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Eric Gordon, MD is President of Gordon Medical Research Center and clinical director of Gordon Medical Associates which specializes in complex chronic illness. In addition to being in clinical practice for over 40 years, Dr. Gordon is engaged in clinical research focused on bringing together leading international medical researchers and... Read More
Ritchie Shoemaker, MD, specializes in mold-triggered illnesses, in particular Chronic Inflammatory Response Syndrome acquired following exposure to the interior environment of Water-Damaged Buildings (CIRS-WDB). He is located in Pocomoke City, MD on the Eastern Shore in Maryland. Read More
Eric Gordon, M.D.
Yeah, so welcome, welcome back. This is another edition of Mycotoxins and Chronic Illness, and my pleasure to continue a conversation with Dr. Ritchie Shoemaker. For those of you who don’t know, Dr. Shoemaker is the pioneer in mycotoxin illness, but especially in the areas of water damage and just chronic inflammatory response syndrome. I mean, he is the man who coined the term, and he’s the man who has developed the treatment tools that we all use every day, and someone who I have learned from, and continuing to learn quite a bit. He has developed, with the help of Jimmy Ryan, a PhD scientist, he has been working on the GENIE test. And we talked about that at length our first episode, we’re gonna talk just a few more minutes about it, because I wanna talk a little bit about, touch upon COVID, hypocoagulation, and then a few minutes on glucose. And then we’ll talk a little bit about and wrap up talking about water damaged buildings and what is it in them that may be causing our problems.
So, Ritch, COVID. I mean, I said I’ve had not much experience with COVID patients, I guess, thankfully, though I do feel like I’ve been left out, but when I did see a handful and I got blood work on them within the first week of either symptoms or exposure or positive tests, and I was very impressed with how elevated their D-dimers were and their ferritins right off the bat. I mean, in some of these people, their D-dimers were, you know, not high enough to get a hospital excited. They were only like two times normal or three times normal, but they were essentially asymptomatic. And so to me, it looked like, perhaps a lot of long-term COVID symptoms are because of these maybe initially silent microemboli or micro-thrombotic events. And I was wondering what your take is on that and if you’ve seen anything that correlates with that, looking at COVID patients and the GENIE test.
Ritchie Shoemaker, M.D.
I’m looking at a graph or a table, excuse me, that is in our new paper, on post-COVID syndrome. And there I asked the question is post-COVID syndrome, really just a CIRS, and as far as multiple markers, it is a CIRS.
Eric Gordon, M.D.
I think so.
Ritchie Shoemaker, M.D.
We look at our percentage of control patients who have coagulation abnormalities and gene upregulation, 5%. That’s not zero, but it’s not 10% either. In our full-blown CIRS people, water damaged buildings, 54%. So big difference cases versus controls, but interestingly other people who had COVID and six weeks later did not have symptoms impairing activities, daily life, the coagulation abnormalities was 14%.
Eric Gordon, M.D.
Okay, little bit.
Ritchie Shoemaker, M.D.
The people that did have impairment of their daily life, 36%. So the p-value is less than 0.0, 0.0, ah! 0.4. So it’s not as good as we want. 36 versus 14 sounds impressive. We had mentioned the null hypothesis, but it’s not enough to show that the COAG is the main problem that we see in COVID, compared to CIRS where it’s much more dramatic.
Eric Gordon, M.D.
Right, okay. Well, I said that was a very small end of mine and just an observation, but–
Ritchie Shoemaker, M.D.
Should also look at illness patients. I’m looking at people six weeks after their COVID is over, after they’ve had a negative test, they feel well enough to do, go back to work. But yet, if you’re well enough to work and don’t have impairment activities in daily life and you had COVID, you still have COAG abnormalities 14% of the time, that’s not a small number, it’s a lot. So when we look at what Jimmy showed in 2016, with cytokine elevation and COAG elevation in our CIRS patients, yes, 54 is more than 36, but our control patients were five and the control patients here was 14. The control patients were a flawed group, for example symptoms, control patients out of 37 symptoms, 2.7 is the mean, we’ve published that, CIRS 22.3, that’s a lot, published that, but PCS negative people were not, they weren’t back to work, what have you, 8.2 symptoms compared to cases of PCS positive, 18.2. Now that was significant at 0.013, 18 versus 8.
Eric Gordon, M.D.
