Chronic Inflammatory Response Syndrome (CIRCLRS) is a problem that affects about 20% of the population, and is the result of exposure to environmental toxins in buildings. In this episode, Dr. Richie Shoemaker and Dr. Scott McMahon discuss what they believe to be the cause of this problem, and why they believe there may be a link between environmental toxins and CIRCS. They also discuss the potential role that environmental stressors can play in the problem. Dr. Shoemaker is a professor of psychology at the University of Wisconsin-Madison, and Scott is a postdoctoral researcher at the Center for Integrative Biology and Toxicology at the Johns Hopkins University, where he is a member of the National Academy of Toxicology, and the National Institute of Occupational Toxicology and Microbiological Engineering, which is a division of the Department of Defense. Dr. Shoeemaker and McMahon are both members of the Defense Advanced Research Projects Agency (DARPA), a joint venture between the Defense Department and the Joint Improvised Explosive Device Defeat Program (JIEDP) at the Joint Functional Genome Project at the National Center for Defense Biology and Chemistry, a joint effort by the Joint Defeat Program and the Army Research Institute, and a joint research project with the Joint Program for Defense and Engineering Research, Inc. (JCRP). is a joint project between the Army and JCRP, which focuses on the problem of chronic inflammation and environmental toxins. . and the U.S. Army Research and Defense Department, which has been identified as a major contributor to the problem, along with other environmental toxins found in military buildings and buildings, including mold, soil, soil and water damage, and soil used to produce environmental toxins, soil remediation, and other materials used to create these toxins. Let this be the first step towards the brighter future you deserve! with Dr. Jordan B. Peterson, who offers a unique understanding of why you might be feeling this way, and offers a roadmap towards healing. In his new series Dr. Peterson provides a roadmap toward healing, showing that while the journey isn t easy, it s absolutely possible to find your way forward. If you re suffering, please know you are not alone, there s hope, and there s a path to feeling better. Go to Daily Wire Plus now and start watching Dr. B.B. Peterson on Depression and Anxiety: A Path to Feeling Better, Let This Be the First Step towards the Bright Future You Deserve.
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00:01:10.440I'm talking today to Dr. Richie Shoemaker and Dr. Scott McMahon, and they are cardinal investigators into a problem known as chronic inflammatory response syndrome.
00:01:22.840And you probably haven't heard that before, but you may have heard about conditions like sick building syndrome or fibromyalgia or chronic fatigue syndrome,
00:01:34.320and you've certainly heard of conditions like Alzheimer's and other degenerative neurological conditions.
00:01:39.440Doctors Shoemaker and McMahon think that they have discovered, with the help of other people, obviously,
00:01:47.940at least one potential pathway to such conditions, and that has to do with toxins in buildings.
00:01:56.900So the basic theory is something like this.
00:01:59.860A substantial number of buildings, especially those built with drywall, using antifungal paints,
00:08:39.480So you're going after a host of immunological diseases,
00:08:44.360including extraordinarily widespread conditions like Alzheimer's.
00:08:48.240Dr. McMahon, do you want to explain to everybody what this has to do with where they live?
00:08:53.200So there are a number of potential triggers that can cause the innate immune system to activate.
00:08:59.320And as Dr. Shoemaker pointed out, these people, or at least around 90% of them,
00:09:06.100don't have adequate or effective antibody production to help mitigate when there is chronic exposure.
00:09:14.560So the innate immune system is then basically left to handle this by itself without the antibody cavalry coming in and reducing the burden.
00:09:25.080And if you are living or working or going to school in a water-damaged building where there is increased dampness or increased microbial growth from molds or bacteria or actinobacteria or all of the above,
00:09:40.860when you inhale those, your body recognizes those as being foreign antigens.
00:09:47.880And it's not just, for instance, say, mold spores.
00:09:50.980It can be old, dead mold spores that have lost their integrity.
00:09:57.020Their cell wall is broken apart into hundreds of fragments.
00:10:00.840And in fact, those fragments, when you inhale them, go even deeper down your respiratory tract into your lung.
00:10:06.840And again, trigger the innate immune system.
00:10:09.340As response to that, the innate immune system will overproduce cytokines.
00:10:15.080In 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.
00:10:23.840And these fragments trigger the innate immune system and the overproduction of the cytokines.
00:10:29.480And 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.
00:10:48.220Okay, so let me get the whole sequence of this straight.
00:10:52.400So what you guys have been studying is sometimes, and stop me at any point if I get any of this wrong.
00:10:59.440Sometimes people refer to this as sick building syndrome.
00:11:02.440You've brought in conditions like Alzheimer's and other immunological diseases, chronic fatigue syndrome.
00:11:08.180I know you've concentrated to some degree, too, on fibromyalgia.
00:11:12.600So 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.
00:11:24.940That's much more likely in buildings that have been water damaged and not properly remediated.
00:11:30.500The 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.
00:11:40.460And some people, when that immune response is triggered, they're not producing antibodies in a proper manner.
00:11:48.880And there are genetic reasons for that and possibly metabolic reasons as well.
