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

00:00:00.940 Hey everyone, real quick before you skip, I want to talk to you about something serious and important.

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00:00:57.420 Hello, everyone.

00:01:10.440 I'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.

00:01:22.840 And you probably haven't heard that before, but you may have heard about conditions like sick building syndrome or fibromyalgia or chronic fatigue syndrome,

00:01:34.320 and you've certainly heard of conditions like Alzheimer's and other degenerative neurological conditions.

00:01:39.440 Doctors Shoemaker and McMahon think that they have discovered, with the help of other people, obviously,

00:01:47.940 at least one potential pathway to such conditions, and that has to do with toxins in buildings.

00:01:56.900 So the basic theory is something like this.

00:01:59.860 A substantial number of buildings, especially those built with drywall, using antifungal paints,

00:02:08.420 have water damage.

00:02:10.380 That water damage produces biotoxins of various sorts.

00:02:13.700 For a substantial proportion of the population, about 25%, exposure to those biotoxins produces an immunological response

00:02:23.520 that has all sorts of neurological and behavioral negative consequences.

00:02:28.500 And so I found out about this through my daughter, who's been wrestling with health disorders of various sorts for her whole life.

00:02:35.500 She's convinced me that it was at least worth some investigation, and that's what I'm doing.

00:02:41.860 And so I decided to, I read some of these gentlemen's research papers, and they struck me as highly credible.

00:02:47.980 And so I'm talking to them today to find out just what there is to this.

00:02:53.300 If they're right, about 20% of the population is suffering from all sorts of conditions,

00:02:58.720 often diagnosed as other illnesses, depression included.

00:03:02.280 And that's actually a consequence of exposure to biotoxins in water-damaged buildings.

00:03:08.940 And this also seems to be a particular problem, by the way, among the military.

00:03:13.420 Low-grade military housing, much of it water-damaged and mold-infested.

00:03:17.880 And the government, by the way, seems to agree with that assessment,

00:03:20.500 even though not enough has been done about that so far.

00:03:23.420 So anyways, come along for the ride.

00:03:25.880 That's what we're talking about today.

00:03:27.180 Dr. Shoemaker, Dr. McMahon, welcome to the program.

00:03:33.080 I'm very interested in talking to you guys today.

00:03:35.640 My daughter has alerted me to your work, and I've been looking into it for the last four or five months.

00:03:41.460 You guys have been studying something called chronic inflammatory response syndrome.

00:03:45.980 And the more I've looked into this, the deeper the rabbit hole goes, I suppose you could say that.

00:03:51.620 And I thought the best way to educate myself and potentially everyone else who's listening and watching

00:03:56.640 would be to have you guys on this podcast so I could ask you all sorts of questions.

00:04:01.900 And so I'm going to take a friendly, skeptical approach, if you don't mind,

00:04:08.220 because what you're studying is of such magnitude that if you're correct, it's a catastrophe.

00:04:13.540 And so we could all hope that you're not correct so that it isn't a catastrophe.

00:04:17.720 But I know you've accumulated a substantial amount of evidence.

00:04:21.180 And so maybe we'll start with you, Dr. Shoemaker.

00:04:23.380 Do you want to just tell everybody what it is you've been studying and why you started studying it

00:04:29.540 and how widespread you think the problem is?

00:04:33.160 Most people have a sense of what inflammation is.

00:04:37.720 Our body is looking at environmental stressors that must be dealt with.

00:04:43.720 And the inflammatory process, as a general rule, is part of the environmental response to the trauma or stress.

00:04:53.180 Inflammation can be of two kinds.

00:04:54.820 One is acquired or allergy or kind of the adaptive way that the body will learn how to make antibodies

00:05:04.040 and respond to stressors with memory.

00:05:07.000 So there's things will be experienced once and then the twice as the next time is very quick.

00:05:12.800 But we're looking at a different form, the left hand, if you will, compared to the right hand,

00:05:17.540 of innate immune responses in which the response to an antigen or a foreign particle

00:05:24.940 that's introduced in the body in many different ways.

00:05:27.940 Inhalation is certainly the big way I worry about, but it could be elsewhere.

00:05:31.980 But specifically, once there is antigen detection by the innate immune response system,

00:05:41.540 there should be processing of an antigen and putting on a HLA molecule or histocompatically

00:05:49.540 locus A molecule on the antigen and packaging it in the antigen-presenting cells to a naive lymphocyte,

00:05:58.940 just waiting for something to happen.

00:06:00.660 And when the naive lymphocyte sees this tasty little morsel packaged with HLA and an antigen on it,

00:06:06.720 it should turn on a kind of T cell, or a B cell, excuse me, to make an antibody.

00:06:15.060 The problem with the illness that we have is that over 95% of the patients do not have antigen processing correctly

00:06:22.560 so that antibodies are made in a reduced fashion, if at all.

00:06:27.040 And when we look at now, what control do we have on inflammation if the stimulus is not stopped?

00:06:37.640 And it doesn't have to be ongoing exposure.

00:06:40.420 It is now in this world of antigen interaction with antigen-presenting cells and T lymphocytes

00:06:45.300 that has gone awry.

00:06:47.320 And the illnesses that we see become chronic because the antibody formation does not occur.

00:06:54.860 Now, over the years, we knew about problems with antigen presentation,

00:06:59.880 but now we know the gene mechanisms behind defective antigen presentation

00:07:05.840 and the gene mechanisms to not only include inflammation in our venues,

00:07:12.100 but also abnormalities in metabolism.

00:07:16.500 So if we look at metabolic problems combined with inflammation,

00:07:21.180 we have molecular hypometabolism,

00:07:23.980 which is a fancy way of saying that 95% of patients with chronic fatigue

00:07:29.980 have a specific abnormality and inflammation and metabolism that we can show with genetic makeup.

00:07:38.580 And then with Scott's work and my work,

00:07:41.240 we've been able to show that we can correct the gene activation

00:07:46.320 when it's not supposed to be activated

00:07:47.900 and you correct gene suppression when it's not supposed to be suppressed.

00:07:51.380 So what we're looking at is the transcriptomic or gene representative theory

00:07:58.540 of illness causation and illness correction.

00:08:03.200 Our last paper, and I hope you had a chance to take a look at it,

00:08:06.080 but it's in your inbox.

00:08:08.180 The next question is now looking at, to me, the Holy Grail,

00:08:14.560 and that's correction of dieback central nervous system degeneration.

00:08:19.440 You may hear it called Alzheimer's.

00:08:21.200 You may hear it called Parkinson's.

00:08:22.580 You may hear that same called peratrophic myotrophic lateral sclerosis or ALS.

00:08:28.300 But we are there.

00:08:29.960 We're there with gene activation and correction with our therapies

00:08:35.520 that have been developed over the last 27 years.

00:08:39.260 Okay.

00:08:39.480 So you're going after a host of immunological diseases,

00:08:44.360 including extraordinarily widespread conditions like Alzheimer's.

00:08:48.240 Dr. McMahon, do you want to explain to everybody what this has to do with where they live?

00:08:53.200 So there are a number of potential triggers that can cause the innate immune system to activate.

00:08:59.320 And as Dr. Shoemaker pointed out, these people, or at least around 90% of them,

00:09:06.100 don't have adequate or effective antibody production to help mitigate when there is chronic exposure.

00:09:14.560 So the innate immune system is then basically left to handle this by itself without the antibody cavalry coming in and reducing the burden.

00:09:25.080 And 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,

00:09:40.860 when you inhale those, your body recognizes those as being foreign antigens.

00:09:47.880 And it's not just, for instance, say, mold spores.

00:09:50.980 It can be old, dead mold spores that have lost their integrity.

00:09:57.020 Their cell wall is broken apart into hundreds of fragments.

00:10:00.840 And in fact, those fragments, when you inhale them, go even deeper down your respiratory tract into your lung.

00:10:06.840 And again, trigger the innate immune system.

00:10:09.340 As response to that, the innate immune system will overproduce cytokines.

00:10:15.080 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.

00:10:23.840 And these fragments trigger the innate immune system and the overproduction of the cytokines.

00:10:29.480 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.

00:10:48.220 Okay, so let me get the whole sequence of this straight.

00:10:52.400 So what you guys have been studying is sometimes, and stop me at any point if I get any of this wrong.

00:10:59.440 Sometimes people refer to this as sick building syndrome.

00:11:02.440 You've brought in conditions like Alzheimer's and other immunological diseases, chronic fatigue syndrome.

00:11:08.180 I know you've concentrated to some degree, too, on fibromyalgia.

00:11:12.600 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.

00:11:24.940 That's much more likely in buildings that have been water damaged and not properly remediated.

00:11:30.500 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.

00:11:40.460 And some people, when that immune response is triggered, they're not producing antibodies in a proper manner.

00:11:48.880 And there are genetic reasons for that and possibly metabolic reasons as well.

00:11:53.980 And then is it the combination of the pathogens that are in the local environment plus the genetic weakness or the metabolic problems that produce this cytokine storm that you associated with flu-like symptoms and pain and chronic inflammation?

00:12:08.740 And have I got all that right? Is that the way this lays itself out?

00:12:13.700 You're doing great. Keep on.

00:12:15.360 That is excellent.

00:12:16.680 Okay, okay, good. So let's go through that one by one then.

00:12:20.880 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?

00:12:30.440 And if it's a large number of buildings, that's obviously a catastrophe.

00:12:35.100 So what's the evidence for this and why did you guys become convinced of this?

00:12:39.960 What we have seen is a similarity of the syndrome of acute exposure followed by chronic exposure wherever the person might live.

00:12:52.560 It's not confined to Florida or Hawaii, could be in Nepal or could be in Stuttgart.

00:13:00.880 This worldwide exposure to an environment that pretty much is 62 to 78 degrees year-round.

00:13:09.940 No wind, no rain, no change of the seasons indoors.

00:13:15.300 And the mark of every one of these indoor places is water intrusion.

00:13:18.760 So if we look to see, is there a water-damaged building, we should be able to find an ecosystem of organisms.

00:13:28.120 Now, 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.

00:13:36.040 We know that fungi have a role, but we also know that endotoxins from bacteria are second on the list, and first is actinobacteria.

00:13:44.620 And when you look at every building that's water-damaged that has these ecologic parameters, you find the same symptoms, the same laboratory findings.

00:13:57.460 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.

00:14:08.620 In some of Scott's work, he's published that the likelihood is that you've got a p-value of less than, p is less than, than one to the minus 50th power.

00:14:20.400 So 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.

00:14:29.820 Okay, 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?

00:14:44.780 And are there specific kinds of buildings that appear more susceptible?

00:14:49.360 I read in some of the work of yours that I reviewed, for example, that drywall seems to be a particular problem.

00:14:54.580 So, what kind of, how widespread is this problem, do you suppose?

00:14:59.760 And what buildings are particularly affected?

00:15:02.600 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.

00:15:16.580 The buildings that are involved are not due to one era of construction or another.

00:15:23.040 With 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.

00:15:34.740 Construction defects for new homes are a real bugaboo.

00:15:38.080 But 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.

00:15:57.020 And 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.

00:16:08.720 It was actually not, because what we were using were paints and sealants to keep down mold growth.

00:16:15.320 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.

00:16:25.000 So before 1970, it usually was a paint building that was retrofitted or retrograde corrected or modern construction.

00:16:35.220 The safest buildings, even though they're water-damaged, are the old buildings with no paint.

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00:18:19.280 Okay, so there's no specific form of building that's amenable, per se, to water damage and the intrusion of toxins in consequence.

00:18:31.120 But you talk about buildings after 1970.

00:18:34.180 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.

00:18:45.920 And I remember when people started talking about sick building syndrome, I guess this went back as far, in my knowledge, as far back as the 80s.

00:18:53.240 They were concerned about these hyper-sealed buildings.

00:18:55.280 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.

00:19:07.360 Now, hypothetically, the reason they put those antifungals and antimold chemicals in the paints was to keep the fungus and mold down.

00:19:13.860 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.

00:19:29.260 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?

00:19:40.820 And what's your evidence for that?

00:19:43.100 Fungi also have a response to environmental hazards.

00:19:47.320 And 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.

00:19:58.880 The main role of a mycotoxin, for example, has nothing to do with defense.

00:20:04.040 It has everything to do with predation.

00:20:06.000 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.

00:20:13.520 And the fungi make compounds to eliminate the fungi.

00:20:16.740 They eliminate the peroxidase, therefore eliminate the plant defenses.

00:20:20.420 But it's predation of fungi on its prey.

00:20:25.920 That's foremost where all this goes on.

00:20:28.200 Meanwhile, 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.

00:20:46.640 So that as you see an initial building, the initial colonization will be with fungi, it'll be replaced by actinobacteria as time goes on.

00:20:57.000 But 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,

00:21:07.520 will initially let in organisms that like very saturated conditions, or AW of 0.9 to its maximum of 1.0 or 100%.

00:21:17.360 So 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.

00:21:27.580 And in the end, then we'll see sources that have very dry buildings, but it's where the moisture has changed the ecosystem.

00:21:37.520 Now, 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.

00:21:50.080 There are also architectural design features that make a building more likely to become water damaged than others.

00:21:58.720 Flat roofs are more likely to leak than pitched roofs are.

00:22:02.280 Or basements and crawl spaces are more likely to have water intrusions than you would see in homes that are built on a slab.

00:22:14.040 We know that drywall is more likely to have problems than plaster on the lathe.

00:22:20.880 So there are a number of different materials and architectural styles that can make a house or a commercial building more vulnerable or less vulnerable.

00:22:30.440 Right. Well, you could imagine, you know, when I'm thinking my paranoid thoughts, I know, here's an example.

00:22:36.480 So one of the reasons that the Roman Empire fell was because the Romans used lead to seal their wine amphora.

00:22:43.020 And lead is a known neurotoxin.

00:22:45.420 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.

00:22:56.980 It was really quite a catastrophe.

00:22:58.360 And that was, it was also the case that in relatively low, let's see, in older houses that had used a plethora of lead paint where the paint was allowed to deteriorate and young children were therefore ingesting lead paint powder,

00:23:15.700 they were also impaired in terms of their intelligence and also much more likely to be antisocial and criminal.

