Brain Fog, Fatigue & No Answers? This Doctor Found the Missing Link (Part 2)

Welcome back, senergy listeners. We are so excited you've joined us again for part two of an amazing series that we're talking with Dr. Richie Shoemaker about Chronic inflammatory response syndrome. This particular episode is going to be filled with his emotions as well as just why he's done what he's done. But we want you to grab a piece of paper, have a pencil, take plenty of notes, and we can't wait to hear what your thoughts were about this episode.

I don't know if you want me to share more about my story, but my story was I got all the way through Shoemaker protocol and then went on VIP and could not tolerate vip. It aggravated my pancreas. But more to my story is I found out. I found out a lot about myself I didn't know. Through this process. I found out I was born with an annular pancreas. So my pancreas is wrapped around my duodenum. And I had poor feeding as a baby, like in the hospital for three weeks because of feeding issues. They never discovered it. I had hyperemesis during pregnancies. Like really, really sick hyperemesis during pregnancies. The whole nine months still wasn't discovered. And so it took having SIRS and failing VIP before that was figured out.

Excuse me, interrupting with your annular pancreas, do you have pressure on the pancreatic duct?

No, I do not. All of my studies as far as flow look really good, but I'm wondering if it's positional or if there's something going on there when stressed.

But again, very similar to what he has done over the years is that it took you to the next window or the next crack in the door. Right. Which gave you insight to the next thing. And it's that persistence that keeps you in this, with an optimism that you know there's hope on the horizon. Right.

And you've been on the low dose VIP protocol.

Yes. Microdosing, 1 100th concentration.

1, 100,000.

Yeah.

And same, same things.

Yeah. And I'm willing to retry because my pancreas, you know, it has calmed down. So, I mean, I'm willing to retry that at some point when it's appropriate, if that's what we need to do.

Yeah, well, I've got a new drug I'm playing with. I'll just let you know. Check with me in six weeks because I want you to try it. I'm not interested in seeing you stay sick.

No, I'm not interested in that either. Yeah, especially after the last. After the Last reports, I was like, okay, you have my attention now. This is. Yeah. Even though. Even though functionality is way better. And I think people need to hear that too, because a lot of times we settle for being fine. And I do a lot to mitigate a whole lot. I'm on binders, continu continuously, air filters everywhere, you know, great food, all the things sleep, all the things that you need to do to take care of yourself. And I'm fine.

Well, your problem is not just a positive army. Didn't you also have actinos?

No, it was endotoxins.

The paper that we published last month, a novel therapeutic approach to Parkinson's disease using transcriptomics to identify unique patterns of gene expression, including triple positives, toll receptors, denotoxin exposure. At Christmas time, we published a fingerprint with Jeannie. One of your questions to talk about was the future. And I'm jumping to the future. Getting fingerprints. Transcriptomic fingerprints of illnesses is going to help us a lot, especially when they're neurodegenerative. But we have used the fingerprint to now add three more biomarkers to our. To our list of what do endotoxins do to microglial cells and to autophagy in the central nervous system. And by fixing those, we're fixing Parkinson's minus far better than it ever was. Alzheimer's. Don't know what's going to work, but it looks promising. But the point is, is that it's patients with illnesses that had no answer, like, like the Fiesteria patients, like the. Like the mold patients, like the dinoflagellate patients, like the blue green algae patients. Those people are the stimulation that says, learn more, learn more, learn more. And when I get someone like you who's still functional but has got a whole upper layer of window that we can go. The future of SIRS research is to fix folks like you. The easy ones are easy ones. The hard ones. We now know how quickly it takes, especially with endotoxins and actinos. By far and away, the most common organisms that make people sick are Actinos, 42% and 28% for endos. But we're also now seeing a beyond beta glucans, the fourth module. We're seeing a fifth one. And this is the triple positives of a direct abnormality in the genes that are involved with coagulation. Because they are involved with each other, they set off one coagulation pathway after another. And at the CERS conference, we met the owners of Neuroquant. They are ready to bring Forward the neuroquant findings. That will give us microclot and microbleed. That may not be affecting you because you don't have triple positives. But where we're going began with doing an autopsy of a fish and now it's looking at the mechanisms of axonal injury. Paper a year ago was looking at tuba 4A and another tubulin, tubb one. You've got the cell body attached to an axon, attached to a synapse, and that's the functioning element in a neuron. The axon is full of tubules and if you've got tubular abnormalities, those tubules will not and you will get deficiency of delivery of ions and nutrients to the synapse and the synapse will die back. And this is called dieback degenerative CNS disease. And we fix that by fixing the tubules. It's just so exciting.