00:11:53.980And then is it the combination of the pathogens that are in the local environment plus the genetic weakness or the metabolic problems that produce this cytokine storm that you associated with flu-like symptoms and pain and chronic inflammation?
00:12:08.740And have I got all that right? Is that the way this lays itself out?
00:12:16.680Okay, okay, good. So let's go through that one by one then.
00:12:20.880The first issue is then, what percentage of buildings in North America and elsewhere in the world do you think are suffering from this problem?
00:12:30.440And if it's a large number of buildings, that's obviously a catastrophe.
00:12:35.100So what's the evidence for this and why did you guys become convinced of this?
00:12:39.960What we have seen is a similarity of the syndrome of acute exposure followed by chronic exposure wherever the person might live.
00:12:52.560It's not confined to Florida or Hawaii, could be in Nepal or could be in Stuttgart.
00:13:00.880This worldwide exposure to an environment that pretty much is 62 to 78 degrees year-round.
00:13:09.940No wind, no rain, no change of the seasons indoors.
00:13:15.300And the mark of every one of these indoor places is water intrusion.
00:13:18.760So if we look to see, is there a water-damaged building, we should be able to find an ecosystem of organisms.
00:13:28.120Now, 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.
00:13:36.040We know that fungi have a role, but we also know that endotoxins from bacteria are second on the list, and first is actinobacteria.
00:13:44.620And when you look at every building that's water-damaged that has these ecologic parameters, you find the same symptoms, the same laboratory findings.
00:13:57.460And 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.
00:14:08.620In some of Scott's work, he's published that the likelihood is that you've got a p-value of less than, p is less than, than one to the minus 50th power.
00:14:20.400So it could be the same in Stuttgart if the lowest was the same, but actually, statistically, the idea that it's not the same is so remote to be impossible.
00:14:29.820Okay, so, Scott, what proportion of modern buildings, first of all, is it modern buildings that are particularly affected, and if not, or if so, what proportion of buildings in general are we talking about?
00:14:44.780And are there specific kinds of buildings that appear more susceptible?
00:14:49.360I read in some of the work of yours that I reviewed, for example, that drywall seems to be a particular problem.
00:14:54.580So, what kind of, how widespread is this problem, do you suppose?
00:14:59.760And what buildings are particularly affected?
00:15:02.600Well, 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.
00:15:16.580The buildings that are involved are not due to one era of construction or another.
00:15:23.040With modern structures put up quickly, contractors investing money, wants to turn over the house sale quickly, so you may not wait for a master plumber to put in the bathroom, and a plumbing leak can develop.
00:15:34.740Construction defects for new homes are a real bugaboo.
00:15:38.080But even when we were in Scotland and the castles from the 1200s and before, we saw the same kinds of problems, 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.
00:15:57.020And about in 1970, when the population got all upset with oil embargoes and houses were made to be tighter, we thought that that was the reason for the problem.
00:16:08.720It was actually not, because what we were using were paints and sealants to keep down mold growth.
00:16:15.320What 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.
00:16:25.000So before 1970, it usually was a paint building that was retrofitted or retrograde corrected or modern construction.
00:16:35.220The safest buildings, even though they're water-damaged, are the old buildings with no paint.
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00:18:19.280Okay, so there's no specific form of building that's amenable, per se, to water damage and the intrusion of toxins in consequence.
00:18:31.120But you talk about buildings after 1970.
00:18:34.180You 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.
00:18:45.920And I remember when people started talking about sick building syndrome, I guess this went back as far, in my knowledge, as far back as the 80s.
00:18:53.240They were concerned about these hyper-sealed buildings.
00:18:55.280But 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.
00:19:07.360Now, hypothetically, the reason they put those antifungals and antimold chemicals in the paints was to keep the fungus and mold down.
00:19:13.860But 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.
00:19:29.260So 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?
00:19:43.100Fungi also have a response to environmental hazards.
00:19:47.320And the environmental hazards of being killed will cause normal activation of genes in fungal species, such that they'll make toxins where beforehand they didn't.
00:19:58.880The main role of a mycotoxin, for example, has nothing to do with defense.
00:20:04.040It has everything to do with predation.
00:20:06.000So 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.
00:20:13.520And the fungi make compounds to eliminate the fungi.
00:20:16.740They eliminate the peroxidase, therefore eliminate the plant defenses.
00:20:20.420But it's predation of fungi on its prey.
00:20:25.920That's foremost where all this goes on.
00:20:28.200Meanwhile, actinobacteria love an alkaline environment, molds like an acid environment, and the alkaline environment from actino is created by a manufacturer of substances that will kill off fungi and change the pH of the drywall.
00:20:46.640So that as you see an initial building, the initial colonization will be with fungi, it'll be replaced by actinobacteria as time goes on.
00:20:57.000But meanwhile, if there's a flood or a hurricane event or a natural disaster, the water saturation, or AW, as people should say, activity of water,
00:21:07.520will initially let in organisms that like very saturated conditions, or AW of 0.9 to its maximum of 1.0 or 100%.
00:21:17.360So we see one group of fungi of water damage that's acute, or different species, or we'll be grouping of water damage that's less acute.