Yeah. So just to remind people is PC is post-COVID and PCS is the post-COVID syndrome, just so they know who we’re talking about.
Ritchie Shoemaker, M.D.
Thank you.
Eric Gordon, M.D.
Yeah. And so this is what I, what we’ll see over time, I hope it doesn’t happen, but those people with the 14% with the abnormalities in the coagulation pathway, what happens when they then walk into a water damaged building?
Ritchie Shoemaker, M.D.
The point is, is that we’re likely to find in our PCS negative group, 14% reactivity, but we end up here with 56% of those with full blown illness and 87.5% had precise, specific causation. We were really looking now at a landscape approach. What happens to a COVID patient who walks into a wet building and stays there. You stay more than two days, you’re gonna have some normality. The turbulent enclosure that I mentioned is 66% in CIRS patients, less than 5% of controls. That’s probably pretty dramatic, but in PCS positive cases, 50%. Wow.
Eric Gordon, M.D.
Wow.
Ritchie Shoemaker, M.D.
50% have got problems. But then we say, well, that says, there’s gonna be a lot of proliferative physiology. Yeah, I’m saving the best for last. If we have zero in our control patients, 0% have molecular hypermetabolism and 85% of untreated CIRS patients that are treatment naive have molecular hypermetabolism. Now how about PCS negative? Do you think they’ll have a low number of molecular hypermetabolism?
Eric Gordon, M.D.
I would hope so, but I have a feeling the answer is no.
Ritchie Shoemaker, M.D.
The answer is zero.
Eric Gordon, M.D.
Oh really.
Ritchie Shoemaker, M.D.
I thought it might be near 10, but how about the PCS positive? What percent of our 14 patients, this is a small study, had PCS positive and hypometabolism? 100%.
Eric Gordon, M.D.
Wow, okay. So these people, yeah, these are your patients. I mean, that’s been my feeling from as soon as post-COVID hit. I mean, it’s like, you know, it’s chronic fatigue all over again. And to me, chronic fatigue is the same thing as chronic inflammatory response syndrome, with different flavors sometimes, but pretty close, so.
Ritchie Shoemaker, M.D.
What was surprising, it goes back in with the PCS positive versus PCS negative for CD3D defective antigen presentation, 86% of PCS positive patients had suppression at CD3D, 86%. In our CIRS patients, we had 96%, look at that. PCS negative, still 14% defective antigen presentation. And we’re telling every one of those patients to get a COVID vaccine.
Eric Gordon, M.D.
Let’s see what happens. Do they, have you checked? Do they develop titers or you don’t know?
Ritchie Shoemaker, M.D.
No one’s doing titers that I know of.
Eric Gordon, M.D.
Yeah, it’d be interesting, or T-cell activation tests and see, so do you require, yeah, okay. I won’t go into that now, but this is amazing. And you know, I mean, there’s so much money. So what, the NIH is gonna spend $1.5 billion or something on post-COVID syndrome. Do you think I’ll throw you a few pennies?
Ritchie Shoemaker, M.D.
That’s the number I got, but still, if they spent the 1.5 doing some GENIE testing, they would know as fast as I did that doing what they’ve been doing is just wrong headed. And yet you can’t tell the NIH because it’s not invented here, it means they didn’t think of it. So who knows what that means?
Eric Gordon, M.D.
Yeah, yeah no, that that’s really a shame.
Ritchie Shoemaker, M.D.
Why don’t have decent answers? ‘Cause people are protecting their turf.
Eric Gordon, M.D.
Yeah, well, and many times, if people don’t understand, you know, like they only know their turf. I mean, that is always the problem with the NIH is that, when you bring something new to them, they don’t know what it is, you know? So they just judge, it’s the old story. If I didn’t hear of it, it can’t possibly be true. I mean, we see this in medicine all the time, and it’s just, until I heard about it from the person who I know knows something, but the problem I always say with experts in chronic diseases, myself included, is that we’re often expert in what doesn’t work. ‘Cause if we knew what worked, we wouldn’t have chronic diseases, we’d have treated them. Anyway, so talk a little bit, I just want a few minutes about glucose control. ‘Cause you know, blood sugar, well, insulin, I mean really to my mind is the bigger issue. Tell me a little bit about what you’ve been finding about insulin and control of insulin production and how it affects the fat cells, and yeah, metabolism .