00:23:21.240 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.

00:23:32.360 You know, experimental vaccines come to mind, by the way.

00:23:36.080 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.

00:23:43.180 And it sounds like that's a case that you're making for drywall, is that it's extraordinarily light, easy to work with, cheap building substance, but it isn't, we don't have a lot of historical experience with it.

00:23:55.480 It was introduced in a very widespread manner in the latter half of the 20th century.

00:23:59.940 And so, and then you're saying that in combination with the fungicides and so forth that was put in the paint, that we put ourselves in a situation where we've contaminated something approximating 50 to 80% of buildings?

00:24:12.760 So that's really quite the bloody catastrophe.

00:24:15.240 So now, let's take that apart a little bit.

00:24:18.380 If it's 50 to 80% of buildings, how many of them, in your estimation, are contaminated to the point where that actually constitutes a serious health problem?

00:24:28.780 Like, you know, I know that that's a threshold issue, but there's lots of threats that people have to contend with, obviously.

00:24:36.420 And if your house is contaminated with mold and water damage, that's a big deal.

00:24:41.140 It's a really difficult thing to fix, or it can be.

00:24:43.800 And so, under what conditions should people be prioritizing this as a actionable risk factor?

00:24:52.200 And how widespread do you think this problem is in its more serious forms?

00:24:58.780 Study after study has looked at individual susceptibility, which underlies who gets sick and who doesn't.

00:25:06.200 The 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.

00:25:18.600 And the percentage of not having SIRS, HLA, but having an illness is less than 5% of the total.

00:25:26.440 So 95% were broken out into six separate haplotypes.

00:25:31.420 There are 54 available.

00:25:33.780 And out of those six, it's 24% of the population.

00:25:36.940 When 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.

00:25:54.000 We're seeing this exactly the same way with COVID.

00:25:58.180 COVID creates an inflammatory response that turns on innate immune responses, which turns on gene-based susceptibility.

00:26:05.360 So long COVID has the same genetic makeup, and we've published a paper on this in June of last year as well, that creates a new illness, a new target where once wasn't before.

00:26:19.280 And 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.

00:26:30.700 And 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.

00:26:39.660 It was just a different initiator.

00:26:41.580 It could be a horde of yellow jackets, stinging people at a picnic, creating an inflammatory response, or it could be an illness.

00:26:51.700 In this case, COVID fills the bill.

00:26:55.920 Okay, okay.

00:26:56.940 So you could imagine that there's a manner of conceptualization that allows for two kinds of disease processes.

00:27:05.580 There's disease processes that are associated with pathogens per se, and then there are disease processes associated with an anti-disease response or an immunological response gone astray.

00:27:17.360 So if I'm following you correctly, we have a situation where, let's say, 75% of our buildings are contaminated.

00:27:24.560 And so three-quarters of the population is exposed to the pathogens that could produce an immune hyper-response.

00:27:29.740 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.

00:27:45.080 Or is that a more general susceptibility to immune overreaction?

00:27:49.560 You seem to be implying that in relationship to the COVID issue.

00:27:52.620 So it's 25% of 75%, essentially, is the number of people who are hypothetically affected.

00:28:00.500 So that's about 25%.

00:28:02.420 That's about 20% of people, all things considered, might be experiencing this as a serious problem.

00:28:08.880 So have I got all that right?

00:28:12.220 Yes, you do.

00:28:13.300 And you picked it up very quickly.

00:28:14.760 I thank you for that.

00:28:15.480 One 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.

00:28:31.080 What are children not doing well in school?

00:28:33.360 Is it the lead paint that they swallowed?

00:28:35.380 Is it the lead in the applesauce that they've been taking in?

00:28:38.980 Are there environmental factors that are creating this overall systemic illness of which the brain is the injury I worry most about in adults?

00:28:51.640 Scott sees children more than I did, so we can let him speak about children with cognitive issues.

00:28:57.080 But the issues are that when we look carefully at chronic fatigue syndrome, we find SIRS.

00:29:02.760 And I'd like you, sir, if you could, to identify one significant biomarker that distinguishes fibromyalgia from not.

00:29:10.780 We have 30 biomarkers for SIRS and zero for fibromyalgia.

00:29:15.580 Why does fibromyalgia have such a preponderance of people?

00:29:18.920 And how many people, adults, have fibromyalgia?

00:29:21.700 10% and 3% for chronic fatigue syndrome?

00:29:25.900 How about post-Lyne syndrome?

00:29:27.280 How about depression?

00:29:28.500 Boy, we've got 25% all of a sudden.

00:29:31.320 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.

00:29:47.340 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.

00:30:02.440 And so let's take depression as a case in point.

00:30:05.540 Now, when I was assessing my clients for depression, the first thing I always tried to figure out was, are they just ill?

00:30:13.420 Because there's all sorts of evidence associating depression, particularly with immunological dysfunction.

00:30:20.120 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.

00:30:34.520 And depression is a relatively non-specific cluster of syndromes.

00:30:38.600 Now, you're pointing to a whole set of syndromes that have relatively non-specific symptoms, some of them even more difficult to diagnose and easier to be skeptical about in relationship even to their existence as, say, fibromyalgia and chronic fatigue syndrome.

00:30:57.820 So, right, that's hard to dissociate from general depression and anxiety and a kind of global neuroticism or even a hypochondriasis.

00:31:07.200 Now, you're saying, you know, your first claim is that 20% of the population is likely to be experiencing these symptoms, but we don't see that, we don't see this Sears chronic inflammatory response syndrome in 20% of people because essentially we're placing them in the wrong bins.

00:31:23.640 Now, and so how much of, so let's walk through, let's walk through what the symptom constellation is for chronic inflammatory response syndrome, that's 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.

00:31:45.840 And 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?

00:32:02.440 Because, 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.

00:32:30.720 Like, including absolutely devastating diseases, like Alzheimer's, so what is it, let's go through, first of all, what are the symptoms that point to Sears, as far as you're concerned, and then what do you use to prove that that's the condition?

00:32:46.940 As 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.

00:32:58.820 We have roughly 30 of them, and all of them have been validated to show that they separate cases from controls.

00:33:06.720 When we look at the diagnosis of Sears, you have to have objective evidence that shows that you have several of these biomarkers.

00:33:16.520 You know, I mean, at least four, or maybe five or more, before you can actually even make the diagnosis.

00:33:23.700 The statistical likelihood of finding a healthy person who had five abnormal biomarkers out of the five we draw, or the 10 that we obtain, it is so small.

00:33:35.780 I mean, it's in the one to a million range.

00:33:37.540 Then when you start looking at a larger group of people, maybe several people in the same hall, or in the same office building, or in the same school, when you start looking at that, and each person's probability of having those abnormal biomarkers multiplies by the next person's, and then multiplies by the next person's.

00:33:59.500 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.

00:34:09.400 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.

00:34:26.100 We are looking specifically at the innate immune system as a possible root cause for these different symptoms.

00:34:32.040 And if they ran the tests that we do, they would see the same kind of data that we have.

00:34:38.640 My data is very similar to Dr. Shoemaker's.

00:34:41.860 I've seen roughly 2,000 patients.

00:34:44.440 2,000 that I've evaluated this.

00:34:46.380 For him, it's much more, because he's been doing it much longer than I have.

00:34:49.780 And our data is very similar.

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00:35:59.080 Okay, so your argument basically is, and I just want to walk through this very carefully so that everyone listening understands,

00:36:07.600 is that you've identified a number of biomarkers.

00:36:11.580 You said 30 overall, but apparently you concentrate on something like 5 to 10.

00:36:15.800 Now, there's a probability that any given test is going to produce a result that's positive falsely.

00:36:23.080 So someone will be diagnosed as abnormal on that evaluated dimension.

00:36:27.820 But in truth, not be abnormal.

00:36:30.260 But that probability declines as a function of the number of tests administered.

00:36:36.760 So maybe there's a 1 in 20 chance that any given test will show that you have the condition.

00:36:43.160 But there's a 1 in 400 chance that two tests would show that.

00:36:46.940 And a 1 in 8,000 chance that three tests would show that.

00:36:49.900 And so your case basically is that as you accumulate evidence of the biomarkers,

00:36:54.320 you decrease the probability of a false diagnosis.

00:36:57.160 And there aren't biomarkers, as far as I know, there certainly aren't biomarkers for depression.

00:37:02.640 So that's not specific, what would you say, physical or chemical biomarkers.

00:37:08.780 You know, sometimes there's elevated cortisol or decreased cortisol, but the markers are very nonspecific.

00:37:13.600 So 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.

00:37:26.480 And so what are the prime biomarkers that you guys use to make the diagnosis?

00:37:32.640 And why did you pick those, and how valid do you think they are, and why?

00:37:38.460 We need to start with a case definition.

00:37:41.620 The case definition in 2003 that our group came up with was modified in 2008 by the U.S. Government Accountability Office.

00:37:49.560 And when they looked at the potential for exposure, this is what CDC used with Fisteria back in 1997, 1996.

00:37:58.140 You didn't get sick from a microalgal bloom unless you were exposed to it.

00:38:03.760 So the potential for exposure is number one.

00:38:06.340 Number two is symptoms the same or similar to those seen in published peer-reviewed literature.

00:38:11.480 The third element is laboratory findings, the same or similar to those seen in published literature.

00:38:18.440 And then the fourth is objective response of biomarkers to treatment.

00:38:23.560 So if we then say what biomarkers have stood the test of time, back in 2000, it was trial and error.

00:38:31.340 By finding HLA was the explanation of why did some people get sick and other people didn't.

00:38:36.540 Was there a risk factor like cigarette smoking or alcohol use or age or underlying illness with diabetes?

00:38:44.860 No, no, no, no.

00:38:46.360 It was based on genetic markers.

00:38:48.500 So individually immune responses became our first biomarker.

00:38:53.140 Actually, the first biomarker came from the EPA with Ken Hodnell.

00:38:56.660 We've been studying the neurotoxicologic features of visual contrast sensitivity, which is a mechanism to see an abnormal neurologic function of vision.

00:39:09.220 Contrast 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.

00:39:20.240 So VCS was our first.

00:39:22.720 HLA was our next.

00:39:23.860 In that group, there was a regulatory neuropeptide, melanocyte-stimulating hormone, which is essentially negative in all cases and normal in all controls.

00:39:35.340 And then with treatment, we saw improvement in MSH, not as much as what we wanted, and that was the impetus to keep on.

00:39:42.480 Scott mentioned cytokines.

00:39:44.320 In 1986, 1985 was the first publication of a paper on cytokines.

00:39:48.780 And here we are in 1996 postulating that this cytokine effect could be huge.

00:39:55.080 And now if we fast forward to COVID, it's a cytokine storm, and everyone in the drug store knows what a cytokine storm is.

00:40:01.040 They're buying COVID tests.

00:40:02.680 They're looking for mechanisms that we have been studying.

00:40:06.660 And cytokine storms are part of innate immune response, so you'll have it in COVID, but you have it in SARS, too.

00:40:12.920 And COVID doesn't have the same HLA that we know of yet, but we'll probably find it doesn't have the same PCS.

00:40:19.740 And it's a sorting process.

00:40:22.440 So we took then inflammatory markers, TGF-beta-1.

00:40:25.980 No lab was running that, so I hired a lab to prove that there was such a marker, and then we showed it with the abnormal and showed it in its height with some of the worst illnesses of all.

00:40:38.060 And then we treated it with medications that were available over-the-counter or with informed consent.

00:40:47.080 And then every time we had re-exposure, here we came to the prospective acquisition of illness, proof of causation.

00:40:56.140 We took people that could have been sick from one building, fixed them all day.

00:41:00.200 And then with informed consent, they stopped all medicines and stayed away at the suspect building.

00:41:07.020 Three days, nothing.

00:41:09.440 Put them back in the building on day one.

00:41:12.220 At the end of day one, laboratory findings changed.

00:41:15.520 Day two, laboratory findings changed again.

00:41:19.060 Day three, we had the exact syndrome of labs, PCS, and symptoms prospectively, proven upon re-exposure only.

00:41:29.120 No other choices could have been affected.

00:41:31.340 It wasn't depression in three days.

00:41:33.040 It was SIRS in three days.

00:41:35.160 Okay, so let me elaborate on the story now.

00:41:39.580 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 quite dramatically.

00:41:49.060 And so there's an online test, which is a visual contrast sensitivity test.

00:41:53.500 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 visual acuity in relationship to closely spaced lines on a diagram, essentially.

00:42:09.760 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?

00:42:22.720 So there is an online test, visual contrast sensitivity, that people can take.

00:42:27.320 See, it's a strange test, because it seems like it's so far removed from the symptom set that people would be experiencing.

00:42:35.640 It's very difficult for someone like myself.

00:42:38.420 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.

00:42:50.260 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.

00:42:58.400 It almost seems like voodoo.

00:42:59.620 Now, 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.

00:43:10.560 And so, have I got that right?

00:43:11.860 We 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.

00:43:26.580 We can measure objectively with a Heidelberg retinal flow meter how fast red blood cells move.

00:43:32.140 And they move more slowly if the inflammatory response promotes production of what are called adhesions, which is one mechanism to decrease flow in the area of hyper-inflammation.

00:43:44.700 And treatment will be shown to improve flow as the environmental stimulus is fixed and is corrected with treatment.

00:43:53.140 So, sick patients, you have reduced flow.

00:43:57.920 Healed patients have restored to normal flow to equal controls.

00:44:02.140 But 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.

00:44:24.300 This in and out, in and out, and constant answers to the critics, how could this possibly be true?

00:44:31.480 Well, here are the data.

00:44:34.340 And if people want to argue with me, they can argue with my data.

00:44:38.080 Okay, so let me elaborate on that a little bit before I return to the biomarkers per se.

00:44:43.500 Okay, so I know that the closest tissue that's deeply analogous to the brain itself is retinal tissue.

00:44:53.260 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?

00:45:00.820 With the visual acuity test, visual contrast sensitivity test, you're measuring retinal dysfunction.

00:45:10.740 What are the implications of that measured retinal dysfunction for broader central nervous system dysfunction or brain dysfunction?

