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Hello everyone. I’m pleased to announce my new tour for 2024. Beginning in early February and running through June, Tammy and I and an assortment of special guests are going to visit 51 cities in the U.S. You can find out more information about this on my website jordanbpeterson.com as well as accessing all relevant ticketing information. I’m going to use the tour to walk through some of the ideas I’ve been working on. My forthcoming book out November 2024, We Who Wrestle with God. I’m looking forward to this. I’m thrilled to be able to do it again and I’ll be pleased to see all of you again soon. Bye bye. One of the reasons that the Roman Empire fell was because the Romans used lead to seal their wine amphora and lead is a known neurotoxin and when we introduced lead into gasoline to stop the gas from from our internal combustion engines from knocking, we lowered the IQ of people around the world by a substantial margin. Hello everyone. 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 and you probably haven’t heard that before but you may have heard about conditions like sick building syndrome or fibromyalgia or chronic fatigue syndrome and you’ve certainly heard of conditions like Alzheimer’s and other degenerative neurological conditions. Doctors Shoemaker and McMahon think that they have discovered with the help of other people obviously at least one potential pathway to such conditions and that has to do with toxins in buildings. So the basic theory is something like this, a substantial number of buildings especially those built with drywall using anti-fungal paints have water damage. That water damage produces biotoxins of various sorts for a substantial proportion of the population about 25 percent exposure to those biotoxins produces an immunological response that has all sorts of neurological and behavioral negative consequences and so I found out about this through my daughter who’s been wrestling with health disorders of various sorts for her whole life. She’s convinced me that it was at least worth some investigation and that’s what I’m doing and so I decided to read some of these gentleman’s research papers and they struck me as highly credible and so I’m talking to them today to find out just what there is to this. If they’re right about 20 percent of the population is suffering from all sorts of conditions often diagnosed as other illnesses depression included and that’s actually a consequence of exposure to biotoxins in in water damaged buildings and this also seems to be a particular problem by the way among the military low-grade military housing much of it water damaged and mold infested and the government by the way seems to agree with that assessment even though not enough has been done about that so far. So anyways come along for the ride that’s what we’re talking about today. Dr. Shoemaker, Dr. McMahon, welcome to the program. I’m very interested in talking to you guys today. My daughter has alerted me to your work and I’ve been looking into it for the last four or five months. You guys have been studying something called chronic inflammatory response syndrome and the more I’ve looked into this the deeper the rabbit hole goes I suppose you could say that and I thought the best way to educate myself and potentially everyone else who’s listening and watching would be to have you guys on this podcast so I could ask you all sorts of questions and so I’m going to take a friendly skeptical approach if you don’t mind because what you’re studying is of such magnitude that if you’re correct it’s a catastrophe and so we could all hope that you’re not correct so that it isn’t a catastrophe but I know you’ve accumulated a substantial amount of evidence and so maybe we’ll start with you Dr. Shoemaker. Do you want to just tell everybody what it is you’ve been studying and why you started studying it and how widespread you think the problem is? Most people have a sense of what inflammation is. Our body is looking at environmental stressors that must be dealt with and the inflammatory process as a general rule is part of the environmental response to the trauma or stress. Inflammation can be of two kinds one is acquired or allergy or kind of the adaptive way that the body will learn how to make antibodies and respond to stressors with memories so these things will be experienced once and then the twice is the next time is very quick but we’re looking at a different form the left hand if you will compared to the right hand of innate immune responses in which the response to an antigen or foreign particle that’s introduced in the body in many different ways inhalation is certainly the big way I worry about but it could be elsewhere but specifically once there is antigen detection by the innate immune response system there should be processing of an antigen and putting on a HLA molecule or a histocopatic locus a molecule on the antigen and packaging it in the antigen presenting cells to a naive lymphocyte just waiting for something to happen and when the naive lymphocyte sees this tasty little morsel package with HLA and an antigen on it it should turn on a kind of Z cell or a B cell excuse me to make an antibody the problem with the illness that we have is that over 95 percent of the patients do not have antigen processing correctly so that antibodies are made in a reduced fashion if at all when we look at now what control do we have on inflammation if the stimulus is not stopped and it doesn’t have to be ongoing exposure it is now in this world of antigen interaction with antigen presenting cells and t lymphocytes that has gone awry and the illnesses that we see become chronic because the antibody formation does not occur now over the years we knew about problems with antigen presentation but now we know the gene mechanisms behind defective antigen presentation and the gene mechanisms to not only include inflammation in our in our venues but also abnormalities in metabolism so if we look at metabolic problems combined with inflammation we have molecular hypometabolism which is a fancy way of saying that 95 percent of patients with chronic fatigue have a specific abnormality and inflammation and metabolism that we can show with genetic makeup and then with scott’s work and my work we’ve been able to show that we can correct the gene activation when it’s not supposed to be activated and correct gene suppression when it’s not supposed to be suppressed so what we’re looking at is the transcriptomic or gene representative theory of illness causation and illness correction our last paper and i hope you had a chance to take a look at it but it’s in your inbox if you didn’t the next question is now when i’m looking at to me the the holy grail and that’s correction of dieback central nervous system degeneration you may hear it called alzheimer’s you may hear called parkinson’s you may hear that same called for atrophic myotrophic lateral sclerosis or als but we are there we’re there with gene activation and correction with our therapies that have been developed over the last 27 years okay so you’re you’re going after a host of the mutological diseases including extraordinarily widespread conditions like alzheimer’s dr mcmahon do you want to explain to everybody what this has to do with where they live so there are a number of potential triggers that can cause the innate immune system to activate and as dr shoemaker pointed out these people are at least around 90 of them don’t have adequate or effective antibody production to help mitigate when there is chronic exposure so the innate immune system is then basically left to handle this by itself without the antibody cavalry coming in and and reducing the burden 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 when you inhale those your body recognizes those as being foreign antigens and it’s not just for instance say mold spores it can be old dead mold spores that have lost their integrity their cell wall is broken apart into hundreds of fragments and in fact those fragments when you inhale them go even deeper down your respiratory tract into your lung and again trigger the innate immune system as response to that the innate immune system will overproduce cytokines in the same way that you would overproduce cytokines if you got the flu or if you got covid or some other kind of viral infection and these fragments trigger the innate immune system and the overproduction of the cytokines and then the cytokines cause the symptoms that we commonly relate to with the flu which could include headaches muscle aches joint pains fatigue malaise difficulty sleeping coughing other respiratory issues brain fog etc etc okay so let me let me get the whole sequence of this straight so what you guys have been studying is sometimes just and stop me you know at any point if i get any of this wrong sometimes people refer to this as sick building syndrome you’ve you’ve brought in conditions like Alzheimer’s and other immunological diseases chronic fatigue syndrome i know you’ve concentrated to some degree too on fibromyalgia so the idea is that there are many buildings and we’ll talk about how many but there are many buildings that harbor airborne pathogens mold being first and foremost among them perhaps that’s much more likely in buildings that have been water damaged and not properly remediated the consequence of that is that if people are in those buildings living in them or or working in them that they’re chronically exposed to pathogens that can trigger an immune response and some people when that immune response is triggered they’re not producing antibodies in a proper manner and there are genetic reasons for that and possibly metabolic reasons as all as well and then is it the combination of the pathogens that are in the local environment plus the genetic weakness or the metabolic problems that produce this cytokine storm that you associated with flu-like symptoms and pain and chronic inflammation now and have i got all that right is that is that the way this lays itself out you’re doing great keep on that is excellent okay okay good so so let’s let’s go through that one by one then the first issue is then what percentage of buildings in north america and elsewhere in the world do you think are suffering from this problem and if it’s a large number of buildings that’s obviously a catastrophe so what’s the evidence for this and why did you guys become convinced of this what we have seen is a similarity of the syndrome of acute exposure followed by chronic exposure wherever the person might live it’s not confined to florida or hawaii could be in in nepal or could be in in in stuttgart this worldwide exposure to an environment that pretty much has 62 to 78 degrees year-round no wind no rain no change of the seasons indoors and the mark of every one of these indoor places is water intrusion so if we look to see is there a water damage building we should be able to find an ecosystem of organisms 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 we know that fungi have a role but we also know that endotoxins from bacteria are second on the list and first is actinobacteria and when you look at every building that’s water damage that has these ecologic parameters you find the same symptoms the same and laboratory findings and now that we have access to gene evaluation the same gene activation and the likelihood that this would be due to something else becomes a statistical problem in some of scott’s work he’s published that the likelihood is you’ve got a p value of less