Metabolomics, the Cell Danger Response, and Peptide Therapy

He created a series of medical symposia, uh, bringing together thought leaders and the international medical community, uh, focusing on chronic fatigue syndrome, um, Emmy Lyme disease, autoimmune disease autism, uh, in a collaborative mode. And he really loves collaborate and as innovative medical practice, uh, as he’s a university researcher, uh, which has been his lifelong dream is collaborating with, uh, multiple forces. Uh, he did a amazing paper with dr. Uh, uh, Robert [inaudible] on [inaudible] and we’ll, we’ll talk about what the heck that is a mitochondrial function, chronic inflammatory disease, uh, and is really bringing his dream to life with all this, uh, amazing new stuff and new ways of looking at things. Uh, in 2016, as I mentioned, he, uh, uh, coauthored a paper groundbreaking, uh, uh, paper with dr. [inaudible], um, the metabolic features of chronic fatigue syndrome published in the proceedings of national Academy of science or prestigious journal. Uh, he’s a medical advisor detect bio-science and is the GMA, uh, his, a collection site for Lyme disease, biobank providing samples for researchers. 

So it’s really doing the right thing and really searching for, uh, you know, what new ways look at things and, and researching, define, you know, cures and treatments for these illnesses that people don’t believe in. And it’s interesting if a doctor doesn’t understand it or doesn’t treat it, it doesn’t exist. It’s the patient’s fault. And it’s, it’s interesting. We’ll get into it where they did a study that, uh, you know, they could tell the history of chronic fatigue syndrome, five, five normals, uh, or doctors. Oh, there’s no, although we do our, just our panel, we can pick out someone with chronic fatigue syndrome, fibromyalgia, chronic Lyme versus a normal about 70, 80% of the time in how bad it is. So it’s kind of like, I think the chronic fatigue syndrome diagnosis, fibromyalgia diagnosis did a disservice to the patients, allowed doctors not to look at an anything underlying. So you’ve got this here’s nanny depressant, but, um, I’d like to welcome dr. Gordon, thank you for coming on our summit. Uh, uh, really looking forward to, uh, uh, talking about all your, uh, information, wonderful knowledge base and sharing that with.

Eric Gordon, M.D.

Thank you, Ken. Thank you again, it’s a, it’s a pleasure. It was really nice to hear how you, um, you know, just how difficult it is, treating people who are not respected because the doctor doesn’t understand. I mean, that, that, that’s, that’s been the bane of my existence. I got into, um, what we used to call alternative medicine and about 1990, 92. And, uh, it always, and it always amazed me how, um, you know, the sicker, the patient, the more the automatic eye roll of the doctor, Oh, plan B you know, um, the positive review of systems. And we have so many nice ways of saying that, uh, a patient is, um, you know, not stick on a Mylene green or, and it, it just broke my heart over the years to watch that. And, you know, we’d see these people and the more you saw her, the more you, the more you saw, you know, cause in the beginning I was kind of the same way. It’s like, can this be real? You know?

Kent Holtorf, M.D.

Yeah. And more and more, you know, doctors have one patient to choose an ICU and the doctor orders, a psych consult says it’s all psychological.

Eric Gordon, M.D.

Yeah. This site console that I just had a patient, unfortunately passed away last year, a young woman, 39. Um, and you know, that, that was, um, you know, she had been told at least 50 times that, you know, she needed psych consults. I mean, they, you know, in all the best places.

Kent Holtorf, M.D.

Oh yeah. And it’s like, you know, I’m sure you have the same as that. We have people start crying. Just the fact we’re working them up and believe them. And we’re like, yes, we’ve seen this before. Like, but you know, they told me this is crazy, you know, and I’m crazy. And then they start wondering if they are crazy, you know?

Eric Gordon, M.D.

Well, that, that, that, that, that is, is, is, is a problem. And that’s what so excited me about this Metalogix okay. Because, um, I had been looking my whole life as you four markers, what can we measure for people? You know? And, um, and we all, you know, we jumped down, you know, we, we, we always jump on the bandwagon of measuring this test and that test, but at the end of the day, they still just tell us if the patient is sick. You know, we have a lot of innate immune markers now thanks to dr. Shoemaker, you know, rich has been a great help, but I have a little disagreement. I just don’t think there’s specific markers. You know, these are just markers that you’re in

Kent Holtorf, M.D.

A lot of, a lot of things. Yeah, yeah,

Eric Gordon, M.D.

