don't test for actinobacteria, you've made a mistake.

[545] But if you don't have fungi, is that because you never had them?

[546] Or is it because it's overrun with actinobacteria that are making the drywall surface alkaline and fungi don't live very well?

[547] And then if that's not the case, what about the water saturation with endotoxins?

[548] Because of the three things that cause the greatest amount of damage to the brain, endotoxins lead the list.

[549] specifically for every abdermality that we find in a gene that shows us about specific causation.

[550] That's the building contractors' words.

[551] Specific causation for endotoxins we've identified in neuroquant.

[552] We've also identified in combination with the genie testing or genomic testing.

[553] So the two go together.

[554] But then we want to know, do you have endotoxins?

[555] Do you have bacterial bacteria?

[556] do you have fungi?

[557] 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, there's license, it's not a fly -by -night insure and shyness your organization.

[558] But there are those that are out there, they really are.

[559] But specifically, if we've got a reputable lab that shows us the abnormalities.

[560] You've defined the illness parameters.

[561] You divide the environmental parameters.

[562] Now we divine the treatment.

[563] Do you want to go for treatment, Scott?

[564] Sure.

[565] The first part of treatment is taking care of the exposures.

[566] So if you're living in a home that's water damaged or if it's your workplace or maybe it's school that you're attending, you need to either fix that or mediate that or leave that.

[567] The most important step of any kind of treatment for any kind of immunologic illness is getting away from exposure.

[568] That is the most important step.

[569] It's probably the most difficult step for many people.

[570] Great.

[571] Expensive and it's mind bending.

[572] 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 remediators, too.

[573] So you want to make sure that you are working with somebody that has stood the test of time and actually knows to some degree about this illness.

[574] But that is the most important step.

[575] The second step that we initiate for almost all patients is the use of a binder.

[576] And there are different kinds of binders.

[577] Dr. Shoemaker pioneered the use of colostyramine and colisevelin, also known as well -call.

[578] They are very effective.

[579] And typically, we will see improvements within two to three months if you can get that first step taken care of.

[580] There are a host of other people that will use other, what I would consider, less effective binders like charcoal and okrapepsin and, different kinds of clays and things like that.

[581] I find in my experience that those work, but they take much longer.

[582] Most people would like to get better faster.

[583] So we use the more aggressive therapy.

[584] 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.

[585] We usually draw some blood, work to look at the tests that you had previously that were abnormal.

[586] And based on which ones continue to be abnormal, the rest of the therapy is follows Dr. Shoemaker's called the pyramid.

[587] And we just go up the pyramid.

[588] 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 contemplate, whether usage of intranasal VIP is useful.

[589] For most patients, it is.

[590] Certainly, in my experience, if you have not recovered at least 70 % of your energy, 70 % of 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.

[591] Instead, if you have or haven't?

[592] If you have not.

[593] So I'm anticipating every one of, of my patients will recover at least 70 and up to 90 % of their previous capability, if they can follow the protocol as I just outlined.

[594] Okay, so I've been trying this call of styramine, and 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 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.

[595] So it was harder for me to do things.

[596] I was thinking more slowly.

[597] I had more pain, especially in the morning, more depressive malaise, none of which, as you obviously know, is particularly pleasant.

[598] And if I decreased the dose enough, that went away.

[599] A week ago, I increased the dose again, and then those symptoms came back.

[600] And so 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.

[601] So what does the binder do and why might it, why might it be the case that it would make symptoms worse and who would be susceptible particularly to that worsening of symptoms?

[602] When we have intensification, which is the word that I used were people who got worse when they took colostyramine.

[603] We found that pre -treatment, usually with compounds that would reduce inflammatory responses, reduced cytokines.

[604] Pre -treatment was, say, five to seven days, and then restarting colostiramine at low dose for another five to seven days, increased the dose, five or seven days.

[605] And at the end of the month, you get up to the full dose of colostiramine, and you go off the extra medications.

[606] Omega -3 fatty acids are widely used for this.

[607] They work very nicely.

[608] Actos was a beautiful drug.

[609] It's got an FDA black box on it for another reason, but that's still available for people that are worse.

[610] Now, most commonly, when people intensify, there are either two problems pre -existing.