And by doing the testing that you're doing, these are things that predictively will alter the course of a person's future by knowing it now, because these aren't things that immediately show up.

We have found three year olds who have the triple positive gene array and they're going to develop Parkinson's when they're 55 years old. Well, here was one person, 10 years old, first got ill, got sick, is now 44, hasn't got out of bed in 34 years, who's got triple positives. Here is an index case for saying these genes were there, they were waiting to be activated. It took 10 years to deactivate them and 34 years, we're going to fix those. We're going to correct those correction of gene abnormalities. Not with crispr, not with tinkering with the genes of God. But we're looking at the makeup of certain genes that are way off the standard deviation list. You're way off the standard deviation list and yet it is you and the 10 year old with his triple positives that bring the future of GENIE and future of sirs to the bedside.

Now, we always say in medicine, you know, it's the genes that load the gun, but it's the environment that pulls the trigger. So the gene, the gene testing you're talking about right now, just for our listeners to discriminate between the standard gene testing that's done and things like, you know, 23andMe or whatever else, genes testing, you're talking about the genie, which is transcriptomics, right? Which is the, the way the genes express themselves based on environmental changes. Is that, did I explain that right?

Yes, you did perfectly. We'll get you to get up there and give you a lecture next time.

So you mentioned earlier kind of the hallmark of chronic inflammatory response syndrome is hypometabolism. So let's go in a little bit to that to have people understand, because this is what creates the fatigue process and the ongoing challenges with the inability of the patient to recover.

When I mentioned the different organisms involved with sers, mold and actinobacteria, most people have not heard of actinos endotoxins coming from gram negative rods. What we're looking at is that each one of these organisms makes a very small molecule that disrupts what's called the sarcin ricin loop. Now rice you're gonna say, oh yeah, that's, that's that plant toxin that released in the subways of Tokyo and killed all these people. Yeah. What the source and ricin loop will do is insert an amino acid according to the gene program. So one amino acid and the next amino acid, the next amino acid. After 28amino acids, you've got 28amino acid protein. But the small molecules disrupt this number 15 in this ring in this loop, it's a ribosomal inhibitory protein or the destruction of the sarcin ricin loop. We now know we can fix the sarcin ricin loop and restore number 15, which is an alanine, to its normal place and correct the gene abnormalities. But 95% of SIRS patients or chronic fatigue patients, fibromyalgia patients and chronic fatigue patients all have SARS and ricin loop dysfunction. With the nuclear transcription factors for the mitochondrial genes that left the mitochondria 3 billion years ago. And now setting up housekeeping in the nucleus, they are affecting ATP synthase, making ATP cyclooxygenase, kind of electron transport chain and then translocases. Translocases remove pyruvate. As I mentioned to you in my excitement, talked about it too fast, sorry, but translocases will move pyruvate into the mitochondria where they're broken down into ATP, CO2 and sugar. But remember, we've got the genes of metabolism affecting these things. I'm sure you've used the keto diet in some people and some people works beautifully. And if the insulin receptor substrate is not over reactive, the keto diet works beautifully. But if IRS 2 insulin receptor substrate is elevated, keto won't work because everything, every protein will get converted over to glucose. You can have all the fat you want, all the ketogenic foods you want, it doesn't matter, It Gets overwhelmed. So GENIE has so many things. What we've got with GENIE is, goes back to my question for you. You had Hertzme 2 and Ermie done. We know that moles back wrong. Actinos can be found out and those can be found out. But specific causation, here's where the lawyers come in. We know that if we have specific causation we'll buy Ando's for example. We are going to have downstream gain genes and these people who've got these genes, CD14, TOL2, that's the big one, TOL4 less big. But these are specific and precise in saying what is making this person sick. As we expand specific causation to triple positives, as we expand it to get rid of Parkinson's and as we expand it to get rid of Alzheimer's, we're looking at neurodegenerative processes that have genes makeup that say this is what is going on wrong. I didn't know what was going on wrong. I knew I had cholestine. I mean I had my little pop gun, I'm going to fire it. But we now can know what else in the environment we don't know about. These little, these microplastics, are they setting off gene activation? And it's the inquiring mind that'll start getting government grants now. No, you won't get them from the NIH for a few more years, but you will eventually. But in the meantime it's patients and physicians at the bedside that make all the difference in the new paper. Really it's a triple paper. It's the history of sers, it's the medical legal aspect of sers. Andy Heyman's got the molecular biology, David Lark has got the microbiology. Eric Dorninger is going to do sophisticated work on what the treatment is. But with that paper in mind, that's 40 pages. Michael Schrantz and David Lark and Larry Schwartz and John Banta are coming with their 40 page paper. They've been accepted. Eric's got his 40 page paper on treatment. We're going to have three legal ready briefs to give to the politicians to give to the other doctors to say here it is what we know. We came from a dark place or lack of knowledge and now we've got fingerprints for what's going to be Alzheimer's and our way of fixing it. We won't give up.

