Brain Fog, Fatigue & No Answers? This Doctor Found the Missing Link (Part 1)

Foreign.

Listeners, it's Lori and Kelly here. As always, today's episode is a little bit different. We've been anticipating this for such a long time. This discussion brings both depth and the science and heart of healing into focus.

We are so honored, truly honored, aren't we? To welcome Dr. Richie Shoemaker to the Synergy podcast today. If you have been touched by chronic fatigue, brain fog, unexplained illness, or you're a practitioner who feels overwhelmed navigating complex care plans, this episode is for you.

Yeah. Dr. Shoemaker has been a pioneer in the world of biotoxic illness, Chronic Inflammatory Response syndrome, for a long time, long before most of the medical community even had a language for these conditions. He didn't just name the problem, he built a pathway out. And his protocol has helped providers like myself and Lori bring hope and answers to patients who felt unseen, unheard, and unwell for far too long.

Way too long. I want to invite you to listen to this episode with an open mind and a posture of respect. The content may feel dense. In fact, it's going to feel dense. I'm just going to say it, but stay with us. Please stay with us. What you're going to hear could completely change how you understand fatigue, mold, illness, and the root causes of many complex fatiguing conditions.

Dr. Shoemaker continues to push forward, refining, researching, and expanding the science behind what we know now as Chronic Inflammatory Response Syndrome, or sirs. His commitment to truth and healing is unmatched, and I know you'll walk away with both insight and inspiration. So grab a notebook, take a deep breath, join us for a long conversation that just might reframe everything you thought you knew about chronic illness and disease.

So before digging into this podcast that you're gonna absolutely love, we felt like it was really, really important to kind of talk about some of the definitions around Chronic Inflammatory Response syndrome and just give you a little bit of context and knowledge around that so that you're prepared to listen.

Yeah, the conversation with Dr. Shoemaker is very technical. And so we just thought it would be a good idea to talk about, just globally, someone that's showing up with or if you're experiencing chronic fatigue, illnesses, or an illness that kind of comes, and then you may relent and have a few good days, and then you're back where you were and you think you're making progress and you're not really sure. So complex chronic illnesses that just are not fully resolving, oftentimes that falls into a category of Chronic Inflammatory Response syndrome.

Also known as sirs.

C I R S. Yeah, Sirs, it's very similar to someone that's in the ICU struggling with systemic inflammation, sepsis. It's a very similar biochemistry that happens internally. It's just in a slower motion. And so it looks very similar on lab work, although their expression may look more chronic. And so I give it the analogy. It's like you're standing in 65 mile an hour winds every day with inflammation being hit, hit, hit. And it really, it's your response to that hit is going to be dictated by your foundation. How well have you built your foundation, how resilient are you? And then what else is driving inflammation in your body at that time? And then you may have times where you dip over or you tump over or whatever. So it's like a waxing and waning condition for a lot of patients. And so oftentimes we either think you're sick or you're well. And in this condition that's not always the case. And it can be really confusing for you, it can be confusing for your family because there are times where you're performing and you're doing well and everything looks great and then the very next day things are not so well. And it's like, how do I explain that I don't think anything changed overnight? Right. And so as we dig into this conversation with Dr. Shoemaker, we want you to have those things in mind. His work to validate this condition and to bring structured testing that we can do that's reliable and reproducible is so important to giving validity to this diagnosis. And so even though the conversation gets really, really technical, it's important that you hear it, it's important that your family hear it and have some understanding of where did this come from. Because for you, maybe you just heard about chronic inflammatory response today or yesterday or last week, but he's been working on this case definition, as you'll hear today, for many, many decades. So this didn't just happen out of nowhere.

And sirs, honestly, I think it's really important for everyone to understand is that it can't just be put in a box. It is a very multi symptom, multi system condition. So it's complex. And most of the time if you've walked through this, maybe you don't know that you've walked through it yet. You have a myriad of symptoms that has led you to be dismissed. You've had multiple times that you've gone maybe to the ER or gone to doctor's offices and you didn't get an answer, and you were waiting for a diagnosis. And what we're going to talk about today is that it's not just waiting on the diagnosis necessarily, necessarily. It's understanding causation to that because it's complex, it's difficult. And also, most providers of care are not trained to do this. And so it wasn't that they. That they purposely dismissed you. It wasn't because they wanted to not help you. They may not have the tools in their toolbox to help you. And so we want you to walk away from today's podcast feeling hope, feeling encouraged to know that these providers of care do exist and that it's been an evolution of knowledge building over time. We're still learning as each other have experienced it ourselves. We've walked out this condition and continue to walk this out and are learning every day. But as a result of that, many providers of care have not necessarily been trained to, number one, recognize it and for sure treat it.