00:45:18.820 And does that lead us logically into a discussion of degenerative neurological conditions like Alzheimer's?

00:45:25.380 Yes, it does.

00:45:26.860 The 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.

00:45:39.220 But 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.

00:45:52.220 It'll happen in kidneys. 0.67

00:45:53.880 It happens in lung. 0.52

00:45:54.840 It happens in liver.

00:45:56.120 And it happens in the neural rim of the optic nerve head, which is the first part of the central nervous system.

00:46:02.440 We've added countless additions to that.

00:46:05.280 But that was the beginning.

00:46:06.100 That was 1998, after studying this for one and a half years, we finally had our first biomarker that showed led the way to cytokines.

00:46:15.160 We could separate with treatment.

00:46:16.700 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.

00:46:26.620 We'll see who's going to do works better.

00:46:28.240 When yours doesn't and mine does, then I'm going to say I win the battle.

00:46:31.800 Right, well, that's particularly powerful, as you pointed out, in combination with evidence that you can reinstantiate the illness once treated with re-exposure.

00:46:41.960 Because then you have direct causality, right?

00:46:44.440 Instead of the weak sort of correlations that often go to hypothetically prove the existence of a given condition.

00:46:51.500 Okay, so let me get this straight again.

00:46:54.180 So 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.

00:47:03.820 So that's four, are those the four primary biomarkers?

00:47:07.280 Vision, HLA.

00:47:07.660 We also saw, you mentioned cortisol and depression.

00:47:11.300 Yeah.

00:47:11.560 We 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.

00:47:27.020 They're all melanocortins.

00:47:28.580 MSH and ACTH are melanocortins.

00:47:31.200 So 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.

00:47:42.660 So dysregulation of ACTH and cortisol is one.

00:47:46.060 We found antidiuretic hormone doing the same thing.

00:47:49.260 People walk around with chronic headaches.

00:47:50.940 They said they had migraine constantly.

00:47:53.240 But we find out they were all functionally dehydrated with elevated osmolality and reduced ADH.

00:47:59.540 That was another measurement.

00:48:02.360 We looked at pulmonary hypertension as a very common cardiac condition that's mistaken for cardiovascular disease.

00:48:10.240 People are short of breath and have chest pain with exertion.

00:48:13.620 We think that it's from due to coronary disease.

00:48:16.380 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.

00:48:26.920 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.

00:48:37.420 And it hits just one after another.

00:48:39.940 When 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.

00:48:51.940 Okay, well, I'll return to the genomics issue.

00:48:56.440 And don't let me forget that if we don't get there.

00:49:00.340 Okay, so we've basically walked through, we've done a reasonable overview of the biomarker space.

00:49:05.660 So let's do this now.

00:49:06.920 Let's talk about behavioral and cognitive, behavioral, emotional, and cognitive symptoms.

00:49:15.360 Like, 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.

00:49:29.640 So what are the fundamental symptoms that people should be alert to, and do they differ in adults and children?

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00:50:33.120 Well, as we were talking about decreased red blood cell flow to the optic disc, you have to understand that there's decreased red blood flow to different places in the body, not just to the optic disc.

00:50:45.820 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.

00:50:54.780 Our patients will often have cold hands or cold feet or both.

00:50:59.160 They can have cramping in their hands.

00:51:01.500 They can have pains in their hands.

00:51:02.940 Even sometimes discoloration, you know, that looks like cyanosis.

00:51:07.240 And we see that that goes away with treatment.

00:51:09.720 Dr. Shoemaker was talking about the lungs.

00:51:11.860 We also need to talk about the brain.

00:51:14.200 The brain will also have a decreased blood flow.

00:51:18.280 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 increase in lactic acid in certain areas of the brain.

00:51:31.320 And 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.

00:51:41.920 So why is that important?

00:51:43.560 Well, the blood carries the oxygen and the sugar, the glucose, that's necessary for production of energy at a cellular level.

00:51:54.920 It chronically reduced the amount of oxygen that is getting to any cell.

00:52:00.720 It will stop making energy as well.

00:52:03.660 And then we get into genomics findings.

00:52:05.960 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.

00:52:15.940 And 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.

00:52:27.220 Now, you also, how do you directly evaluate brain state and brain function?

00:52:36.940 If I remember correctly, I mean, I've been investigating this with my daughter and my wife for some time, and some of the details are unclear to me.

00:52:44.580 We've also had brain scans specifically done to look for neurological damage that might be associated with this exposure and sensitivity.

00:52:54.580 And so for everyone who's watching and listening, I mean, I might as well tell you why I'm particularly interested in this.

00:53:01.040 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.

00:53:14.180 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.

00:53:22.760 And she's treated a lot of those successfully with a very restricted diet, as have my wife and I.

00:53:28.220 But she's become convinced more recently that the cause of the food sensitivity that's driving her immunological conditions might be associated, might be attributed to sensitivity to these biotoxins that Dr. Shoemaker and McMahon are talking about.

00:53:45.200 And so, well, that's what we're trying to track down at the moment, because this has been a multi-generational catastrophe in my family, and I would like to get to the bottom of it.

00:53:53.500 And so we did some of these neurological tests that did indicate some neurological damage, hypothetically, as a consequence of toxin exposure.

00:54:04.140 And so can you walk everybody through those tests and what they indicate?

00:54:07.900 And then maybe we could talk a little bit about treatment before turning to genomics.

00:54:13.200 We skipped over symptoms.

00:54:14.960 You asked a couple times.

00:54:15.640 Yes, right.

00:54:16.420 Yes.

00:54:16.800 Let's pick up that loose end before we hit into NeuroQuant and all that.

00:54:21.660 The symptom reporting that I did when I had visual contrast as my only biomarker was compulsive logging down of what symptoms that people have.

00:54:31.080 Maybe symptoms that I elicited in an interview wasn't a self-form or questionnaire that the patient would fill out.

00:54:39.340 It's the process of doing a medical history that we're all trained to do in the four years of medical school or longer if we specialize.

00:54:47.040 But 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.

00:55:02.000 And it was hard to extend fingers because the muscles were in spasm.

00:55:05.940 Basically, that was the end of circulation.

00:55:10.380 The fingers and the toes were the end.

00:55:12.120 That's where the accumulation of lactic acid was greater.

00:55:14.280 So that's where the muscle spasm was.

00:55:15.520 It was respiratory issues, cough, shortness of breath, sinus congestion that was chronic, not related to seasons necessarily.

00:55:24.540 Eye findings, we'd have red eyes, blurred vision, tearing, sensitivity to bright light.

00:55:30.160 With cough and shortness of breath and difficulty with exertion, we had lung involvement.

00:55:34.740 Didn't have a lot of speed in production.

00:55:36.760 And the biomarker was restrictive lung disease, not obstructive.

00:55:40.940 It wasn't asthma.

00:55:41.900 It was called asthma by some, but it's not.

00:55:44.580 It's restrictive.

00:55:45.520 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.

00:55:58.440 The cognitive issues were there.

00:56:01.780 Difficulty with memory, difficulty with assimilation of new knowledge, difficulty with concentration, difficulty with disorientation.

00:56:10.020 And the executive cognitive functions were six.

00:56:12.740 Hypothalamic system.

00:56:14.340 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.

00:56:27.340 Those are all the MSH related things.

00:56:29.260 So let me ask you a technical question about that.

00:56:32.700 So when you're going through that as a psychologist, so what I would think would be helpful in relationship to that diagnosis would be to make a list, like a questionnaire, of all you listed off about 40 symptoms.

00:56:45.340 I think that's about how many you covered.

00:56:46.980 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.

00:56:59.400 Have you guys done any questionnaire development that's oriented towards symptom identification?

00:57:04.920 Yes.

00:57:05.280 Every person that takes their visual contrast test will undergo a symptom analysis and a symptom discussion, and we look to see if there's cluster analysis, a statistical function of saying yes or no based on visual contrast and symptoms alone without any of the other biomarkers.

00:57:24.460 Just statistically, we can tell you 98.5% likelihood of SIRS just on VCS and symptom clusters.

00:57:32.240 It's incredible.

00:57:32.980 No one believes it until they take it, and they say, my God, my symptom cluster's gone from 8 down to 6 down to 4.

00:57:39.440 You're halfway there.

00:57:40.500 We want you down to 1.

00:57:42.040 Have you done a factor analysis of the symptoms by any chance?

00:57:46.340 Yes, it was published in 2006.

00:57:48.640 Okay, okay, okay.

00:57:50.100 All right, all right.

00:57:51.300 All right, so we've covered symptoms now.

00:57:53.520 There's about 40 of them.

00:57:54.640 We covered biomarkers.

00:57:56.360 What, and we talked a little bit about illnesses that are hypothetically attributable to that, but let's go through that in some more detail.

00:58:05.920 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.

00:58:23.520 And that that was associated in this paper with a particularity of, if I remember correctly, a Finnish architectural design that made their houses more susceptible to these biotoxins that you describe.

00:58:35.980 And that's produced a statistically significant increase in the rate of Alzheimer's in Finland.

00:58:41.020 Was that your work?

00:58:42.240 I got that right.

00:58:43.100 I'm familiar with that work.

00:58:45.120 All I wanted the Finnish people to show is that treatment will correct the abnormalities and then correct the Alzheimer's. 1.00

00:58:53.600 By the time it gets to be Alzheimer's, we're 20 years late.

00:58:56.620 We can pick up the difficulties of tubulin A4A and TUBB1 in ALS on a congenital basis.

00:59:04.640 We can identify that at very young ages.

00:59:07.620 Certainly by the time we've got people, when grandma's getting in trouble with her cognition, we think it's old age.

00:59:15.480 Her problems got started when she was 30 and 40.

00:59:19.080 Right, right.

00:59:19.720 It was recognizable then and all the other.

00:59:22.180 Scott, I've been manipulating you and talking too much.

00:59:25.240 Your turn.

00:59:26.500 Have you guys ever tried a verbal fluency test by any chance?

00:59:30.860 Because verbal fluency seems quite susceptible to disruption by, well, there's certain forms of neurological degeneration that interfere with verbal fluency quite dramatically.

00:59:39.560 And it might be a good marker for cognitive interference.

00:59:44.640 They're very easy to administer.

00:59:46.720 Lynn Gratton from the University of Maryland published on Fisteria, the neurocognitive abnormalities.

00:59:53.140 Verbal processing was one of the panel they had.

00:59:56.400 It was published in the Lancet in 1998.

00:59:59.400 It was worth taking a look at.

01:00:00.800 I don't have your skills, but she did and those abnormalities were found.

01:00:06.380 When 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.

01:00:21.020 And one of the complaints that we very commonly see is that people are still able to do the functions of their job.

01:00:27.460 It just takes them much longer than it used to.

01:00:30.420 So 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.

01:00:39.620 See, that's why verbal fluency might be a real useful marker, because it's a time test, right?

01:00:44.680 How many words can you write down that begin with the letter S in three minutes?

01:00:48.300 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.

01:01:01.520 So that's really why it sprang to mind.

01:01:04.680 Well, it's also an unbelievably easy test to administer, and there's wide individual variability.

01:01:09.380 And it'd be very interesting to see if that was associated with the genomic markers that you described.

01:01:14.880 And maybe we could turn to those now.

01:01:18.060 And then I want to delve a bit more into, you know, we brushed over this very quickly, the idea that the symptoms that culminate in Alzheimer's decades later can be detected decades previously.

01:01:30.500 I know, for example, by the way, this is another reason the verbal fluency test popped into mind.

01:01:35.620 I know there was a study of nuns.

01:01:38.280 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.

01:01:48.420 It's the longest longitudinal study.

01:01:50.120 Yeah, exactly.

01:01:50.760 So another reason verbal fluency might be an interesting marker.

01:01:54.320 So, okay, now, and we just, so I wanted to go in two directions.

01:01:58.360 One direction was, okay, what is the panoply of neurological, degenerative neurological conditions that you think are likely to be associated with SIRS?

01:02:10.740 We didn't have a assumption-based discussion about symptoms and neurological abnormalities that we thought were for SIRS.

01:02:21.620 We 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.

01:02:35.400 We couldn't measure abnormalities in brain.

01:02:38.180 And 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.

01:02:51.080 And 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.

01:03:04.620 But the beauty in 2017 was we could actually fix multi-nuclear atrophy.

01:03:12.340 So our treatment was nonspecific, nondegenerative, but instead of just fixing the hippocampus, we were fixing hippocampus, amygdala, and caudate.

01:03:22.120 We were fixing pallidum.

01:03:23.480 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, cases equal to controls.

01:03:35.340 So NeuroQuant early on became of interest, but the final change was NeuroQuant associated with genomics.

01:03:44.880 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.

01:03:55.360 In fact, there's more than one.

01:03:57.000 If 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.

01:04:08.440 We see that, or enlarged, I should say.

01:04:11.040 We'll see that the cortical gray matter will be enlarged and that the caudate nucleus will be atrophic, will be smaller.

01:04:18.100 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.

01:04:29.880 And that pattern is that the right thalus is enlarged and that the putamen is smaller and atrophic.

01:04:36.980 And we showed that on two different studies.

01:04:39.520 And then in the third study that Dr. Shoemaker and I published together looked at different treatment.

01:04:45.500 And 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.

01:05:02.340 But we didn't see improvement in the multinuclear atrophy.

01:05:07.020 The 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.

01:05:23.300 It's a neuroregulatory peptide that brings your activated immune system back down to normal when it's appropriate to do that.

01:05:31.980 And 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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01:07:01.420 Have you guys used that same treatment protocol for conditions like Alzheimer's or other degenerative neurological diseases?

01:07:09.760 Obviously, there's an overlap there, which we've discussed, or hypothetically, there's an overlap there with SIRS.

01:07:15.420 Has anybody been looking at the application of this particular treatment protocol to these degenerative neurological diseases?

01:07:22.000 Yes, we published one study just a few weeks ago.

01:07:25.780 But 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.

01:07:34.880 Stage 3, treated with VIP.

01:07:37.160 But stage 4, that's where we had the off VIP and doing well.