And I love what you said about looking for causation because I do really believe that oftentimes we're operating from the you know, just a set of symptoms and it's. People just want an answer. They want like a diagnosis. And at the end of the day we have to understand what's causing the problem to help a person.

So on the genie, I'm super curious, I've never asked you this, but we have ability to see causation from mold, endotoxins, etinomyces, now beta glucans. Why, why don't we in Lyme, Right. But we're not seeing ciguatera and we're not seeing piesteria on the list. Is there a reason for that?

They have their own specific causation. We just haven't had enough people to do the genie on them.

Okay.

It's just a matter of not enough genie. We'll find it. It's a great question.

It has to be statistically significant for you to report out and have something to build from. Is that what you're saying?

We don't have a specific neuroquant that we know of now for dinoflagel illness, for blue green algae illness.

Just think that's probably more prevalent than we're realizing. You know, I live on a reservoir in Mississippi, like the Pearl river runs through. And I just feel like there may be some issues possibly, you know full well.

If you create an environment, could. It's an ecosystem and that ecosystem has got nutrients or, or poison altering compounds like, like copper and carbonates were, you know, if you build it, they will come. If, if you put it poison in the water, things will grow. As this country enters its climate change problems. You got too much water from floods and not enough for fires.

I think too often I kind of want to talk a little bit about mold being a small fraction of this whole equation. The naive, either consumer being a patient or a client or a physician or medical provider, sirs has automatically, for those naive providers have meant mold. And actually, from what I understand, that's only a small fraction. Right. That's kind of what we've been talking about as causation. Yes.

I think water damage and mold oftentimes get lumped in the same language. And I think it can be challenging, especially as we work with our remediators. But they'll go into an environment and they'll do their remediation. And no, it doesn't have mold. Well, no small particle cleaning was done. Nothing was done for actinos. Nothing was done for endoscopy. They're not looking for any sewage leaks in the home. Like, it's just, it's a, it's a hard conversation to drive when the conversation is mold specific. So I know that's been a process of evolution, but just curious on your perspective.

Next week you will have the paper from the environment, environmental groups together with the, the history and all the other stuff after CERS next meeting. On, on. On June 8th, the European Medical Society sponsored a symposium on environmental illness and the built environment. And they said, would you like to submit a paper? And I said yes. It took 10 of us three weeks to write three 40 page papers and they're all accepted, they're all going to be published. You will have things to flop down on the desk of your fellow that wants to do an air sample or flop it down on a fellow that thinks that nothing's wrong with the sump pump in the crawl space and somebody who's ignored that leaky, leaky sewage seal on the toilet. You know it's going to be published in the highest frame. I think the environmental guys have got 191 references. I think you want the answers you gotta publish. Don't give me your opinion, give me your data. Publish your data, then we'll listen to your opinion. It's kind of dogmatic and I've been that way for all my life. But you know, a long triumphant proof was with my explanation point of the fifth grade math problem. A long triumphant proof is what this has been here. And we're just getting started with molecular biology and extensions that we have. It's folks like you on the front lines taking care of patients who are going to be challenged to read. Challenged to read and read and read and read. You know, I'll write the paper but you got to read it. People are using part of my protocol. Well, he's wrong. I did part of the protocol just didn't work. Oh yeah, how much well call did you use? Well, it's easier to take the colostyramine. We were able to get one a day. What happened to two, three times a day? Oh no, we don't want to do that. But the protocol doesn't work. Well, it doesn't work because you didn't do it.

