10: CIRS and the Bio Toxin Pathway: A Deep Dive into Detoxification and Healing with Dr. Jenski

Biotoxin pathway. Ultimately what it is is it kind of draws out how our bodies get exposed to biotoxins which we described as it can be mold related biotoxins, it can be particulates in a water damage building, bacterial toxins in water damage building. But it also can be biotoxins from things like fastera ciguatera. We've also talked about how the lime, lime, it gets really bigger and bigger and bigger. So when we say biotoxin it's a really, really big big world, broad term. Welcome back. Once again we are talking again about chronic inflammatory response syndrome. And today we're going to talk about the biotoxin pathway. It's going to be a little nerdy. This is the basic science. Yeah, I know a little nerdy. It's the basic science behind chrono phantom response and what it does. So if you like this information, follow us like us, ask your questions below. As we're going through one of our goals towards end this will be do some Q and A sessions. We'll be answering people's questions. So if you want to be informed about that, you have to make sure you're following us and liking us and all that kind of stuff. So we're going to start with the biotoxin pathway. You both kind of joked about that because it's who's going first, who starts with the bioticomi come up, that's fine. Well the biotoxin pathway ultimately what it is is it kind of draws out how our bodies get exposed to biotoxins which we described as it can be mold related biotoxins, it can be particulates in a water damage building, it can be different chemicals in a water damage building. It can be bacterial toxins in water damage building. But it also can be biotoxins from things like fastera ciguatera. We've also talked about how the Lyme it gets really bigger and bigger and bigger. It can be a biotoxin actually related to traumatic brain injury is now part of the service world. It can be related to overexertion. There's an overtraining syndrome where you actually break your muscles down and you relate these damage associated molecular patterns that activate your immune system. So when we say biotoxin it's a really, really big big world. Broad term, Broad term what happens is that gets released and your body has to clean to clear these out. And so one of the first things that happens and all by the way this is on our, we actually on our series we did on this, I actually have a picture of the biotoxin pathway on our website for those who want to look at that. And it kind of walks this whole process through. So. But your body's supposed to clear these things, right? And that's where the genes come into play. Yeah, the HLA DRDQ gene. If you don't have the right, if you have this mutation, it's harder for your body to clear these biotoxins.

Yeah. So I think I like explaining this one because I explain this to my patients all the time and I think sinks in better to help them understand beyond all the gobbledygook of these biomarkers is really simply, we'll do a quick immunology lecture.

Okay.

Just a brief immunology lecture. So there's the innate immune system and there's the adaptive immune system. And the innate is quick and nonspecific and it is the prehistoric branch and ultimately I call it surveillance snitch. Right. It's looking around all day and then it's going to tell on it. It's going to tell the adaptive, which is a little bit slower and more specialized and very specific and the more modern branch of the immune system. So innate informs adaptive that there's a problem. Adaptive meets the innate on the battlefield. They sort the issue out. There's some debris that's left behind. The tolerogenic T cells come in and clear it up and you go back to homeostasis or immuno immunologic balance. And now your immune system is stronger physiologically, you have more reserves, et cetera, et cetera. So ultimately, if you have the HLA DRDQ issue where you're multiceptable, multi susceptible, etc. Your innate immune system still works. It's seeing toxins, it's throwing inflammation at them in the form of cytokines, little chemical messengers, tries to quarantine. It takes a little piece of whatever that toxin is and it presents. It scout snitches to the adaptive and the adaptive normally would take that and make antibodies with the B cells that become plasma memory cells. And it would make specialized T cells to meet on the battlefield, clear the toxin out, tap the innate on the shoulder and say we're here, we got it, you calm down and we're going to make this go away. And then resolution. Like I mentioned, when you have this issue, the innate does what it's supposed to do and it takes a little piece, it presents and the adaptive says that's a problem, but I can't help you that handoff is broken. It's dysfunctional. Your antigen presentation does not work. You do not recruit the adaptive immune system. B cells, T cells do not meet on the battlefield. More importantly, they do not tap the innate on the shoulder and say, we got it. So the scout goes back and says, we're not gonna get any help. And they say, well, we're just gonna do what we do, which is inflame, inflame, inflame. And so you wind up filling up this proverbial bucket of toxins and you stay inflamed and you get exposed and you get more inflamed and the process potentiates. Now you've initiated that cascade of events of biotoxicity because you didn't do what you're supposed to do to no fault of your own. Because, because of genetics, you don't get that adaptive recruitment. That's the biggest part to understand with this whole HLA dysfunction. That's what the genetics mean at its core. What's the next step?