00:21:27.580And in the end, then we'll see sources that have very dry buildings, but it's where the moisture has changed the ecosystem.
00:21:37.520Now, actinobacteria are famous for creating a smell, and interestingly, the musty smell or musty odor we've long associated with fungal colonization is coming from actinous.
00:21:50.080There are also architectural design features that make a building more likely to become water damaged than others.
00:21:58.720Flat roofs are more likely to leak than pitched roofs are.
00:22:02.280Or basements and crawl spaces are more likely to have water intrusions than you would see in homes that are built on a slab.
00:22:14.040We know that drywall is more likely to have problems than plaster on the lathe.
00:22:20.880So there are a number of different materials and architectural styles that can make a house or a commercial building more vulnerable or less vulnerable.
00:22:30.440Right. Well, you could imagine, you know, when I'm thinking my paranoid thoughts, I know, here's an example.
00:22:36.480So one of the reasons that the Roman Empire fell was because the Romans used lead to seal their wine amphora.
00:22:45.420And 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.
00:22:58.360And that was, it was also the case that in relatively low, let's see, in older houses that had used a plethora of lead paint where the paint was allowed to deteriorate and young children were therefore ingesting lead paint powder,
00:23:15.700they were also impaired in terms of their intelligence and also much more likely to be antisocial and criminal.
00:23:21.240And 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.
00:23:32.360You know, experimental vaccines come to mind, by the way.
00:23:36.080And 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.
00:23:43.180And it sounds like that's a case that you're making for drywall, is that it's extraordinarily light, easy to work with, cheap building substance, but it isn't, we don't have a lot of historical experience with it.
00:23:55.480It was introduced in a very widespread manner in the latter half of the 20th century.
00:23:59.940And so, and then you're saying that in combination with the fungicides and so forth that was put in the paint, that we put ourselves in a situation where we've contaminated something approximating 50 to 80% of buildings?
00:24:12.760So that's really quite the bloody catastrophe.
00:24:15.240So now, let's take that apart a little bit.
00:24:18.380If it's 50 to 80% of buildings, how many of them, in your estimation, are contaminated to the point where that actually constitutes a serious health problem?
00:24:28.780Like, you know, I know that that's a threshold issue, but there's lots of threats that people have to contend with, obviously.
00:24:36.420And if your house is contaminated with mold and water damage, that's a big deal.
00:24:41.140It's a really difficult thing to fix, or it can be.
00:24:43.800And so, under what conditions should people be prioritizing this as a actionable risk factor?
00:24:52.200And how widespread do you think this problem is in its more serious forms?
00:24:58.780Study after study has looked at individual susceptibility, which underlies who gets sick and who doesn't.
00:25:06.200The individual susceptibility of the immune response genes found in chromosome 6 or HLA-DR was shown to be present in just about every person who had SIRS.
00:25:18.600And the percentage of not having SIRS, HLA, but having an illness is less than 5% of the total.
00:25:26.440So 95% were broken out into six separate haplotypes.
00:25:33.780And out of those six, it's 24% of the population.
00:25:36.940When we look at this 24%, if we put them into exposure and follow them prospectively, we can show that the initial responses, once a priming event has taken place, is essentially 100% of those with individual susceptibility.
00:25:54.000We're seeing this exactly the same way with COVID.
00:25:58.180COVID creates an inflammatory response that turns on innate immune responses, which turns on gene-based susceptibility.
00:26:05.360So long COVID has the same genetic makeup, and we've published a paper on this in June of last year as well, that creates a new illness, a new target where once wasn't before.
00:26:19.280And we looked at people who were living in a building and fine, got COVID, got better from COVID, but then that turned on the innate immune response system that didn't stop.
00:26:30.700And 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.
00:26:56.940So you could imagine that there's a manner of conceptualization that allows for two kinds of disease processes.
00:27:05.580There's disease processes that are associated with pathogens per se, and then there are disease processes associated with an anti-disease response or an immunological response gone astray.
00:27:17.360So if I'm following you correctly, we have a situation where, let's say, 75% of our buildings are contaminated.
00:27:24.560And so three-quarters of the population is exposed to the pathogens that could produce an immune hyper-response.
00:27:29.740But 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.
00:27:45.080Or is that a more general susceptibility to immune overreaction?
00:27:49.560You seem to be implying that in relationship to the COVID issue.
00:27:52.620So it's 25% of 75%, essentially, is the number of people who are hypothetically affected.
00:28:15.480One of the reasons that it's so important is that we look at illnesses that are SIRS, that actually are SIRS, and add up who has chronic fatigue syndrome, who has fibromyalgia, who has depression, who's just getting older because their cognitive effects are moving forward.
00:28:31.080What are children not doing well in school?
00:28:33.360Is it the lead paint that they swallowed?
00:28:35.380Is it the lead in the applesauce that they've been taking in?
00:28:38.980Are there environmental factors that are creating this overall systemic illness of which the brain is the injury I worry most about in adults?
00:28:51.640Scott sees children more than I did, so we can let him speak about children with cognitive issues.