Ritchie Shoemaker, M.D.
In the metabolism paper that was published in September of 2020, we to go through that in some detail, it’s a free download from Surviving Mold website, in your spare time, maybe you can take a quick read. It’s the densest–
Eric Gordon, M.D.
We do, of course.
Ritchie Shoemaker, M.D.
Jargon-filled paper I’ve ever written in my life. But having said all that, what was interesting is that the problem with proliferative physiology is it’s bad for people with molecular hypermetabolism. But the problem with proliferative physiology is truncated tremendously if you don’t have MHM. And what I mean by that is that if you are not breaking down pyruvate in the mitochondria, which are delivering glucose into the cell, what will happen is some of the glucose is diverted as it’s metabolized into the biosynthetic pathway that’s designed to treat and create the availability for cells to divide. Look at the mucus membranes we have in our body. How often do those cells get replaced? Well, if there’s one on one corner and one on another corner and another on another corner, that’s four corners. One of the cell’ll be replaced every four days. And how come our mucus membranes don’t fall apart? Because apoptosis is proceeding along nice and beautifully.
But if you have apoptosis, you’ve got to be making another mucus membrane cell. You’ve got to have proliferative physiology to a certain extent. So if you look at N-Acetylglucosamine, it is able to bring about ubiquitination and phosphorylation and all these different changes in proteins, including proteins that are involved with insulin resistance and fat cells. It’s not in monocytes, it’s not in anywhere else, it’s in fat cells, but that situation is now giving rise to our ability to measure genes that are found in white blood cells, OTA and OTG. If you want to have the insulin resistance, turn on OTA, if you don’t wanna insulin resistance, turn on OTG, and all these different mechanisms the cell has that we can access. And if we can diagnose it and show the abnormalities, then we will be able to create gene solutions that we haven’t had for obesity and diabetes type II.
Eric Gordon, M.D.
Hmm. Yeah, this makes me real, I mean, just one of the things you said about, you know, how often we see either a failure to turn on or off apoptosis in, I mean, we always think of it in terms of cancers, but my God, almost every, you know, just even things like osteoarthritis and degenerative tissue disease of all kinds. We’re failing to turn it on or turn it off, keeping it in balanced, balance seems to be the key.
Ritchie Shoemaker, M.D.
I had a lady yesterday that I had not talked to for nearly 39 years, and her husband has passed away. And so she’s been kind of doing other things, but her problem is osteoporosis, and she’s taking some Prolia or some drug advertised on TV, a shot every six weeks. But then the question is, where did the osteoporosis come from? And I said, “Have you had your TGF beta 1 measured?” “No, what’s that?” Well TGF beta 1 turns off osteoblasts and turns on osteoclasts.
Eric Gordon, M.D.
That’ll do it.
Ritchie Shoemaker, M.D.
So if you wanna rot your bone, she’s gonna have a hip surgery done ’cause of osteoporosis, she just had a lumbar spine fusion with rods put in six weeks ago, and your shoulders are falling apart and rotator cuff problems, and this actually is kind of a malignant form of osteoporosis and they could be using Calcimar, and it turns out that she was gonna have her TGF beta 1, it’s probably gonna be 20,000.
Eric Gordon, M.D.
Wow, wow.
Ritchie Shoemaker, M.D.
Inflammatory response syndrome and how to treat that? I’m gonna be able to help her with the IPA through Prozar.
Eric Gordon, M.D.
Yup. You know, it’s just, I mean, I think that’s another course in itself for you to, I don’t know if you’ve done this one or not, but just all the places in medicine where we should be thinking, which is basically everywhere. CIRS is happening.
Ritchie Shoemaker, M.D.
The review article in JAMA that not too long ago, maybe six months, time’s going by fast, but it was “COVID: The View from Cardiology.” “COVID: The View from Urology,” “COVID: The View from Pulmonology,” a bunch of ologies, and every single one was something that my docs take care of every single day .
Eric Gordon, M.D.
Yeah, no, this is what we see and this is what we treat, but since these are patients who’ve always had normal blood counts, conventional medicine has usually ignored them until they get to the point where their system is broken and then they can give something else to suppress it. Anyway, so yeah, so fat and glucose and glucose metabolism is just such a huge issue, I mean, that was something that you talked about early, early on in your career.
Ritchie Shoemaker, M.D.