Well, the next. Well, I want to stop there real quick.

Yeah, okay.

So I think this is one of the things where, like, why are we having this issue now more so than we had in the past? Why is it such a big deal? I think part of that is like, how does your body overcome that? How does your body detoxify? You poop stuff out. You breathe it out. Sweat. Sweat it out. Pee. You pee it out. And so the average Americans chronically dehydrate, so our kidneys aren't helping out as much.

Constipated.

We get constipated. Well, what's nature's. What's nature's biotoxin? Binder? Fiber. The average American eats 12 grams of fiber a day.

Is it that much that it was less? I thought it was like nine.

That's nine, though. Okay. And we should get between 40 and 60. And in Sub Saharan Africa, they're getting 80 plus grams, you know, sweating like Americans don't sweat anymore. And there's certain chemicals, and particularly solvents, when you get into the different types of biotoxins that are not biotoxins, but chemical toxins that are only sweat out. So all of a sudden now it's almost like the setup. We don't directly constipate. Our guts are messed up, not enough fiber. Nutritional status is low. We don't get enough protein. Protein is part of detoxification. Phase two detox. Right. And so it's. All this stuff builds up. And the reason I like to talk to patients about that Is because you can't actually. Your body was made to survive in this world. And if you get the right environment, you can actually overcome some of these genetic things. But when people don't sweat for years, when we don't have fiber, we're all chronically malnourished. We have this new thing overfeeded. We have this overfeeding syndrome. It just sets us up for something like this. Yeah. To go overboard.

Not to mention the. The shoddy way in which homes are built or the paints impregnated with antifungals that made super molds and all the other things that we can. We can go on a combustion sidebar.

That'S in the textbook.

Yeah. I mean, it's like it's a combination of things that led us to this point. And. And by not sweating, we basically mean people aren't exercising, people aren't going to saunas, that kind of stuff. Or they're trying and they're not sweating because their detox pathways are all clamped down. Is that vascular? Is that lymphatic? Is that just. The toxic burden is so high the body just doesn't know what to do with it. But. All right, so we've established that we live in a toxic soup and that our systems don't work like they should. Then you layer in that genetic component, and now you know that you're not getting that adaptive recruitment. The innate immune system is inflamed and on fire and mad. And now what happens?

So now what happens is the regulatory system in your body, the hypothalamus, has these things called leptin receptors. And one of the things you get is leptin receptor resistance. So it's really interesting. You know, you check patients that are obese, and this is where some of the obesity comes into play, leptin resistance. But people know about insulin. Insulin's like the storage hormone. You put energy into your cells, or leptin's a hormone to actually get the energy out. So what happens is because of some of this, the metabolic stuff you've talked about already, you can store energy, but you can't utilize it. And this is driven by the selective resistance in your peripheral body, metabolic syndrome in your liver, PCOS in your ovary. It means all kinds of stuff throughout your body, in your hypothalamus. Leptin resistance drives dysregulation of neuropeptides. So all of a sudden, your msh, your vip, adh. There we go. And so the lab test you do, looking for ADH and MSH Is one of the master ones that when that gets down, you mentioned it briefly before how that helps with pain regulation in your reverse spinal tract. That when that's low part of your innate system fighting off infections. So it sets people up for this thing called morcons. So all of a sudden this dysregulation of hypothalamus driven by leptin resistance comes forward to that and then you start getting all the downward stuff. The vip which is vasoactive intestinal peptide was found in the GI tract but now we know it helps with leaky gut. It can be used with traumatic brain injuries. It actually helps a lot of different brain neuro, inflammatory immune regulatory processes going back to multi system, multi symptom, right?