[611] We would know if we had done the evaluation, if you have a more, ultimately antibiotic resistant coagulase 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 a toxin, a polycystic ether toxin, polycyclic ether toxin, that is released when it's disturbed in its ecosystem.

[612] And there's a binding coefficient looking at other toxins that are bound to a receptor.

[613] And when you start pulling the toxin off with colostiramine binding it in the gut, there will be a response of the receptor to suddenly release all cytokines that are bound.

[614] And so you frequently will create a cytokine storm.

[615] Now, the paradigm illness for this is post -lime syndrome.

[616] 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, Sard low -dose colostyramine, and away you go.

[617] Now, for other people who don't have Marcones and who don't have Lyme disease, we found that paradoxically the last step, or VIP, can be used in low doses, microdoses, as the first step.

[618] And this is from a textbook that Scott and I wrote on the art and science of service.

[619] medicine.

[620] It's called the low VIDs protein VIP protocol, and we can start people on that, get through the intensification, decrease the VIP, increase the colostyromina well call, and people sail on.

[621] But they've got to be willing to take things slowly and defeat the intensification monster, because it is horrible.

[622] It is absolutely horrible, having experienced it myself.

[623] So what does it mean for people?

[624] So, you know, when I'm contemplating this and, and contemplating, doing something about it, I'm wondering, well, you know, what, what's the implication here for travel, for visiting other people's houses?

[625] I mean, I already almost eat nothing, which makes me, you know, an annoying guest in many ways.

[626] 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.

[627] 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?

[628] If MSH levels don't rise, which is the most common situation, the susceptibility has not changed because your HLA has not changed.

[629] With low MSH, if you go somewhere to a hotel or an airplane and you reacquire markons because they're ubiquitous in the environment and the Marcon starts to grow, you will relapse and recrude us with your symptoms within three days.

[630] Folks who travel extensively, like I used to, will be on medications on a prophylactic basis and take them on a regular basis.

[631] I have a room sanitizer that I use when I travel, and I would go to the hotel room and plug that in to clean out the hotel room because whether the kind of heating devices they might have in the corner underneath the window that has some humidity coming out.

[632] We try to keep up with heat or the air cooling system.

[633] But hotels are notoriously with carpets next to bathrooms and kids playing in the bathroom.

[634] Oh, let's play hockey and saturate the rug.

[635] And you don't know it was there saturated a week ago.

[636] And you walk into it, it looks fine.

[637] But you are basically re -exposing yourself.

[638] It means that you need to manipulate your environment.

[639] as best you can is your first guess, but then you need to take medication on a regular basis.

[640] Fortunately, the side effects of low -dose VIP are essentially zero.

[641] So that's a way you can live.

[642] As far as a 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 will be something helpful unless you expand your diet once you have retrieves the maximum medical improvement from the carnivore diet.

[643] 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?

[644] Oh, my goodness, you're describing leptin deficit, left resistance.

[645] Leptin is made by a GP -130 cytokine receptor in the brain, right in the hypothalamus, where MSH is involved.

[646] And leptin must bind to its receptor, send off a stat 1 signal to turn on production of POMC, pro opio melanocortin, to make MSH.

[647] So if you're leptin -resistant because of weight problems, you don't turn on MSH.

[648] And so that by itself will turn on fatigue, pain, and then now obesity.

[649] And what a triad.

[650] And a good day, a good months, a good months for a leptid -resistant patient, not to mention an insulin -resistant patient, and one of the MSH deficient, is half a pound per month.

[651] That's not a good day.

[652] Wow, wow, wow.

[653] Well, okay, so what do you think about this?

[654] 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 to its rate of increase.

[655] And the last projection I read was something like 40 % of Americans will be grossly obese, morbidly obese by the year 2030.

[656] 40%.

[657] You know, and that's, well, it's impossible to overstate what a catastrophe that is.

[658] That's half a surge patients.

[659] If you look at someone who weighs 300 pounds, we're not going to use pedantic terms like morbidly obese.

[660] Yes, yeah, yeah, yeah.

[661] specifically when weights a problem, what's leptin, what are adipocytokines doing, what's insulin doing, and more importantly, what's molecular hypometabolism doing?

[662] Because we've got a prescription now we've been using it that will defeat the mechanisms, the physiologic mechanism for weight storage and fat storage.