00:28:57.080But the issues are that when we look carefully at chronic fatigue syndrome, we find SIRS.
00:29:02.760And I'd like you, sir, if you could, to identify one significant biomarker that distinguishes fibromyalgia from not.
00:29:10.780We have 30 biomarkers for SIRS and zero for fibromyalgia.
00:29:15.580Why does fibromyalgia have such a preponderance of people?
00:29:18.920And how many people, adults, have fibromyalgia?
00:29:21.70010% and 3% for chronic fatigue syndrome?
00:29:31.320And 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.
00:29:47.340Okay, 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.
00:30:02.440And so let's take depression as a case in point.
00:30:05.540Now, when I was assessing my clients for depression, the first thing I always tried to figure out was, are they just ill?
00:30:13.420Because there's all sorts of evidence associating depression, particularly with immunological dysfunction.
00:30:20.120And 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.
00:30:34.520And depression is a relatively non-specific cluster of syndromes.
00:30:38.600Now, you're pointing to a whole set of syndromes that have relatively non-specific symptoms, some of them even more difficult to diagnose and easier to be skeptical about in relationship even to their existence as, say, fibromyalgia and chronic fatigue syndrome.
00:30:57.820So, right, that's hard to dissociate from general depression and anxiety and a kind of global neuroticism or even a hypochondriasis.
00:31:07.200Now, you're saying, you know, your first claim is that 20% of the population is likely to be experiencing these symptoms, but we don't see that, we don't see this Sears chronic inflammatory response syndrome in 20% of people because essentially we're placing them in the wrong bins.
00:31:23.640Now, and so how much of, so let's walk through, let's walk through what the symptom constellation is for chronic inflammatory response syndrome, that's Sears, 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.
00:31:45.840And why do you think that your category system, which 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?
00:32:02.440Because, I mean, you're making a lot of radical claims here, and I'm certainly not in a position to dispute them, but you know what they say, radical claims require radical evidence, and you're saying, well, first of all, that 80% of our buildings are in serious trouble, that 20% of the population is suffering dreadfully as a consequence, and that there are genetic predispositions to this, and that many, many people with many other disorders are fundamentally misdiagnosed, and that this is actually the root cause of their symptoms.
00:32:30.720Like, including absolutely devastating diseases, like Alzheimer's, so what is it, let's go through, first of all, what are the symptoms that point to Sears, as far as you're concerned, and then what do you use to prove that that's the condition?
00:32:46.940As Dr. Shoemaker said, we have roughly 30 biomarkers. These are tests which can distinguish ill people, or what we call cases, from healthy people, what we call controls.
00:32:58.820We have roughly 30 of them, and all of them have been validated to show that they separate cases from controls.
00:33:06.720When we look at the diagnosis of Sears, you have to have objective evidence that shows that you have several of these biomarkers.
00:33:16.520You know, I mean, at least four, or maybe five or more, before you can actually even make the diagnosis.
00:33:23.700The statistical likelihood of finding a healthy person who had five abnormal biomarkers out of the five we draw, or the 10 that we obtain, it is so small.
00:33:35.780I mean, it's in the one to a million range.
00:33:37.540Then when you start looking at a larger group of people, maybe several people in the same hall, or in the same office building, or in the same school, when you start looking at that, and each person's probability of having those abnormal biomarkers multiplies by the next person's, and then multiplies by the next person's.
00:33:59.500By 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.
00:34:09.400I 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.
00:34:26.100We are looking specifically at the innate immune system as a possible root cause for these different symptoms.
00:34:32.040And if they ran the tests that we do, they would see the same kind of data that we have.
00:34:38.640My data is very similar to Dr. Shoemaker's.
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00:36:30.260But that probability declines as a function of the number of tests administered.
00:36:36.760So maybe there's a 1 in 20 chance that any given test will show that you have the condition.
00:36:43.160But there's a 1 in 400 chance that two tests would show that.
00:36:46.940And a 1 in 8,000 chance that three tests would show that.
00:36:49.900And so your case basically is that as you accumulate evidence of the biomarkers,
00:36:54.320you decrease the probability of a false diagnosis.
00:36:57.160And there aren't biomarkers, as far as I know, there certainly aren't biomarkers for depression.
00:37:02.640So that's not specific, what would you say, physical or chemical biomarkers.
00:37:08.780You know, sometimes there's elevated cortisol or decreased cortisol, but the markers are very nonspecific.
00:37:13.600So if you're correct, and there are specific biomarkers for SIRS, that implies that it can be more accurately diagnosed than the other conditions with which it might be confused.
00:37:26.480And so what are the prime biomarkers that you guys use to make the diagnosis?
00:37:32.640And why did you pick those, and how valid do you think they are, and why?
00:37:38.460We need to start with a case definition.
00:37:41.620The case definition in 2003 that our group came up with was modified in 2008 by the U.S. Government Accountability Office.
00:37:49.560And when they looked at the potential for exposure, this is what CDC used with Fisteria back in 1997, 1996.
00:37:58.140You didn't get sick from a microalgal bloom unless you were exposed to it.
00:38:03.760So the potential for exposure is number one.