One thing is thinking about is that if it’s a good thing for proliferative physiology to have the biosynthetic pathway active, that’s gonna be necessary, if you’ve got pyruvate reduced entry into the mitochondria, if pyrubate is increased in the entry to mitochondria, then we don’t need the biosynthetic pathway at all, but that’s not the only way that insulin gives us trouble. IRS II, Insulin Receptor Substrate II, opens glucose channel I, gluc I, and glucose channel IV, gluc IV. These solute pathways let glucose increase entry to the cell through wide open pores in its cell membrane. But the other mechanism where it really has to do with water-damaged buildings and insulin resistance has to do with insulin bound to an insulin receptor on the cell surface, holding onto a glucose in the hot little hands, that grouping, that moiety of three different structures is engulfed, pinocytosis or endocytosis, whatever you wanna say.
And that little bubble will come into the cell where it’ll stay a bubble, keeping insulin away from being recycled until that bubble is acidified. And if the cell pumps hydrogen into that bubble, the bubble will open up, release glucose for metabolism, release the receptor, be recycled, release insulin receptor, the insulin to be recycled. But what if there is monensin or valanimycin present in that cell, they’re actinomycin compounds. They work by preventing acidification of that vesicle. So if you don’t acidify the vesicle, you don’t release, you don’t recycle insulin, insulin receptors. So what happens is that with normal blood glucose, you are insulin resistant.
Eric Gordon, M.D.
Right, okay.
Ritchie Shoemaker, M.D.
That was big back in the 80s back when they put monensin in chicken feed. I used to laugh at people who had weight loss desires. They would go on diets, they’d eliminate red meat, but they still would eat each chicken. So they’re guaranteed when they eat the chicken, to eat monensin, 100 milligrams per ton in chicken feed, that’s a lot, and you go through the bunch of tons of chicken feed, and that monensin in nanomolar amounts will hurt you. They’re actually creating more insulin resistance by eating chicken than they were by eating fatty beef.
Eric Gordon, M.D.
Wow. That is no longer being used in chicken feed?
Ritchie Shoemaker, M.D.
No, no, hardly at all. Well, they switched over to using inoculations and vaccinations, and someone’s gonna be upset about vaccinations, but that also has taken a toll because now we don’t have monensin killing eimeria, which is an apicomplexan parasite that kills little chickens and little pigs. We also have in avian cells, the sarcocystis being a problem, And we’re seeing an explosion of BCI, IgG, and IgM positive tests that are false positive because they’re not killing eimeria with an antibiotic like monensin.
Eric Gordon, M.D.
Oh, okay . We can’t wait, it’s interesting. So yeah, acidifying those makes me start thinking about, I won’t go there . We used to use Plaquenil to do that in the old days when we use, actually, we still do sometimes, when we use the macrolide antibiotics. I wonder if it has the same effect, that would be an interesting thought. So getting back to, I said the real heart of the matter for a lot of our listeners is the, you know, everyone has focused really on mycotoxins, and you know, your recent papers and your work the last years has been that, wait a minute, it’s water-damaged buildings. It’s these Actinomyces species that are producing the chronic inflammatory response syndrome. And the problem that most of our patients are having, just real quickly. How did that metamorphosis happen? How did you see, how did you realize what was going on?
Ritchie Shoemaker, M.D.
The expression we’ve used a couple of times today is that we go as far as science lets us, and the newer diagnostic techniques that are either the basis for new insights into causation of these illnesses is something we didn’t have four or five years ago. So we are told and taught and being in our head that mycotoxins were pro-inflammatory. And then if you had exposure of instilled mycotoxins into test animals, usually a rat or a mouse, there’ll be this surge of inflammatory responses, and then rats did poorly and they died. If they had done those same studies in pigs, they would have seen even more efficacy of mycotoxins killing things.
The Chinese were able to show that, that pigs are the most sensitive mammal to the effects of mycotoxins. But if they supplement it with glutamine, that the mycotoxin toxicity disappeared. So I think in the normal American diet about eight ounces approaching a day, how many milligrams of glutamine are there that we’re eating? At least five milligrams a day. And who gets mycotoxin toxicity is primarily, the papers say, this is a horrible thing, but starving horses in Russia, or people were getting aflatoxin in Africa. And what do the people look like who get aflatoxin in Africa, they’ve got bloated stomached and they’ve got their protein . If we give them five milligrams a day of glutamine, then the mycotoxin toxicity clears up.