Right, right. But that takes a provider that's willing to sit with that patient and educate and re educate because a lot of times they don't because of the neurological challenges of this condition. They don't always. They don't have the best ability to follow instructions the first time you tell in.

Right, Right.

So this is a labor of love as a provider treating patients with SS as well. Just being patient with the evolution of the process of walking them through a treatment plan.

And a perfect example that healing is not linear in your case. You will hit walls. You will hit. I don't know, let's figure it out. And they have to be willing to understand that it is not a black or a white answer. You're navigating causation, environment and re exposure.

Right. And I think the other thing, when.

I was talking about fixing exposure, get out of exposure is number one, as you've already mentioned. One lady said, well, I'd be happy to send the dust samples, but I heard it cost $450 to get the answer. What's wrong? I said, that's right. How much have you spent so far? $100,000. Well, it's not free. You're gonna have to do it. Genie's not free. We're getting ready. Johnny Rossini at Envirobiomics is going to be making by PCR available rela, TOL2 and AKT. We're going to have these new biomarkers readily available so you don't have to buy all the whole Genie. Genie's $750. It's. It's, it's expensive to do jeans from.

Gene work, but it's less expensive than it used to be.

Yes, it is.

When I did my first genie, I think I paid quite over more than that.

Yeah, it was $2,000 when we were doing all the jeans.

Yeah, yeah, yeah.

People are pretty desperate to do that. But getting, Getting back to this team approach, I talk too fast, I leave too fast. And I'm more of a research mentality and someone to sit and figuratively hold the hand of the patient who's angry, the patient who's lost everything, patient who hasn't gotten anything and all she's got is misery in her life. Maybe her kids like her, maybe her husband still does, but not necessarily. It's. It ruins, ruins life. And so me Talking about tubulin A4A as the gene for brain injury is going to be second to someone having human compassion by saying, you're not alone. Here's hope. Remember Pandora's box? She opened it. She was told not to. And all the flies and mosquitoes and beetles and bugs and all the bad things got let loose on earth. And you know what? The bottom of Pandora's box? A little butterfly. And that butterfly was hope. And that hope is what providers like you guys do is better than I ever did, that's for sure. And the more coaches we bring in, the more compassion things we bring in the better off we are because we're after healing the whole person.

Yes.

Person is more than the genes. The whole person has got caring. The whole person's got family members that love. The whole person's life has been taken from them by a little tiny particle made by a mold made by an actino. It was growing in a house where it shouldn't have been. It was let. What was wrong was criminal. Renters aren't allowed to be exposed to bad things. But, you know, when we started certifying coaches, I said, well, you know, look out. They're gonna try to act like they're doctors. No, as a matter of fact, they're acting what doctors don't do.

That's right.

Bringing in the humanity to the human.

Yep. And that. That personal touch. And I think more and more are getting into the field in space. I know Kelly shared with me, you know, even someone in the licensed mental health arena who is there to counsel couples going through it, because oftentimes, I mean, I've. I've lived some of this where they, they. They dismiss too. Right. Because they just don't know what they don't know. And so I love that more coaches with a diverse background are coming into this space. But sadly, in some respects, they're usually getting into it because they, too, have had a personal journey through it, which makes them relatable. Which makes them relatable, too. But, yeah, people have been so dismissed and they're broke. Typically, at the point at which they come to providers I can speak to, for me, and you could probably speak for you, is they have tried everything. Everything. They've been a lot of places they've been dismissed. They've lost trust in the traditional medical people that they have sought out. They have felt unlistened to, and they've spent every dollar. And the thought of having to move from their home or from their business. I remember you going home that weekend that you left that conference and you were faced with a weekend decision of having to move out because staying in your practice wasn't going to be possible for you. And I admired the fact that you were willing to do that. But you knew because you saw firsthand what it would be like if you stayed in that.

Yeah.

You know.

Yeah. And luckily they tore the building down. Later. Later. I was worried that someone else would move right into that space and have a problem as well. But they did tear the building down, which was, I think, epic and very healing for me to see that gone.