Yeah. And we want you to leave today with some resources. Right. Dr. Shoemaker has a website that he developed called survivingmold.com there's a lot of information on that website regarding Chronic Inflammatory Response Syndrome. You can find links to a lot of the research that's been done that supports this diagnosis, and you can also find a map of providers that treat this diagnosis. And I think that's really important. Depending on where you are, it's always best to have someone in your community that you can see face to face. But there are practices because there aren't always providers in your state that can treat this also remotely. So lean in. We are going to break this podcast up into segments, probably two segments, if I had to guess. And so just know there will be several parts, at least part one and part two to this podcast series. And the first part is going to be really technical. And so I want you prepared for that. I think it's important we did that for a reason. I just feel like that that needs some validity here. We needed the space for that and really to honor Dr. Shoemaker and all the work that he done and continues to do for this community. So dig in and we can't wait to hear what you think about this. Okay, before we get started, Lori is going to read Dr. Shoemaker's bio. And we cannot possibly sum up his bio in 45 seconds, but Lori is going to do her best. We will put in the show notes, his full bio, because I do think it's important to understand everything that he's been able to do.

Dr. Richie Shoemaker is a nationally recognized physician and researcher known for pioneering work in the biotoxin related illness, particularly chronic inflammatory response syndrome. Since 1997, he's helped uncover toxins from molds, bacteria, and other environmental sources and sources that trigger these complex chronic conditions, often misdiagnosed as fatigue, fibromyalgia, or autoimmune disease. With a foundation in rigorous science and patient advocacy, Dr. Shoemaker has published extensively, he's advised lawmakers, and he continues to lead in clinical care and education, transforming lives by revealing what others have overlooked. We welcome Dr. Richie Shoemaker, and we're.

Just so thrilled to have him. So if you've been struggling with chronic fatigue, a chronic illness that you just can't figure out, or if you're a healthcare provider who treats patients with chronic illness and are struggling to get to root cause, this podcast is for you. I strongly recommend that you get a notebook and a pen and maybe listen to this two or three times. I know I'm going to go back and listen again. We're just so honored, Dr. Shoemaker, to have you here.

Well, it's absolutely my pleasure to be speaking to such beautiful ladies. My goodness gracious, I am blessed for sure.

So can you tell us what got you interested in chronic illness? I mean, I want to go into the history of chronic inflammatory response syndrome and your role in kind of mapping this out in the way of diagnosis and treatment. But what got you interested in this?

When I was in medical school at Duke and graduated in 1977, seems like a long time ago, but it was a long time ago. I had wanted to be a rural primary care physician and there's one other freak like that besides me and medical school class. But when I got time to say the oath of Hippocrates, the Duke has a ceremony and the Duke Chapel and all that, I said, I'm not going to go there. Apollo is the God that we say the oath of photography to. So I went to Delphi to say my oath in the temple of Apollo. It was kind of, it's a cloudy, misty day and the ride up from Athens was kind of rocky and queasy and I was glad to have some motion sickness pills, but God walked up on, onto the, the floor of the temple and it was just cloudy. And then I said, well, this, this is not right. So I'll just go walking around. And so we see what the oracle was supposed to be doing and where the games had been and sometimes passed. And, you know, the bus was going back to Athens, leaving at 5:00 and 4:30, nothing had happened. And you know, I was sure that something was going to happen, some sign. So I went back down the hill and walked out onto the floor of the temple. And just then the clouds parted in a shaft of light. Came down, I'm not kidding, you came down from the sky, hit me right in the eyes and I said, this is my sign. So I said my oath. And it was goosebumpy day and still is goosebumpy for me. But dedication of me to my craft was something that I wanted to be prepared for. And I had thought that the best physicians that were graduating from medical school should be in the areas of least available care. So I had done National Service Corps and was going to be in a medically underserved area. But this was, this was really special to be, you know, there's only one physician for 30 miles. And when things started getting a little funny about chronic fatigue syndrome, 1984, Paul Chaney and Dan Peterson had made their discovery of being in the right place in the right time. And 1985, CDC got involved and said, well, it's, it's not Epstein Barr virus, but we don't know what it is. And you know, I didn't know what it is, but started looking at it and reading about it and tried creatine and did this and that. And it was like, oh, well, you know, I'm just a regular family practice doctor. 1995, fast forward. Something strange started happening coming out of Nank's Head and the Outer Banks that people were seeing fish kills. And what was killing the fish was a dinoflagel, this little algae like creature called Pfiesteria. And the state was adamant, nobody's made sick by Pfiesteria can kill the fish, but it won't harm. Fish are safe to eat and it's safe to come down and be a tourist. Don't worry about it. Well, in 1995 we started seeing the first inklings that we had Pfiesteria, just, you know, two hours by car north from, from, from Nangstead. And, and sure enough, there is occasional fish kills. And people that work on the water are called watermen because they catch crabs and oysters. Got to say oysters, right? It's not oysters, oysters, but, and, and fish. And they started saying things. The fish were looking funny. And I started looking and said, well, this is strange. What's going on? 1996, people are getting sick and the fish kills are getting more common. What's going on? And 1990 was really a big deal. And I started seeing some people who were sick and politically incorrect like I usually am. I just said, well, I got sick people. No, you don't. No, you don't. You're just some wacko and hysteria. Hysteria. Nobody believed it. And everybody said the water was safe, and it's just a little extra nutrient enrichment in the water. Well, the water nutrient measurements that were done were no different than the last 20 years. And this was not nutrient enrichment. And what could be going on? Well, about that time, there's news that tobacco plants in North Carolina and tomato plantations along the Chesapeake Bay were having an outbreak of a new fungus called blue mold. And it was resistant to all standard fungicides. So we had two water events. We. We had fungicide use. We had hysteria. We had sick people. And I started looking at it and started doing autopsies in fish to see what I could figure out. And, you know, these. These are my friends. These. These are. These are my patients. But I'd see them in Walmart and, hey, how you doing? And, you know, saying, jack Howard, what's. What's with that rash that you got? And, well, it's just. It's all that hysteria. Well, nobody believed him, but I believed them and started looking around. And sure enough, I ended up having six patients all coming in one day with the same story. And the third patient had terrible secretory diarrhea. And she had the same memory problems and fatigue and cough and shortness of breath and muscle aches, not real joint legs. It wasn't arthritis, but knee surgery. But I said, well, I can't fix the rest of this, but I can fix the secretory diarrhea that's having bowel movements without having had something to eat. And here's your cholestyramine. We in the woods always know about stopping secretory diarrhea. And sure enough, the next day, Sleepy says, well, thank you. I had a good night's sleep. Didn't have to wake up going through the bathroom three or four times. And I said, well, that's great. And she goes, you know, but what's strange is my memory's better. I said, what? He remembers better. Yeah, my cough's gone. Well, how's your energy? Well, you got up, and I walked two miles this morning. I said, wait a minute. So, I mean, Kelly, what would you do? Would you have started treating other patients without a database with cholestyramine?