than p is less than than one to the minus 50th power so it could be the same in stuttgart if the noise was the same but actually statistically the idea that it’s not the same is so remote to be impossible okay so what scott what proportion of modern buildings first of all isn’t modern buildings that are particularly affected and and if not or if so what proportion of buildings in general are we talking about and are there specific kinds of buildings that appear more susceptible i read in some of the work of yours that i reviewed for example that drywall seems to be a particular problem so what what what kind of how widespread is this problem do you suppose and and what buildings are particularly affected well the epa has published the united states environmental protection agency has published that at least 50 percent of the buildings and up to 85 percent of the buildings in the united states are historically water damaged buildings that are involved are not due to one year of construction or another with modern structures put up quickly contractors investing money wants to turn over the house sale quickly so you may not wait for a master plumber to put in the bathroom and a plumbing leak can develop instruction defects for new homes are a real bugaboo 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 and about in 1970 when the population got all upset with the oil embargoes and houses were made to be tighter we thought that that was the reason for the problem it was actually not because what we were using were were paints and sealants to keep down mold growth what we did was create natural selection to kill off molds that could be killed and if with the molds that survived became toxin formers were before they didn’t so before 1970 it usually was a paint one building that was retrofitted or retrograde corrected or modern construction the safest buildings even though they’re water water damaged are the old buildings with no paint okay so there there’s no specific form of building that can be that’s amenable per se to to water damage and the intrusion of toxins in it in consequence but you talk about buildings after 1970 you said your first hypothesis was these buildings were arguably more dangerous because they were more airtight as a consequence of panic over declining fossil fuel availability and i remember when people started talking about sick building syndrome i guess this is this went back as far in my knowledge as far back as the 80s they were concerned about these hypersealed buildings but you said that your further investigations revealed that it wasn’t the ceiling of the buildings per se so much as the use of modern paints and sealants that had anti-fungal chemicals embedded in them now hypothetically the reason they put those anti-fungals and anti-mold chemicals in the paints was to keep the fungus and mold down but you said or you’re implying i think you said directly that the consequence of that the unintended consequence of that was that we produced molds and other toxins that were more toxic rather than less as a consequence of natural selection so why did natural selection which was obviously selecting molds and other biohazards that could tolerate the exposure to this poison why did they become more toxic and what’s your evidence for that fungi also have a response to environmental hazards and the environmental hazards of being killed will cause act normal activation of genes in fungal species such that they’ll make toxins where beforehand they didn’t with the main role of a micro toxin for example has nothing to do with defense it has everything to do with predation so the fungus wants to be eating a plant and the plant doesn’t want to be eaten so it’ll release things like a peroxidase and the fungi make compounds who eliminate the fungi they eliminate the proxidase therefore eliminate the plant defenses but it’s predation of fungi on on its prey that’s foremost where all this goes on meanwhile actinobacteria love an alkaline environment molds like an acid environment and the alkaline environment from actinone is created by manufacturer of substances that will kill off fungi and change the ph of the drywall so that as you see a initial building the initial colonization will be with fungi it’ll be replaced by actinobacteria as time goes on but meanwhile if there’s a flood or a hurricane event or natural disaster the water saturation or aw as people should say activity of water will initially let in organisms that like very saturated conditions or aw 0.9 to its maximum of 1.0 or 100 so we see one group of fungi of water damage that’s acute one different species will be grouping of water damage that’s less acute and in the end then we’ll see of sources that have very dry buildings but where the moisture has changed the ecosystem now actinobacteria are famous for creating most smell and interestingly the musty smell or musty odor we’ve long associated with fungal colonization is coming from actinose geosman there are also architectural design features that make a building more likely to become water damaged than others flat roofs are more likely to leak than than pitched roofs are basements and crawl spaces are more likely to have water intrusions than you would see in homes that are built on a slab we know that that drywall is more likely to have problems than plaster on laid and so there are a number of different materials and architectural styles that can make a house or a commercial building more vulnerable or less right well you could imagine you know when i’m thinking my paranoid thoughts i know here here’s an example so one of the reasons that the roman empire fell was because the romans used lead to seal their wine amphora and lead is a known neurotoxin and when we introduced lead into gasoline to stop the gas from from our our internal combustion engines from knocking we lowered the iq of people around the world by a substantial margin it was really quite a catastrophe and that was it was also the case that in relatively low let’s see it in how in older houses that had used a plethora of lead paint where the paint was allowed to deteriorate and young children were therefore ingesting lead paint powder they were also impaired in terms of their intelligence and also much more likely to be anti-social and criminal and so the reason i’m bringing this up is because it’s possible for a society to introduce something into their myths that’s then distributed in an extraordinarily widespread fashion you know experimental vaccines come to mind by the way and all of a sudden all sorts of things that we didn’t that weren’t understood about that thing that’s being introduced make themselves manifest and it sounds like that’s a case that you’re making for drywall is that it’s extraordinarily light easy to work with cheap building substance but it isn’t we don’t have a lot of historical experience with it it was introduced in a very widespread manner in the latter half of the 20th century and so and then you’re saying that in combination with the fungicides and so forth that was put in the paint that we put ourselves in a situation where we’ve contaminated something approximating 50 to 80 percent of buildings so that’s really quite the bloody catastrophe so now let’s take that apart a little bit if it’s 50 to 80 percent of buildings how many of them in your estimation are contaminated to the point where that actually constitutes a serious health problem like you know i know that that’s a threshold issue but there’s lots of threats that people have to contend with obviously and and if your house is contaminated with mold and water damage that’s a big deal it’s a really difficult thing to fix or it can be and so under what conditions should be should people be prioritizing this as a actionable risk factor and and how widespread do you think this problem is in its more serious forms study after study has looked at individual susceptibility which underlies who gets sick and who doesn’t the individual’s susceptibility of the immune response genes phenochromosome 6 hla dr was shown to be present in in just about every person who had SIRS and the percentage of not having SIRS hla but having an illness is less than five percent of the total so 95 percent were broken out into six separate haplotypes there are 54 available and out of those six it’s 24 of the population when we look at this 24 percent we put them in exposure and follow them prospectively we can show that the initial responses once the priming event has taken place is essentially 100 percent in those with individual susceptibility we’re seeing this exactly with the same way with coven coven creates an inflammatory response it turns on innate immune responses which turns on gene-based susceptibility so long coven has the same genetic makeup and we’ve published a paper on this in june of last year as well that it creates a new illness a new target where once wasn’t before and we looked at people who had were living in a building and find got coven got better from coven but then that turned on the innate immune response system that didn’t stop and lo and behold a month later two months later three months later they had long coven syndrome when actually what they had was a chronic inflammatory and metabolic response syndrome it was just a different initiator it could be a whole horde of of yellow jackets stinging people in a picnic creating inflammatory response or it could be an illness in this case coven feels the bill last year because of you preborn’s network of clinics saved over 58 000 babies thank you to all who made this possible let’s celebrate these precious babies when charlotte found out she was pregnant she was seven weeks along in the back of her mind she thought abortion was the best solution she went into a preborn clinic and after hearing her baby’s heartbeat and seeing her beautiful baby on ultrasound she chose life her heart is filled with gratitude for all of you who made this possible each of these babies is truly miraculous and every day preborn celebrates 200 miracles just 28 dollars can be the difference between the life and death of a child when a mother meets her baby on ultrasound and hears that heartbeat it’s a divine connection that doubles that baby’s chance at life let’s join together and help mothers choose life to donate dial pound 250 and say the keyword baby that’s pound 250 baby or go to preborn.com slash jordan that’s preborn.com slash jordan okay okay so you could imagine that there’s a manner of conceptualization that allows for two kinds of disease processes there’s disease processes that are associated with pathogens per se and then there are disease processes associated with an anti-disease response or an immunological response gone astray so if i’m following you correctly we have a situation where let’s say 75 percent of our buildings are contaminated and so three quarters of the population is exposed to the pathogens that could produce an immune hyper response but 25 percent of the population in those buildings is particularly susceptible to that because they have a genetic predisposition to immune overreaction in response to the specific kinds of pathogens we’re describing or is that a more general susceptibility to immune overreaction you’re you seem to be implying that in relationship to the covid issue so so it’s 25 percent of 75 essentially is the number of people who are hypothetically affected so that’s about 25 that’s about 20 percent of people all things considered might be experiencing this as a serious problem so so have i got that have i got all