Eric Gordon, M.D.
Wow, and have you tried that clinically?
Ritchie Shoemaker, M.D.
I have everybody getting extra protein. It works.
Eric Gordon, M.D.
Okay . And right, but yet we’re still seeing–
Ritchie Shoemaker, M.D.
Let me just continue.
Eric Gordon, M.D.
Yeah sure, please go.
Ritchie Shoemaker, M.D.
Issue was still dominant despite the Chinese finding about glutamine and protein deficiency creating a problem. But when we finally started finding that actinos were present hugely in buildings, and it turns out that literature started in 2010, it was not a new literature. But when I wrote “Surviving Mold” in 2005, correction, wrote “Mold Wars” in 2005, we didn’t have the information about actions. We certainly didn’t know about endotoxins. And in 2010, when I wrote “Surviving Mold,” we’re just starting to barely see that remediation by ways we’ve approached it for years didn’t work, mycotoxins would be removed, but people still would stay sick. What was left was actinos. You would knock down some of their substance, but not much. Actinos are different than mycotoxins. Actinos like an alkaline environment, but they also like company for being sitting there by themselves on a piece of drywall.
They release a compound, a fair amount, if you will, called trimethylamine or TMA. And you know about other kinds of trimethylamine, oxide compound in smelly fish and histamine release and all that. But specifically TMA will attract other actinos, other bacterial species, to grow a pseudopod, a fake leg, so to speak, that let them rise up and explore, they can cross over glass membranes that are barriers. They’ve traveled great distances to join to their friend who releases TMA. TMA released locally creates an alkaline environment. Do mycotoxins grow well in alkaline environments? No, but what you have is actinos that you can’t see versus mycotoxins, mold you can see lot of the time, but actinos you can’t. But what are there is the species diversity of 16 plus, showing the TMA is active. Now if TMA is active, then the mycotoxins are involved in secondary metabolism, making ribotoxins like crazy. They also turn on compounds that turn on TGF beta 1 signaling devices. Oh my God, these organisms make every antibiotic know to man and every biochemical known to man, but they also turn on TGF beta 1. And what TGF beta 1 does is then create the precise, specific causation of the presence of actinos. So, I mean–
Eric Gordon, M.D.
Big circle.
Ritchie Shoemaker, M.D.
What we’re doing is using the physiology and growth phases of actinos to answer questions of why are they so common in buildings? Why do they hurt people so much? Why do they cause so much pulmonary fibrosis? Well, there you are. TGF beta 1 signaling mechanisms involve turning on some of the exact same genes that insulin does. So if insulin is developing resistance, how come we’re not seeing resistant TGF beta 1 signaling? Well, maybe we are, fascinating.
Eric Gordon, M.D.
Yeah, I mean, you know, another conversation, someday, is just the whole, I mean, TGF beta 1 is one of those fascinating molecules. It does so many different things. It’s milieu dependent, it’s just amazing.
Ritchie Shoemaker, M.D.
ability to send T regulatory cells in the tissue that’s inflamed at will. And if the tissue has retinoic acid receptor, that signal will change the T-reg cell into a T effector cell, it’s called plasticity. And the plasticized T effector cell releases more TGF beta 1 to send more T-reg cells to their death and conversion, so what do we get? Rising TGF beta 1 and lowering T-reg cells. As I said, we can start measuring that with GENIE now. And TH17 will follow from rising TGF beta 1 and T-reg deficiency will give an increased quotient to TH17 over T-reg cells. What happens? Various cardiovascular, acute coronary syndromes, acute aneurysm syndromes like crazy. And the days are coming because of the proteomics of TH17, T-reg imbalance look like CIRS, but it’s not CIRS, they don’t have the same mechanisms. They don’t have the same proteomics necessarily. They certainly don’t have, they have a group of the same symptoms, but they’re not the same thing. So as we learn more about CIRS, we’re learning more about lookalikes and the ability to manipulate T regulatory cells has got to be something we go to in the future.
Eric Gordon, M.D.
Yeah, no, I mean, I think you said it in the beginning of our first conversation of regulation, lack of regulation, lack of regulation, lack of regulation, of lack of regulation, and yeah, your immune dysregulation to me is where I get these chronic illnesses all have in common, is you’ve got inflammation that should be transitory, and is not, I mean, if we can get it to go, you know, it’s what keeps us alive. If we can turn it on and turn it off.