Right. Yeah. I mean, you think about. I mean, you're a curious provider. You're a compassionate provider. You're seeing something happen that you haven't seen happen before. And it was a tool that you used off label that worked, right?

So, yeah, well, I called around and nobody else was seeing anything. And just, you know, well, I'll just try some cold starting. Five patients in a row were better. I wrote them up later on for publication in the fall. But, you know, this was a big deal. The Baltimore media were here, the DC Media were here. We had all kinds of people coming over. They wanted to know. And, you know, the state of Maryland had the Secretary of Health, Marty Wasserman's daughter had gone to Duke, and we hit it off for a little while, but he said, there's nothing wrong. I'll go swimming with Pokemon. I said, I will too. He goes, well, I forgot my bathing suit, but maybe next time.

So, Dr. Schumacher, I want to stop right there though, because you did bring up a good point about providers trying things that they really don't know if it's going to work. We know it's not going to harm, but is it going to help? But you took the time not only to do that, but also to write these cases up and to get attention to what was really going on, like what was causing the problem. Not just quietly treating, hoping that things got better. Right. I mean, there's, there's. I mean, you're, you're a hero for that, in my opinion, because without you doing that, we wouldn't be where we are today.

Well, I actually, I think that's true.

Yeah.

You know, it didn't take too long before the State of Maryland said, well, we'll hold a, a meeting of bringing all of all the stakeholders. You can tell they're bureaucrats. Stakeholders. How about people? You know, but anyway, and we'll, we'll put an end to all this nonsense and that, that fellow from Pokemon, we'll just let him go quietly out the Western front. Well, there was a big fish kill the day before, and I had one of my friends, Bob Hughey's photographer, and he took pictures of sick people and lesions and all this stuff and developed them. And I had 8 by 10 color glossies walking in that meeting. And I tell you, I bro that meeting up. Everybody saying, well, the heck with the state. What's this guy got? Oh, look at that. Look at that.

Well, you know, disruption is necessary to make change.

Would you. I mean, we'd agree with that, right?

Well, yeah, for sure. Anyway, sure enough, the state of Maryland decided they would, they would, they would have their experts from Hopkins and University of Maryland to come down and show everybody that I was wrong, that there was nothing wrong at all. But as you can imagine, the politicians couldn't agree which university they're going to come from, so they decided they would do both. And I had written everything up and they came down and held a clinic. And the end of the day they go, holy God, we see what he sees.

Right?

And that was the lid of the kettle bouncing off. And it wasn't too long before I had 200 patients treated with cold siame. And just about all of them got better. Some didn't. But how come some people though would be recreating in the Williams Point area and out of 10 people that are swimming that day, all in the same water, the same, same lesion, fish, seven of them were sick and three weren't.

So that comes in the HLA typing, right? The genotype that makes people more susceptible.

That's exactly right. I had no biomarkers, I had nothing to go on. I had exposure, I had symptoms. There's a ton of symptoms. It took a while to do a history. Good gracious, 20 some symptoms as an average. And I had response to colostyramine. I had three things. Well, later on, here comes news of a fellow from North Carolina. Ken Hodnell was a neurotoxicologist for the U.S. ePA Research by national Health Environmental Effects Research Lab. And he had done a test I never heard of called visual contra sensitivity in, in, in people from, from North Carolina who exposed to, to fish kills and it showed an abnormality. And I said, oh, what is it? What is this? Found Debbie, got his number. Debbie is such a good person. She's been working for me for 43 years.

And I love Debbie, I love Debbie. I just reach out to Debbie, she takes care of me.

Yeah, we all need people like Debbie in our lives.

Well if, if, if I could clone her and then distribute her to the mold community, we would have.

Right, so you connected the dots with the visual contrast screening and this was before the Internet was a thing, guys. Yeah, that's also part of the story that I think sometimes we miss because we're so used to being able to just do Google searches and PubMed searches and you know, we didn't have. You didn't have any of those easy access tools. Yeah. To get to.