00:38:06.340Number two is symptoms the same or similar to those seen in published peer-reviewed literature.
00:38:11.480The third element is laboratory findings, the same or similar to those seen in published literature.
00:38:18.440And then the fourth is objective response of biomarkers to treatment.
00:38:23.560So if we then say what biomarkers have stood the test of time, back in 2000, it was trial and error.
00:38:31.340By finding HLA was the explanation of why did some people get sick and other people didn't.
00:38:36.540Was there a risk factor like cigarette smoking or alcohol use or age or underlying illness with diabetes?
00:38:48.500So individually immune responses became our first biomarker.
00:38:53.140Actually, the first biomarker came from the EPA with Ken Hodnell.
00:38:56.660We've been studying the neurotoxicologic features of visual contrast sensitivity, which is a mechanism to see an abnormal neurologic function of vision.
00:39:09.220Contrast is one that's stabilized over time and is adversely affected as velocity of flow of red cells and retina and neural rim of the optic nerve head increases.
00:39:23.860In that group, there was a regulatory neuropeptide, melanocyte-stimulating hormone, which is essentially negative in all cases and normal in all controls.
00:39:35.340And then with treatment, we saw improvement in MSH, not as much as what we wanted, and that was the impetus to keep on.
00:40:22.440So we took then inflammatory markers, TGF-beta-1.
00:40:25.980No lab was running that, so I hired a lab to prove that there was such a marker, and then we showed it with the abnormal and showed it in its height with some of the worst illnesses of all.
00:40:38.060And then we treated it with medications that were available over-the-counter or with informed consent.
00:40:47.080And then every time we had re-exposure, here we came to the prospective acquisition of illness, proof of causation.
00:40:56.140We took people that could have been sick from one building, fixed them all day.
00:41:00.200And then with informed consent, they stopped all medicines and stayed away at the suspect building.
00:41:35.160Okay, so let me elaborate on the story now.
00:41:39.580So 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 quite dramatically.
00:41:49.060And so there's an online test, which is a visual contrast sensitivity test.
00:41:53.500And 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 visual acuity in relationship to closely spaced lines on a diagram, essentially.
00:42:09.760And 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?
00:42:22.720So there is an online test, visual contrast sensitivity, that people can take.
00:42:27.320See, it's a strange test, because it seems like it's so far removed from the symptom set that people would be experiencing.
00:42:35.640It's very difficult for someone like myself.
00:42:38.420I'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.
00:42:50.260This 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.
00:42:59.620Now, you said that the reason that this visual contrast sensitivity test works is because the retina itself is compromised as a consequence of immunological malfunction.
00:43:11.860We have an objective parameter, and that's velocity of flow of red blood cells in the retina blood vessels, in the capillary beds, as well as the neural ramdiopic nerve head.
00:43:26.580We can measure objectively with a Heidelberg retinal flow meter how fast red blood cells move.
00:43:32.140And they move more slowly if the inflammatory response promotes production of what are called adhesions, which is one mechanism to decrease flow in the area of hyper-inflammation.
00:43:44.700And treatment will be shown to improve flow as the environmental stimulus is fixed and is corrected with treatment.
00:43:53.140So, sick patients, you have reduced flow.
00:43:57.920Healed patients have restored to normal flow to equal controls.
00:44:02.140But re-exposure, here we go, prospective exposure again, this is how we determine risk in all of medicine and science, prospectively, not an association, but prospectively re-exposed people, get the same findings back again, we fix them, we get them back to the same mechanism they were when they were healed to equal to controls.
00:44:24.300This in and out, in and out, and constant answers to the critics, how could this possibly be true?
00:44:34.340And if people want to argue with me, they can argue with my data.
00:44:38.080Okay, so let me elaborate on that a little bit before I return to the biomarkers per se.
00:44:43.500Okay, so I know that the closest tissue that's deeply analogous to the brain itself is retinal tissue.
00:44:53.260And 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?
00:45:26.860The same mechanism of cytokine response in capillary beds is the same whether it started with a fungus, whether it started with an actinobacteria, whether it started with the flu.
00:45:39.220But this innate immune response is nonspecific in how it responds, but it will respond, and we can measure its tendency to recur regardless of where it happens.
00:46:16.700But 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.
00:46:26.620We'll see who's going to do works better.
00:46:28.240When yours doesn't and mine does, then I'm going to say I win the battle.
00:46:31.800Right, well, that's particularly powerful, as you pointed out, in combination with evidence that you can reinstantiate the illness once treated with re-exposure.
00:46:41.960Because then you have direct causality, right?
00:46:44.440Instead of the weak sort of correlations that often go to hypothetically prove the existence of a given condition.
00:46:51.500Okay, so let me get this straight again.
00:46:54.180So you have the vision test, you have HLA, maybe you can tell us again what that is, was it melatonin-stimulating hormone, and cytokine detection.
00:47:03.820So that's four, are those the four primary biomarkers?
00:47:11.560We measured simultaneous ACTH 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.
00:47:31.200So if we have disruption of MSH, we're going to have disruption of ACTH, and cortisol can either follow in step, which it often will, or create its own marker.