that right if yes you do and you picked it up very quickly i thank you for that one of the reasons that it’s so important is that we look at illnesses that are sers that actually are sers and add up who has chronic fatigue syndrome who has fibromyalgia who has depression who’s just getting older because their cognitive refraction right for children not doing well in school is it the lead paint that they swallowed is it the lead in the applesauce that they’ve been they’ve indeed been taking in are there environmental factors that are creating this overall systemic illness of which the brain is the injury i worry most about in adults scott sees children more than i did so we can let him speak about children’s with cognitive issues but the issues are that when we look carefully at chronic fatigue syndrome we find sers and i’d like you sir if you could to identify one significant biomarker that distinguishes fibromyalgia from not we have 30 biomarkers for sers and zero for fibromyalgia why does fibromyalgia have such a preponderance of people and how many people adults have fibromyalgia 10 and 3 for for chronic fatigue syndrome how about post-line syndrome how about depression boy we’ve got 25 all of a sudden and we’ve started 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 okay so one of the things that the non-medical listeners and watchers of this podcast might not know is that there’s a lot of overlap in symptoms between different hypothetically different illnesses and so let’s take depression as a case in point now when i was assessing my clients for depression the first thing i always tried to figure out was are they just ill because there’s all sorts of evidence associating depression particularly with immunological dysfunction and so i would inquire into their sleep habits and their eating habits and also their associated health conditions to find out if we could because my sense was before we diagnosed something as psychological we should take a look and see if there’s actually something causing it and depression is a relatively non specific cluster of syndromes now you’re pointing to a whole set of syndromes that have relatively non-specific symptoms some of them even more difficult to diagnose and and easier to be skeptical about in relationship even to their existence as say fibromyalgia and chronic fatigue syndrome right that’s hard to dissociate from general depression and anxiety and and and a kind of global neuroticism or even a hypochondriasis now you’re saying you know your first claim is that 20 percent of the population is likely to be experiencing these symptoms but we don’t see that that we don’t see this sears chronic inflammatory response syndrome in 20 percent of people because essentially we’re placing them in the wrong bins now and so how much of so let’s walk through let’s walk through what the symptom constellation is for chronic inflammatory response syndrome that’s 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 and and why do you think that your category your category system which put places all these people in the in the box of chronic inflammatory response syndrome why do you think that that’s preferable to the approach that’s being used by physicians now because you 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 percent of our buildings are in serious trouble that 20 percent 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 maldi misdiagnosed and that this is actually the root cause of their of their symptoms like including absolutely devastating diseases like Alzheimer’s so 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 as dr shoemaker said we have roughly 30 biomarkers these are these are tests which can distinguish ill people or what we call cases from healthy people what we call controls we have roughly 30 of them and all of them have been validated to show that they separate cases from controls when we look at the diagnosis of surge you have to have objective evidence that shows that you have several of these biomarkers you know i mean at least four or maybe five or more before you can actually even make the diagnosis the statistical likelihood of finding a healthy person who had five abnormal biomarkers out of the five we draw or the 10 that we obtained it is so small i mean it’s in the one to a million then when you start looking at a larger group of people maybe several people in the same hall or in the same office building or in the same school when you start looking at that and and each person’s probability of having those abnormal biomarkers multiplies by the next person’s and then multiplies by the next person’s 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 what the i think what the main problem is and why this hasn’t been seen before in chronic fatigue patients or irritable bowel patients or fibromyalgia patients is because most physicians or many physicians don’t run the tests that we do we are looking specifically at the innate immune system as the possible root cause for these different symptoms and if they ran the tests that we do they would see the same kind of data that we my data is very similar to dr shumakers i’ve seen roughly 2 000 patients 2 000 that i’ve evaluated this for him it’s much more because he’s been doing it much longer than i have and our data is is very similar okay so your argument basically is and i just want to walk through this very carefully so that everyone listening understands is that you’ve identified a number of biomarkers you said 30 overall but apparently you concentrate on something like five to ten now there’s a probability that any given test is going to produce a result that’s positive falsely so someone will be diagnosed as abnormal on that evaluated dimension but in truth not be abnormal but that probability declines as a function of the number of tests administered so maybe there’s a one in 20 chance that any given test will show that you have the condition but there’s a one in 400 chance that two tests would show that and a one in 8 000 chance that three tests would show that and so your case basically is that as you accumulate evidence of the biomarkers you decrease the probability of a false diagnosis and there aren’t biomarkers as far as i know there aren’t there certainly aren’t biomarkers for depression so that’s not not specific uh what would you say physical or chemical biomarkers you know there’s sometimes there’s elevated cortisol or decreased cortisol but it’s very non the markers are very non-specific so if you’re correct and there are specific biomarkers for sers that implies that that it can be more accurately diagnosed than the other conditions with which be confused and so what are the what are the prime biomarkers that you guys use to to make the diagnosis and why did you pick those and how how valid do you think they are and why we need to start with the case definition the case definition in 2003 that our group came up with was modified in 2008 by the u.s government accountability office when they looked at the potential for exposure this is what cdc used with hysteria back in 1997 1996 you didn’t get sick from a microalgal bloom unless you’re exposed to it so the potential for exposure is number one number two is symptoms the same or similar to those seen in published peer-reviewed literature the third element is laboratory findings the same or similar to those in published literature and then the fourth is objective response of biomarkers to treatment so if we then say what biomarkers have stood the test of time back in in in 2000 it was trial and error by finding hla was the explanation of why did some people get sick and other people didn’t was there a risk factor like cigarette smoking or alcohol use or age or or underlying the illness with diabetes no no no no it was based on genetic markers so individually immune responses became our first biomarker the actually the first biomarker came from the epa with ken hudnell been studying the neurotoxic logic features of visual contrast sensitivity which is a mechanism to see an abnormal neurologic function of vision contrast is one that’s going to stabilized over time and is adversely affected as velocity of flow of red cells and retina and neuro-rhymbe optic nerve head increases so vcs was our first hla was our next in that group there was a regulatory neuropeptide melanocytes stimulating hormone which is essentially negative in all cases and normal in all controls and then with treatment we saw improvement in msh not as much as what we wanted and that was the impetus to keep on scott mentioned cytokines in 1986 1985 was the first publication of a paper on cytokines and here we are in 1996 postulating that this cytokine effect could be huge and now if we fast forward to covid it’s a cytokine storm and everyone the drugs store knows what a cytokine storm is they’re buying covid tests they’re looking for mechanisms that we have been studying and cytokine storms can are part of innate immune response so you’ll have it in covid but you have it in service too and covid doesn’t have the same hla that we know of yet but we’ll probably find it doesn’t have the same vcs and it’s a it’s a sorting process so we took them inflammatory markers tgf beta 1 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 abnormality showed it in its its height with some of the worst illnesses of all and then we treated it with medications that were available over the counter or with with uh any informed consent and then every time we had re-exposure here we came to the prospective acquisition of illness proof of causation we took people that could have been sick from one building fixed and all the lab markers were the same and then with informed consent they stopped all medicines and stayed away the suspect building three days nothing put them back in the day in the building on day one at the end of day one laboratory findings changed day two laboratory changes finding changed again day three we had the exact syndrome of labs vcs and symptoms prospectively proven upon re-exposure only no other choices could have been affected it wasn’t depression in three days it was sers in three days okay so so let me let me elaborate on the story now so the biomarkers that you described the first one which is a very odd one i’ve taken this test by the way and failed it and quite dramatically and so there’s an online test which is a visual contrast sensitivity test and basically what you’re doing and stop me if i get this wrong because it’s been a while is you’re you’re testing people’s sensitivity to what visual acuity in relationship to closely spaced lines on a on a diagram essentially and the hypothesis that you’re putting forward is that in the presence of these inflammatory syndromes retinal acuity is compromised and i don’t understand the mechanism there but that’s basically the issue right so you have an there is an online test visual contrast sensitivity that people can take um see it’s a it’s a strange test because it seems like it’s so far removed from the symptom set that people would be experiencing it’s very difficult for someone like myself i’m scientifically trained you know and any and all of this stuff that i’ve encountered as a consequence all of the findings i’ve encountered as a consequence of going through your material have really come as a as a shock to me this visual contrast sensitivity test being one of them because it’s so far removed from the symptoms that it’s hard to believe that there could be a relationship it almost seems like voodoo now you said that the reason that this visual