Well, sure enough, Ken told me how to use it and I bought the little device and talked to Stereo Optical who made it and I said, well this is fun. And because I could show that the people who had this illness, this biotoxin illness is all I knew to call it neurotoxic mediated illness. If I gave them cholestyramine, the defect in VCS went away. And VCS was normal. But people, if they're normal, most of them were employees of the Department of Environment, State of Maryland. They would go back in because they had a job. They get sick again. And the visual contrast test got bad again and I gave him cholestyramine and it got better again. And I said, oh, this is Koch's postulates. My goodness, this is great.

So Dr. Shoemaker, can you go into the visual contrast screening? Because a lot of our audience won't know what that is and how to access that test. And that's something that you can do.

From home if you think about an edge in vision. Contrast is the ability to see an edge. So you could have a white background against a black symbol in the front. Well, that's the extreme contrast we use for measuring visual acuity. The Snellen test. Back then there was a big to do worldwide. US fighter planes had flown low over a ski resort in Italy and clipped the cables of the gondola and people were killed and they came there as court martial and everything. But they were let off because the gray light and the gray cable could not be distinguished. You couldn't see the contrast was zero. And what Hudnell's test started at full contrast in row one and then A, B, C all the way down through nine gradations. They decreased the contrast by 0.3 log units as you went from left to right or left the near frequency to higher frequencies. And we could come up with a point, we could see the point of extinction where you couldn't see contrast anymore. And that was an endpoint. So that was, that was fun. And this is a little card. You put it in front of 18 inches in front of your eyes and you cover one eye and takes five minutes to do. And it's not a fancy technology thing, but it turns out to be very sophisticated in what it is. And the people from Stereo Optical said, we've talked to the Heidelberg engineering folks and you can borrow their dual laser Doppler for about six weeks and see what you can find about people with visual contrast that's abnormal. And then visual contrast is normal. Well, I mean me and computers, if you listen, Debbie can do this stuff. But anyway, they sent down an expert and showed me how to do it and I could focus in on the retina, just these pretty pictures you see in the retina. But there was the optic nerve head coming out of the brain. And the neural rim was as this thin little area that I was looking at the brain. Oh, man, is that cool. So anyway, the velocity of flow of red blood cells was reduced markedly in the retina, in the neural rim of the optic nerve head. In people who are sick, it improved when they were better. It took a day to see improvement, a week to see resolution, and this. And then Carnell was a big wheel with epa. He wrote it up. Now come on and get credit for Ken. He says, you will on your time. Anyway, so by this time, it's February of 1998. So I wrote up, I already written the illness diagnosis, I wrote up treatment. And the phone started going nuts. And here people from the St. Lucie river in Florida, they had a. Outbreak of lesion fish. And I went down there and Cryptoperidiniopsis, I still remember how to pronounce that word, was there. And what happened is that when Lake Okeechobee, 28 miles in diameter level rose with hurricane water and all this other stuff. It's the dam is what it is. And they were worried that if they don't vent some of the water through to the St. Lucie, there'll be a problem with flooding and dam break and all that. But as soon as the water hit lock 73 and 74, coming all the way from Okeechobee and you know about Okeechobee, probably been in vacation there. But here's this, this very wealthy community, a steward and in St. Lucie started getting sick and fish got lesions and all this stuff. And I said visual contrast. I had symptoms, I had exposure, I cholestyramine, but I didn't have the fact I now had two dinoflagellate species. And darn. If the fellow from Woods Hole, Donald Anderson, calls up and he goes, I've got people with ciguatera, they're still sick. See what you can do with them. Well, if you had acute ciguatera, which you get from eating, eating fish with lesions and they grow on the reef and also this stuff, you can get a dinoflagellate illness and get all the same things, symptoms, vcs, responsive treatment, but the chronic people didn't get better. I'm going, well, how come acute is different than chronic? And meanwhile I got a call from someone with, with blue green algae problems. And like Eustace and Dora and Harris and Griffin and Apopka, I mean, the chain of lakes, all the water flows north into the, into the St. John river and then out into the Atlantic Ocean in Jacksonville, but they just had all the same things. And you could see people driving on over the bridges over the St. John's river in Jacksonville and the water looked muddy, blue, green. I'm driving over this is going to make me sick and exposed to this. Well, it turned out we published a paper later on that it did make people sick and that was very unpopular in Florida. They kept the lid on, on red tide pretty well, but they couldn't keep the riddle on blue green algae. So anyway, but, so I'm still in Kelly, just like you said. I was worried about it, I couldn't figure out why. And it was, was eating at me. And there's something about this that said, you know, I, I can read more. And I was reading about where the Dinoflagellus will bloom and we started doing GPS data points and doing sampling of poor water. Improve that in where the, the fish kills were in the emergent vegetation of, of the, the marshes and all this stuff in the estuary. We could predict where the outbreak was going to be. And copper was there. It's a number one EPVA biocide. And copper was used and put into chicken feed. And chicken feed would run off the farms and into the river and the copper would precipitate into poor water. If you've ever a kid and you had a mud pie and you squeezed it, all this water comes out. That's poor water. That's the water between the particles of the mud pie. Well, in that was copper. And when he got stirred up in a rain event, that's when you got the kills. That's when we would have problems with Pfiesteria changing his life form because the cryptomonads of Hysteria likes to eat were being killed by copper in the runoff. So then I said, wait a minute, what if hysteria changes into a life form for feeding and breeding? It's, it's moving fast. How can, how come we get blooms? Well, you know, the issue is that the Pfiesteria life form was being eaten in the feeding, breeding fast by rotifers. So we had a bloom situation set up with a one, two punch. And what killed the rotifers were dithiocarbonates, the fungicide that's 25 years old, never been used or worked on blood milk. So suddenly I had the causative agents that I could measure. And here comes Florida. Florida with the Southwest Water Management District. Top quality science. Good gracious. They measured diethylcarbonates, they measured fungicides in the St. Lucie River. I said, oh, here it is. So I came up with a copper theory and boy I really got criticized for that. I used to say my back didn't bleed anymore. It's been carved up so many times, it's all scar tissue.