Preventing target in organ damage that sometimes is misdiagnosed as dementia or Parkinson's and is actually reversible. S But what's Marcons? You mentioned Marcons.

So Marcons is a, is a multi drug resistant staphorious that you get exposed to in water damage, buildings. And so it's a very, very slow growing staph. So you have to have a special culture that's a slow seven day culture for it which most nasal sweats actually grows in. Your sinuses won't pick up because they don't have the right kind of media and you're not looking at it. And so with this, this, this bacteria that colonizes your sinuses because most people's sciences are colonized with staph aureus, it's actually very normal. You've heard of mrsa, right? Yeah. Multi drug resistance, Staph aureus. That's one version of an abnormal staph in our sinuses. Marcons is a different version. And with, with Marcons one of the things it does, it releases these things called hemolysins which are these little bitty dysregulatory proteins that go up into and they actually, if it's in your sinuses, in your ethmoid plate, it goes right up to your ethmoid plate. And basically if you can visualize the brain, this regulatory center hypothalamus, like literally it's like right on top of that ethmoid plate. And all of a sudden now these hemolycin go in and disrupt your pomp C molecule which turns into affects cortisol, affects msh. And so all of a sudden now the exposure might cause that downward stuff with leptin resistance you get the Marcons, it kind of hits you from a blow and then all of a sudden now you're Getting stuck. And you might remove yourself from the building, you might do the binders. But if you still have that mark on growing, causing more dysregulation and still.

Having toxins made from within and suppressing msh, the mark. So MSH gets suppressed and then you get Marcons when MSH is low enough, and then Marcons suppresses MSH even more. And so it's giving you kind of diving you deeper into this, into this hole. So we have the genetic predisposition, biotoxin exposure, poor antigen presentation, broken bridge, inflamed innate immune system, which we're going to talk about next. We start to get leptin resistance, we start to get suppressed msh, dysregulation of the hypothalamic loops, Marcons pushing MSH down even more. MSH in itself affecting pain and energy and sleep and androgens and other things. Gut, leaky gut. So you get zonulin release and intestinal permeability that we call leaky gut. And then you activate these alternate complement pathways of inflammation. That's where the C4A and the C3A come in. And what else is going on?

Well, part of that activation of complement, like you mentioned, is that you start chewing up the complement System and create C4A. I think that the thing that's really interesting about that is that in the, the rheumatology world, they've known for years, like you can check a C3A, C4A, CH50, which is a test for the, the totality of your complement immune system when those are low immunity. Being chewed up by something. Yeah. Actually is one of the ways you can actually diagnose lupus, for example. So this is kind of like connection with other autoimmune. Well, other, with autoimmune diseases like that, where there's this complement cascade, this is part of your immune system which tags cells, puts holes in them, makes them spontaneously combust. There's actually a bridge between other autoimmune issues. And so what will happen though, however, now I've actually tested lots of my patients on this and I will see the Ch 50s high, but I've not seen C3a, C3 and C4 levels consumed by patients. That's more the Lyme stuff is you'll see the C4A pop up and that's a marker that this part of the immune system is being overactive. So they're actually creating more of these damage associated molecular patterns because they're making cells spontaneously combust, releasing their contents. And now you get inflammation on inflammation. Yeah. And then you can start spilling over and get this epiphenomena. So now your body starts seeing all this stuff and goes, wait a second, I see thyroid, let me make some thyroid antibodies. I see, I see a little bit of lupus. And this is what's interesting about the lupus anticoagulant. The, the lupus anticoagulant actually is attacking a phospholipid that's actually on the inside of your cell membranes. So what has to happen is you have to have dysregulation these cell membranes that flip that thing out. Anticory lipid antibody is what it's called to expose that to immune system. Right. So all of a sudden this is where I love about the lipid therapy because part of the lipid therapy does actually flushes those toxins off the cell wall membranes and allows them to kind of flip back in. But now all of a sudden like there's this crazy science behind the chronic fatigue and the fibro and the brain falls and all kinds ties it all together. And it's inflammation on inflammation. It's the initial inflammation exposure that activates stuff. It's then the next inflammation with disregulation of your presentation. TH17. It's in this complement activation part and you get this dysregulation dysregulation that then feeds over into things like hypoxia inducible factor alpha, which we didn't really talk about, but it's basically something that happens. You get decreased blood flow to cells. You mentioned VEGF before, which is not one of the official labs, but what initially happens, it gets upregulated. So you can see VEGF increasing because your body wants to adjust, make new.