01:07:43.440 We had a reduction of the basic mechanism of dieback CNS degeneration, looking at changes in TUBA for a 44% reduction in three months.

01:07:59.600 That's, that's not been published yet, but it's high on our list.

01:08:03.220 Yeah, I bet it's high on your list, yeah.

01:08:06.000 It's like, we've got to get going on this one.

01:08:09.900 There are other things that other people are doing or aware this is a complex field and no one illness parameter will fit everybody.

01:08:19.100 But 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%.

01:08:38.000 And that's just in three months of work.

01:08:40.480 Okay, so I would like to take this in two directions now, and we've got about half an hour left in this segment, although we can run a little longer if, you know, if that seems appropriate.

01:08:50.140 I want to know about, you know, what people should do, you know, what constitutes treatment.

01:08:55.740 And so that would be building testing, building remediation, and then the interventions that you described.

01:09:01.600 But I would also like to talk about, I know, Dr. Shoemaker, that you and Dr. McMahon have brought this problem to the attention of government officials.

01:09:09.900 And I believe particularly in relationship to military housing, but not only that.

01:09:15.060 So let's start with, everybody who's listening to this is going to be thinking, well, I know people who have this cluster of symptoms, you know, what in the world should I do about it?

01:09:24.880 So let's talk, we had our houses mold tested, and, you know, the results were rather dismal.

01:09:31.100 And I'm not exactly sure what to do about that, because I have properties now that appear to be quite mold saturated.

01:09:38.260 And, you know, the step after that's not exactly clear.

01:09:42.580 One of them was just remodeled, and I'm not that inclined to bloody well do the whole thing again, you know.

01:09:47.100 But that's partly why I'm investigating this to the degree that I am.

01:09:50.400 But what is it, what are the steps that people should take in order to determine, first of all, that they have this problem, and then in order to do something about it?

01:10:02.560 We first need to make sure the patient satisfies the case definition.

01:10:07.260 If they don't satisfy the case definition, this doesn't apply.

01:10:13.260 But if you satisfy the case definition, then we want to define the ecological parameters within the building.

01:10:21.900 If 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.

01:10:30.580 But 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?

01:10:43.360 And then if that's not the case, what about the water saturation with endotoxins?

01:10:47.880 Because of the three things that cause the greatest amount of damage to the brain, endotoxins lead the list.

01:10:53.900 Specifically for every abnormality that we find in the gene that shows us about specific causation.

01:11:03.760 That's the building contractor's word.

01:11:06.980 Specific causation for endotoxins we've identified in neuroquant.

01:11:13.260 We've also identified in combination with the genie testing or genomic testing.

01:11:18.060 So the two go together.

01:11:20.040 But then we want to know, do you have endotoxins?

01:11:22.340 Do you have actinobacteria?

01:11:24.160 Do you have fungi?

01:11:25.660 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, that's licensed, that's not a fly-by-night, and sure, it's your organization.

01:11:45.280 But there are those that are out there.

01:11:47.200 Sure, 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.

01:12:00.700 Do you want to go for treatment, Scott?

01:12:02.480 Sure, the first part of treatment is taking care of the exposure.

01:12:07.460 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, remediate that, or leave that.

01:12:21.180 The most important step of any kind of treatment for any kind of immunologic illness is getting away from exposure.

01:12:30.880 That is the most important step.

01:12:33.220 It's probably the most difficult step for many people, also.

01:12:36.860 Right.

01:12:37.120 Because 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.

01:12:55.720 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.

01:13:04.520 But that is the most important step.

01:13:07.580 The second step that we initiate for almost all patients is the use of a binder.

01:13:14.880 And there are different kinds of binders.

01:13:17.720 Dr. Shoemaker pioneered the use of cholestyramine and cholestevolam, also known as Wellcol.

01:13:25.480 They are very effective.

01:13:27.440 And typically, we will see improvements within two to three months if you can get that first step taken care of.

01:13:33.320 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.

01:13:49.300 I find, in my experience, that those work, but they take much longer.

01:13:54.880 Most people would like to get better faster.

01:13:57.140 So we use the more aggressive therapy.

01:13:59.320 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,

01:14:12.980 we usually draw some blood work to look at the tests that you had previously that were abnormal.

01:14:18.680 And based on which ones continue to be abnormal, the rest of the therapy follows, Dr. Shoemaker, what's called the pyramid.

01:14:29.780 And we just go up the pyramid.

01:14:32.180 And 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,

01:14:42.580 after that, we contemplate whether usage of intranasal VIP is useful.

01:14:48.880 For most patients, it is.

01:14:51.040 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,

01:15:03.520 if you haven't recovered, if you haven't recovered those from the rest of the therapy, then it's time for VIP.

01:15:08.980 You said if you have or haven't?

01:15:11.260 If you have not.

01:15:12.440 So I'm anticipating every one of my patients will recover at least 70% and up to 90% of their previous function, previous capability,

01:15:22.920 if they can follow the protocol as I just outlined.

01:15:26.860 Okay, so I've been trying this cholestyramine.

01:15:30.180 And so what I've found with it, and this is still a tentative conclusion on my part,

01:15:35.360 but to begin with, it seemed to make my symptoms quite a bit worse, even at a relatively low dose.

01:15:43.240 And then I moved the dose up and down for a while, and I seemed to find a dose that wasn't disturbing me.

01:15:49.040 So what it was doing to me was producing symptoms of psychomotor slowing.

01:15:53.140 So it was harder for me to do things.

01:15:54.840 I was thinking more slowly.

01:15:56.040 I had more pain, especially in the morning, more depressive malaise, none of which, as you obviously know, is particularly pleasant.

01:16:05.460 And if I decreased the dose enough, that went away.

01:16:08.300 A week ago, I increased the dose again, and then those symptoms came back.

01:16:12.820 And so why?

01:16:15.020 I know that that's not uncommon, that return of symptom, and that that means that the dose should be decreased.

01:16:20.320 But that obviously makes treating this even more complicated, because when you first start using the binder,

01:16:25.240 it can make what's wrong with you worse.

01:16:27.940 So what does the binder do, and why might it be the case that it would make symptoms worse,

01:16:35.220 and who would be susceptible particularly to that worsening of symptoms?

01:16:39.200 When we have intensification, which is the word that I use for people who got worse when they took cholestyramine,

01:16:47.380 we found that pretreatment, usually with compounds that would reduce inflammatory responses, reduce cytokines,

01:16:55.980 pretreatment with, say, five to seven days, and then restarting cholestyramine at low dose for another five to seven days,

01:17:04.500 increase the dose five or seven days.

01:17:06.520 And at the end of the month, you get up to the full dose of cholestyramine, and you go off the extra medications.

01:17:12.160 Omega-3 fatty acids are widely used for this.

01:17:16.540 They work very nicely.

01:17:18.060 Actos was a beautiful drug.

01:17:19.600 It's got an FDA black box on it for another reason, but that's still available for people that are worse.

01:17:26.740 Now, most commonly, when people intensify, there are either two problems preexisting.

01:17:33.060 We would know, if we had done the evaluation, if you have a multiply-antibiotic-resistant coagulase-negative staph colonizing your nose,

01:17:43.280 not infecting your nose, not creating symptoms, but colonizing your nose, and you treat with binders,

01:17:49.980 there can be intensification because this organism makes a toxin, a polycyclic ether toxin,

01:17:58.480 that is released when it's disturbed in its ecosystem.

01:18:01.680 And there's a binding coefficient looking at other toxins that are bound to a receptor.

01:18:07.600 And when you start pulling the toxin off with cholestyramine binding it in the gut,

01:18:13.460 there will be a response of the receptor to suddenly release all cytokines that are bound.

01:18:20.600 And so you frequently will create a cytokine storm.

01:18:25.640 Now, the paradigm illness for this is post-Lyme syndrome.

01:18:28.340 Post-Lyme syndrome, if you've got Lyme disease and the diagnosis is difficult to prove,

01:18:34.500 but specifically you pre-treat with omega-3s for five days, start low-dose cholestyramine, and away you go.

01:18:42.720 Now, for other people who don't have Marcon's and who don't have Lyme disease,

01:18:46.340 we found that paradoxically the last step, or VIP, can be used in low doses, micro doses, as the first step.

01:18:56.540 And this is from a textbook that Scott and I wrote on the art and science of SARS-Medicine.

01:19:02.500 It's called the Low VIDS, VIP protocol, and we can start people on that,

01:19:07.720 get through the intensification, decrease the VIP, increase the cholestyramine or well call,

01:19:14.360 and people sail on.

01:19:15.900 But they've got to be willing to take things slowly and defeat the intensification monster,

01:19:20.800 because it is horrible.

01:19:22.120 It is absolutely horrible having experienced it myself.

01:19:25.800 So what does it mean for people?

01:19:27.580 So, you know, when I'm contemplating this and contemplating doing something about it,

01:19:33.240 I'm wondering, well, you know, what's the implication here for travel, for visiting other people's houses?

01:19:40.200 I mean, I already almost eat nothing, which makes me, you know, an annoying guest in many ways.

01:19:45.140 And now, you know, if I'm sensitive to these sorts of toxins, that also means that,

01:19:52.440 in principle, it's going to be more difficult for me to travel and to visit people.

01:19:55.860 And if you recover, if you're in a clean environment and you recover,

01:20:00.200 and you use the treatment protocol that you described,

01:20:03.060 what does that do in terms of people's, you know, relative long-term resistance,

01:20:08.420 assuming they're not living in an absolutely mold-saturated house?

01:20:12.620 If MSH levels don't rise, which is the most common situation,

01:20:17.480 the susceptibility has not changed because your HLA has not changed.

01:20:21.180 With low MSH, if you go somewhere to a hotel or an airplane and you reacquire Marcon's,

01:20:28.340 because they're ubiquitous in the environment, and the Marcon starts to grow,

01:20:33.440 you will relapse and recrudesce with your symptoms within three days.

01:20:37.300 Folks who travel extensively, like I used to, will be on medications on a prophylactic basis

01:20:42.780 and take them on a regular basis.

01:20:45.560 I have a room sanitizer that I use when I travel, and I would go to the hotel room and plug that in

01:20:53.500 to clean out the hotel room, because whether the kind of heating devices they might have in the corner

01:20:58.800 underneath the window that has some humidity coming out to try to keep up with heat,

01:21:04.460 or the air cooling system, but hotels are notoriously with carpets next to bathrooms

01:21:11.160 and kids playing in the bathroom.

01:21:13.160 Oh, let's play hockey and saturate the rug, and you don't know it was there saturated a week ago,

01:21:20.840 and you walk into it and it looks fine, but you are basically re-exposing yourself.

01:21:25.120 It means that you need to manipulate your environment as best you can, as your first guess,

01:21:32.140 but then you need to take medication on a regular basis.

01:21:35.960 Fortunately, the side effects of low-dose VIP are essentially zero, so that's a way you can live.

01:21:42.620 As far as a carnivore diet, as you reduce the inflammatory result of using veggies

01:21:50.860 and other things that are not carnivore food,

01:21:52.760 you will find that VIP is your good friend, and it will be something helpful to let you expand your

01:21:58.420 diet once you have achieved the maximum medical improvement from the carnivore diet.

01:22:05.020 Do you think, this is a slight sideways move, and I won't pursue it for long,

01:22:09.640 but do you think that there's any association between SIRS and the obesity epidemic?

01:22:16.500 Oh my goodness, you're describing leptin resistance.

01:22:19.680 For instance, leptin is made by a GP130 cytokine receptor in the brain,

01:22:25.200 right in the hypothalamus where MSH is involved,

01:22:28.040 and leptin must bind to its receptor, send off a STAT1 signal to turn on production of POMC,

01:22:36.760 pro-opio-melanocortin, to make MSH.

01:22:39.380 So if you're leptin-resistant because of weight problems, you don't turn on MSH,

01:22:45.020 and so that by itself will turn on fatigue, pain, and then now obesity.

01:22:52.380 And what a triad.

01:22:53.840 And a good day, a good month, a good month for a leptin-resistant patient,

01:22:58.660 not to mention an insulin-resistant patient on an MSH deficient,

01:23:02.000 is half a pound per month.

01:23:04.500 That's not a good day.

01:23:05.540 Wow, wow.

01:23:07.000 Well, okay, so what do you think about this?

01:23:09.900 Okay, well, you know, I've been reviewing the statistics lately,

01:23:13.380 not only with regard to the prevalence of obesity, let's say, in the United States,

01:23:17.960 but also to its rate of increase.

01:23:19.940 And the last projection I read was something like 40% of Americans will be grossly obese,

01:23:26.540 morbidly obese by the year 2030.

01:23:28.480 40%, you know, and that's, well, it's impossible to overstate what a catastrophe that is.

01:23:37.400 That's half a SERS patients.

01:23:40.080 If you look at someone who weighs 300 pounds,

01:23:43.020 we're not going to use pedantic terms like morbidly obese.

01:23:46.060 Yeah, yeah, yeah.

01:23:47.480 Specifically, when weight's a problem, what's leptin, what are adipocytokines doing,

01:23:53.120 what's insulin doing, and more importantly, what's molecular hypometabolism doing?

01:23:57.760 Because we've got a prescription now, we've been using it,

01:24:01.400 that will defeat the mechanisms, the physiologic mechanism for weight storage and fat storage.

01:24:08.440 We looked at adipocytokines and brown fat, and we wanted to turn on brown fat.

01:24:14.800 Uncoupling protein 1, 2, and 3 were found.

01:24:17.440 It used to be just 1, but uncoupling 1, 2, and 3 are found.

01:24:20.620 We can convert base fat to brown fat and have increased metabolic consumption

01:24:25.500 of energy by turning on brown fat activation.

01:24:29.640 This is one of the advantages from Finland again. 1.00

01:24:32.440 Here we heat you up and you have a nice sauna,

01:24:35.300 and then we always tend to let you go out and jump into a snowbank.

01:24:39.480 Without making shivering, that turns on brown fat physiology, 0.97

01:24:43.660 that turns on energy production like crazy.

01:24:46.900 It's wasting heat.

01:24:48.340 Non-shivering thermogenesis is what that is.