You didn't know you were going to need to become a marine biologist as you're, as a physician. Right. Trying to piece all this together.

I was, I was saying that the other, the experts were wrong. Yeah, I said the politicians were wrong. They said well look at all the pile of chicken manure. That's the problem. It's, it's nutrients. Same as the Gulf of Mexico. Well they made the sacred Gulf of Mexico. Yeah, but then I got a call, the guy was, was sick. He had symptoms. Yeah, he did visual contrast sensitivity that was positive. But he hadn't been to Florida, he wasn't in the St. Lucie river, it wasn't the Pilk Mc River. All he had was this black stuff growing in a mold and roof leaked. And I said well let me, let me just see what I could find. So I did a tape lift and got stachy buttress and so whoa, look at this. Well I said let's, let's try you. Well he got better but when he been back into his house he got sick again. Well he's got to have all these other things coming back again. But he didn't get better as well the second time. Well, something's going on. And meanwhile then I'm reading about msh, Melanocyte stimulating hormone. It's a regulatory neuropeptide. I got hla, the immune response genes. He had the right hla, I'm looking at msh. Called up the FDA and said look, I've got all these people with hysteria, can't we use MSH with them? Because the US was going to use MSH in some of its battles with Sadomas in Kuwait because it's an anti inflammatory neuropeptide which treats inflammation, treats circadian rhythms and all this good stuff.

So Dr. Shoemaker, what year was that when MSH was a thing as far as using MSH as a peptide?

It would be given to, it was in the process darpa, the Defense Research Program association was ready to use msh. But the FDA next it they said you haven't done the, the toxicology studies, you haven't done the rat studies, you haven't done primate studies. When you do that, after you spend $5 million and we'll talk to you. I didn't just have $5 million to spend on, on MSH. And so James Lipton called me up and he was the master of msh. He and Anna Catania, they were going private. He says, do you want my DARPA grant? I said, oh, yeah, yeah, I want my darpa. DARPA grant. And the DARPA just. People just kind of laughed. Me says, sure you do. So have a nice day. Bye. Bye. But I had now mold problems. And now I started getting phone calls with people with mold, right. And gave cold styrene and found out that some people didn't get better. And meanwhile, I'm reading about what will grow in low MSA situation were Marcons, multi antibiotic resistant coagulation, negative staphylocation. And I said, well, let's see if we can find those. And bingo. We came up with Dennis Case and I figured out how to kill the Marcons. And we killed them with big spray. We couldn't use that anymore later on because there's all the folks that use pests, use fungicides and ruin the danger, the ability to. We're killing Markhans as it was. But anyway, we found Marcons could be eradicated with a spray, with nasal spray. And that helped fix the people that weren't much better. So that was, that was good. Then I still found more people that were still sick and they had the same things. And meanwhile I'm finding other, other markers. And MMP9 was a cytokine. It's a measure of all the other cytokines that are pro inflammatory compounds. And MMP9 was, was the marker. And I found that I could fix that with cholestyramine. And MMP9 was, was the next marker. VEGF was the next marker. And I'm suddenly getting this, this whole pattern, this systemic illness with multiple symptoms is being driven by inflammation. And inflammation was not just you scratch your knee and then you got a little red line and maybe a little bit of swelling. That's the information we learned about. This is from innate immune responses. And TNF was discovered in 1985. And this is now, you know, 2000. Is TNF a role in this? Yes, TNF was a role in this. This was just really exciting. So I started trying to put it together and people would come for a visit and I had nice table paper and I was drawing out all the lines and arrows. Well, this does this and this does this. And finally one guy was sophisticated with computers. He goes, you need something better than your scribbles on a piece of paper. He made me a little card biotoxic pathway in 2004, and boy, was that a hit because it had everything all there and all these other things and meanwhile other people calling me and we're trying to do things. Hudnail and I were writing papers like crazy. We had one paper that was made grand rounds of environmental medicine on the National Institute of Environmental Health Sciences and EHP environmental report. I got to be the main guy for grand rounds. Then they had their meeting because we had done a double blinded placebo controlled trial. I mean, you've got to do things, right. That got published. But this was held in Stone Mountain and they had, you know, a nice dinner set up and a buffet line for people and they had a big pile of grouper and looked beautiful. I said, I'm not eating that. Fella says, why aren't you eating the grouper? I said, dinoflagellus? Are you kidding me? A secretary carrier? What are you talking about? He said, well, I, I don't think too much of you and I'm gonn Grouper and a bunch more had their group or two. The next day I had all these people stopping me in the hallway. How do you fix the sibo terra, by the way? Don't, don't tell anybody. You're asking. I'm asking you. But you know, we know you're a kook. And I said, well, I'm not going to tell you.