Ritchie Shoemaker, M.D.
There’s an analogy from biology, just to throw in, just for the sake of discussion. And that is the toxin anti-toxin system, perhaps you’ve heard of those, there were 6,000 different species of bacteria that will use a toxin to survive intracellular life or a stressed life. And then they can turn on an antitoxin to block their toxins and to stop the hibernation or torpor. Now one of your papers with Bob Naviaux had a summary about dauer, you and Neil had something to do with that paper, but what you had was dauer, which you were describing as an aerobic glycolysis. It’s not, it’s an anaerobic glycolysis. So a fundamental mechanism because dauer does not do the same things that hypermetabolism does. You’re talking about dauer, and dauer is not the same as what we’re talking about.
Eric Gordon, M.D.
Right, well, I think it’s just stages, I think that that is the point is that, I think what Bob was referring by, the hypometabolism, but he was, I think, fully aware of and interested in the area you’re talking about… ‘Cause with the aerobic metabolism, aerobic hypometabolism is what he describes very clearly.
Ritchie Shoemaker, M.D.
He didn’t talk about DNA at all in his paper, I don’t think.
Eric Gordon, M.D.
No, no, no, he wasn’t talking, but he was looking at it from metabolites. And I said, that’s something that you two, I think it would be a great conversation, in that it will shed a lot of light on other fields. But I think at the end of the day, it’s one of those chicken or the egg conversations.
Ritchie Shoemaker, M.D.
I’m not so sure.
Eric Gordon, M.D.
Well, it’s, you know, whether the metabolite is the primary, is the first signal or the change in in gene transcription is the first signal. It’s like, they both signal each other. So it’s really hard to, you know, like you need them both.
Ritchie Shoemaker, M.D.
Bob could control for translocations and control for VDAC, that would make a big difference because those are two external factors that were not discussed that have a great deal to do with entering pyruvate into the mitochondria.
Eric Gordon, M.D.
Right, but I mean, he’s just saying it’s the mitochondria sensing the difference in the pyruvate levels, amongst other things, that then get the mitochondria to change their shape and change their function. And we’ll get you into that hypo, what?
Ritchie Shoemaker, M.D.
Involving nuclear-encoded mitochondrial genes.
Eric Gordon, M.D.
Yeah, that’s what I’m saying. It’s like you’re saying, it is the chicken or the egg, which came first, and you know, I think what would interest me is not so much which came first, but how each one will illuminate the other is because we might find things that we can modulate through the metabolites and ways that we can also realize with your model is know which level to be addressing, because you’re looking at–
Ritchie Shoemaker, M.D.
All he needs to do is to fix translocations and VDAC. And I think his worries will go away.
Eric Gordon, M.D.
Well, the question is how to go about doing that, is how to restore cellular regulation. That is the question. VIP is one of those ways that that obviously does it, we’re using a lot more other peptides. The thing that’s interesting is, you know, VIP is one of those peptides that actually has genetic control, direct genetic control. A lot of the peptides that we’re using clinically now are probably more derivatives of albumin and other proteins. So, I mean, that’s what makes VIP so interesting, is that it’s got direct genetic control.
Ritchie Shoemaker, M.D.
Right.
Eric Gordon, M.D.
But my point is that I just think it’s the chicken or the egg and the real issue is what’s gonna give us the ability to modulate the system. I mean, for Bob’s world, you know, he’s looking to control, to modulate the ATP receptors or the purinergic receptors, and just give the cell a time-out, a chance to return back to a more normal physiology. But I’d like to leave that conversation for the two of you. I think you’d be much deeper, and you know, I think you’d both, you’d both see things .
Ritchie Shoemaker, M.D.
To finish up, I just wanted to share a couple of words about the future.
Eric Gordon, M.D.
Yes.
Ritchie Shoemaker, M.D.
We’ve been in this business for a long time. This is my 25th year. And I think you were probably do in chronic fatigue before I was in 1996, I started, and I’ve seen a lot of ideas come and go, and at one time, I had kept track of Paul Chaini’s ideas. And when there was 12 references to what was the new guy on the block, and XMRV was–
Eric Gordon, M.D.
Oh, Judy.
Ritchie Shoemaker, M.D.