contrast sensitivity test works is because the retinal the retina itself is compromised as a consequence of immunological malfunction and so have i got that right we have a objective parameter and that’s velocity of flow of red blood cells in the the retina blood vessels and the capillary beds as well as the neuro-rheumatoid nerve head we can measure objectively with the heidelberg retinal flow meter how fast red blood cells move and they move more slowly if the inflammatory response promotes production of what are called adhesions which is one mechanism to decrease flow in an area of hyper inflammation and treatment will be shown to improve flow as the environmental stimulus is fixed and is corrected with treatment so with sick patients you have reduced flow healed patients have restored the normal flow to equal controls but re-exposure here we go prospective exposure again that’s this is how we determine risk in all of medicine and science prospectively not an association but both 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 this is in and out in and out and constant answers to the critics how could this possibly be true well here are the data and if people want to argue with me they can argue with my data okay so let let me elaborate on that a little bit before i return to the biomarkers per se so i know that the closest tissue that’s deeply analogous to the brain itself is retinal tissue and and so i i don’t know if that’s relevant in this regard but it seems to me that if what you’re measuring with the visual what does it mean you’re with the retinal with the visual acuity test visual sensitivity visual contrast sensitivity test you’re measuring retinal dysfunction what are the implications of that measured retinal dysfunction for broader central nervous system dysfunction or brain dysfunction and does that lead us logically into a discussion of degenerative neurological conditions like Alzheimer’s it does the same mechanism of cytokine response in capillary beds is the same whether it started with the fungus whether it started with the bacterial bacteria whether it started with the flu but this innate immune response is nonspecific in how its response but it will respond and we can measure its tendency to reoccur regardless of where it happens it’ll happen in kidneys it happens in lung it happens in liver and it happens in the neural rim of the optic nerve head which is the first part of the central nervous system we’ve added countless additions to that but that was the beginning that was 1998 after studying this for for one and a half years we finally had our first biomarker that showed led the way to cytokines we could separate with treatment but by having treatment we had the way around the skeptics because i can say all right you use your view do medicine for a week and i’ll use my view do medicine for a week we’ll see who’s gonna do works better when yours doesn’t and mine does then i’m going to say i win the battle right well that’s particularly powerful as you pointed out in combination with evidence that you can reinstance the ill reinstantiate the illness once treated with re-exposure because then you have direct causality right instead of the weak sort of correlations that often go to to hypothetically prove the existence of a given condition okay so let let me get this straight again so you have the vision test you have hla maybe you can tell us again what that is uh mel was it melatonin stimulating hormone and cytokine detection so that’s four are those the four primary biomarkers we also saw you mentioned cortisol and depression yeah we measure simultaneous a cth and cortisol because lo and behold there was dysregulation of a cth which is made by the same set of of environmental and metabolic pathways in the brain they’re all melanocortins msh and a cth are melanocortins so if we have disruption of msh we’re going to have disruption of a cth and cortisol can either follow in step which it often will or can create in its own marker so dysregulation of a cth and cortisol is one we found anti-diuretic hormone doing the same thing people walk around with chronic headaches they said they had migraine they’re constantly but we find out they were they were all functionally dehydrated with elevated osmolality and reduced adh that was another measurement we looked at at pulmonary hypertension is a very common cardiac conditions mistaken for cardiovascular disease people are short of breath and have chest pain with exertion we think that it’s from doing a coronary disease when in fact we measure the velocity of flow coming in the force of the flow coming from the right ventricle to the lung that’s reduced if the pulmonary pressure is increased when we measure that we find that over 60 percent of our cases have pulmonary hypertension that’s alluded to cardiologists because they didn’t do the echocardiogram to show it and it hits just one after another when we get to genomics and i hope we’ll have time for today if not we should do this tomorrow or another day the gene mechanisms are the real gold line for the researcher and for the clinician alike have you ever heard of data brokers they’re the middlemen collecting and selling all those digital footprints you leave online they can stitch together detailed profiles which includes your browsing history online searches and location data they then sell your profile to a company that delivers you a targeted ad no biggie right well you might be surprised to learn that these same data brokers are also selling your information to the department of homeland security and the irs so to mask my digital footprints i protect myself with express vpn one of the easiest ways for brokers to aggregate data and tie it back to you is through your device’s unique ip address which also reveals information about your location when you’re connected to express vpn your ip address is hidden that makes it much more difficult for data brokers to identify who you are express vpn also encrypts 100 of network traffic to keep your data safe from hackers on public wi-fi that’s why i have the express vpn app downloaded on all of my devices phone computer and even my home wi-fi router all i do is tap one button to turn it on and i’m protected it’s that easy make sure your online activity and data is protected with the best vpn buy secure your online data today by visiting expressvpn.com slash jordan that’s exp ressvpn.com slash jordan and you can get an extra three months free expressvpn.com slash jordan okay well i’ll return to to the genomics issue and don’t let me forget that if i if if we don’t get there i want to okay so we’ve basically walked through we’ve done a reasonable overview of the biomarker space so let’s do this now let’s let’s talk about behavioral and cognitive behavioral emotional and cognitive symptoms like what are people what are people who have sirs going to experience in their day-to-day life that they might confuse with chronic fatigue syndrome or or depression or fibromyalgia for example or or you said pulmonary hypertension as well so what what are the fundamental symptoms that people should be alert to and do they differ in adults and children well as we were talking about decreased red blood cell flow to to the optic disc you have to understand that there’s decreased red blood flow to different places in the body not just to the optic disc so for instance you know peripherally as you look at the hands and feet we’ll see that there’s reduced red cell flow there too our patients will often have cold hands or cold feet or both they can have cramping in their hands they can have pains in their hands even sometimes discoloration you know that looks like cyanosis and we see that that goes away with treatment dr schumacher was talking about the lungs we also need to talk about the brain the brain will will also have a decreased blood flow and dr schumacher actually demonstrated that in unpublished data back in the late 2000s when he was doing mr spectroscopy and showed that there was an increasing lactic acid in certain areas of the brain there was the abnormality in the glutamate glutamine ratio both of which suggested that there was hypoperfusion or a reduction of that red blood cell flow so why is that important well the blood carries the oxygen and the sugar the glucose that’s necessary for for production of energy at a cellular level it can chronically reduce the amount of oxygen that is getting to any cell it will stop making energy as well and then we get into genomics findings but what we know is when you’re not making enough energy then you have to ration the energy that you have and the cell will underperform in in different areas and so that will lead into brain fog and potentially into cellular death which can then lead into things like you know dieback regeneration and the neurologic illnesses now you you you also how do you directly evaluate brain state and brain function if i remember correctly i mean i’ve been investigating this with my daughter and my wife for some time and some of the details are unclear to me we’ve also had brain scans specifically done to look for neurological damage that might be associated with this this exposure and and sensitivity and so for everyone who’s watching and listening i mean i might as well tell you why i’m particularly interested in this i mean there’s a long-standing history of depression in my family and my suspicions are strong that it has a physiological basis because first of all it has a seasonal component and that indicates something physiological right off the bat but it’s also associated with a lot of immunological trouble which seemed to culminate in this case of my daughter who had endless numbers of immunological problems and she’s treated a lot of those successfully with a very restricted diet as have my wife and i but she’s become convinced more recently that the cause of the food sensitivity that’s driving her immunological conditions might be associated might be attributed to sensitivity to these biotoxins that dr shoemaker and mcmahon are talking about and so well that’s what we’re trying to track down at the moment because this has been a multi-generational catastrophe in my family and i would like to get to the bottom of it and so we did some of these neurological tests that did indicate some some neurological damage hypothetically as a consequence of toxin exposure and so can you can you walk everybody through those tests and what they indicate and then maybe we could talk a little bit about treatment before turning to genomics we skipped over symptoms you asked a couple yes right yes all right let’s pick up that loose end before we hit in his neurocon and all that the reporting that i did when i had visual contrast is my only biomarker was compulsive logging down of what symptoms that people have maybe symptoms that i listed in an interview wasn’t a self uh form or question here the patient would fill out it’s the process of doing a medical history that we’re all trained to do in in four years of medical school or longer if we’ve specialized but specifically fatigue and weakness were nonspecific didn’t have to with the others aching and cramping unusual cramping of the legs when you’d get spasms at night time and get a charlie horse or in the hands and it was hard to extend fingers because the muscles were in spasm basically that was the end of of circulation the fingers and the toes were the end that’s where the accumulation lactic acid was greater so that’s where the muscle spasm was respiratory issues cough shortest of breath