How ironic, right, that they would serve grouper at an event like that. That's crazy.

Patient got sick and fortunately acute illness with secretary gets better real quickly.

But I just, I kind of want to just stop for a minute and go back and just first of all, thank you for the, just obviously a relentless amount of opposition in your journey to. And your, your just dedication, ongoing persistence to keep going, looking at data, hearing and listening and modifying and looking for answers and like we just lack that. Overall, I believe in our medical community and you have been such a pioneer and a beacon of light for those that definitely need to continue this on.

Right.

But just listening to you, I can only imagine the opposition. I can only imagine what you faced in criticism. I mean, you make light of it, but. And I love, you know what you.

Said about your back, right.

Like that was such a true. But I can only imagine what you endured through all of that.

Well, it wasn't all fun and games. The key issue is I knew I was right. People that criticized me couldn't even spell cat twice. Right. You know, I said, I'm not going to give up for that.

Yeah.

My wife is supportive and in 2002 I had enough of a practice that I said, I'm going to stop being a family practice doctor. I'm going to be a biotoxin doctor. And my wife, who got breast cancer and passed away, bless her heart, but she said, are you sure you're going to make a living like this? I said, oh, yeah, it'll work. And it did. But that's when I would come to work in the morning and look to see what the computer had spat out as far as labs from the night before, because it was. HLA was one of the first ones in MSH and MMP9 and VEGF and C3A and C4A and all this stuff. We started with no biomarkers. And at the conference, the SIRS X conference, where I talked about your case a little bit because you had given me permission, and one of the slides actually didn't fit on one slide. We now have 64 reproducibly reliable biomarkers for Sergioma. 64. And I'm looking at chronic fatigue syndrome. One of the things that kind of got me started thinking this way. How many biomarkers do we have for chronic fatigue? None. How about fibromyalgia? I had great fun with them. None. I got 64. How many y' all got?

So let's go back. I want to really dig into the HLA because you brought it up a couple of times how 7 people can be in the water or 10 people can be in the water and, you know, only three or four get sick. Right? So what is that about? And you, you kind of stumbled upon the HLA typing. When did. How did that come about? And then let's go through the types, not individually, but just kind of globally.

Well, I read a lot and I never heard of hla. I saw a paper on HLA and I said, well, what's this? The immune response genes on chromosome 6. You know, you learn about ankylosing spondylitis with HLA B27. And HLA's got some things, and HLA C's got some things, and Hla Doctor's got some things. Oh, my DRB one. You know, I started seeing that the people who had a given HLA were the sick ones and they weren't the same. The mold patients weren't the same as the dinoflagellate patients. They weren't the same as the blue green algae patients. They sure weren't the same as the Ly Lyme patients. And, you know, the line was another story because I thought, well, if I've got The biomarkers are all positive, and I give cholestye. I mean, we can put up with. With the constipation. I mean, that's how I discovered use of it. But, you know, nausea and vomiting and all this other stuff. But the. The line people, when they took it, they got slammed. Their visual contrast sensitivity. I said, well, what. What does that show? Maybe that's got something to show. That showed a fall in column E followed by a fall in column D. Like clockwork, a day to day. When the fall and D MMP9 was released, I was. I was bringing on this. This. This cytokine storm.

So you're saying cola in. In the Lyme positive patient, untreated Lyme cholestarmine made them worse. Is that what you're saying?

Yeah. And I call it intensification. It's not a Herxheimer. It's intensifying. But I was able to show it's coming from a toxin.

Right.