[663] We look at adipocytokines and brown fat, and we wanted to turn on brown fat on coupling protein one, two, and three were found.

[664] It used to be just one, but coupling one, two, and three are found.

[665] We can convert base fat to brown fat and have increased metabolic consumption of energy by turning on brown fat activation.

[666] This is one of the advantages from Finland again.

[667] Here we heat you up and you have a nice sauna and then we tend to let you go out and jump into a snowbank.

[668] Without making shivering, that turns on brown fat physiology, that turns out energy production like crazy, is wasting heat.

[669] Non -shivering thermogenesis is what that is.

[670] Okay.

[671] How many papers have you two published between you that are related specifically to this topic, approximately?

[672] Over 30.

[673] Okay, okay.

[674] So we're two together.

[675] We're 60.

[676] Okay, okay.

[677] So 60 papers.

[678] All right.

[679] So you've brought your findings to the attention of various government.

[680] bureaus.

[681] What has been, what has been, what have you delivered in terms of reports?

[682] What has been the consequence of that?

[683] Hold on nothing.

[684] Well, I had the privilege of speaking before adjuncts at the House and Senate Art and Services Committee in December of 2019.

[685] And then they made a report to the full Congress.

[686] And 16 days later, they appropriated $300 million to look into military housing, particularly as it pertain to troop readiness and suicide in the military.

[687] And you probably didn't hear about that because the next day, they impeached President Trump for the first time.

[688] And when that news cycle was over, we had this little thing called COVID.

[689] And then after that, it's like everybody seems to have forgotten.

[690] 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.

[691] And three, like, I can't imagine how you could spend $300 million testing military housing.

[692] I mean, that's an insane amount of money.

[693] But it does indicate, regardless of that, it does indicate that they took what you were pointing out seriously.

[694] 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?

[695] The people that I was meeting with had visited a number of military bases and had seen the military housing.

[696] So they were already aware of the rat and infestations and the mold growing on the walls and whatnot.

[697] I mean, they'd seen it with their own eyes.

[698] What I presented was that this was definitely causing problems with troop readiness.

[699] 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.

[700] If 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, and it can be reversed very quickly.

[701] Yeah, well, it's not uncommon for the patient's psychological problems to be a direct consequence of the fact that they've been misdiagnosed by a physician.

[702] You know, like I was always extremely loath in my practice to attribute any serious physiological alterations to psychological condition, you know, because it just strikes me as highly unlikely.

[703] And so it's very easy to assume that if you don't know how to diagnose something, it's a consequence of the malfunctioning psyche of your patient or your client.

[704] And that's an easy thing to fall into.

[705] I don't want to be cynical about this.

[706] 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.

[707] Right.

[708] 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.

[709] So, you know, I can, 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 malfunctioning psychological processes.

[710] This might be particularly relevant with kids.

[711] 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.

[712] Yes, at this point, I've seen about a thousand children for that.

[713] For 28 years, I had my own private practice, so I worked with a nurse practitioner.

[714] In the last 10 years, I evaluated the children there that had chronic illnesses for serves also and found that, again, the majority of children that had chronic headaches.

[715] And we're talking 10 million children in the United States alone.

[716] The majority of those, the large majority, they had serves when I evaluated them for that.

[717] And when I treated them for that, their headaches would either go away or they would become much less severe, much less frequent.

[718] It's the same with chronic abdominal pains.

[719] I was taught in residency, and I went to a fantastic residency.

[720] But I was taught that stomach pains that were recurrent in children, maybe 10 % of the time you can make a diagnosis of urinary tract infections or constipation, Or, you know, maybe there's some visceral problem with their liver or some other organ in their abdomen.

[721] But that the majority of times that the children were actually seeking either a primary or a secondary gain.

[722] And that's psychological.

[723] But what I saw in my patients when I started evaluating them for SARS is that about 90 % outside of that 10%.

[724] So we're talking closer to 80, 81 % of these patients had four or more biomarkers for, served.

[725] And then when we treated them, their abdominal pains either went away completely or became much less frequent and much less severe.

[726] So, I mean, it's a really fundamental game changer.

[727] These are two of the most common visits for pediatricians is children with chronic headaches, children with chronic abdominal pains.