Blood vessels, deliver oxygen to the blood.

Right, exactly. Because you got this hypoxia inducible factor going on. So then your body's like after a while gets tired, then it bottoms out, which is more common to see later on. It does. It does freak some of my patients out there if they see their veg up high. Because it can also be a market for cancer. Yeah, yeah.

So but the HIF1 Alpha is, it's, it's often. I mean it's not something that we can measure, but it's often something that's abnormal because of just relative states of hypoxia. You don't need to be anemic. You don't need to be a COPD patient who's hypoxic.

Exactly.

You can have a relative state of hypoxia in the tissue itself. And if that's because of inflammation and oxidative stress, HIF1alpha gets released, which then leads to the final common pathway of inflammation, which is NF kappa beta. And now you got problems. And when you're saying inflammation on top of inflammation, I mean, that's what you're kind of alluding to. It's a cascade. It's an array of events that almost like dominoes, one topples the other and it just continues on down. And the reality is when you're talking about things like damage associated molecular patterns, we call those damps. There's also pathogen associated molecular patterns that we call pamps.

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The best thing to understand from a layperson standpoint is that it's just creating a debris field. And where there's tissue debris, there's also endogenous tissue. So your own soft tissue, where that debris field is, the immune system is there trying to figure out what's going on. And it's going to pick some of that tissue up and eventually it's going to get curious enough to say, maybe we should present this and see about it. And when it's presenting it and there's CO stimulation, you've now triggered antibody production. And if that's your thyroid, you now have thyroiditis or graves. And if that's your joints, you now have rheumatoid and it's the process of am I inflamed? Okay, that's bad at its core. But now am I inflamed and creating tissue debris, and now am I inflamed, creating tissue Debris and activating my immune system. And is my immune system confused at baseline. Now everything is getting presented bad and good and I'm losing that tolerogenic immune response. The differentiation between good, bad self and foreign. And now I have an autoimmune phenomenon. And you can trace it all the way back. And, and if you can reverse that condition, you can put the autoimmunity into remission. And that's pretty awesome.

And now I'm confused because this is so much stuff. It's all over the place. And so just to kind of take it home. Like the cool thing about all this, which is kind of complicated for people to understand, is that ultimately to start the process of healing, you have to limit the exposure. Yeah. And we're gonna talk about this more later in the treatment section. Start your body to detoxifying with lipids. We talked about binders. Okay. If you have this, this infection, you're testing for the Marcons. If you have it, retreating it, removing it. If you have issues with positive gliadin antibodies, which a lot of people do. Yeah. Do you all do you actually do a lot of. I guess we'll talk about this. Do a lot of low amylose diet or how do you. Dietary. Because that's one of the traditional things.

MMP9 and some of the other things. So I have all my source patients go gluten free. That's for sure.

Course.

Because every one of my source patients by nature has got leaky gut. You, you have intestinal permeability as long as your MSH is low. And, and you don't need a zonulin test to prove that. You can just know it based on, based on the literature. And, and I do do celiac testing if they're actively eating gluten. Because if they're not, then what's the point? That's the treatment anyway. You're going to get a false negative if they were. Were to be positive. So I have them not eat gluten to potentiate the problem. But MMP9 that you talked about in another video. Metallo matrix. Metallo proteinase number nine. It's kind of leaky gut. Leaky membrane, tissue destruction activation in those white cells. As you were talking about some of the treatment, or at least one of the treatments used to be actos, which is an old school diabetic medicine. And then low amylose diet and low amylose diet can sometimes help with some of the inflammation and immune stuff. I don't do that a lot. But if patients are hitting a Wall and I have them on high dose Omega 3s and I have them on boswellia or some of the other treatments that we use to lower it. It's not, I might say, hey, maybe we should try this and give it a go.