I said, well, if it's coming from a toxin, I should be able to prevent the intensification by stabilizing the pool of cytokines before we give them colostyramine. So I use actose, which is fabulous drug. It was given a bad reputation, and then that was proved to be bogus. And you can get lactose to use it, but we use Omega 3s now without arguing about the politics. But I said, this should work. So I took five days of actors follow my no amylose diet. And I used to do weight loss. And the diet book was. I must have sold 100 copies. So I thought I could retire on that. But no, Amy's diet is fantastic. Yeah. Oh, you didn't reach out yet? Okay. Yeah. The issue was that I could give them a drug safely. It would block the intensification. And it blocked the intensification. It was blocking cytokines. So working backwards, did I block cytokines? Yes. I stabilized MMP9. And people with Lyme could take that and sail through. Well, Lyme's pretty controversial. And, you know, I got tired of some of the people that I met in ILS and just said, no, I don't. I'll do something different. I had gotten contacted by GlaxoSmithKline, and they wanted me to look at people who had Lyme and Babesia co infection. And so I said, well, that's. That's good. I. I got plenty of patients with Lyman Babesia. Well, it took 300 patients for me to find 30 that actually did have Babesia. People were doing different things. And, you know, Andy Spielen was my co worker. He was the chairman of tropical medicine at Harvard. He says, you know, do the thick films, the right stains. You know, you can see the Babesia mirazoids showing in bright red in red blood cells and every red blood cell that's, that's that Babesia in it will hemolyze so that haptoglobins will rise and bind hemoglobin. So haptic hypoglobins will be low and free urinary hemoglobin will be marker. We had those three markers for Babesia. We got our 30 patients and we used cholestyramine and the drug that GlaxoSmithKline was making. And we were able to show that Babesia makes a GPI toxin. Glycerophosphoenidotoacetal and malaria makes it. Other ap chemplexans make it. Toxoplasmosis makes it. I, Maria makes this Babesia in little chickens and pigs and then Sarcocystis in birds. And so if you do, if you think you've got Babesia and you do a test with an ELISA aspect to it, all you're going to look at is false positives coming from sarcocystis and toxoplasmosis and malaria and all that. And I married, I married is fascinating. It will kill little chickens. And here on the Eastern shore, while chicken farming is a big industry and more in the center of the country is a lot bigger chicken farms. But if you've got him area, it'll kill the chicken. So if you've got I Maria, you need to worry about, you can kill the Imeria with a polycyclic ether toxin called Monensa. And every ton of chicken feed had 100 milligrams of Monenson in it. So all these people were worried about chicken, they're worried about beef and cholesterol. And they started, I'll eat chicken and I'll eat pork, knowing they were eating my Maria first. Then they were eating Monenson. Monensin will take sugar coming out through glucose transfer proteins 1 and 4 and getting into the endosome and fused with the endosome. And that endosome, if it's acidified, will release glucose and the glute in the insulin receptor and insulin into the cytoplasm and then insulin will be recycled back to the cell membrane and all that. But if you didn't acidify the endosome, you didn't get, you didn't get release of insulin and glucose and all this other stuff. You functionally were developing insulin resistance by keeping it in the endosome, the cell. Well, it's like, oh my. So now we, we know that's one of the big deals because I hadn't forgotten that, that this is 1986. We're doing that work on moments. And flipping forward to 2016. Jimmy Ryan, who's absolutely brilliant, a cell biologist, to beat all cell biologists. We were doing next generation sequencing of, of human genome, trying to see what genes were going on, right. And you know, here we, we come along and we find out that the genes that are involved most with this illness are ones that are, are MRNA that affect ribosomes. And if ribosome protein production is, is compromised and, and it is, then people are making drugs, they're not making proteins at all. And then there's 37 genes left in the, in the, in the mitochondria. And those mitochondrial genes, they could be doing good things. Well, they weren't. And it turns out we're able to show is that pyruvate was blocked from entering into mitochondria. If pyruvate was not blocked or the entry didn't go across the, the outer membrane got sequestered in the outer membrane side, it didn't get into the mitochondrial matrix. ATPase and cyclooxygenase didn't make ATP out of this and people would be tired. But it took 16, no, it took 20 years before Jimmy discovered that this gene basis was one that I had been working on for 20 years and didn't find the holy, holy grail. And Jimmy found it and we started looking at a smaller number of genes because 50,000 genes was too much, it was too expensive. Nobody would pay for a test. We couldn't handle that much. We didn't have the computer capacity to do that. So we found 2,000 genes that were upregulated, that looked like they were inflammatory and metabolic in nature. Picked 200 out of there. And we have now what we have genie. But the beginnings of GENIE started with an observation of a polycyclic ether of the dinoflagellate toxin. So what goes around comes around. And all that reading I'd done, a multidisciplinary reading, now has paid off because now we can see that there are drugs that will work for people with these mitochondrial gene problems and, and ribosomal gene problems. And if we gave them vip, we'd get them better. Unless they couldn't take vip.

Yes, that's where my story is hindered. Right. And the reason why we need ongoing research and ongoing efforts and why I'm so enamored by the persistence that you have exhibited over the course of. Of, you know, your career in pursuit of that. Right. VIP is amazing. VIP works. But there are people that can't do vip.

This talk.

Yes. Brainstorm. Yes.

Yeah, that's you.

Yeah.

And I presented your case, and I. I wanted people. I've had 10,000 patients on VIP. It's the last step of my 12 step protocol. And I had six dropouts, and you. You made. You made seven. The other lady, the other people that were dropouts. So I had them take their gallbladder out, and they did fine. And you still got your gallbladder.

No, I had my gallbladder out. I did all the things. I did all the things.

Did anybody call you from that conference? Just. Just.

Yes, yes. Dr. Doinger reached out, and we're. We're connecting and we're gonna pursue other things. And so I can't wait to have that consult with him. I have not. Have not had it yet. But to back up, you've said a few things that I want to make sure our audience really understands. Number one, we have a community called SRS X. And that's an ongoing community of providers treating SIRS, and it encompasses remediators. So part of Dr. Shoemaker's protocol, step one is removing from exposure whatever that exposure is. Right. So our remediators are extremely important in creating a safe environment for people to have an opportunity to recover and repair from water damage and chronic inflammatory response syndrome. The second part is we have providers there and all multidisciplinary providers. So physicians, we have nurse practitioners, PAs, psychologists, psychiatrists, you know, the gamut of people really walking alongside of patients because oftentimes it does take a village to heal and repair. This is a chronic condition that there is hope for recovery. And I live a very full life. I mean, despite the challenges that I've had, I am living a very full life. And I owe that to you guys, because without the work that you've done, that would not be possible for me. I think I would be in a wheelchair today if it weren't for the work that you've done. Because at the onset of my diagnosis, I was very neurologically impaired. And so I lead a very, I would say, normal life in spite of a chronic condition because of that. And so these guys are true warriors out there doing the work, listening to patients, you know, really hearing what they're saying. And, you know, I Didn't get dismissed because I'm one of the six patients that can't tolerate VIP on your list. It's just more to come. Right.