Yeah, I mean, it was just one, but there was one after another.
Eric Gordon, M.D.
Yeah.
Ritchie Shoemaker, M.D.
And the constancy in my approach has still been to avoid exposure and remember that we are mutating organisms inside water-damaged buildings constantly. So we heard a lot about mutations and variants for COVID, I think they call ’em variants ’cause they don’t wanna alarm people by saying mutations, but we are creating monsters in our indoor environment by the chemicals we use, we saw what Benomyl and substituted Benzimidazole would do to bacterial resistance and mutation. We’re doing that with Fungiconazol as well, which is a Benomyl congener. It’s wrong-headed so that as long as we’re gonna have concern about human health I think we need to have concern about environmental health.
That means that physicians need to be more aware of what’s going on in the environment compared to what they do and what they don’t do. So that as we go forward, I think it’s gonna be important to expand the training, not only of the patient population, but of the medical population to know what the difference is. And not just say pesticides. We come up with mechanisms for insecticides and herbicides and fungicides. Those are three main classes, and patients should be demanding that physicians who are involved in giving them chronic care have a broader, more landscape approach to what environmental illness really means.
Eric Gordon, M.D.
Oh, absolutely, absolutely. And I think that’s where, you know, I think the naturopaths have been leading the way, trying to for years, you know, Lyn Patrick, and, you know, before her, Crinnion, who just unfortunately passed away a few years ago, really trying to get that knowledge out there and getting people to ask and environmental history, really, really where you live, what you’re exposed to, what’s in your kitchen cabinets, what are you cleaning with? What are you using for the common household things? I mean, this is an area that, yes, I think by and large physicians have, they just, you know, haven’t paid attention, if the FDA says you can sell it, they assume that it’s safe. And I think we can really see the results of that. It has not bode well, I mean, on some level, I believe that that’s why, the level of these chronic diseases has skyrocketed, you know, and also the autoimmune diseases. I mean, we just didn’t see these, back in the 70s and 80s, we just didn’t see this level of autoimmune diseases. I mean it just, and sick kids.
Ritchie Shoemaker, M.D.
And I’m not willing to concede that point. I think that the mechanism of awareness in society has changed. For example, the word gomer was one I heard a lot of in medical school–
Eric Gordon, M.D.
Oh, sure .
Ritchie Shoemaker, M.D.
Who was a gomer? Gomer was someone who had 25 symptoms and nothing was wrong that they could find in standard measurements, and gomer stands for get out of my emergency room. So the medical profession as a whole is acting with this sense of arrogance in terms of illnesses they don’t understand and creating examples one after another with psychiatric diagnosis when they just didn’t know what objective parameters were real. That’s where GENIE is coming in and making a big difference. GENIE II will make more of a difference. This is gonna be the way the future. When people in the medical practice and medical profession are involved in learning and resistant to learning new things, then we really have trouble, ’cause there’s something new coming out of the woods every single day.
Eric Gordon, M.D.
Yeah, oh, absolutely. But I’m hopeful because we have a lot of young physicians who are excited and really wanna learn new things. I’m always a little less optimistic because we have a system that is now run by accountants and doctors are no longer running the show, you know, accountants and lawyers are running medicine, and many doctors who have taken on administrative functions often think the same way as the accountants and lawyers do with how to minimize risks rather than how to optimize therapies for people.
Ritchie Shoemaker, M.D.
So on that note, my friend, I’ve got to move along.
Eric Gordon, M.D.
Yes. A pleasure to talk with you. I’m looking forward to seeing you soon. I’m gonna make sure I sign up for your training. I think you’re gonna do a short one for people. Was it June 4th for doctors?
Ritchie Shoemaker, M.D.
That’s right. So that’s the next big event for Surviving Mold. You can get information attending Friday afternoon. There’s gonna be some really good things, Jimmy’s gonna present the GENIE II, I’m gonna to present the PCS paper. We’ve got a host of other good speakers. It’ll be quick, it’ll be factual. It will be your data-driven, opinions nah, sorry. If you don’t have data, it doesn’t mean very much.
Eric Gordon, M.D.
Anyways, thank you again. I really appreciate your work. It’s been something that has changed my life and the life of my patients, so thank you very much, Rich.
Ritchie Shoemaker, M.D.
Take care Eric, bye.
Eric Gordon, M.D.
Okay, bye-bye.
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