[728] There's another 10 million who have chronic abdominal pains.

[729] And then you can also expand that to adults.

[730] 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.

[731] They actually have a term, functional abdominal pain syndrome.

[732] And again, if you were doing the correct testing looking at the in -a -d -ean system, again, my experience is about 90 % of those people with this functional pain will have the biomarkers consistent with the diagnosis of sers.

[733] And then treatment, you know, just follows along.

[734] Dr. Shoemaker, you insisted earlier in the discussion that we returned to the issue of genomics and genetic susceptibility, and so I don't feel that we've covered that inadequate depth.

[735] So do you want to expound on that for a moment or two?

[736] And so for everyone watching and listening, so the causal pathway is an affected building.

[737] That's a building affected by water damage.

[738] That's increased.

[739] The probability that that will be problematic is increased if it's drywall and the drywall is all.

[740] also sealed or painted with an antifungal chemical.

[741] And then that isn't sufficient altogether to produce the syndrome.

[742] 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.

[743] And so we're going to delve into the genetic markers for a moment and the genomics aspect of that.

[744] So Dr. Shoemaker, you want to take that away?

[745] When we look at the role of metabolism in this illness, it was been under, under, studied for years, but now it's risen to the head of the cream of the crop.

[746] The structure that makes proteins, and there's a million of these in every cell, it's called a ribosome.

[747] And if you remember your high school biology, ribosomes make proteins and mitochondria make energy.

[748] But the mechanism of protein production comes from RNA copied in fossil DNA.

[749] and traveling from the nucleus into the cytoplasm of the cell, and that messenger RNA gives a signal to the ribosome to assemble one amino acid at a time a given protein that's coded for by the RNA.

[750] So a DNA message transcribe to RNA, transcribed to RNA, makes a protein.

[751] What happens in chronic fatiguing illnesses is that the structure, they call the Sarsen -Rison -Loop, and that's getting a little complicated here, it's present in every living creature.

[752] Every creature known to God has got a Sarsen -Rison -Looping.

[753] And at the one point, the 15 nucleotide, where there's an adenosine moiety, a toxin can cause replacement or elimination of that one plane adenosine, and the loop won't work.

[754] So suddenly, a million ribosomes losing half a million of his capability won't make the protein needed for cell functioning and the cell stops functioning normally.

[755] Meanwhile, glucose is being driven into the cell by two transporters and their glycolysis or breakdown of glucose, a six -carbon chain, a circle or chain, excuse me, or circular compound, is broken into two, three -carbon fragments in a chain called pyruvate.

[756] 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 cyclo -oxygenase pathway to make energy.

[757] So if you don't get pyruvate going into the nucleus, you don't make the 36 ATP or 38 ATP the nucleus can bring.

[758] So Otto Warburg studied this in 1928, in 1955 and finally passed away.

[759] But he studied cancer, and he found that pyruvate was readily available, but it was not being metabolized in the binachondria.

[760] It was being broken down from pyruvate, a three -carbon chain, into lactic acid, a three -carbon chain.

[761] Lactic acid was secreted outside the gradient into the capillary beds, and lactic acidosis became common.

[762] We see this proliferative physiology of lactic acidosis in 85 % of our cirrhizant.

[763] patients.

[764] We have ribosomal attack on protein.

[765] We've got lack of proper energy metabolism going on.

[766] But at the same time, in addition to metabolic acidosis, will have lack of a regulatory T -cell population, thymus -derived T -cells, will have increased gray matter and nuclear atrophy.

[767] We'll get pulmonary hypertension.

[768] We'll get, here's your obesity.

[769] We'll get insulin resistance.

[770] You get five complications of metabolism abnormality in 95 % of the patients who've got molecular hypometabolism.

[771] That is a prescription for a disaster.

[772] So we start looking at insulin receptor substrate too.

[773] That will increase delivery of glucose regardless of what the diet has it involved.

[774] A lot of people will be on a diet called a keto diet.

[775] With keto diets, they want to make themselves burning fat.

[776] Well, if IRS 2 is increased, then that keto doesn't get into the cell.

[777] It'll be turning on uptake of glucose.

[778] So you've wasted the keto function if irs2 is elevated.

[779] So if you're going to get serious about a diet, and the carnivore diet also gives tremendous source of glucose.