00:47:42.660So dysregulation of ACTH and cortisol is one.
00:47:46.060We found antidiuretic hormone doing the same thing.
00:47:49.260People walk around with chronic headaches.
00:47:50.940They said they had migraine constantly.
00:47:53.240But we find out they were all functionally dehydrated with elevated osmolality and reduced ADH.
00:48:02.360We looked at pulmonary hypertension as a very common cardiac condition that's mistaken for cardiovascular disease.
00:48:10.240People are short of breath and have chest pain with exertion.
00:48:13.620We think that it's from due to coronary disease.
00:48:16.380When, 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.
00:48:26.920When 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.
00:48:39.940When we get to genomics, and I hope we'll have time for today, if not, we should do this tomorrow or another day, the gene mechanisms are the real goldmine for the researcher and for the clinician alike.
00:48:51.940Okay, well, I'll return to the genomics issue.
00:48:56.440And don't let me forget that if we don't get there.
00:49:00.340Okay, so we've basically walked through, we've done a reasonable overview of the biomarker space.
00:49:06.920Let's talk about behavioral and cognitive, behavioral, emotional, and cognitive symptoms.
00:49:15.360Like, what are people, what are people who have SIRS 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.
00:49:29.640So what are the fundamental symptoms that people should be alert to, and do they differ in adults and children?
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00:50:33.120Well, as we were talking about decreased red blood cell flow to the optic disc, you have to understand that there's decreased red blood flow to different places in the body, not just to the optic disc.
00:50:45.820So, 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.
00:50:54.780Our patients will often have cold hands or cold feet or both.
00:50:59.160They can have cramping in their hands.
00:51:14.200The brain will also have a decreased blood flow.
00:51:18.280And 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 increase in lactic acid in certain areas of the brain.
00:51:31.320And there was an abnormality in the glutamate-glutamine ratio, both of which suggested that there was hypoperfusion or a reduction of that red blood cell flow.
00:52:03.660And then we get into genomics findings.
00:52:05.960But 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.
00:52:15.940And so that will lead into brain fog and potentially into cellular death, which can then lead into things like, you know, dieback regeneration and the neurologic illnesses.
00:52:27.220Now, you also, how do you directly evaluate brain state and brain function?
00:52:36.940If I remember correctly, I mean, I've been investigating this with my daughter and my wife for some time, and some of the details are unclear to me.
00:52:44.580We've also had brain scans specifically done to look for neurological damage that might be associated with this exposure and sensitivity.
00:52:54.580And so for everyone who's watching and listening, I mean, I might as well tell you why I'm particularly interested in this.
00:53:01.040I 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.
00:53:14.180But 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.
00:53:22.760And she's treated a lot of those successfully with a very restricted diet, as have my wife and I.
00:53:28.220But she's become convinced more recently that the cause of the food sensitivity that's driving her immunological conditions might be associated, might be attributed to sensitivity to these biotoxins that Dr. Shoemaker and McMahon are talking about.
00:53:45.200And so, well, that's what we're trying to track down at the moment, because this has been a multi-generational catastrophe in my family, and I would like to get to the bottom of it.
00:53:53.500And so we did some of these neurological tests that did indicate some neurological damage, hypothetically, as a consequence of toxin exposure.
00:54:04.140And so can you walk everybody through those tests and what they indicate?
00:54:07.900And then maybe we could talk a little bit about treatment before turning to genomics.
00:54:16.800Let's pick up that loose end before we hit into NeuroQuant and all that.
00:54:21.660The symptom reporting that I did when I had visual contrast as my only biomarker was compulsive logging down of what symptoms that people have.
00:54:31.080Maybe symptoms that I elicited in an interview wasn't a self-form or questionnaire that the patient would fill out.
00:54:39.340It's the process of doing a medical history that we're all trained to do in the four years of medical school or longer if we specialize.
00:54:47.040But specifically, fatigue and weakness were not specific, didn't have two or the others, aching and cramping, unusual cramping of the legs when you'd get spasms at nighttime and get a charley horse or in the hands.
00:55:02.000And it was hard to extend fingers because the muscles were in spasm.
00:55:05.940Basically, that was the end of circulation.
00:55:10.380The fingers and the toes were the end.
00:55:12.120That's where the accumulation of lactic acid was greater.
00:55:45.520Abdominal 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.
00:56:14.340We 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.
00:56:29.260So let me ask you a technical question about that.
00:56:32.700So when you're going through that as a psychologist, so what I would think would be helpful in relationship to that diagnosis would be to make a list, like a questionnaire, of all you listed off about 40 symptoms.
00:56:45.340I think that's about how many you covered.
00:56:46.980So 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.
00:56:59.400Have you guys done any questionnaire development that's oriented towards symptom identification?
00:57:05.280Every person that takes their visual contrast test will undergo a symptom analysis and a symptom discussion, and we look to see if there's cluster analysis, a statistical function of saying yes or no based on visual contrast and symptoms alone without any of the other biomarkers.
00:57:24.460Just statistically, we can tell you 98.5% likelihood of SIRS just on VCS and symptom clusters.