Yeah. You know, I mean, we started do measuring his stuff back in 2004 and you know, there they were, they are exciting, but there’s so much like that out there. You know, we have so many tests that tell us the person is sick, but we don’t know the sills and really tell us what’s wrong. Just their immune system is triggered, you know? And, um, and, and that that’s been the problem with getting our patients respect without a test we’re kind of left to that. Will we know that these people are sick. There’s there are very few diseases as, I mean, Horowitz, who’s very good at pointing out. There are very few diseases that give you transitory arthralgia. This just doesn’t happen. That’s why, you know,

Kent Holtorf, M.D.

They’ll basically say a standard infectious disease doc. Nope. They don’t have Lyme, but they’ve lost the power of basically exam and review of systems and history like, Hey, what else does that? Well, nothing else. Well, now your test is negative, you know? So what’s explaining it. I don’t know. It must be psychological. Yeah. So you know what the heck is metabolic.

Eric Gordon, M.D.

Okay. So , I mean, you can say it any which way you want. I don’t know the product a lot. I don’t know myself, but I, I guess it comes out of me as the metabolic mix. Um,

Kent Holtorf, M.D.

And then we did a George Bush there. Yeah.

Eric Gordon, M.D.

Nuclear. Yeah. Okay. Uh, um, this is looking at the small molecules in the body. These, they call them small, they lay about less than a thousand dolphins, which make them, um, you know, like the amino acids, uh, the glucose, um, the small, the smaller, um, small proteins, but most, and, um, and the fats, you know, and these are, we always looked at those as your, basically your raw materials for the body, but they’re also the end products of metabolism. So metabolomics measures, you know, the raw materials and metabolism and most of the end products, uh, you know, if you think of it, the genes are the blueprints. Okay. The enzymes tend to be the machines and the metal and the metabolites. 

Cause that’s what we’re measuring with. Metalogix its metabolites are the raw materials and the end products. And what has been so interesting about looking at better below mix is you start to see that, um, they are, what is controlling a lot of the information, the, this is the mechanism that allows for epigenetics. Okay. We talk a lot about epigenetics, but basically is the, um, you know, whether you met the late or assimilate or D methylator Tia stipulate, the histone. So you begin to expose different parts of DNA, which then will, um, give you, uh, another, um,

Kent Holtorf, M.D.

Just so the viewers, like with epigenetics, it’s how the environment affects the genes. So if you have a gene for like diabetes, let’s say that, um, if you, someone, two people on the same gene, one person eats great, you know, but other person, not so much that person will get it. But if someone who doesn’t have a gene, but they eat terrible, they’ll still get it. So the environment affects the genes that are, uh, uh, produced. But yes,

Eric Gordon, M.D.

Blow mix is the way that this is, um, is the intervening step. Okay. Um, like, cause I said, if you have too much glucose, you begin to like, like, like, um, cause glycosylation of proteins and you also, um, change how much insulin is made, you know, that happens because you’re turning genes on and off. Um, and so the dr NAVIO, um, got into this because he initially was doing a lot of work with inborn errors of metabolism. That’s, that’s usually lipid disorders in kids, things that will often cause death in the early, in the first 10 years of life. Um, and if you, of course, he was doing a lot of genetic work. That’s what he’s mostly doing. But as the more he did, the more he saw that genetics doesn’t predict much. Okay. Cause even two kids with the same gene defect have vastly different prognosis. And we see that all the time take, you know, um, Fallacemia or any, you know, anything, you know, you have the gene, but some people have symptoms and many people are asymptomatic. Um, it depends on whatever else is happening in the environment. And that’s where the metabolome directly talks to the genes turns them on and off.

Kent Holtorf, M.D.

And, and when you’re looking at the metabolome the metabolomics, are you looking at, like, it’s basically taking all these things, uh, measuring the amount of certain things. Are you looking at specific markers because there are so many, how do you interpret that?

Eric Gordon, M.D.

Well, that’s the thing is that, I mean, whether there’s 2000, 3000 or 5,000, they’re still arguing. Um, what, uh, generally what can be measured is somewhere between 500 and a thousand relatively easily, um, you can measure them and know what they are cause in, in Metalogix you can do, um, metabolomics is, is done using these days, using mass spectra of mass specs. And, uh, you know, it’s the kind of device that you can get a ton of information, but you just know something is there. You don’t know what it is, but when we, you miss your chemicals and identify them, usually you’re measuring about four or 500 and you can really identify what the chemical is. Um, and what we’ve been looking at. And the two we’ll take the chronic fatigue as an example is, um, at that point a doctor. And I just want to make it very clear that paper, which is a brilliant paper, right.