sinus congestion that was chronic not related to seasons necessarily eye findings we have red eyes blurred vision tearing sensitivity bright light with cough and shortness of breath and difficulty with exertion we had lung involvement didn’t have a lot of speed of production and the biomarker was restrictive lung disease not not obstructive it wasn’t asthma was called asthma by some it’s not it’s restrictive abdominal pain secretory diarrhea vomiting nausea also present joint problems soreness stiffness first thing in the morning and throughout after sitting in a chair for two hours the cognitive issues were there difficulty with memory difficulty with assimilation of new knowledge difficulty with concentration difficulty with with disorientation the executive cognitive functions are six hypothalamic system we had change in appetite change in in in weight suddenly and then what weight gain out of the blue change in sweats and night sweats especially change in bio and temperature regulation those are all the msh related things so let me ask you a technical question about that so when you’re going through that as a psychologist so what i would think would be helpful in relationship to that diagnosis would be to make a list like a questionnaire of all you you listed off about 40 symptoms i think that’s about how many you covered so you could imagine that you had people fill out a questionnaire and then you could associate each questionnaire item with the with the biomarkers and you could find out which of the symptoms were cardinal with a factor analysis have you guys done any questionnaire development that’s oriented towards symptom identification yes every person that takes their visual contrast test will undergo a symptom analysis in 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 yeah just statistically we can tell you 98.5 likelihood of sers just on vcs and symptom clusters it’s incredible no one believes it until they take it and they say my god well my symptom cluster is gone from eight down to six down to four you’re halfway there we want you down to one have you done a factor analysis of the of the symptoms by any chance yes it was published in 2006 okay okay okay all right all right all right so we’ve covered symptoms now there’s about 40 of them we covered biomarkers what and we we talked a little bit about illnesses that are hypothetically attributable to that but let’s go through that in some more detail what common illnesses now i don’t remember for you if it’s you guys or not but i read a paper here recently while i was doing background research that showed that there’s a much higher risk than in most countries in finland for the development of of elsheimers 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 and that’s produced a statistically significant increase in the rate of elsheimers in in finland was that your work i got that right i’m familiar with that work all i want to do the finnish people to show is that fainting will correct the abnormalities and then create the correct the osmers by the time it gets to the osmers we’re 20 years late we can pick up the difficulties attributed in a4a and tubb1 in als on a congenital basis we can identify that it’s very young ages certainly by the time we’ve got people when when when grandma’s getting trouble with her her cognition we think it’s old age her problems got started when she was 30 and 40 right recognizable then and all the other scott i’ve been manipulating talking too much your turn have you guys ever tried a verbal fluency test by any chance because verbal fluency seems quite susceptible to disruption by there’s certain forms of neurological degeneration that interfere with verbal fluency quite dramatically and it might be a good marker for cognitive for cognitive interference they’re very easy to administer lynn gratton probably from university of maryland published on fisteria the neuro cognitive abnormalities verbal processing was one of the panel they had it was published in the lancet in 1998 we were taking a look at i don’t have your skills but uh she did and those abnormalities were found when you ate neuropsychological testing of patients the the two most common abnormalities that i see are deficits in working and memory deficits in processing speed overall and one of the complaints that we very commonly see is that people are still able to do the functions of their job it just takes them much longer than it used to so what they used to be able to wrap up three or four hours which right i looked at way unproductive and eventually they end up on disability see that’s why verbal fluency might be a real useful marker because it’s a time test right how many words can you write down that begin with the letter s in three minutes and so it’s because it’s a speeded test it might exactly pinpoint that interference with with ongoing process processing say rather than long-term memory or crystallized intelligence so that’s that’s really widespread well that’s why it’s spring to mind well it’s also an unbelievably easy test to administer and there’s wide individual variability and it’d be very interesting to see if that was associated with the genomic markers that you described and maybe we could we could turn to those now and then i want to delve a bit more into you know the we brushed over this very quickly the idea that the symptoms that culminate in alzheimer’s decades later can be detected decades previously i know for example by the way this is another reason the verbal fluency test popped into mind i know there was a study of nuns they looked at their writing samples from when they were in their 20s and they could tell by an analysis of verbal fluency which nuns were most likely to develop alzheimer’s in in old age it’s the longest longitudinal study yeah exactly so another reason verbal fluency might be an interesting marker so okay now and we just so i wanted to go in two directions one direction was okay yeah what is the panoply of neurological degenerative neurological conditions that you think are likely to be associated with sIRS we didn’t have a assumption-based discussion about symptoms and neurological abnormalities that we thought were for sIRS we had recorded executive cognitive function we recorded tremors recorded metallic taste dizziness vertigo tremors but we didn’t have any way of assessing what was going on with the brain we couldn’t measure abnormalities in brain and 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 and by 2015 scott and i had both published papers looking that they were reproducible abnormalities in neuroquant in sIRS patients and with treatment we can fix those but the beauty in 2017 was we could actually fix multi-nuclear atrophy so our treatment was non-specific non-degenerative but instead of just fixing the hippocampus we were fixing hippocampus amygdala and caudate we were fixing paladin we were fixing of the 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 controls so neuroquant early on became of interest but the final change was neuroquant associated with genomics and before we go there i should just mention that there’s there’s a pattern of damage that we see in the brains of people that have chronic inflammatory response syndrome in fact there’s more than one if if you developed your chronic inflammatory response syndrome as a result of water damage buildings we tend to see that the forebrain parenchyma will be swollen we see that or enlarged i should say we’ll see that the critical gray matter will be enlarged and that the caudate nucleus will be atrophic will be smaller if you develop chronic inflammatory response syndrome as a result of of lyme disease and post treatment lyme disease syndrome we see a completely different pattern and and that pattern is that the right thallus is enlarged and that the putamen is is smaller and atrophic and we showed that on two different studies and then in the third study that dr shoemaker and i published together looked at different treatment 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 full values but we didn’t see improvement in in the in the multinuclear atrophy the next paper though did and that was with use of vip basoactive intestinal polypeptide which is a substance that your body makes and is key for um it’s an anti-inflammatory peptide it’s a neuro regulatory peptide that brings your activated immune system back down to normal when it’s appropriate to do that and so with vip therapy which dr shoemaker we have seen caudate nucleus and multinuclear atrophy either stopping or reverting back toward normal have you guys used that same treatment protocol for conditions like alzheimer’s or other degenerative neurological diseases obviously there’s an overlap there which we’ve discussed or hypothetically there’s an overlap there with sers has anybody been looking at the application of this particular treatment protocol to to these degenerative neurological diseases yes we published one study just a few weeks ago but what we didn’t have was looking at people that were untreated or stage one patients compared to stage two which is treating with the first part of the protocol stage three treatment with vip with stage four that’s where we had the off vip and and doing well we had a reduction of the basic mechanism of dieback cns degeneration looking at changes in tub-a4a 44 reduction in three months that’s not been published yet but it’s high on our list but yeah i bet it’s high on your list yeah it’s it’s like we’ve we’ve we’ve we’ve got to get going on this one there are other things that other people are doing or where this is a complex field and not no no one illness parameter will fit and fit everybody but if you’ve got the microtubular dysfunction that we had alluded to with tub-a4a and tub-b1 if you have that as a marker and you have cognitive issues and you use and you respond to vip the reduction is 44 percent and that’s just in three months of work okay so i would like to take this in two directions now and we’ve got about half an hour left in this segment although we can run a little longer if you know if that seems appropriate i want to know about you know what people should do you know what constitutes treatment and so that would be building testing building remediation and then the interventions that you described but i would also like to talk about i know dr shoemaker that you and dr mcmahon have brought this problem to the attention of government officials and i believe particularly in relationship to military housing but not only that so let’s start with everybody who’s listening to this is going to be thinking well i know people who have this cluster of symptoms you know what in the world should i do about it so let’s talk we had our houses mold tested and you know the results were rather dismal and i’m not exactly sure what to do about that because i have properties now that appear to be quite mold saturated and you know the step after that’s not exactly clear one of them was just remodeled and i’m not that inclined to bloody well do the whole thing again you know but that’s partly why i’m investigating this to the degree that i am but what is it what are the steps that people should take in order to determine first of all that they have this problem and then and then in order to do something about it we first need to make sure the patient satisfies the case definition if they don’t satisfy the case definition of the sirs this this doesn’t apply okay but if you satisfy the case definition then we want to define the ecological parameters within the building if the