01:24:51.000 Okay, how many papers have you two published between you

01:24:56.140 that are related specifically to this topic, approximately?

01:25:00.040 Over 30.

01:25:00.600 60.

01:25:01.940 Okay, okay, so...

01:25:03.780 We're two together, we're 60.

01:25:05.900 Okay, okay, so 60 papers.

01:25:07.700 All right, so you've brought your findings to the attention of various government bureaus.

01:25:13.600 What has been, what has been, what have you delivered in terms of reports?

01:25:18.620 What has been the consequence of that?

01:25:21.080 A whole lot of nothing.

01:25:22.840 Well, I had the privilege of speaking before adjuncts of the House and Senate Armed Services Committee

01:25:29.440 in December of 2019, and then they made a report to the full Congress.

01:25:35.860 And 16 days later, they appropriated $300 million to look into military housing,

01:25:43.600 particularly as it pertained to troop readiness and suicide in the military.

01:25:51.340 And you probably didn't hear about that because the next day,

01:25:54.940 they impeached President Trump for the first time.

01:25:58.200 And when that news cycle was over, we had this little thing called COVID.

01:26:02.280 And then after that, it's like everybody seems to have forgotten.

01:26:07.260 Yeah, well, I read big chunks of that report.

01:26:12.420 And my conclusion was that the people to whom you presented this report

01:26:18.860 regarded your findings as credible.

01:26:22.120 And three, like, I can't imagine how you could spend $300 million testing military housing.

01:26:27.580 I mean, that's an insane amount of money.

01:26:29.280 But it does indicate, regardless of that, it does indicate that they took what you were pointing out seriously.

01:26:35.460 What did you find in relationship to military housing?

01:26:38.540 And what do you think the consequences of that are for, let's say, military readiness

01:26:44.040 and for the mental and physical health of the servicemen?

01:26:47.260 The people that I was meeting with had visited a number of military bases

01:26:54.140 and had seen the military housing.

01:26:56.840 So they were already aware of the rad and infestations and the mold growing on the walls and whatnot.

01:27:06.420 I mean, they'd seen it with their own eyes.

01:27:08.720 What I presented was that this was definitely causing problems with troop readiness.

01:27:15.780 Even when the GI is living there and going and being deployed, 0.95

01:27:20.900 just being aware that your family is living in that and that your family is getting sick and chronically fatigued

01:27:26.760 and your children are having cognitive issues and chronic headaches and chronic stomach pains

01:27:34.760 It's that local pediatricians will usually say are psychological symptoms

01:27:40.360 because they don't know what biomarkers to check for it.

01:27:45.000 If they did, they'd find that somewhere between 80 and 90 percent of those children,

01:27:49.020 both with chronic headaches and chronic stomach problems,

01:27:52.740 that they really have SIRS and it's treatable and it can be reversed very quickly.

01:27:57.100 Yeah, well, it's not uncommon for the patient's psychological problems to be a direct consequence

01:28:04.720 of the fact that they've been misdiagnosed by a physician.

01:28:07.760 You know, like I was always extremely loath in my practice to attribute

01:28:11.620 any serious physiological alterations to psychological condition, you know,

01:28:16.320 because it just strikes me as highly unlikely.

01:28:18.700 And so it's very easy to assume that if you don't know how to diagnose something,

01:28:22.800 it's a consequence of the malfunctioning psyche of your patient or your client.

01:28:29.080 And that's an easy thing to fall into.

01:28:31.040 I don't want to be cynical about this.

01:28:32.340 That's an easy thing to fall into if it's also associated with, let's say, depression and anxiety

01:28:36.880 because those are pretty nonspecific symptoms of most psychological conditions, right?

01:28:42.760 And depression, which is essentially a pain-like condition,

01:28:46.100 and anxiety are very easy to attribute to psychological factors,

01:28:49.580 even though they have a profound underlying psychophysiological substrate.

01:28:54.700 So, you know, I have some sympathy for the physicians,

01:28:59.520 but it's all too easy to attribute an illness to someone's malfunctioning psychological processes.

01:29:07.600 This might be particularly relevant with kids.

01:29:09.860 I understand, Dr. McMahon, you've spent a fair time looking into the problem of SERS with children,

01:29:15.060 so maybe we could just touch on that briefly.

01:29:16.840 Yes, at this point, I've seen about 1,000 children for that.

01:29:23.420 For 28 years, I had my own private practice, so I worked with a nurse practitioner.

01:29:29.480 In the last 10 years, I evaluated the children there that had chronic illnesses for SERS also

01:29:35.960 and found that, again, the majority of children that had chronic headaches,

01:29:40.340 and we're talking 10 million children in the United States alone,

01:29:44.180 the majority of those, the large majority, they had SERS when I evaluated them for that.

01:29:50.220 And when I treated them for that, their headaches would either go away

01:29:53.600 or they would become much less severe, much less frequent.

01:29:57.220 It's the same with chronic abdominal pains.

01:29:59.660 I was taught in residency, and I went to a fantastic residency,

01:30:03.760 but I was taught that stomach pains that were recurrent in children,

01:30:07.820 maybe 10% of the time you could make a diagnosis of urinary tract infections or constipation,

01:30:14.200 or maybe there's some visceral problem with their liver or some other organ in their abdomen.

01:30:20.220 But that the majority of times, the children were actually seeking either a primary or a secondary gain,

01:30:26.860 and that was psychological.

01:30:28.540 But what I saw in my patients when I started evaluating them for SERS is that about 90% outside of that 10%,

01:30:37.040 so we're talking closer to 80%, 81% of these patients had four or more biomarkers for SERS.

01:30:44.820 And then when we treated them, their abdominal pains either went away completely

01:30:48.620 or became much less frequent and much less severe.

01:30:52.440 So, I mean, it's a really fundamental game changer.

01:30:54.780 These are two of the most common visits for pediatricians is children with chronic headaches,

01:31:00.580 children with chronic abdominal pains.

01:31:02.580 There's another 10 million who have chronic abdominal pains.

01:31:06.340 And then you can also expand that to adults.

01:31:10.760 The number one reason in my reading for a visit to your primary care physician is chronic stomach pains,

01:31:17.780 which are considered functional in most adults.

01:31:20.600 They actually have a term, functional abdominal pain syndrome.

01:31:23.360 And again, if you were doing the correct testing, looking at the innate immune system,

01:31:29.260 again, my experience is about 90% of those people with this functional pain

01:31:33.740 will have the biomarkers consistent with the diagnosis of SERS.

01:31:38.660 And then treatment, you know, just follows along.

01:31:41.160 Dr. Shoemaker, you insisted earlier in the discussion that we return to the issue of genomics

01:31:48.960 and genetic susceptibility.

01:31:51.140 And so I don't feel that we've covered that inadequate depth.

01:31:53.540 So do you want to expound on that for a moment or two?

01:31:56.600 And so for everyone watching and listening,

01:31:59.100 so the causal pathway is an affected building.

01:32:02.120 That's a building affected by water damage.

01:32:04.320 That's increased.

01:32:05.460 The probability that that will be problematic is increased if it's drywalled

01:32:09.300 and the drywall is also sealed or painted with an antifungal chemical.

01:32:15.780 And then that isn't sufficient altogether to produce the syndrome.

01:32:19.400 You also need a person who's susceptible, and that's about 25% of people.

01:32:23.700 And they're susceptible for a variety of physiological and genetic reasons.

01:32:27.420 And so we're going to delve into the genetic markers for a moment

01:32:29.900 and the genomics aspect of that.

01:32:32.420 So Dr. Shoemaker, you want to take that away?

01:32:35.020 When we look at the role of metabolism in this illness,

01:32:39.420 it's been understudied for years,

01:32:43.180 but now it's risen to the head of the cream of the crop.

01:32:46.240 The structure that makes proteins,

01:32:50.360 and there's a million of these in every cell,

01:32:52.620 it's called a ribosome.

01:32:55.120 And if you remember your high school biology,

01:32:56.860 ribosomes make proteins and mitochondria make energy.

01:33:00.080 But the mechanism of protein production comes from RNA copied in off of DNA

01:33:10.840 and traveling from the nucleus into the cytoplasm of the cell.

01:33:16.120 And that messenger RNA gives a signal to the ribosome

01:33:19.660 to assemble one amino acid at a time,

01:33:23.260 a given protein that's coded for by the RNA.

01:33:25.560 So DNA message transcribed to RNA transcribed to RNA makes a protein.

01:33:33.060 What happens in chronic fatiguing illnesses

01:33:36.140 is that the structure we call the sarsen-ricin loop,

01:33:42.520 and it's getting a little complicated here,

01:33:46.080 it's present in every living creature.

01:33:48.200 Every creature known to God has got a sarsen-ricin loop in it.

01:33:52.560 And at the one point, the 15 nucleotide,

01:33:55.500 where there's an adenosine moiety,

01:33:57.580 a toxin can cause replacement or elimination of that one-plane adenosine,

01:34:03.220 and the loop won't work.

01:34:06.020 So suddenly, a million ribosomes,

01:34:08.960 losing half a million of its capability,

01:34:12.080 won't make the protein needed for cell functioning,

01:34:14.540 and the cell stops functioning normally.

01:34:16.280 Meanwhile, glucose is being driven into the cell by two transporters,

01:34:22.440 and their glycolysis, or breakdown of glucose,

01:34:25.180 a six-carbon circle, or chain, excuse me,

01:34:29.000 circular compound,

01:34:30.680 is broken into two three-carbon fragments in a chain called pyruvate.

01:34:35.260 Pyruvate must be delivered across an outer membrane of the mitochondria

01:34:39.280 to get into the middle membrane across the inner membrane

01:34:44.700 to get to the cyclooxygenase pathway to make energy.

01:34:49.800 So if you don't get pyruvate going into the nucleus,

01:34:53.640 you don't make the 36 ATP or 38 ATP the nucleus can break.

01:34:58.420 So Otto Warburg studied this in 1928.

01:35:02.180 In 1955, he finally passed away.

01:35:04.520 But he studied cancer.

01:35:07.080 And he found that pyruvate was readily available,

01:35:10.700 but it was not being metabolized in the mitochondria.

01:35:14.260 It was being broken down from pyruvate,

01:35:17.420 a three-carbon chain,

01:35:18.840 into lactic acid, a three-carbon chain.

01:35:21.240 Lactic acid was secreted outside of the gradient,

01:35:23.540 into the capillary beds,

01:35:24.980 and lactic acidosis became common.

01:35:27.920 We see this proliferative physiology

01:35:31.340 of lactic acidosis in 85% of our SIRS patients.

01:35:35.740 We have ribosomal attack on protein. 0.93

01:35:39.540 We've got lack of proper energy metabolism going on.

01:35:44.320 But at the same time,

01:35:45.800 in addition to metabolic acidosis,

01:35:48.040 we'll have lack of a regulatory T-cell population, 0.52

01:35:51.360 thymus-derived T-cells.

01:35:52.740 We'll have increased gray matter and nuclear atrophy.

01:35:55.740 We'll get pulmonary hypertension.

01:35:57.740 We'll get, here's your obesity,

01:36:00.660 we'll get insulin resistance.

01:36:01.960 You get five complications of metabolism abnormality

01:36:05.380 in 95% of the patients

01:36:08.060 who've got molecular hypometabolism.

01:36:11.000 That is prescription for disaster.

01:36:13.360 So we start looking at insulin receptor substrate too.

01:36:17.520 That will increase delivery of glucose

01:36:20.560 regardless of what the diet has involved.

01:36:23.600 A lot of people will be on a diet called a keto diet.

01:36:26.140 With keto diets,

01:36:27.480 they want to make themselves burning fat.

01:36:29.680 Well, if IRS-2 is increased,

01:36:33.380 then that keto doesn't get into the cell.

01:36:36.980 It'll be turning on uptake of glucose.

01:36:39.680 So you've wasted the keto function

01:36:41.760 if IRS-2 is elevated.

01:36:44.240 So if you're going to get serious about a diet,

01:36:47.520 and the carnivore diet also gives tremendous source of glucose.

01:36:52.740 Remember, aspartate and glutamate

01:36:54.560 are broke down in glucose very quickly

01:36:56.480 when your energy is low.

01:36:58.800 And so that protein wasting

01:37:00.320 goes along with the carnivore diet if IRS-2 is up.

01:37:04.320 And having done a little bit of work with the carnivore diet,

01:37:07.540 I would just urge people to know what your IRS-2 is

01:37:10.300 before you stop eating all carbohydrates.

01:37:13.100 But secondarily,

01:37:14.620 we start seeing disruptions of apoptosis.

01:37:20.220 This is programmed cell death,

01:37:22.180 where cells should die,

01:37:23.600 normally being with fragments of cells,

01:37:25.580 be coated with membrane,

01:37:27.020 released into the circulation,

01:37:28.780 but not causing inflammation.

01:37:30.880 But here in this illness,

01:37:32.820 with apoptosis,

01:37:34.540 we have defective apoptosis,

01:37:36.780 where the cell is laced without coating

01:37:38.600 of the internal fragments that are antigens.

01:37:41.860 So we get now a surge of antigen load

01:37:45.720 in bloodstream with apoptosis

01:37:48.000 in someone who's got defective apoptosis genes.

01:37:51.700 RIPK-1, we can tell you that. 0.62

01:37:54.060 And that will create an endogenous source for SIRS.

01:37:58.140 I realize I'm getting a little technical,

01:38:00.100 but then we look at coagulation factors.

01:38:03.520 These genes are upregulated like crazy,

01:38:06.040 and they will bind to tau and tau beta in the brain

01:38:11.020 and then create a microclot,

01:38:13.460 which will lice, you know, microbleed.

01:38:15.960 And that's where Alzheimer's gets its start.

01:38:18.560 But it begins with extra coagulation factors.

01:38:22.520 Cytokines, we mentioned

01:38:23.660 the tremendous increase in cytokines.

01:38:25.980 We also mentioned there's a specific causation

01:38:28.820 for endotoxins.

01:38:30.260 There are three markers that we use

01:38:32.200 in addition to environmental samples,

01:38:33.860 for actinobacteria.