Do you in that case ever use on PM use?

Those are amazing.

Yeah, these are pretty cool. Yeah. So. So part of this inflammation is giving anti inflammatory. And so there's the omega 3, there's the O3 and O6 derivatives in your immune system. Right. You get these Prostaglandins, right. The three series and the six series. So Omega 3s and Omega sixes. Right. So if you make lots of the threes, they're anti inflammatory. If you make lots of the sixes, they're pro inflammatory. So what could happen is if you get the sixes up, which is the typical American diet, I think the ratio right now is 16 to 1. Omega sixes to threes, it should be anywhere from 1 to 1 to 4 to 1 to 1. Depending on what, depending on what you read.

I try to get them to four. A four to one ratio I think is excellent.

That's from, from your ear Schumer fields work. That's the number. But then you read other things. But anyway that's the body balance oral. That's the number. But so what happens is, is ultimately the omega 3s and 6s downstream will make these, these iosanoids which are the actual infl. The anti inflammatory molecules. So SPMs, pro resolving mediators. So pro resolving mediators, what they do. And you actually said this perfectly before, once you get the inflammation, everything gets crazy. Then the tap out happens. Right. The way you said it, I don't 100% remember, but the tap out you said calm things down.

Yeah.

Well the way your body calms things down is making these pro resolve immediate. These things that actually say it's time to chill out. Well, if that's not the handoff isn't happening, what happens is the chill out doesn't happen. SPMs are the chill out signal.

Yeah.

And they actually act kind of sort of like steroids do. Yeah, but they're not steroids. And so I have great responses to patients with all kinds of issues with these.

They're the anti inflammatory magic that's kind of extracted from fish oil. Like theoretically, when you take fish oil or eat omega 3s in your diet, your body should make these, but you're not getting them in this therapeutic dose that when you take SPMs or specialized protozole. High doses. High doses, yeah. And and it's the, the moraisens and the protectants and all these different kinds that are made and they're just pretty incredible. But they also flip your macrophages. Talk about that from M1, M2 state and what that means.

So it's the M1, M2. And like the phenotype of M2 is a pro inflammatory and M1 is, is, is more like the presenting macrophage. And these actual. Flip it from the M2, M1 which is huge. Now we don't have ways that we don't have ways to test for that, do we? It's, it's just the basic science. Yeah. So we can't really test for that. But you know, if someone has chronic inflammatory response syndrome, they have this. And so a lot of times, and I'm not sure how you do it, but depending on where the patient's at, sometimes when they don't tolerate the cold styrene, they don't tolerate the. Well call. You put them on the, the, on the, on other binders that these lipids with the phospholipids and these SPMs can actually be really super helpful to calm the inflammation down. Yeah. That then later you can actually add.

Back in the cold start curcumin is great for that. Cursor curcumin, especially certain types that cross the blood brain barrier. But then like SPMs, high dose fish oil, like those are my go to anti inflammatories. And you're absolutely right. Like that'll bring a lot of that down so that you can do the binding with more efficiency without side effects, detox die off, all that, all that stuff.

And one thing to add to that, a lot of times when people have these Herx reactions, it's actually in this case technically what's happening is when you start detoxifying, they actually have a cytokine flare.

Yeah.

So it's almost like a miniature, miniature cytokine storm. Which I think most people know what that is now. Yeah. And so what happens is these people can't tolerate the, the binders. You actually have to go in and give them high doses of mega 3s first for a month, do what you mentioned, maybe add some SPMs and then once you calm that part down so they don't release all these things that cause that miniature cytokine response, you can then go back in and add the binder. But the point is, I think we could ramble on about this. Is that this, this actually this, this is like deep science. Yeah. It's crazy. But at the same time, the treatments, once you understand what you're doing, it's, it's, I would say it's not templated. That's pretty like.