building is water damaged and you should have fungi but doesn’t and you don’t test for actinobacteria you’ve made a mistake but if you don’t have fungi is that because you never had them or is it because it’s overrun with with actinobacteria that are making the dry wall surface alkaline and fungi don’t live very well and then if that’s not the case what about the water saturation with endotoxins because of the three things that cause the greatest amount of damage to the brain endotoxins lead to list specifically for every abnormality that we find in the gene that that shows us the specific causation that’s the building contractor’s word specific causation for endotoxins we’ve identified in neuroquant we’ve also identified in combination with the genie testing or genomic testing so the two go together but then we want to know do you have endotoxins do you have actinobacteria do you have fungi and you can do that on one dust sample collected at home by someone who can put a glove on one hand and wipe the swiffer cloth in one direction over 10 to 30 surfaces that are horizontal above the floor and send that off to a lab that’s reputable there’s license it’s not a fly-by-night insuring and strikes your organization but you there are those that are out there they really are but specifically if we’ve got a reputable lab that shows us the abnormalities you’ve defined the illness parameters you divide the environmental parameters now we divide the treatment do you want to go for treatment scott sure first part of treatment is taking care of the exposures so if you’re living in a home that’s water damaged or uh or if it’s your workplace or maybe a school that you’re attending you need to either fix that or mediate that or or leave that the most important step of any kind of treatment for any kind of immunologic illness is getting away from exposure that is the most important step it’s probably the most difficult step for many people all expensive and it’s it’s mind-bending and and as there is a certain variation in knowledge of this illness amongst physicians there is also a variation in knowledge of this illness of amongst mold testers and mold remediators too 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 but that is the most important step the second step that that we initiate for almost all patients is the use of a binder and there are different kinds of binders dr shoemaker pioneered the use of colostyramine and and colostevalm also known as well call they are very effective and typically we will see improvements within two to three months if you can get that first step taken care of there are a host of other people that will use other what i would consider less effective binders like charcoal and okra pepsin and different kinds of clays and things like that i find in my experience that those work but they take much longer most people would like to get better faster so we use the more aggressive therapy after you go through those two steps and we see that you’re improving usually your vcs test that was previously negative is now positive or is is normal we usually draw some blood work to look at the tests that you had previously that were abnormal and based on which ones continue to be abnormal the rest of the therapy is follows back to she made the what’s called the pyramid and we just go up the pyramid and when we’ve gone through all of those steps and and corrected or attempted to correct the various different systems of inflammation that were still causing abnormalities in the lab test after that we contemplate whether usage of intranasal vip is useful for most patients it is certainly in my experience if you have not recovered at least 70 of your energy 70 of your cognitive ability 70 of of your exercise tolerance if you haven’t recovered those from the rest of the therapy then it’s time for vip instead if you have or haven’t if you have not so i’m anticipating every one of my patients will recover at least 70 and up to 90 percent of their previous previous capability if they can follow the protocol as as i just outlined okay so i’ve been trying this call of styramine and so what i’ve found with it and this is still tentative conclusion on my part but um first to begin with it seemed to make my symptoms quite a bit worse even at a relatively low dose and then i moved the dose up and down for a while and i seemed to find a dose that wasn’t disturbing me so what it was doing to me was producing symptoms of psychomotor slowing so it was harder for me to do things i was thinking more slowly i had more pain especially in the morning more depressive malaise none of which as you obviously know is particularly pleasant and if i decreased the dose enough that went away a week ago i increased the dose again and then those symptoms came back and so why why i know that that’s not uncommon that return of symptom and that that means that the dose should be decreased but that obviously makes treating this even more complicated because when you first start using the binder it can make what’s wrong with you worse so why does the bind what does the binder do and why might it why might it be the case that would make symptoms worse and who would be susceptible particularly to that worsening of symptoms when we have intensification which is the word that i use for people who got worse when they took colostrum we found that pretreatment usually with compounds that would reduce inflammatory responses reduce cytokines pretreatment would say five to seven days and then restarting colostrum at low dose for another five to seven days increase the dose five or seven days at the end of the month you get up to the full full dose of colostrum and you go off the the extra medications omega-3 fatty acids are widely used for this they work very nicely actos was a beautiful drug it’s got an fta black box on it for another reason but that’s still available and as for people that are worse now most commonly when people intensify there are either two problems pre-existing that we would know if we had done the evaluation if you have a multiply antibiotic resistant coagulase negative staph colonizing your nose not infecting your nose not creating symptoms but colonizing your nose and you treat with binders there can be intensification because this organism makes a toxin a polycyclic ether toxin that is released when it’s disturbed in its ecosystem and there’s a binding coefficient looking at other toxins that are bound to a receptor and when you start pulling the toxin off with colostiamine binding it in the gut there will be a response of the receptor to suddenly release all cytokines that are bound and so you frequently will create a cytokine storm now the paradigm illness for this is post-lime syndrome post-lime syndrome if you’ve got Lyme disease and the diagnosis is difficult to prove but specifically you pre-treat with omega-3s for five days start low dose colostiamine and away you go now for other people who don’t have marcons and don’t have Lyme disease we found that paradoxically the last step or vip can be used in low doses micro doses as the first step and this is from a textbook that scott and i wrote on the art and sciences serves medicine it’s called the low vids protein vip protocol and we can start people on that get through the intensification decrease the vip increase the colostiamine or well call and people sail on but they’ve got to be willing to take things slowly and defeat the intensification monster because it is horrible it is absolutely horrible having to experience it myself so what does it mean for people so you know when i’m contemplating this and and contemplating doing something about it i’m wondering well you know what’s the implication here for for travel for visiting other people’s houses i mean i’ll already almost eat nothing which makes me you know an annoying guest in many ways and now you know if i’m sensitive to these sorts of toxins that also means that in principle it’s going to be more difficult for me to travel and to visit people and if you recover if you’re in a clean environment and you recover and you use the treatment protocol that you describe what does that do in terms of people’s you know relative long-term resistance assuming they’re not living in an absolutely mold saturated house if msh levels don’t rise which is the most common situation the susceptibility has not changed because your hla has not changed with low msh if you get it you go somewhere to a hotel or an airplane and you reacquire mark ons because they’re ubiquitous in the environment and the marcon starts to grow you will relapse and recrudesce with your symptoms within three days folks who travel extensively like i used to will be on medications on a prophylactic basis and take them on a regular basis i have a room sanitizer that i use that i use when i travel and i would go to the hotel room and plug that in to clean out the hotel room because whether the kind of heating devices they might have in the corner underneath the window that has some humidity coming out we’re trying to keep up with with heat or the clear cooling system but hotels are notoriously with carpets next to bathrooms and kids playing in the bathroom oh let’s let’s play let’s let’s let’s play hockey and and saturate the rug and you don’t know it was there saturated a week ago and you walk in and it looks fine but you are basically re-exposing yourself it means that you need to manipulate your environment as best you can as your first guess but then you need to take medication on a regular basis fortunately the side effects of low-dose vip are essentially zero so that’s a way you can live as far as a carnivore diet as you reduce the inflammatory result of using veggies and other things that are not carnivore food you will find that vip is your good friend and it will be something helpful to let you expand your diet once you have achieved the maximum medical improvement from the carnivore diet do you think this is a slight sideways move and i won’t pursue it for long but do you think that there’s any association between sers and the obesity epidemic oh my goodness you’re describing leptin resistance leptin is made by gp 130 cytokine receptor in the brain right in the hypothalamus where msh is involved and leptin must bind to its receptor send off a stat one signal to turn on production of pomc pro-opio melanoquartan to make msh so if you’re leptin resistant because of weight problems you don’t turn on msh and so that by itself will turn on fatigue pain and then now obesity and what a triad and a good day a good month a good month for a leptin resistant patient not to mention an insulin resistant patient and one of the msh deficient is half a pound per month that’s not a good day wow wow well okay so so so what do you think about this okay well you know i’ve been reviewing the statistics lately not only with regard to the prevalence of obesity let’s say in the united states but also to its rate of increase and the last projection i read was something like 40 percent of americans will be grossly obese morbidly obese by the year 2030 40 you know and that’s that’s well it’s impossible to overstate what a catastrophe that is that’s half of sers patients if you look at someone who weighs 300 pounds we’re not going to use pedantic terms like morbidly obese yeah yeah yeah yeah specifically when weight’s a problem what’s leptin what are adipocytokines doing what’s insulin doing and more importantly what’s molecular hypometabolism doing because we’ve got a prescription now we’ve been using it that will defeat the mechanisms