01:38:36.220 We use TGFBR1 and 2

01:38:38.220 that will turn on fibrosis

01:38:40.440 as a way to tell about actinial injury.

01:38:43.980 And then we look at MAP kinases

01:38:45.280 that does its own bad things

01:38:46.880 being turned on by actinobacteria.

01:38:50.780 Fungi, we'll have apoptosis,

01:38:52.900 and then you'll have the findings in the brainstem.

01:38:56.140 So all of these findings,

01:38:58.760 and there's more, honestly,

01:39:00.160 it's been a two-hour lecture.

01:39:02.480 Yeah, yeah.

01:39:04.320 Lessons from Jeannie available 0.75

01:39:05.640 on its free downloads

01:39:06.960 from Surviving Mold website.

01:39:08.320 You just take a look.

01:39:09.400 You don't have to pay a doctor.

01:39:10.640 You can just get it read yourself.

01:39:12.600 Let me ask you a question about the,

01:39:16.400 is there an association

01:39:17.400 between the genetic markers

01:39:18.960 that interfere with celloptosis

01:39:20.740 in the way you described

01:39:21.640 and susceptibility to Alzheimer's?

01:39:23.780 Does anyone know that?

01:39:25.200 What we have shown

01:39:26.140 is that the susceptibility is separate.

01:39:27.860 The cytoskeleton or microtubule genes,

01:39:31.500 T-U-B-A-4-A and D-U-B-B-1,

01:39:33.840 that's the one associated with dieback loss.

01:39:36.680 Remember, every neuron of every eukaryote

01:39:41.180 has got a cell body connected to

01:39:43.460 a series of tubes called an axon.

01:39:46.680 The tubes convey ions and nutrients

01:39:49.020 that must get from the cell body

01:39:50.820 down to the end of the road of the axon

01:39:52.940 to the synapse.

01:39:55.100 Energy demands like crazy.

01:39:56.800 You've got to maintain a gradient

01:39:58.120 of sodium-potassium.

01:39:59.540 That costs energy.

01:40:01.180 But if the microtubules are disrupted,

01:40:03.920 as there are in dieback neuropathy,

01:40:06.720 what you will see is loss of this neuron

01:40:10.640 and then the next neuron,

01:40:12.300 the next neuron is going on.

01:40:14.180 Meanwhile, coagulation is going on

01:40:16.240 and you're getting the vascular phenomenon

01:40:18.500 that leads to cognitive impairment.

01:40:20.920 They're both gone at the same time.

01:40:22.340 And if you don't have blood supply

01:40:23.820 bringing energy in

01:40:25.260 to the already damaged nervous system,

01:40:27.920 it just piles up.

01:40:29.240 It is a positive feedback loop

01:40:31.100 of abnormalities in blood flow,

01:40:33.580 abnormalities in energy flow,

01:40:35.700 abnormalities can be identified in genie.

01:40:39.200 Now, we were talking about the government.

01:40:41.360 I just want to remind you

01:40:42.180 that in 2004,

01:40:43.820 John Conyers convened

01:40:45.480 at a special session of Congress.

01:40:48.660 Sharon Kramer was the contact person

01:40:50.700 and she's been a real fighter

01:40:53.100 on all these years

01:40:54.300 for mold rights,

01:40:55.120 for mold patients and all that. 0.67

01:40:56.740 She's the one that first blew the whistle

01:40:58.120 on military housing problems

01:40:59.460 around the Norfolk energy base.

01:41:03.040 And $3 billion later,

01:41:04.760 those lawsuits have been settled.

01:41:06.800 But along the way,

01:41:08.380 Sharon also ran, 0.99

01:41:10.140 blew the whistle,

01:41:10.740 and Ted Kennedy's HEL Committee,

01:41:12.740 Health Education and Labor Committee,

01:41:14.700 sent a group of physicians,

01:41:16.560 including me,

01:41:17.140 down to New Orleans

01:41:18.100 to look to see what happened

01:41:19.600 with Katrina and Rita.

01:41:21.120 And there,

01:41:21.520 most of New Orleans,

01:41:22.400 this was in February 2006,

01:41:24.380 was still underwater

01:41:25.520 and as moldy as can be

01:41:26.560 and FEMA was doing things.

01:41:28.760 But we had a ship,

01:41:30.300 the Scotia Prince

01:41:31.140 was our control group.

01:41:33.280 None of these people

01:41:33.900 had been involved

01:41:35.200 with New Orleans in any way,

01:41:36.660 but they were there

01:41:37.400 and our controls for the group.

01:41:40.800 And we had people

01:41:41.640 being stashed on the boat

01:41:43.480 that were from firemen,

01:41:45.740 they're from children,

01:41:46.440 they're homeless people,

01:41:47.780 people from St. Bernard Parish.

01:41:49.360 And I had a case control study

01:41:50.860 I did over the weekend.

01:41:51.800 All we did was symptoms

01:41:53.460 and visual contrasts

01:41:55.220 on 250 patients.

01:41:56.860 And we showed distinct markers.

01:41:58.860 If you had more than five symptoms,

01:42:00.280 you were a case.

01:42:01.500 It was incredible.

01:42:02.460 That report was released

01:42:04.400 to St. Bernard Parish

01:42:05.980 on a Monday.

01:42:07.120 It was taken down on Tuesday.

01:42:08.380 And that's the last I've heard of it.

01:42:10.480 Well, it's not surprising

01:42:11.920 as far as I'm concerned,

01:42:13.100 because if this problem

01:42:14.780 is as severe and as widespread

01:42:16.600 as you described,

01:42:18.900 then it makes the asbestos problem

01:42:20.720 look trivial by comparison.

01:42:22.800 It takes a long time

01:42:23.720 to kill you from asbestos.

01:42:25.300 The mold just makes you feel

01:42:26.400 like you want to die. 0.85

01:42:27.880 Right, yes, yes. 0.52

01:42:28.860 Right, right.

01:42:29.540 Well, but it's so unbelievably prevalent.

01:42:32.280 And it's so...

01:42:33.340 I mean, you lay out very carefully

01:42:35.180 what the treatment course is,

01:42:36.580 but it's certainly...

01:42:38.480 It's a complicated

01:42:40.260 and life-altering process

01:42:42.680 to undergo the diagnosis,

01:42:46.720 the house remediation,

01:42:48.220 which can be expensive,

01:42:49.180 and then the lifestyle

01:42:50.580 and other alterations

01:42:51.600 that would be necessary

01:42:52.540 to bring this under control.

01:42:53.960 And if it's as widespread

01:42:54.920 and severe as you claim,

01:42:56.300 it's no wonder

01:42:56.800 that there's tremendous resistance.

01:42:58.600 Let's speak about that

01:42:59.500 to maybe bring this to a close.

01:43:01.040 You guys have been hard at this

01:43:02.580 for quite a long time,

01:43:03.500 and you said some 60 papers published,

01:43:06.100 which is quite a substantial...

01:43:08.540 That's for everyone

01:43:09.140 watching and listening.

01:43:10.040 That's about the equivalent

01:43:10.880 of 20 PhD thesis, by the way.

01:43:13.760 So you can get a PhD thesis

01:43:15.060 essentially for three publications.

01:43:17.000 It's a lot of work.

01:43:18.780 And what sort of response

01:43:20.840 have you had

01:43:22.140 from the broad medical community?

01:43:25.740 Like, how is your work being received?

01:43:28.600 Do people know this?

01:43:29.760 Are you on the fringe

01:43:31.800 and outer edges

01:43:32.560 of what's regarded

01:43:33.620 as acceptable medicine?

01:43:35.340 How have you been received?

01:43:37.180 There is a derogatory term

01:43:39.560 that is still widespread use.

01:43:43.080 I have done a study

01:43:43.840 about emergency room physicians

01:43:45.960 called a patient

01:43:47.700 they would see

01:43:48.240 with multiple symptoms

01:43:49.280 called a gomer.

01:43:51.180 Yeah.

01:43:52.100 Get out of my emergency room.

01:43:54.480 Yeah.

01:43:55.420 Because these people take time.

01:43:57.020 And when you have

01:43:57.840 a healthcare system

01:43:58.700 that gives you 10 or 15 minutes

01:44:00.140 to see a patient

01:44:00.860 in primary care facilities,

01:44:02.560 and you've got someone

01:44:03.440 who needs two hours of time,

01:44:05.260 who's going to lose?

01:44:06.280 The two-hour patient

01:44:07.180 or the 10-minute patient?

01:44:08.800 And who's going to go without care?

01:44:10.620 So I think it's a systemic approach

01:44:12.620 and not an individual approach.

01:44:13.880 I think our healthcare system

01:44:15.340 has some of the best physicians

01:44:16.620 in the world.

01:44:17.840 But I'm biased

01:44:18.540 because I've seen this

01:44:19.620 in action for 40 years.

01:44:20.800 But specifically,

01:44:22.000 when we look to see

01:44:23.260 who's doing the caring,

01:44:25.300 it's the primary care doctors.

01:44:27.360 The specialists,

01:44:28.820 there's a hand

01:44:29.620 in the waiting room.

01:44:30.680 There's a heart

01:44:31.920 in the cath lab.

01:44:33.600 But that's a person

01:44:34.560 with a hand.

01:44:35.440 That's a person

01:44:36.140 with a heart.

01:44:36.940 That's a person

01:44:37.620 with a brain.

01:44:38.780 Let's look at what

01:44:39.600 the fundamental unit

01:44:40.920 of care has got to be.

01:44:42.540 It's a person.

01:44:43.440 Scott and I

01:44:43.900 spent all day long,

01:44:44.840 two-hour visits,

01:44:46.100 and listened to people.

01:44:46.920 I had one rheumatologist

01:44:50.100 give me a hard time

01:44:50.960 at University of Washington

01:44:51.940 in Seattle.

01:44:52.960 I sent a patient in

01:44:54.100 from Coeur d'Alene

01:44:54.920 who needed to have

01:44:56.260 a TGF-beta-1 done

01:44:57.580 because he had

01:44:58.680 juvenile rheumatoid arthritis

01:45:00.480 who was going blind.

01:45:01.800 And TGF-beta-1

01:45:02.560 was the cause of that.

01:45:03.780 And he goes,

01:45:04.360 well, I've never heard

01:45:05.300 of a TGF-beta-1.

01:45:06.660 This was years ago.

01:45:07.800 And being a smartass,

01:45:08.820 I said,

01:45:09.220 there's only 75,000 papers

01:45:11.820 published on TGF-beta-1.

01:45:13.120 I would not admit that.

01:45:14.040 You didn't know any of them

01:45:14.900 in public if I were you.

01:45:17.340 Well, needless to say,

01:45:18.680 he got the TGF-beta-1

01:45:19.620 and the child can see now.

01:45:21.040 But the point is,

01:45:22.380 it's hard to read everything.

01:45:24.420 We're asking you

01:45:25.140 to be an expert

01:45:25.820 in endocrinology,

01:45:27.060 an expert in metabolism,

01:45:28.460 an expert in cardiology,

01:45:29.640 an expert in pulmonology.

01:45:30.780 We want you to be an expert

01:45:32.160 in pre-renal azotemia

01:45:34.060 and POTS and PANS.

01:45:35.560 We want you to do all of it

01:45:37.220 all day long.

01:45:39.100 Yeah, yeah.

01:45:39.820 Well, when I was first introduced

01:45:41.220 to this by my daughter,

01:45:42.700 I started to read it

01:45:44.220 and I thought,

01:45:44.680 oh my God,

01:45:45.240 it's going to take me

01:45:46.180 two years

01:45:47.360 just to get on top

01:45:48.220 of this conceptually

01:45:49.260 to figure out,

01:45:50.280 well, first of all,

01:45:51.060 if it's credible information

01:45:52.260 and second of all,

01:45:53.540 to really understand

01:45:54.880 how I would possibly

01:45:55.960 reorganize my life

01:45:57.000 to deal with it.

01:45:57.740 So it's really,

01:45:58.720 it's a major,

01:46:00.660 but on the other hand,

01:46:01.720 you know,

01:46:02.220 a long-term prognosis

01:46:03.460 of chronic depression

01:46:04.620 and immunological trouble

01:46:05.880 plus Alzheimer's

01:46:06.860 sounds like a pretty dismal

01:46:07.920 way to conduct,

01:46:09.280 you know,

01:46:09.660 conduct life.

01:46:10.620 So,

01:46:11.240 you always have to read.

01:46:13.740 Right, well,

01:46:14.440 right, well,

01:46:15.080 right.

01:46:15.360 And I've already discovered

01:46:16.400 some things about,

01:46:17.540 you know,

01:46:18.180 how immunological systems work.

01:46:21.180 I mean,

01:46:21.360 I've been struck to the core

01:46:22.520 by how effective

01:46:23.260 this carnivore diet

01:46:24.140 has been for so many people.

01:46:25.460 And I would have never,

01:46:27.120 I would have never believed that,

01:46:29.500 you know,

01:46:29.820 20 years ago,

01:46:30.720 the probability that,

01:46:32.160 like,

01:46:32.460 just the very idea

01:46:33.420 that people could live

01:46:34.240 on nothing but meat

01:46:35.020 would have struck me as,

01:46:36.140 like,

01:46:37.460 outright preposterous

01:46:38.600 and that it was the actual,

01:46:40.400 that food sensitivity

01:46:41.400 was the cause

01:46:42.220 of so much immunological suffering

01:46:43.840 or at least a cause

01:46:45.460 also struck me

01:46:46.560 as highly improbable.

01:46:47.760 But, you know,

01:46:48.460 here we are.

01:46:49.160 It does seem to be the case.

01:46:50.540 And certainly,

01:46:52.160 the body of data

01:46:53.160 that you guys have accumulated

01:46:54.420 in the studies you've done

01:46:55.440 they're difficult to,

01:46:57.520 once you go through them,

01:46:58.860 they're very difficult

01:46:59.640 to just shunt away 0.81

01:47:00.720 and ignore.

01:47:01.620 And I really think

01:47:02.280 that's too bad

01:47:02.980 because I would have

01:47:03.660 just as soon

01:47:04.220 shunted them away

01:47:05.220 and ignored them

01:47:05.920 if I had my druthers.