[780] Remember, aspartate and glutamator broke down in glucose very quickly when your energy is low.

[781] 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 carbon carbohydrates.

[782] But secondarily we start seeing disruptions of apoptosis.

[783] This is programmed cell death where cells should die normally be in the fragments of cells be coated with membrane released into the circulation, but not causing inflammation.

[784] But here in this illness, apoptosis, we have defective apoptosis, where the cell is lice without coating of the internal fragments that are antigens, so we get now a surge of antigen load in bloodstream with apoptosis and someone who's got defective apoptosis genes.

[785] RAPK1, we can tell you that, and that will create an endogenous source for sers.

[786] I realize they're getting a little technical, but then we look at coagulation factors.

[787] These genes are upregulated like crazy, and they will bind to tall and tall beta in the brain and then create a microclot, which will lice, you know, microbleed, and that's where Alzheimer's gets at start.

[788] But it begins with extra quagulation factors.

[789] Cytokines, we mentioned the tremendous increase in cytokines.

[790] We also mentioned there's a specific causation for endotoxins.

[791] There are three markers that we use in addition to environmental samples for actinobacteria.

[792] We use KGFBR 1 and 2 that will turn on fibrosis as a way to tell about actino injury.

[793] And then we look at map kinases that does its own bad things being turned on by actinobacteria.

[794] Fungi will have apoptosis and then you'll have the findings in the brain.

[795] So all of these findings, and there's more.

[796] Honestly, there's this, it's been a two -hour lecture.

[797] Yeah, yeah.

[798] Lessons from Jeannie available on free downloads from Surviving One website.

[799] You just take a look.

[800] You don't have to pay a doctor, and you can just get it read yourself.

[801] 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?

[802] Does anyone know that?

[803] What we have shown is the susceptibility is separate.

[804] The cytoskeleton or microtubial genes, TUBA4A and DUBBB1, that's the one associated with dieback loss.

[805] Remember, every neuron of every eukaryote has got a cell body connected to a series of tubes called an axon.

[806] The tubes convey ions and nutrients that must get from the cell body down to the end of the road of the axon to the synapse.

[807] Energy demands like crazy.

[808] You've got to maintain a gradient of sodium potassium that costs energy.

[809] But if the microtubules are disrupted, as there are in die -backed neuropathy, what you will see is loss of this neuron and then the next neuron, the next neuron is going on.

[810] Meanwhile, coagulation is going on and you're getting the vascular phenomenon that leads to cognitive impairment.

[811] They're both gone at the same time.

[812] And if you don't have have blood supply, bringing energy in to an already damaged nervous system, it just piles up.

[813] It is a positive feedback loop of abnormalities in blood flow, abnormalities in energy flow, abnormalities can be identified in chaining.

[814] Now, we were talking about the government.

[815] I just want to remind you that in 2004, John Conyers, convened at a special session of Congress.

[816] Sharon Kramer was the contact person, and she's been a real fighter all these years for mold rights, for mold patients and all that.

[817] She's the one that first blew the whistle in military housing problems around the Norfolk energy base, and $3 billion later those lawsuits have been settled.

[818] But along the way, Sharon also blew the whistle, and Ted Kennedy's HAL Committee, Health Education and Labor Committee, sent a group of physicians, including me, down to New Orleans to look to see what happened with Katrina and Rita.

[819] And there, most of New Orleans, this is in February 2006, was still underwater and as moldy as can be, and FEMA was doing things.

[820] But we had a ship.

[821] The Scotia Prince was our control group.

[822] None of these people had been involved with New Orleans in any way, but they were there at our taking controls for the group, and we had people being stashed on the boat.

[823] They were from firemen.

[824] They're from children.

[825] They're homeless people from St. Bernard Parish.

[826] And I had a case control study I did over the weekend.

[827] All we did was symptoms and visual contrasts, 250 patients, and we showed to stick markers.

[828] If you had more than five symptoms, you were a case.

[829] It was incredible.

[830] The report was released to St. Bernard Parish on a Monday.

[831] It was taken down on Tuesday, and that's the last I've heard of it.

[832] 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.

[833] It takes a long time to kill you from asbestos.

[834] Mold just makes you feel like you want to die.