the physiologic mechanism for weight storage and fat storage we look at the adipocytokines and and brown fat and we wanted to turn on brown fat uncoupling protein one two and three were found it used to be just one but uncoupling one two and three are found we can convert base fat to brown fat and have increased metabolic consumption of energy by turning on brown fat activation this is one of the advantages from finland again here we heat you up and you have a nice sauna and then we tend to let you go out and jump into a snowbank we have yeah without making shivering that turns on brown fat physiology that turns out energy production like crazy is wasting heat non-shivering thermogenesis is what that is okay how many papers have youtube published between you that are related specifically to this topic approximately over 30 okay okay so we can put the two together we’re 60 okay okay so 60 papers all right so you’ve brought your findings to the attention of various government bureaus what has been what has been what have you delivered in terms of reports what has been the consequence of that a whole lot of nothing well i i had the privilege of of speaking before adjuncts of the house of senate art and services committee in december of 2019 and then they made a report the full congress and 16 days later they appropriated 300 million dollars to look into military housing particularly as it as it pertained to uh troop readiness and and suicide in the military and you probably didn’t hear about that because the next day they impeached president trump for the first time and when that news cycle was over we had this little thing called covet and then after that it’s like everybody seems to have forgotten yeah well i i i read big chunks of that report and my conclusion was that the people to whom you presented this report regarded your findings as credible and three like i can’t imagine how you could spend 300 million dollars testing military housing i mean that’s an insane amount of money but but it does indicate regardless of that it does indicate that they took what you were pointing out seriously what did you find in relationship to military housing and what what do you think the consequences of that are for let’s say military readiness and for the mental and physical health of the servicemen the people that that i was meeting with had visited a number of military bases and had seen the military housing so they were already aware of the rad and uh infestations and and the the mold growing on the walls and whatnot i mean they’d seen it with their own eyes what i presented was that this was definitely causing problems with troop readiness even even when the gi is living there and going and and being deployed just being aware that your family is living in that and that your family is getting sick and chronically fatigued and and your children are having cognitive issues and and uh chronic headaches and chronic stomach pains that local pediatricians will usually say are our psychological symptoms because they don’t know what biomarkers to check for if they did they find that somewhere between 80 and 90 percent of those children both with chronic headaches and chronic stomach problems that they really have sers and it’s treatable and it can be reversed very quickly yeah well it’s not it’s not uncommon for the patient’s psychological problems to be a direct consequence of the fact that they’ve been misdiagnosed by a physician you know like i was always extremely loathed in my practice to attribute any serious physiological alterations to psychological condition you know because it just strikes me as highly unlikely and so it’s very easy to assume that if you don’t know how to diagnose something it’s a consequence of the malfunctioning psyche of your of your patient or your client and that’s an easy thing to fall into i don’t want to be cynical about this that’s an easy thing to fall into if it’s also associated with let’s say depression and anxiety because those are pretty non-specific symptoms of most psychological conditions right and and depression which is essentially a pain-like condition and anxiety are very easy to attribute to psychological factors even though they have a profound underlying psychophysiological substrate so you know i can i can feel i can i have some sympathy for the physicians but but it’s all too easy to attribute an illness to someone’s malfunctioning psychological processes this might be particularly relevant with kids i understand dr mcmahon you’ve spent a fair time looking into the problem of sears with children so maybe we could just touch on that briefly yes at this point i’ve seen about a thousand children for that for 28 years i had my own private practice where i worked with a nurse practitioner in the last 10 years i evaluated the children there that had chronic illnesses for sears also and found that again the majority of children that had chronic headaches and and we’re talking 10 million children in the united states alone the majority of those the the large majority they had sears when i evaluated them for that and when i treated them for that their their headaches would either go away or they would become much less severe much less frequent it’s the same with with chronic abdominal pains i was taught in residency and i and i went to a fantastic residency but i was taught that that stomach pains that were recurring in children maybe 10 percent of the time you can make a diagnosis of you know urinary tract infections or constipation or you know maybe there’s some visceral problem with their liver or some other organ in their abdomen but that the majority of times that the children were actually seeking either a primary or a secondary game and that was psychological but what i saw in my patients when i started evaluating them for sears is that about 90 percent outside of that 10 percent so we’re talking closer to 80 81 percent of these patients had four or more biomarkers for sears and then when we treated them their abdominal pains either went away completely or became much less frequent and much less severe so i mean it’s a really fundamental game changer these are two of the most common visits for pediatricians is children with chronic headaches children with chronic abdominal pains there’s another 10 million who have chronic abdominal pains i and then you can also expand that to adults this is the number one reason in my reading for a visit to your primary care physician is chronic stomach pains which are considered functional in most adults they actually have a term functional abdominal pain syndrome and again if you were doing the correct testing looking at the innate immune system again my experience is about 90 of those people with this functional pain will have the biomarkers consistent with the diagnosis of sears and then treatment you know just follows along um doctor shoemaker you you insisted earlier in the discussion that we return to the issue of genomics and and genetic susceptibility and so i don’t feel that we’ve covered that in adequate depth so do you want to expound on that for a moment or two and so for everyone watching and listening so the the causal pathway is an affected building that’s a building affected by water damage that’s increased the probability that that will be problematic is increased if it’s dry walled and that and the dry wall is also sealed or painted with an anti-fungal chemical and then that isn’t sufficient altogether to produce the syndrome you also need a person who’s susceptible and that’s about 25 percent of people and they’re susceptible for a variety of physiological and genetic reasons and so we’re going to delve into the genetic markers for a moment and and the the genomics aspect of that so dr shoemaker you want to take that away when we look at the role of metabolism in this illness it’s it’s been under understudied for years but now it’s risen to the head of the cream of the crop the structure that makes proteins and there’s a million of these in every cell it’s called a ribosome and if you remember your high school biology ribosomes make proteins and mitochondria make energy but the mechanism of protein production comes from RNA copied in off of DNA and traveling from the nucleus into the cytoplasm of the cell and that messenger RNA gives a signal to the ribosome to assemble one amino acid at a time a given protein is coded for by the RNA so a DNA message transcribed to RNA transcribed to RNA makes a protein what happens in chronic fatiguing illnesses is that the structure we call the sarsen ricin loop and it’s getting a little little constant little complicated here it’s present in every living creature every every creature known to god has got a sarsen ricin loop in and at the one point the 15 nucleotide where there’s an adenosine moiety a toxin can cause replacement or elimination of that willing plane adenosine and the loop won’t work so suddenly a million ribosomes losing half a million of this capability won’t make the protein needed for cell functioning and the cell stops functioning normally meanwhile glucose is being driven into the cell by two transporters and their glycolysis or breakdown of glucose a six carbon chain circle or chain excuse me there’s a circular compound is broken into two three carbon fragments in a chain called pyruvate pyruvate must be delivered across an outer membrane of the mitochondria to get into the middle membrane across the inner membrane to get to the cyclo-oxygenase pathway to make energy so if you don’t get pyruvate going into the nucleus you don’t make the 36 ATP or 38 ATP the nucleus can break so Otto Warburg studied this in 1928 in 1955 he finally passed away but he studied cancer and he found that pyruvate was readily available but it was not being metabolized in the mitochondria it was being broken down from pyruvate a three carbon chain into lactic acid a three carbon chain the lactic acid was secreted outside of the gradient into the capillary beds and lactic acidosis became common we see this proliferative physiology and lactic acidosis in 85 percent of our CSRS patients we have ribosomal attack on protein we’ve got lack of proper energy metabolism going on but at the same time in addition to metabolic acidosis well I have lack of a regulatory T cell population thymus derived T cells will have increased gray matter nuclear atrophy we’ll get pulmonary hypertension we’ll get here’s your obesity we’ll get insulin resistance you get five complications of metabolism abnormality and 95 percent of the patients who’ve got molecular hypermetabolism that is prescription for a disaster so we start looking at insulin receptor substrate too that will increase delivery of glucose regardless of what the diet has it involved a lot of people will be on a diet called a keto diet with keto diets they want to make themselves burning fat well if irs2 is increased then that keto doesn’t get into the cell it’ll be turning on uptake of glucose so you’ve wasted the keto function if irs2 is elevated so if you’re going to get a serious about a diet and in the carnivore diet also gives tremendous source of glucose you remember aspartate and glutamate are broke down in glucose very quickly when your energy is low and so that protein wasting goes along with the carnivore diet if irs2 is up and having done a little bit of work with carnivore diet I would just urge people to know what your irs2 is before you stop eating all the carbohydrates but secondarily we start seeing disruptions of apoptosis this is programmed cell death where cells should die normally