01:47:07.440 Is there anything

01:47:08.340 that we haven't covered

01:47:09.460 in this two-hour presentation?

01:47:11.200 Now,

01:47:11.460 I wanted to ask you,

01:47:12.840 the textbook that you said,

01:47:14.140 that was

01:47:14.520 Art and Science of SERS

01:47:17.040 Treatment?

01:47:18.920 Medicine.

01:47:19.460 Art and Science of SERS Medicine.

01:47:21.820 Okay,

01:47:22.100 so that's where

01:47:22.620 medical practitioners

01:47:23.780 can learn about this.

01:47:24.840 What's the best source

01:47:26.400 for just general public people?

01:47:28.580 I know my daughter's put up

01:47:29.680 a big website

01:47:30.520 about SERS-related disorders.

01:47:33.460 And we'll put that

01:47:34.180 in the links.

01:47:36.100 But where should people go

01:47:38.120 online

01:47:39.000 to gather more information

01:47:40.300 about this?

01:47:41.620 There are two websites.

01:47:43.720 Scott,

01:47:44.220 Scott1,

01:47:44.880 SERS-X,

01:47:46.640 Surviving Moles,

01:47:47.880 another one.

01:47:48.320 Scott,

01:47:48.580 tell us about SERS-X.

01:47:49.640 Well,

01:47:50.340 I was going to say

01:47:51.120 the two places

01:47:51.900 where the most knowledge,

01:47:53.540 the most trusted

01:47:54.680 knowledge is,

01:47:57.380 the most literature,

01:47:59.900 the most videos

01:48:00.900 about this

01:48:01.700 are either from

01:48:02.840 Dr. Shoemaker's

01:48:03.920 www.survivingmold

01:48:06.200 or

01:48:06.960 SERS-X,

01:48:07.860 C-I-R-S-X.com.

01:48:10.940 I think you go to

01:48:11.580 those two places,

01:48:12.800 you can find

01:48:13.340 just about anything

01:48:14.220 you need,

01:48:15.140 including

01:48:15.660 a local

01:48:17.300 provider

01:48:18.060 who would know

01:48:18.820 something about this

01:48:19.820 if you think

01:48:20.640 that you have

01:48:21.320 this illness.

01:48:22.560 Okay,

01:48:23.000 okay.

01:48:23.320 So those two places

01:48:24.480 are fairly exhaustive

01:48:25.760 and complimentary.

01:48:27.140 Okay,

01:48:27.540 Dr. McMahon,

01:48:28.820 is there anything

01:48:29.560 that you would like

01:48:30.500 to bring to the attention

01:48:31.420 of people

01:48:31.840 who are watching

01:48:32.420 and listening

01:48:32.840 before,

01:48:33.620 as everybody

01:48:34.080 watching and listening

01:48:34.980 knows we're going

01:48:35.760 to do another

01:48:36.520 half an hour

01:48:37.160 with these two gentlemen

01:48:38.040 behind the Daily

01:48:38.740 Hour Plus platform,

01:48:39.780 but before we turn

01:48:40.560 to that,

01:48:40.960 Dr. McMahon,

01:48:41.540 is there anything

01:48:42.040 else that you

01:48:42.940 would like to bring

01:48:43.540 to the attention

01:48:44.180 of the people

01:48:44.740 who are watching

01:48:45.300 and listening?

01:48:46.200 There's really

01:48:46.780 just one other

01:48:47.700 part of the pathophysiology

01:48:49.260 that we didn't discuss

01:48:50.660 and that is

01:48:51.520 the blood-brain barrier.

01:48:53.800 Most people,

01:48:55.020 including myself,

01:48:56.040 when I was going

01:48:56.600 through medical schools,

01:48:57.860 thought of

01:48:58.620 an artery

01:48:59.900 that carries blood

01:49:01.000 as being like

01:49:01.960 a garden hose.

01:49:03.460 The blood enters

01:49:04.760 one end

01:49:05.220 and it comes

01:49:05.660 out the other,

01:49:06.720 but it turns out

01:49:07.700 that actually

01:49:08.540 the cells

01:49:09.440 that make up

01:49:10.060 the lining

01:49:10.600 of blood vessels

01:49:11.500 is pretty porous

01:49:13.020 and small proteins

01:49:15.340 and fluid

01:49:16.300 can flow

01:49:17.060 outside

01:49:17.840 of the blood vessels

01:49:19.100 and into the body

01:49:20.860 where the cells are.

01:49:21.800 The cells don't seem

01:49:22.840 to mind that.

01:49:24.040 Maybe they get

01:49:24.500 a little extra snack

01:49:25.580 and in addition,

01:49:26.780 you've got the lymph system

01:49:27.820 to clean that up,

01:49:29.340 but the brain

01:49:30.540 is much more

01:49:31.600 sensitive tissue

01:49:32.720 and the brain

01:49:34.420 doesn't want

01:49:35.340 all those

01:49:36.060 potential chemicals

01:49:36.940 and possibly toxins

01:49:38.280 oozing into it.

01:49:39.940 So by five days

01:49:41.120 of life,

01:49:42.420 the brain

01:49:43.000 has sent cells

01:49:44.480 to intercalate

01:49:45.680 into

01:49:46.220 those arteries

01:49:48.620 that are feeding

01:49:49.340 the brain

01:49:49.860 and create

01:49:50.880 what's called

01:49:51.300 the blood-brain barrier.

01:49:53.340 The blood-brain barrier

01:49:54.500 is maintained

01:49:56.060 by chemicals

01:49:57.040 like VIP,

01:49:58.660 maintained

01:49:59.000 by chemicals

01:50:00.000 like vascular

01:50:00.720 endothelial growth factor.

01:50:02.020 And we see

01:50:03.000 that the vast

01:50:03.680 majority

01:50:04.080 of our patients

01:50:04.740 have low levels

01:50:05.560 of VIP

01:50:06.020 and at least

01:50:07.280 a third

01:50:07.700 have low levels

01:50:08.680 of vascular

01:50:09.800 endothelial growth factor.

01:50:11.300 So what is created

01:50:12.520 is actual breaches

01:50:13.720 or changes

01:50:14.800 in permeability

01:50:15.740 in that blood-brain barrier.

01:50:17.420 What other scientists

01:50:18.480 have shown

01:50:18.980 is if you have

01:50:20.160 an excess

01:50:21.120 of cytokines,

01:50:22.740 doesn't matter why,

01:50:23.800 could be from

01:50:24.240 a Th1 process,

01:50:25.620 a Th2 process,

01:50:26.980 or a Th17 process,

01:50:28.940 if you have

01:50:29.720 additional cytokines

01:50:31.400 in your body

01:50:32.120 and you have

01:50:33.400 breaches

01:50:33.900 in your blood-brain barrier,

01:50:35.640 then those cytokines

01:50:37.060 will go into

01:50:38.220 the meat,

01:50:39.400 the parenchyma

01:50:40.100 of your brain

01:50:40.840 and will cause

01:50:42.380 a low-level

01:50:43.940 inflammatory process.

01:50:46.640 And I'm saying

01:50:47.800 that

01:50:48.100 to some degree

01:50:49.680 for

01:50:50.140 the people

01:50:51.760 that might be listening,

01:50:52.760 but especially

01:50:53.480 for you,

01:50:54.420 Dr. Peterson,

01:50:55.320 to understand

01:50:56.080 that now

01:50:56.640 you've got

01:50:57.020 an infiltration

01:50:57.980 of cytokines

01:50:59.020 setting up

01:50:59.580 low-level

01:51:00.120 inflammatory processes.

01:51:02.120 And not only that,

01:51:03.100 but there are

01:51:03.500 a couple of key areas

01:51:05.140 in the hypothalamus

01:51:06.740 that don't even

01:51:07.740 have a blood-brain barrier

01:51:08.940 because they're busy

01:51:10.000 sampling,

01:51:10.980 you know,

01:51:11.460 cortisol

01:51:11.780 or sampling

01:51:12.780 what the serum

01:51:13.540 osmolality is.

01:51:14.860 And so

01:51:15.180 these areas

01:51:16.400 have direct exposure.

01:51:18.240 Now,

01:51:18.480 it doesn't even

01:51:18.900 have to filter through.

01:51:20.320 We can define

01:51:21.540 similar processes

01:51:23.120 in the gut

01:51:24.520 and those processes

01:51:26.480 are maintained

01:51:27.820 primarily

01:51:28.380 by MSH,

01:51:29.860 which is almost

01:51:30.520 universally low

01:51:31.860 in our patients.

01:51:33.400 And so

01:51:33.760 they develop

01:51:34.660 with great frequency

01:51:35.680 food sensitivities,

01:51:37.320 true food allergies

01:51:38.600 and whatnot,

01:51:39.280 and they are

01:51:39.900 often reversible.

01:51:42.120 So if I were going

01:51:42.840 to sum all that up

01:51:44.280 for those

01:51:46.380 who are watching,

01:51:47.580 SIRS is a 1.00

01:51:48.380 terrible disease, 0.98

01:51:50.080 but it's

01:51:50.820 diagnosable

01:51:51.640 and it's

01:51:52.540 treatable

01:51:53.100 and we

01:51:54.000 usually

01:51:54.500 see people

01:51:55.320 recover

01:51:55.860 70 to

01:51:56.880 90 percent

01:51:58.060 of their

01:51:59.280 previous

01:51:59.740 function

01:52:00.220 if they

01:52:01.740 can follow

01:52:02.400 through

01:52:02.700 Dr.

01:52:03.080 Shoemaker's

01:52:03.520 protocol.

01:52:04.520 And then

01:52:04.940 the last

01:52:05.560 point that

01:52:06.040 I would

01:52:06.380 want to

01:52:06.680 make

01:52:06.920 is that

01:52:07.420 I believe

01:52:08.180 that this

01:52:08.640 illness

01:52:08.820 is basically

01:52:10.160 preventable

01:52:10.900 and eventually

01:52:12.300 what I'd like

01:52:13.120 to see

01:52:13.500 is screening

01:52:14.260 of young

01:52:15.280 children,

01:52:15.840 primarily

01:52:16.120 looking at

01:52:16.880 either their

01:52:17.680 HLA to see

01:52:18.560 if they have

01:52:18.880 a predisposition

01:52:19.660 or perhaps

01:52:20.660 their MSH,

01:52:21.720 which again

01:52:22.280 is almost

01:52:22.900 universally low

01:52:23.920 so that you

01:52:24.740 can determine

01:52:25.320 who are the

01:52:25.760 people most

01:52:26.340 likely to

01:52:27.040 develop this

01:52:27.800 and then

01:52:28.940 you also

01:52:29.840 need

01:52:30.300 some sort

01:52:32.680 of process

01:52:33.240 to fix

01:52:34.200 the buildings

01:52:34.880 or build

01:52:35.580 new buildings,

01:52:36.820 the schools.

01:52:38.100 Many of my

01:52:38.880 children,

01:52:39.300 their exposures

01:52:39.920 were in the

01:52:40.960 public schools

01:52:41.760 required by

01:52:43.120 law to go

01:52:43.820 to.

01:52:44.640 We've had

01:52:45.140 as many

01:52:45.480 as four

01:52:45.980 or five

01:52:46.400 children

01:52:46.740 and the

01:52:47.280 teacher

01:52:47.620 in the

01:52:48.520 same room

01:52:49.480 who had

01:52:50.560 problems

01:52:51.320 and once

01:52:52.460 they remediated

01:52:53.240 the room,

01:52:54.240 you know,

01:52:54.440 these children's

01:52:55.080 headaches went

01:52:55.600 away,

01:52:56.440 these teachers'

01:52:57.820 total body

01:52:58.340 syndromes

01:52:59.900 went away.

01:53:01.160 So that would

01:53:02.300 be my

01:53:03.000 message is

01:53:04.580 that awareness

01:53:05.740 has to get

01:53:06.380 out,

01:53:07.060 doctors need

01:53:07.720 to be trained

01:53:08.440 and policies

01:53:10.800 need to be

01:53:11.520 made to

01:53:12.880 eradicate

01:53:13.940 this illness

01:53:14.480 and I believe

01:53:15.140 it's totally

01:53:15.600 possible.

01:53:16.860 Yeah,

01:53:17.080 well that's

01:53:18.340 a pessimistic

01:53:19.560 and an

01:53:20.120 optimistic

01:53:20.600 conclusion.

01:53:21.360 I mean,

01:53:21.480 the pessimistic

01:53:22.100 conclusion is

01:53:22.740 that this

01:53:23.080 is very

01:53:23.440 widespread

01:53:23.920 and it's

01:53:24.460 very serious

01:53:25.220 and the

01:53:25.640 optimistic

01:53:26.060 conclusion is

01:53:26.780 yeah,

01:53:27.560 that's true

01:53:28.020 but we

01:53:28.360 know what

01:53:28.700 causes it

01:53:30.100 and we

01:53:30.280 know how

01:53:30.540 to treat

01:53:30.900 it.

01:53:31.440 And so

01:53:31.680 the news

01:53:32.080 could be

01:53:32.420 a hell of a lot

01:53:32.920 worse.

01:53:33.360 Dr. Shoemaker,

01:53:34.120 do you have

01:53:34.460 anything to say

01:53:35.180 in closing?

01:53:36.500 My greatest

01:53:37.280 concern is

01:53:38.300 that for

01:53:38.980 longer

01:53:39.740 neurologic

01:53:41.080 syndromes

01:53:41.720 like

01:53:42.040 Alzheimer's,

01:53:43.480 like Parkinson's,

01:53:44.460 we are

01:53:46.100 stuck with

01:53:46.900 the lack

01:53:47.580 of a

01:53:48.680 prospective

01:53:49.340 study

01:53:50.260 to prove

01:53:51.540 causation

01:53:52.360 of the

01:53:52.680 physiologic

01:53:53.300 abnormalities

01:53:53.900 we've

01:53:54.180 identified.

01:53:55.060 We can

01:53:55.600 find them

01:53:56.080 and fix

01:53:56.460 them

01:53:56.720 but how

01:53:57.600 do we

01:53:58.100 know

01:53:58.320 we've

01:53:58.920 prevented

01:53:59.500 a disease

01:54:01.120 that wouldn't

01:54:01.440 show up

01:54:01.760 for 25

01:54:02.160 years?