Yeah. I mean it was made into a pyramid.

Yeah.

And the pyramid, as you would expect, is stepwise from bottom up. I don't know. And this is my personal opinion that it's as pragmatic as it was once thought to be. And, and Heyman, as he's kind of collaborated with Shoemaker, has made it a little bit more pragmatic and palatable. And there's more options other than medications. There's more natural stuff that we can do and it doesn't have to be as, hey, I must do this in order to get to this. You still want to move in that sequential fashion, but there's less boxes to check to get to that endpoint treatment. And you have more options and tools in the toolkit to treat if someone is not getting better or not tolerating treatment. Because I mean, let's be real. This is personalized precision medicine. And I don't treat any SURS patient identically. I mean they're very similar because you have to be because you're treating the same condition. But at the same time, how I get to that point is different for every individual. For someone, they don't need much anti inflammatory support. For others, I need to throw everything we listed at them and they still feel like crap. It's like everyone's a little bit different. Most people are somewhere in between. But you just have to do your best. How do you, how do you monitor besides the clinical. Okay, this is better, this is better. How do you monitor how they're doing? Like how are you determining that they're getting better? From, from a physiologic standpoint, we're going.

To actually probably talk about in the treatment protocol. Oh, cool. I'll answer the question now because the next one we'll talk about is actually treatment. But one of the things you, you monitor is are you the vcs? Yeah. Are they the VCS normalizing? Have they cleared the mark ons? Because that you kind of literally are stuck there.

Yeah.

Because of the feedback with MSH and that whole. We talked about the hypothalamic dysregulation. If, if they still are creating these, these hemolysins from the, the Marcons, if they still don't have enough blood flow going to the back of their eyeball, which then leads down to all this other inflammatory stuff, the hypoxic inducible factor so their, their cells aren't getting enough oxygen. All the other stuff just isn't going to start working as well. So the really thing, once you do the basic lab testing and you know where you're at, yes, you track symptoms. Yes. You see how they're feeling. But ultimately you track their DCS and you track the mark ons and they need to be on binder of some sort until you clear, until the DCS normalizes, until the mark on clears. Now many of my patients, some similar years as well, that's like a six month, nine months long process. And so once you get, once you get there, a lot of them like you must keep them on some kind of binder, maybe fiber long term, realizing they're going to keep on getting exposure, you need to help that part of their disposal detoxification system.

Yeah, perfect. And then I'm sure we're going to talk about this a little bit, but I'd just like to allude to it with regards to the mark ons. Are we going to do a section on like myths and some other things as well?

Okay. Yeah, the myth. Yes, that's there. After we finish this, there's a whole section on myths. Okay, cool.

Because I wanted to talk a little bit about how you treat mark ons and then also if the mark on swab is negative but has other bacteria, what does that mean? What do you do about that and that kind of thing? Because there's, there's so many layers to each level of treatment as we go along. And I just feel like the more that we talk about, the more we inform individuals, you're, we're going to cover every possible scenario that might exist.

Actually on the myth section, that's not one of the 10 myths because that was a little too complicated. But we can tell that that is one of myths. So make sure. I'll write. Yeah. Okay, cool. Yeah, you have, you have amazing memories. So cool. So next, next time we're going to talk actually about treating chronic inflammatory response. Synergy, a lot of things we do and it's gonna be maybe more practical cause we've been doing it for years. So talk about like the protocol, what you're supposed to do, but then actually what happens in real life when you take care of patients. So hopefully this was helpful. This was our probably most deep sciency kind of one of these. All of these are basically, we're taking a deep dive into the blogs on our website. So please go there if you want to learn more about, see the images, see the biotoxin pathway. This was helpful. Please, like us, follow us, share this information again. We'll be doing a question and answer after we finish the five to six sessions. So to get your question and answer to be able to follow up with, that'd be great if you could follow us and we'll talk to y' all later.