But Sirs is not a common Household term. And so I think even when we talk about sirs or even bring up that topic, like to us it's what we talk about. Right. But to them it's not common. And I think that we have to make it more common to talk about. And I think I'm trying to figure out how to do that. That's why perhaps this podcast, just like this is so important, because we just hope that they'll click on it and they'll listen. Right. And plant that seed.

And to your point, Dr. Shoemaker, all the technicalities of all of the intricacies of the biochemistry is mind boggling. And oftentimes we just glass over when we start hearing all of the details. But all of those details are so incredibly important for providers to understand for us to do the right thing and not take short shortcuts in the protocol. There is no shortcut. I wish there was a shortcut, but there's not a shortcut. In getting out of exposure, in deloading the body and taking the binders, in working through calming that inflammatory storm that just gets progressively worse as the years go by. There's no shortcut to that. And it's your work and the work of others that are pursuing this research ongoingly that provide hope and a future. And we don't have to struggle like that for a lifetime, despite our genes.

Right.

Despite the genes that we're born with.

Right. And I think about even the development on your behalf of and those that came around you for the proficiency. Right. For creating a proficiency test of sorts or certification that ensured that people, providers of care walking through that journey were proficient at the practice of doing this. And that doesn't mean it's over when it's over. Because what we found is there's more data coming out, right. You got to stay connected, educated.

So, yeah, as Dr. Shoemaker developed his protocol and published his protocol and got the case definition for chronic inflammatory response syndrome, gave us the language that we have today. As Laurie mentioned, he developed a curriculum for providers to follow and become proficient in treating this.

Right.

And it was rigorous. I remember doing that and meeting with you to go over the exam and it was. Yeah, you were a little bit intimidating, Dr. Shoemaker, I'm not going to lie.

A lot intimidating.

A lot intimidating.

But not purposely. And I'm so glad you were. Because it's holding us to a standard. Right? Holding us to a standard of care. Right, Right. That is so important.

And now George Washington University has a curriculum. And now Sirs X is developing, not curriculum, per Se. But coursework ongoing where they're bringing all of these people together once a year for a live conference conference that's also live streamed. So there's no excuse for not continuing your education there because you can do it from the comfort of your own home and not have to travel. And I will say I heard, I heard a lot of chatter around them vetting the hotel. Right. That you guys stayed in. And I thought that was really impressive because we don't often hear that when we go to conferences. It's kind of a crapshoot as far as what we're going to get in the way of quality of space that we're in for, for the patients that we have that have chronic inflammatory response. So good job there too.

What we talked today is come, come back to attitude. Really?

Yeah.

Attitude towards sick people and attitude towards finding answers. I just wanted to, to read the last, last sentence in my essay that's part of this paper coming out. But it must be said that for all the power of innovative tests and technologies available to advanced medical science, no tool proves more value valuable in unraveling sirs, than the timeless skill of truly hearing the patient. That's the attitudinal stuff that I'm hoping will continue to grow by leaps and bounds because it is making a difference if, if, you know, there's a respect issue. If you ever worked in emergency rooms, you would see someone coming in who had 25 health complaints and a big thick wad of patients. And the emergency room doctor, cynically without much respect for the patient, will say, that's a gomer. You know what gomer means, right? You know, get out of my emergency room.

I worked in the er. You're exactly right. You're true. That's true.

There's a hand waiting for you in the, in the exam room. Was the hand waiting to attach to a person.

I mean, they were classified either as a drug seeker or, you know, and you brought me kind of to tears to that, I'll be honest, like I'm wiping my tears. But it's true, because I just think again, you know, that compassion and that doesn't come at a cost. It doesn't come at a cost for practitioners that genuinely care. We're having to continually refine how we do what we do because it can be exhausting, it can be tiresome, you know, and we have to collectively be around other providers of care to lift us up, encourage us, figure out new ways to do what we do so that we have the bandwidth to give. Because you can't give from an empty cup either. You can't pour from an empty cup.