01:54:03.240 We don't.

01:54:04.700 So we

01:54:05.040 have the

01:54:05.340 ethical

01:54:05.660 issue

01:54:06.180 of letting

01:54:07.360 people stay

01:54:07.980 in a

01:54:08.460 water-damaged

01:54:08.960 building

01:54:09.320 for 25

01:54:09.860 years and

01:54:10.400 watch them

01:54:10.780 develop

01:54:11.160 Alzheimer's?

01:54:12.460 I don't

01:54:12.980 think that

01:54:13.260 would be a

01:54:13.560 very nice

01:54:13.940 idea.

01:54:14.240 I would

01:54:14.560 not like

01:54:14.820 to be

01:54:15.000 treated

01:54:15.560 that way

01:54:16.020 and so

01:54:17.060 we could

01:54:17.320 do it

01:54:17.640 with

01:54:17.820 short-term

01:54:18.260 exposure

01:54:18.720 with

01:54:18.960 sequential

01:54:19.320 activation

01:54:19.860 of

01:54:20.040 native

01:54:20.240 immune

01:54:20.380 elements

01:54:20.880 but

01:54:21.700 the

01:54:21.980 changes

01:54:24.000 of

01:54:25.100 environmental

01:54:25.660 toxicology

01:54:26.480 it's not

01:54:27.620 just

01:54:27.800 biotoxins

01:54:28.460 anymore

01:54:28.880 it's

01:54:29.800 other

01:54:30.080 inflammatory

01:54:31.060 situations

01:54:32.220 plasticizers

01:54:33.480 who knows

01:54:34.200 what they're

01:54:34.540 doing

01:54:34.880 it's

01:54:35.740 far

01:54:36.600 greater

01:54:37.040 but the

01:54:38.160 availability

01:54:38.620 of the

01:54:39.380 primary care

01:54:39.840 physician

01:54:40.320 to be

01:54:41.100 the leader

01:54:41.740 of the

01:54:43.160 pack

01:54:43.580 the leader

01:54:44.780 of the

01:54:45.520 cadre

01:54:45.940 that does

01:54:46.580 the work

01:54:47.360 and does

01:54:47.720 the patient

01:54:48.120 oriented

01:54:48.500 research

01:54:49.100 is limited

01:54:50.260 by our

01:54:50.760 current

01:54:51.040 medical

01:54:51.380 system

01:54:51.940 that

01:54:52.560 treasures

01:54:53.000 academics

01:54:53.740 and

01:54:54.500 university

01:54:54.980 appointed

01:54:55.520 specialists

01:54:56.840 and not

01:54:57.760 the primary

01:54:58.180 care

01:54:58.680 person who

01:54:59.780 sees 15,000

01:55:00.700 people a

01:55:01.200 year.

01:55:01.420 All right

01:55:02.960 gentlemen

01:55:03.360 well that

01:55:04.180 was a lot

01:55:04.580 of information

01:55:05.200 I'm going

01:55:05.700 to sum

01:55:06.000 it up

01:55:06.300 here just

01:55:06.980 for the

01:55:07.780 convenience

01:55:08.140 of everybody

01:55:08.700 watching and

01:55:09.320 listening

01:55:09.600 so we're

01:55:10.960 in a

01:55:11.160 situation

01:55:11.620 hypothetically

01:55:12.300 where 50

01:55:13.020 to 85

01:55:13.680 percent of

01:55:14.380 buildings

01:55:14.780 are affected

01:55:16.080 by the

01:55:17.780 invasion of

01:55:18.840 toxic

01:55:19.460 living

01:55:20.500 creatures

01:55:22.180 molds

01:55:22.840 fungi

01:55:23.460 etc

01:55:23.900 bacteria

01:55:24.720 as a

01:55:25.720 consequence

01:55:26.060 of water

01:55:26.580 damage

01:55:26.940 some

01:55:27.260 buildings

01:55:27.600 are more

01:55:28.000 susceptible

01:55:28.460 than others

01:55:29.460 to that

01:55:30.380 particularly

01:55:31.300 those that

01:55:32.080 are made

01:55:32.460 of drywall

01:55:33.420 and drywall

01:55:34.700 that's being

01:55:35.180 painted

01:55:35.580 with substances

01:55:37.900 hypothetically

01:55:38.600 designed to

01:55:39.280 stop those

01:55:40.220 biological organisms

01:55:41.600 from getting

01:55:42.080 a foothold

01:55:42.720 it's had a

01:55:43.360 paradoxical effect

01:55:44.280 that's affecting

01:55:45.340 a lot of

01:55:45.900 people

01:55:46.200 there is a

01:55:46.880 subset of

01:55:47.400 people

01:55:47.640 about 25

01:55:48.280 percent of

01:55:48.880 people who

01:55:49.300 are particularly

01:55:49.880 susceptible

01:55:50.440 to those

01:55:50.900 effects

01:55:51.260 there are

01:55:51.940 various ways

01:55:52.620 of identifying

01:55:53.260 them

01:55:53.680 and there

01:55:54.300 are an

01:55:54.920 array of

01:55:55.320 biomarkers

01:55:56.160 that are

01:55:56.460 available

01:55:56.860 to diagnose

01:55:57.660 this

01:55:58.180 illness

01:55:58.780 there is

01:55:59.680 about 40

01:56:00.300 symptoms

01:56:00.760 that are

01:56:01.100 associated

01:56:01.580 with it

01:56:02.040 and there

01:56:02.420 is a

01:56:02.760 standardized

01:56:03.180 treatment

01:56:03.780 protocol

01:56:04.200 that has

01:56:05.000 been

01:56:05.340 worked on

01:56:06.400 and publicized

01:56:07.720 by Dr.

01:56:08.940 McMahon

01:56:09.180 and Dr.

01:56:09.760 Shoemaker

01:56:10.120 and you can

01:56:10.620 find out

01:56:11.000 about that

01:56:11.600 at the

01:56:13.200 URLs

01:56:13.660 that we

01:56:14.060 put in

01:56:14.480 the description

01:56:14.960 of the

01:56:15.300 website

01:56:15.640 and so

01:56:16.360 that

01:56:18.240 about

01:56:19.220 sums it

01:56:19.740 up

01:56:19.920 it's

01:56:20.180 complicated

01:56:20.680 and

01:56:21.320 the

01:56:22.260 implications

01:56:23.880 are relatively

01:56:24.700 horrifying

01:56:25.280 but the

01:56:25.820 good news

01:56:26.200 is that

01:56:26.580 it's

01:56:26.760 actually

01:56:27.140 identifiable

01:56:28.120 and treatable

01:56:29.180 and that

01:56:29.460 the causal

01:56:29.860 sequence

01:56:30.320 has been

01:56:30.660 pretty well

01:56:31.140 identified

01:56:31.700 so

01:56:32.200 well

01:56:34.300 we'll make

01:56:34.940 of that

01:56:35.260 what we

01:56:35.640 can

01:56:35.960 as we

01:56:36.580 move

01:56:36.780 forward

01:56:37.160 everybody's

01:56:37.780 going to

01:56:38.040 have to

01:56:38.320 evaluate

01:56:38.720 this to

01:56:39.240 some degree

01:56:39.740 for themselves

01:56:40.760 because it's

01:56:41.560 a very

01:56:41.840 complicated

01:56:42.300 topic

01:56:42.740 we talked

01:56:43.700 about this

01:56:44.160 textbook

01:56:44.600 for

01:56:45.000 physicians

01:56:45.700 that's

01:56:46.680 the art

01:56:48.460 and science

01:56:49.180 of

01:56:50.000 SERS 0.88

01:56:50.620 medicine

01:56:51.140 and the

01:56:52.200 websites

01:56:52.560 for public

01:56:53.440 consumption

01:56:53.900 and so

01:56:54.320 I'm going

01:56:54.680 to talk

01:56:55.080 to

01:56:55.420 Drs.

01:56:56.360 McMahon

01:56:56.680 and Shoemaker

01:56:57.140 for another

01:56:57.560 half an hour

01:56:58.060 on the

01:56:58.340 Daily Wire

01:56:58.680 Plus side

01:56:59.240 and so

01:56:59.580 you guys

01:56:59.960 can join

01:57:00.320 us there

01:57:00.680 if you're

01:57:01.020 inclined to

01:57:01.540 and thank

01:57:02.320 you very

01:57:02.620 much gentlemen

01:57:03.260 for walking

01:57:04.400 through all

01:57:04.820 that information

01:57:05.520 for me

01:57:06.540 and for

01:57:06.860 everybody

01:57:07.140 who's

01:57:07.460 watching

01:57:07.800 and listening

01:57:08.260 today

01:57:08.700 thank you

01:57:10.460 you are

01:57:11.020 the best

01:57:11.640 interviewer

01:57:12.200 I've had

01:57:12.740 so I

01:57:13.120 thank you

01:57:13.480 for your

01:57:13.800 skill

01:57:14.100 oh my

01:57:15.000 pleasure

01:57:15.300 man

01:57:15.580 well I

01:57:15.880 wanted to

01:57:16.300 understand

01:57:16.760 what you

01:57:17.160 guys are

01:57:17.500 talking about

01:57:18.000 and I

01:57:18.280 certainly feel

01:57:18.840 like I'm

01:57:19.200 more on top

01:57:19.720 of it

01:57:19.960 now

01:57:20.240 you know

01:57:20.800 the problem

01:57:21.220 I had

01:57:21.760 when this

01:57:22.360 was all

01:57:22.680 brought to

01:57:23.000 my attention

01:57:23.540 my daughter

01:57:24.100 started talking

01:57:24.740 to me

01:57:25.000 about it

01:57:25.320 you know

01:57:25.480 and there's

01:57:25.740 a real

01:57:26.060 difference

01:57:26.520 between

01:57:26.860 someone just

01:57:27.480 telling you

01:57:28.200 something

01:57:28.940 even if it's

01:57:30.020 extraordinarily

01:57:30.600 vital

01:57:31.260 and actually

01:57:32.340 understanding

01:57:33.120 it

01:57:33.300 it was quite

01:57:33.860 frightening

01:57:34.660 to me

01:57:35.080 to encounter

01:57:36.100 this information

01:57:36.820 to begin

01:57:37.240 with

01:57:37.460 because I

01:57:37.880 thought

01:57:38.100 oh my

01:57:38.340 god

01:57:38.580 I'm going

01:57:38.840 to have

01:57:39.080 to dive

01:57:39.520 into

01:57:39.880 this literature

01:57:42.540 and try

01:57:42.880 to understand

01:57:43.360 it

01:57:43.580 just to even

01:57:44.240 interpret

01:57:44.900 for example

01:57:45.580 you know

01:57:45.960 why would I

01:57:46.640 believe that

01:57:47.180 the visual acuity

01:57:48.000 test is a

01:57:48.720 reasonable

01:57:49.100 diagnostic

01:57:50.040 marker

01:57:50.440 that's not

01:57:51.320 simple

01:57:51.800 I mean

01:57:52.200 your logic

01:57:52.820 I think

01:57:53.220 is impeccable

01:57:53.940 in relationship

01:57:54.520 to that

01:57:54.980 but it's

01:57:55.720 just another

01:57:56.160 indication

01:57:56.660 of how

01:57:57.000 complicated

01:57:57.480 it is

01:57:57.900 to get

01:57:58.200 on top

01:57:58.780 of a

01:57:59.140 potential

01:58:00.080 disease

01:58:00.520 process

01:58:00.960 of this

01:58:01.400 complexity

01:58:01.960 my experience

01:58:03.440 is even

01:58:04.280 though it's

01:58:04.760 complicated

01:58:05.400 if you're

01:58:06.300 speaking to

01:58:07.000 a provider

01:58:08.160 physician

01:58:09.140 nurse practitioner

01:58:09.940 whatever

01:58:10.620 who has an

01:58:12.120 open mind

01:58:12.760 and is willing

01:58:13.520 to hear about

01:58:14.140 it

01:58:14.300 it's not

01:58:14.940 very difficult

01:58:15.700 to convince

01:58:16.500 them that

01:58:16.980 this is a

01:58:17.500 reality

01:58:17.960 and it

01:58:18.520 answers a

01:58:19.200 lot of

01:58:19.840 unanswered

01:58:20.600 questions

01:58:20.980 there are

01:58:22.980 always people

01:58:23.540 that don't

01:58:24.240 want to know

01:58:24.720 and don't

01:58:25.080 want to hear

01:58:25.560 and obviously

01:58:26.940 we don't have

01:58:27.420 the same

01:58:27.700 success with

01:58:28.320 them

01:58:28.500 but in

01:58:29.160 people that

01:58:29.580 have an

01:58:29.900 open mind

01:58:30.400 this is

01:58:30.820 actually

01:58:31.320 very enlightening

01:58:33.440 for them

01:58:33.980 all right

01:58:34.920 well I'm

01:58:35.280 very glad to

01:58:35.820 hear that

01:58:36.160 that's a

01:58:36.540 good positive

01:58:37.040 note to end

01:58:37.560 on

01:58:37.700 okay so

01:58:38.100 thanks again

01:58:38.620 gentlemen

01:58:38.980 and to

01:58:39.880 everyone watching

01:58:40.520 and listening

01:58:40.980 your time

01:58:41.460 and attention

01:58:41.880 is always

01:58:42.340 much appreciated

01:58:43.100 to the Daily

01:58:43.960 Wire plus

01:58:44.480 people for

01:58:45.020 making this

01:58:45.440 possible

01:58:45.840 that's much

01:58:46.680 appreciated

01:58:47.180 as well

01:58:47.620 and so

01:58:48.340 we'll see

01:58:48.900 many of you

01:58:49.940 on the next

01:58:51.000 episode

01:58:51.380 thanks again

01:58:52.260 gentlemen

01:58:52.620 thank you

01:58:53.580 thank you very

01:58:54.160 much

01:58:54.480 thank you

The Jordan B. Peterson Podcast - January 18, 2024

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

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