[835] Right, yes, yes, right, right.

[836] Well, but it's so unbelievably prevalent.

[837] 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.

[838] And if it's as widespread and severe as you claim, it's no wonder that there's tremendous resistance.

[839] Let's speak about that to maybe bring this to a close.

[840] You guys have been hard at this for quite a long time, and you said some 60 papers published, which is quite a substantial.

[841] That's for everyone watching and listening.

[842] That's about the equivalent of 20 PhD thesis.

[843] by the way, so you can get a Ph .D. thesis essentially for three publications.

[844] It's a lot of work.

[845] And what sort of response have you had from the broad medical community?

[846] Like, how is your, how is your work being received?

[847] Do people know this?

[848] Or do they, are you on the fringe and outer edges of what's regarded as acceptable medicine?

[849] How have you been received?

[850] There is a derogatory term that is still widespread use.

[851] I have done a study about emergency room physicians called a patient they would see with multiple symptoms called a gomer.

[852] Yeah.

[853] Get out of my emergency room.

[854] Yeah.

[855] Because there's people take time.

[856] And when you have a health care 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?

[857] the two -hour patient or the 10 -minute patient, and who's going to go without care?

[858] So I think it's a systemic approach and not an individual approach.

[859] I think our health care system has some of the best physicians in the world but I'm biased because I've seen this in action for 40 years.

[860] But specifically, when we look to see who's doing the caring, it's the primary care doctors.

[861] The specialists, there's a hand in the waiting room.

[862] There's a heart in the cath lab.

[863] But that's a person with a hand.

[864] that's a person with the heart.

[865] That's a person with the brain.

[866] Let's look at what the fundamental unit of care has got to be.

[867] It's a person.

[868] Scott and I spent all day long, two -hour visits and listen to people.

[869] I had one rheumatologist giving me a hard time at University of Washington in Seattle.

[870] I sent a patient in from Cordoline who needed to have a TGF Beta 1 done because he had juvenile rheumatoid arthritis was going blind, and TGF Beta 1 was the cause of that.

[871] And he goes, Well, I've never heard of a TGF Beta 1.

[872] This was years ago.

[873] And being a smart ass, I said, there's only 75 ,000 papers published on TGF Beta 1.

[874] I would not admit that.

[875] You didn't know any of them in public if I were you.

[876] Well, needless to say, he got the TGF beta 1, the child can see now.

[877] But the point is, it's hard to read everything.

[878] We're asking you to be an expert in endocrinology, an expert of metabolism, an expert in cardiology, an expert in pulmonology.

[879] We want you to be an expert in pre -renelazotemia.

[880] pots and pans.

[881] We want you to do all of it all day long.

[882] Yeah, yeah.

[883] 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.

[884] So it's really, it's a major.

[885] But on the other hand, you know, a long -term prognosis of chronic depression and immunological trouble plus Alzheimer sounds like a pretty dismal way to conduct, you know, conduct life.

[886] So, um, you always have to rain.

[887] Right.

[888] Well, right, well, right.

[889] And I've already discovered some things about, you know, how, how immunological systems work.

[890] I mean, I've been struck to the core by how effective this carnivore diet has been for so many people.

[891] It's, and I would have never, I would have never believed that, you know, 20 years ago that the probability that, like, just the very idea that people could live on nothing but meat would have struck me as, like, 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.

[892] It does seem to be the case.

[893] And certainly the body of data that you guys have accumulated, the studies you've done, they're difficult to, once you go through them, they're very difficult to just shunt away and ignore.

[894] 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.

[895] Is there anything that we haven't covered in this two -hour presentation?

[896] Now, I wanted to ask you, the textbook that you said, that was art and science of SERS treatment, medicine.

[897] Art and science of SERS medicine.

[898] Okay, so that's where medical practitioners can learn about this.

[899] what's the best source for just general public people?

[900] I know my daughter's put up a big website about SERS -related disorders, and we'll put that in the links, but where should people go online to gather more information about this?

[901] There are two of the other sites, Scott, Scott Juan, Sirs -X, surviving mold is another one.

[902] Scott, tell us all about Surz -X.

[903] Well, I was going to say the two places where the most knowledge, the most trusted knowledge is, the most literature, the most videos about this are either from Dr. Shoemaker's www