It goes both ways. There needs to be respect for the physician or the provider who's trying his utmost to help. And folks with a lot of loss, a lot of emotion can't express a lot of anger. And some of the phone calls we get are from people who really are angry. And yet when their brain's fixed and they're thinking normally and acting normally, it's like, oh, my God, I'm so sorry. That's part of the illness. So you need to have that thick skin, like the back that doesn't bleed because you'll get carved up by folks you're trying to help as well. The approach that we've got to keep in mind is that the 24% HLA number comes from a paper I wrote in 2003, by the way, in case you're wondering where that comes from. But we've got OSHA saying that 50% of our buildings and 85% of our office buildings got water damage and water exposure. 24% of people working in 50% of the buildings. Well, let's see. 50% of the US is 160 million people. 25% of those is 40 million people. How many million people are diagnosed with fibromyalgia? How many million people are diagnosed as depression that doesn't respond to antibiotics or antidepressants? How many people are walking around with Lyme disease that doesn't respond to antibiotics? You know, the numbers start adding up, and 40 million sounds like a lot of people with SIRS. But you can almost guarantee that if you work up with a new patient with sirs, that they will say aha near the end of the interview. This is just like Mrs. Jones has. I went to school. I went to high school with her. And the SIRS word may not be around, but the fatigue is around. And feed fatigue, and all that is too real.

And anxiety. Anxiety, that's a common symptom as well, that we see repetitively.

And what do we do for anxious patients? We might look to see what their amygdala looks like on Neuroquant. We might give them a benzo. What really are we doing? Are we helping them with the benzo? Well, you know, hard, hard, hard to say. Some people get hooked and then bad things happen. But the future is you guys. The future is not old guys like me. My job is pass on what I know. My job is to make sure that research questions are asked and more people are taught the more people that are taught, the more people learn, the more people learn, they learn together.

That's right.

That's part of the message of these, these podcasts. Because here you are doing the, the hard work and, and maybe of espousing, and you had a rough day and people were mad at your receptionist because they didn't do something you wanted. And, you know, they come home and, you know, what you're doing is so important. It'll. It'll test your face. But there's, there's reasons that, that we are put here to do things that other people won't. And that's for another day in another podcast. But, you know, when I look to see the inflammatory pathways that are evolutionarily conserved, what does that mean, an evolutionarily conserved pathway? Because everybody's got it. Where did it come from? So, you know, when I, when I went to Galapagos for a nice vacation in 1986 and was beautiful, it was just amazing that Charles Darwin spent 19 days and 12 of them weren't on land, Niners, seven on ship, and he collected finches by shooting them with one of those big old blunderbuss guns they had. And they had pieces of sparrow, pieces of finch. How could he have detected changes from evolution in the beak of a finch? That it was in three pieces and maybe two. Two or one finch and was another finch. I look at one of the teachers and mentors of Darwin was a fellow from Scotland who was a archaeologist and just looking at patterns of rocks that came from South America and from Antarctica to Scotland when Pangea was floating around, all these things that we're looking at, like they're new or not new, it's just us are new, finding what they are. So I'll continue to look for the nuances of Parkinson's disease and triple positives. You'll continue to look on more efficient ways to provide compassion to people quickly and put it in a bottle. We'll give them two, two drops three times a day of compassion.

So, Dr. Shoemaker, I was able to watch the SIRS X conference. Some of that I got to do live, and some of that I watched recorded. I did watch your presentation and your presenting my case study. And as you stood up there in front of the SIRS X community, I could see the pride in you of watching the people in those seats learning and soaking it in. You got really emotional during that time. What was that emotion for you in that moment? It was powerful. You could feel it. Even remotely, you could feel it. So just so much appreciation for that because you have had it hard. And a lot of times I think you are perceived as being a little hard. And so to see you in that light and to see, like, your gift to this community, I think is love. And you could just. You could just see it and feel it. And so I want you to know that. I just really want you to know that. And I just. Thank you for sharing.

Those kind words make a lot of difference. I appreciate that.

You're leaving an incredible legacy, as we would all love to to. Right. I think about what. When I. When I go from this earth, whether that be tomorrow. We never know our time.

Right.

Is the one thing I think about. Having lost my dad this year gave me a lot of reflection on. This is, you know, when they wheeled his body out, right? And you kind of like, gosh, is that what life is about? Or is that all, like, one day here and breathing and then the next day gone? Like it's. Or in a minute, just gone? What are the things that you just wish to leave behind?

Yeah.

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