And it's also raising the standard of care, too. Like, collectively, it requires a village to train to bring back what we're seeing in clinical practice. Because to your point, you know what, what we read in the books isn't typically what is happening in clinical practice.

Right.

So there has to be that collective place where people can come together.

So, yeah, And I want to tell a story, too. It's not a very flattering story, but I think it's a story that other providers need to hear. When I was first introduced to the HLA genotype responsible for chronic inflammatory response syndrome, it was through a 4M. They hosted a genetic course that Lori and I took in Vegas. And it was a long, long, tedious, if you can imagine, going through all of the different genotypes course. And we had had a full morning, we had had break. We had an afternoon session and then another break break. And we came back from that break and there were some other providers sitting there talking about what was to come in the next talk. And I don't remember who was presenting the next talk. I really don't remember. But they were telling us about the dreaded gene and how these patients were just the walking dead, that you would never, ever be able to get them better. And I looked at Lori and I said, I'm never going to see this. I don't want to know about this. This sounds terrible.

She did.

Let's peace out. Well, let's. We're done for the day. So we missed the lecture. Missed the lecture, I mean, and I regret that as a provider, I'm like, why? Why did you leave? Right. So fast forward two years later, we were in the process of repeating all of our modules with a 4M, because they update them, thank goodness. They update content constantly. And Andy Heyman was speaking. It was in 2016, October. And I always, you know, in, in, in the practice of medicine, you have patients that you treat that get better right away. You have patients that you treat that get better, but you know they're not well and you still need some work. And then there are those patients that just don't get well, Right? And so I would always go to conference with a list of patients that I wanted to pursue, asking questions about bringing their labs, getting the ear of mentors while I was there to really dig into. We're sitting in conference and she nudges me, me and I was having, I was having neuro flares. Like I would flare, be really sick for three or four days and then I would be okay. You know, I'd, I would kind of come out of it and be, be better. And then all of a sudden those times were getting closer and closer together and that was becoming my norm and I was losing the ability to walk at times.

And I will never forget this moment.

Yeah. So she looks, she punches me and she says, I think that's you. I think you need to be on the list. And I said, no, that's not me. Like she did. That's just, that's, that's not something.

That's, that's not me.

And I'm like, you should really think about this. She looked at me at the end of the lecture and she said, promise me when you get home that you're going to do the testing. Just do the testing. What can it hurt? So I tested my office, I tested myself. And then December, we were coming back to Congress. I didn't know what any of that meant, Dr. Shoemaker. I had no idea what any of those numbers meant. I took my lab and I took my office, report my army at the time is what we were doing. Took it to Dr. Heyman and he looked at it and he looked at me. He said, who is this? And I said, well, that would be me. And he said, follow me. And I was like, where are we going? He took me up to his hotel room. I was with her. She went with me, put cholestyramine in my hand and said, start on this immediately and do not go back in that building. And that began my journey of just exploring. I later did the proficiency partner course with you and then ongoing work. I did the George Washington course. Csrs, do they still offer that George Washington course through the George Washington University School of Law.

Andy has worked with them.

I think providers need to know that's available because it's a hardcore nose to the grindstone course on cers.

First any I taught had two different phases. The beginner's phase that now is incorporated into the graduate program at gw, the only medical school that's got CSRS education in it. We'll be starting up courses in the fall.

Well, it's not, it's the first, but hopefully it won't be the only because, you know, Back to the HLA, 25%, 24 point something percent of the U.S. population carry an HLA gene. And I believe, and I'm going to rename your gene, do you mind If I rename your gene doctor Shoemaker, or the dreaded gene, can I rename it?

Will you call it Billie Gene?

No, I'm going to call. I'm going to call it the Garden of Eden. Eden Gene. Because I think I should be living in the Garden of Eden. And those genes are made for the Garden of Eden. They're made for pretty everything. And that's not the world we live in today. You know, we live in a very toxic world with indoor air quality being poor, with our lakes and our rivers being contaminated. You know, we just don't live the way that our genes need to be living. Right. And so I'm joking about renaming your gene, but I think of it in that way. I try to think of it in a positive way, you know, instead of dreaded, like, oh, no, this is the worst case scenario.

Well, I think it's a lovely idea and I urge you to write it up. Up.

Scientist.

When we get you better, and it's not going to be long, you write right, right up your paper. Okay, that's gonna. That's gonna be great. That's gonna be great.

Wow, that was incredible. We just had an amazing conversation with Dr. Shoemaker and we hope that you were able to learn something that your paper is of notes that you took.

We're definitely going to have a part two. This part one was so deep and wide and rich, but it was a lot. It was very technical. In our second part that we want to invite you back to, it's going to be heartfelt. We really get into the heart of why Richie Shoemaker does what he does, the things that he's contributed to the service community. Just profound. And I can't wait to see you back for part two.

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