00:57:56.360What, and we talked a little bit about illnesses that are hypothetically attributable to that, but let's go through that in some more detail.
00:58:05.920What 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.
00:58:23.520And that that was associated in this paper with a particularity of, if I remember correctly, a Finnish architectural design that made their houses more susceptible to these biotoxins that you describe.
00:58:35.980And that's produced a statistically significant increase in the rate of Alzheimer's in Finland.
00:59:26.500Have you guys ever tried a verbal fluency test by any chance?
00:59:30.860Because verbal fluency seems quite susceptible to disruption by, well, there's certain forms of neurological degeneration that interfere with verbal fluency quite dramatically.
00:59:39.560And it might be a good marker for cognitive interference.
01:00:00.800I don't have your skills, but she did and those abnormalities were found.
01:00:06.380When you look at neuropsychological testing of patients, the two most common abnormalities that I see are deficits in working and memory and deficits in processing speed overall.
01:00:21.020And one of the complaints that we very commonly see is that people are still able to do the functions of their job.
01:00:27.460It just takes them much longer than it used to.
01:00:30.420So what they used to be able to wrap up in an hour now, three or four hours, which is relatively unproductive, and eventually they end up on disability.
01:00:39.620See, that's why verbal fluency might be a real useful marker, because it's a time test, right?
01:00:44.680How many words can you write down that begin with the letter S in three minutes?
01:00:48.300And 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.
01:01:01.520So that's really why it sprang to mind.
01:01:04.680Well, it's also an unbelievably easy test to administer, and there's wide individual variability.
01:01:09.380And it'd be very interesting to see if that was associated with the genomic markers that you described.
01:01:18.060And then I want to delve a bit more into, you know, we brushed over this very quickly, the idea that the symptoms that culminate in Alzheimer's decades later can be detected decades previously.
01:01:30.500I know, for example, by the way, this is another reason the verbal fluency test popped into mind.
01:01:38.280They 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.
01:01:50.760So another reason verbal fluency might be an interesting marker.
01:01:54.320So, okay, now, and we just, so I wanted to go in two directions.
01:01:58.360One direction was, okay, what is the panoply of neurological, degenerative neurological conditions that you think are likely to be associated with SIRS?
01:02:10.740We didn't have a assumption-based discussion about symptoms and neurological abnormalities that we thought were for SIRS.
01:02:21.620We had recorded executive cognitive function, we recorded tremors, we recorded metallic taste, dizziness, vertigo, tremors, but we didn't have any way of assessing what was going on with the brain.
01:02:35.400We couldn't measure abnormalities in brain.
01:02:38.180And along in 2007 comes NeuroQuant, and NeuroQuant, with one MRI image, can look at 11 different volumes that we then could start to correlate with parameters.
01:02:51.080And by 2015, Scott and I had both published papers looking that there were reproducible abnormalities in NeuroQuant in SIRS patients, and with treatment, we can fix those.
01:03:04.620But the beauty in 2017 was we could actually fix multi-nuclear atrophy.
01:03:12.340So our treatment was nonspecific, nondegenerative, but instead of just fixing the hippocampus, we were fixing hippocampus, amygdala, and caudate.
01:03:23.480We 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, cases equal to controls.
01:03:35.340So NeuroQuant early on became of interest, but the final change was NeuroQuant associated with genomics.
01:03:44.880And 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.
01:03:57.000If you developed your chronic inflammatory response syndrome as a result of water-damaged buildings, we tend to see that the forebrain parenchyma will be swollen.
01:04:08.440We see that, or enlarged, I should say.
01:04:11.040We'll see that the cortical gray matter will be enlarged and that the caudate nucleus will be atrophic, will be smaller.
01:04:18.100If you develop chronic inflammatory response syndrome as a result of Lyme disease and post-treatment Lyme disease syndrome, we see a completely different pattern.
01:04:29.880And that pattern is that the right thalus is enlarged and that the putamen is smaller and atrophic.
01:04:36.980And we showed that on two different studies.
01:04:39.520And then in the third study that Dr. Shoemaker and I published together looked at different treatment.
01:04:45.500And when we used Dr. Shoemaker's treatment protocol up to the next to the last step, we saw that the forebrain parenchyma that had previously been enlarged and the cortical gray that had previously been enlarged came back to control values.
01:05:02.340But we didn't see improvement in the multinuclear atrophy.
01:05:07.020The next paper, though, did, and that was with use of VIP, basalactive intestinal polypeptide, which is a substance that your body makes and is key for, it's an anti-inflammatory peptide.
01:05:23.300It's a neuroregulatory peptide that brings your activated immune system back down to normal when it's appropriate to do that.
01:05:31.980And so with VIP therapy, which Dr. Shoemaker put in hand, we have seen caudate nucleus and multinuclear atrophy either stopping or reverting back toward normal.
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01:07:01.420Have you guys used that same treatment protocol for conditions like Alzheimer's or other degenerative neurological diseases?
01:07:09.760Obviously, there's an overlap there, which we've discussed, or hypothetically, there's an overlap there with SIRS.