being the fragments of cells be coated with membrane released into the circulation but not causing inflammation but here in this illness we have apoptosis we have defective apoptosis where the cell is lice without coating of the internal fragments that are antigens so we get now a surge of antigen load in bloodstream with apoptosis in someone who’s got defective apoptosis genes rpk1 we can tell you that and that will create an endogenous source for sers I realize I get a little technical but then look at coagulation factors these genes are upregulated like crazy and they will bind to tau and in tau beta in the brain and then create a micro clot which will lice you know micro bleed and that’s where Alzheimer’s gets its start but it begins with extra coagulation factors cytokines we mentioned the tremendous increase in cytokines we also mentioned there’s a specific causation for endotoxins there are three markers that we use in addition to environmental samples for actinobacteria we use tgfpr1 and 2 that will turn on fibrosis this is a way to tell about the actinohenery and then we look at map kinases that does its own bad things being turned on by by actinobacteria fungi we’ll have apoptosis and then you’ll have the findings in the in the in the brain stem so all of these findings and there’s more honestly there’s this it’s it’s been a two-hour lecture yeah there’s lessons from Jeannie available on his free downloads from surviving world website you just take a look you don’t have to pay a doctor you can just get it read yourself let me ask you let me ask you a question about the is there an association between the genetic markers that interfere with cell apoptosis in the way you described and susceptibility to Alzheimer’s does anyone know that what we have shown is the susceptibility is separate the the cytoskeleton or microtubule genes tub-a4a and dub-b1 that’s the one associated with dieback loss remember every neuron of every eukaryote has got a cell body connected to a series of tubes called an axon the tubes convey ions and nutrients they must get from the cell body down to the end of the road of the axon to the synapse energy demands like crazy you’ve got to maintain a gradient of sodium potassium that costs energy but if the microtubules are disrupted as there are in dieback neuropathy what you will see is loss of this neuron and then the next neuron the next neuron is going on meanwhile coagulation is going on and you’re getting the vascular phenomenon that leads to cognitive impairment they’re both going at the same time and if you don’t have blood supply bringing energy in to an already damaged nervous system it just piles up it is a positive feedback loop of abnormalities in blood flow abnormalities in energy flow abnormalities can be identified in chaining now we were talking about the government i just want to remind you that 2004 john conyers convened a special session of congress uh sharon kramer was the contact person and she’s been a real real fighter on all these years from old rights from old patients and all that she’s the one that first blew the whistle on military housing problems around the norfolk in an energy base and three billion dollars later that those lawsuits have been settled but along the way she jaren also ran blew the whistle and ted kennedy’s hgal committee health education labor committee sent a group of physicians including me down to new orleans to look to see what happened with katrina and rita and they’re most of norleans this is in february 2006 was still underwater and as moldy as can be and fema was doing things but we had a ship the scotia prince was our control group none of these people have been in involved with new orleans in any way but they were there at our our taking controls for the group and we had people being stashed stashed on the boat they were from firemen they’re from children they’re homeless people people from saint bernard parish and i had a case control study i did over the weekend all we did was was symptoms and visual contrast 250 patients and we showed to state markers if you had more than five symptoms you were a case was incredible with that report was released to saint bernard parish on a monday it was taken down on tuesday and that’s the last i’ve heard of it well it’s not surprising as far as i’m concerned because if this problem is as severe and as widespread as you describe then it makes the asbestos problem look trivial by comparison and you know a long time to kill you from asbestos mold just makes you feel like you want to die right yes yes right right well but it’s so unbelievably prevalent and it’s so it i mean you lay out very carefully what the treatment course is but it’s it’s certainly it’s a complicated and life altering process to undergo the diagnosis the house remediation which can be expensive and then the lifestyle and other alterations that would be necessary to bring this under control and if it’s as widespread and severe as you claim it’s no wonder that there’s tremendous resistance let’s speak about that to maybe bring this to a close you guys have been hard at this for quite a long time and you said some 60 papers published which is quite a substantial that’s for everyone watching and listening that’s about the equivalent of 20 phd thesis by the way so you can get a phd thesis essentially for three publications it’s a lot of work and what sort of response have you had from the from the from the broad medical community like how is your how is your work being received do people know this or do they are you on the fringe and outer edges of what’s regarded as acceptable medicine how have you been received there is a derogatory term that is and still widespread use i have done a study about emergency room physicians called a patient they would see with multiple symptoms called a gomer yeah get out of my emergency room yeah it says people take time and when you have a health care system that gives you 10 or 15 minutes to see a patient in primary care facilities and you’ve got someone who needs two hours of time who’s going to lose the two hour patient or the 10 minute patient and who’s going to go without care so i think it’s a systemic approach not an individual approach i think our health care system has some of the best physicians in the world but i’m biased because i have seen this in action for 40 years but specifically when we look to see who’s doing the caring it’s the primary care doctors the specialists there’s a hand in the waiting room there’s there’s there’s a heart in the in the cath lab but that’s a person with a hand that’s a person with a heart that’s a person with a brain let’s look at what the fundamental unit of care has got to be it’s a person scott and i spent all day long two hour visits and listened to people and i had one rheumatologist give me a hard time at university washington in seattle i sent a patient in from quarterline who needed to have a tgf beta one done because he had uh juvenile rheumatoid arthritis was going blind and tgf beta one was the cause of it and he goes well i’ve never heard of a tgf beta one this is years ago and being a smart ass i said there’s only 75 000 papers published on tgf beta one i would not admit that you didn’t know any of them in public if i were you well right needless to say he got the teachers beta one the child can see now but the point is it’s hard to read everything we’re asking you to be an expert in endocrinology an expert in metabolism an expert in cardiology an expert in pulmonology we want you to be an expert in pre-renalazotemia and pots and pans we want you to do all of it all day long yeah yeah well when i was first introduced to this by my daughter i thought i started to read it and i thought oh my god you know it’s going to take me two years just to get on top of this conceptually to figure out well first of all if it’s credible information and second of all to really understand how i would possibly reorganize my life to deal with it so it’s really a it’s a major but on the other hand you know a long-term prognosis of chronic depression and immunological trouble plus alzheimer sounds like a pretty dismal way to conduct you know conduct life so um you always have to read right well right well right and i’ve already discovered some things about you know how how immunological systems work i mean i’ve been struck to the core by how effective this carnivore diet has been for so many people it’s and i would have never i would have never believed that you know 20 years ago that the probability that like just the very idea that people could live on nothing but meat would have struck me as like outright preposterous and that it was the actual that food sensitivity was the cause of so much immunological suffering or at least a cause also struck me as highly improbable but you know here we are it does seem to be the case and certainly the body of data that you guys have accumulated the studies you’ve done they’re difficult to once you go through them they’re very difficult to just shunt away and ignore and i really think that’s too bad because i would have just assumed shunted them away and ignored them if i had my druthers is there anything that we haven’t covered in this two-hour presentation now i i wanted to ask you the textbook that you said that was um art and science of sirs treatment medicine art and science of sirs medicine okay so that’s where medical practitioners can learn about this what’s the best source for just general public people i know my daughter’s put up a big website about sirs related disorders um and we’ll put that in the in the uh links but what where should people go online to gather more information about this there are two sites from scott scott one sirs x surviving moles another one scott tell us about sirs x well i was going to say the two places where the most knowledge the most uh trusting no trusted knowledge is the most uh literature the most videos about this are either from dr shoemaker’s www.survivingmold or sirs x c i r s x.com then you go to those two places you can find just about anything you need including a local provider who would know something about this if you think that you have this illness okay okay those two places are fairly exhaustive and complementary okay dr mcmahon is there anything that you would like to bring to the attention of people who are watching and listening before as everybody watching and listening knows we’re going to do another half an hour with these two gentlemen behind the daily world plus platform but before we turn to that dr mcmahon is there anything else that you would like to bring to the attention of the people who are watching and listening there’s really just one other part of the pathophysiology that we didn’t discuss and that is the blood brain barrier most people including myself when i was going through medical schools thought of an artery that carries blood as being like a garden hose the blood enters one end and it comes out the other but it turns out that actually the cells that make up the lining of blood vessels is pretty porous and small proteins and fluid can flow outside of the blood vessels and into the body where the cells are the cells don’t seem to mind that maybe they get a little extra snack and in addition you’ve got the lymph system to clean that up but the brain is much more sensitive tissue and the brain doesn’t want all those potential chemicals and possibly toxins oozing into it so by five days of life the brain has sent cells to intercalate into the those arteries that are feeding the brain and create