01:07:15.420Has anybody been looking at the application of this particular treatment protocol to these degenerative neurological diseases?
01:07:22.000Yes, we published one study just a few weeks ago.
01:07:25.780But what we didn't have was looking at people that were untreated or stage 1 patients compared to stage 2, which is treated with the first part of the protocol.
01:07:37.160But stage 4, that's where we had the off VIP and doing well.
01:07:43.440We had a reduction of the basic mechanism of dieback CNS degeneration, looking at changes in TUBA for a 44% reduction in three months.
01:07:59.600That's, that's not been published yet, but it's high on our list.
01:08:03.220Yeah, I bet it's high on your list, yeah.
01:08:06.000It's like, we've got to get going on this one.
01:08:09.900There are other things that other people are doing or aware this is a complex field and no one illness parameter will fit everybody.
01:08:19.100But if you've got the microtubular dysfunction that we had alluded to with TUBA4A and TUBB1, if you have that as a marker and you have cognitive issues and you use and you respond to VIP, the reduction is 44%.
01:08:38.000And that's just in three months of work.
01:08:40.480Okay, so I would like to take this in two directions now, and we've got about half an hour left in this segment, although we can run a little longer if, you know, if that seems appropriate.
01:08:50.140I want to know about, you know, what people should do, you know, what constitutes treatment.
01:08:55.740And so that would be building testing, building remediation, and then the interventions that you described.
01:09:01.600But I would also like to talk about, I know, Dr. Shoemaker, that you and Dr. McMahon have brought this problem to the attention of government officials.
01:09:09.900And I believe particularly in relationship to military housing, but not only that.
01:09:15.060So let's start with, everybody who's listening to this is going to be thinking, well, I know people who have this cluster of symptoms, you know, what in the world should I do about it?
01:09:24.880So let's talk, we had our houses mold tested, and, you know, the results were rather dismal.
01:09:31.100And I'm not exactly sure what to do about that, because I have properties now that appear to be quite mold saturated.
01:09:38.260And, you know, the step after that's not exactly clear.
01:09:42.580One of them was just remodeled, and I'm not that inclined to bloody well do the whole thing again, you know.
01:09:47.100But that's partly why I'm investigating this to the degree that I am.
01:09:50.400But what is it, what are the steps that people should take in order to determine, first of all, that they have this problem, and then in order to do something about it?
01:10:02.560We first need to make sure the patient satisfies the case definition.
01:10:07.260If they don't satisfy the case definition, this doesn't apply.
01:10:13.260But if you satisfy the case definition, then we want to define the ecological parameters within the building.
01:10:21.900If the building is water damaged and it should have fungi, but doesn't, and you don't test for actinobacteria, you've made a mistake.
01:10:30.580But if you don't have fungi, is that because you never had them, or is it because it's overrun with actinobacteria that are making the drywall surface alkaline, and fungi don't live very well?
01:10:43.360And then if that's not the case, what about the water saturation with endotoxins?
01:10:47.880Because of the three things that cause the greatest amount of damage to the brain, endotoxins lead the list.
01:10:53.900Specifically for every abnormality that we find in the gene that shows us about specific causation.
01:11:03.760That's the building contractor's word.
01:11:06.980Specific causation for endotoxins we've identified in neuroquant.
01:11:13.260We've also identified in combination with the genie testing or genomic testing.
01:11:25.660And 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, that's licensed, that's not a fly-by-night, and sure, it's your organization.
01:11:45.280But there are those that are out there.
01:11:47.200Sure, they really are, but specifically, if we've got a reputable lab that shows us the abnormalities, you've defined the illness parameters, you divide the environmental parameters, now we divide the treatment.
01:12:00.700Do you want to go for treatment, Scott?
01:12:02.480Sure, the first part of treatment is taking care of the exposure.
01:12:07.460So 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, remediate that, or leave that.
01:12:21.180The most important step of any kind of treatment for any kind of immunologic illness is getting away from exposure.
01:12:37.120Because it's expensive, and it's mind-bending, and as there is a certain variation in knowledge of this illness amongst mold testers and mold remediators, too.
01:12:55.720So 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.
01:13:27.440And typically, we will see improvements within two to three months if you can get that first step taken care of.
01:13:33.320There 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.
01:13:49.300I find, in my experience, that those work, but they take much longer.
01:13:54.880Most people would like to get better faster.
01:13:57.140So we use the more aggressive therapy.
01:13:59.320After 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,
01:14:12.980we usually draw some blood work to look at the tests that you had previously that were abnormal.
01:14:18.680And based on which ones continue to be abnormal, the rest of the therapy follows, Dr. Shoemaker, what's called the pyramid.
01:14:32.180And when we've gone through all of those steps and corrected or attempted to correct the various different systems of inflammation that were still causing abnormalities in the lab test,
01:14:42.580after that, we contemplate whether usage of intranasal VIP is useful.
01:14:51.040Certainly, in my experience, if you have not recovered at least 70% of your energy, 70% of your cognitive ability, 70% of your exercise tolerance,
01:15:03.520if you haven't recovered, if you haven't recovered those from the rest of the therapy, then it's time for VIP.