Eric Gordon, M.D.

Which is I supplied the patients, dr. NAVIO supplied the brains. It’s like, yeah, I know you did more than that, but basically, you know, I mean, I just want that weaker. Um, it’s uh, he had, he is an amazing thinker. I really think that if, if you actually look at his website and some of his ideas are just really, really, I think groundbreaking, cause he’s got a very eclectic background. He was originally used an MD who was got a PhD in virology and then went into inborn errors of metabolism and has a great interest in evolutionary biology as well. So he very broad and there’s some art, his recent articles, um, that on, um, the cell danger response and uh, on the healing cycle, I think are really worth looking at to get a broad view and we’ll come back to that. But, um, but just some people out there can get a copy of those articles, look up cell danger response. Yeah. It’s nav I a U X, you know, and he pressed it. 

NAVIO if you just stick that in and cell danger or just even CDR, your paper will show up. It’s there have been the same thing, chronic fatigue put chronic fatigue and NAVIO, and the paper will show up. Um, he’s also done a lot of work with autism. Um, and I’ll touch on that at the end if we have a minute. Uh, but what we, what we did in, um, the chronic fatigue, he looked at between four and 500 chemicals in patients, 20 males and 20 females. And that’s one of the important thing about metabolomics is that sex and age matter. Okay. And it’s not just the sex hormones, men and women are significantly different, even subtracting out the sex hormones. Um, and it’s just like they say, women are a little more complicated. 

I think if I remember correctly, if we, if we, we can hit a very good differentiation of chronic fatigue, patients from healthy patients in men looking at about eight chemicals in women that took at least 12. And even then we probably, because they’re a lot more complicated than we are. Um, but that was the beauty is what we saw is that, um, you know, we found basically about 40 chemicals that were two standard deviations from the mean from normal in people with chronic fatigue. Uh, the other thing that’s very interesting about it and he’s done this in, um, PTSD, uh, using, um, uh, people from, you know, in the Navy, uh, before and after this, uh, you know, Afghanistan and Iraq, um, he did it, he’s done it in depression with a large group from, from Denmark. Um, he’s done it in Gulf war syndrome, you know, I’m chronic fatigue and he’s now working on a lime cohort.

Kent Holtorf, M.D.

Yeah. And you know, when we look at our panel, you know, they’re your guys looking at 400 things and we do a 35, they think we’re crazy. We do so many things, but it’s, we see that the Lyme patients, the autistic patients, uh, Gulf war syndrome, patients there look the same, you know, that, I mean, just, um, that, you know, everything just like, wow, it’s they have this common pathophysiology. What we’ll talk about.

Eric Gordon, M.D.

Yeah. The comment is, is, is, is inflammation in different inflammation, stuck in different parts of Pat in different pathways? Because one of the things, I mean, this is just an aside it’s that we’re seeing is that we did two chronic fatigue studies with we buy only one of them has been published so far. The other one is kind of in the cab waiting to come out. And one of them was done almost all with my patients or I wouldn’t take my patients, your patients from my clinic. And, uh, the other one was predominantly patients, Paul Chaney. I don’t know if he knows a lot of people don’t know about Paul anymore because he’s kind of gotten quiet, but Paul was one of the original people, you know, Paul Chaney and, and, um, and Peterson, you know, basically what woke everybody up that this was happening.

Kent Holtorf, M.D.

Yeah. He got a lot of arrows too. Yeah, yeah, yeah.

Eric Gordon, M.D.

But the thing is, but what’s interesting is that Paul doesn’t quite believe as much in chronic Lyme as we do. And one of the things is that I, we did a lot of the people that are in the chronic fatigue group started off with Lyme disease. Years ago, we treated their line and their joint pains went away. There are a lot of their symptomatology went away what they were very, we were very careful to exclude anyone who had typical Lyme symptoms. What they were left with was to me, the hallmark of chronic fatigue, you know, post exertional, malaise, they couldn’t, their lives were limited if they did, you know, whatever it was, if they did two hours, four hours, whatever, if they pass that they crashed the next day or later that day. To me, that’s when they there’s. So many of the academic articles on chronic fatigue are not talking about chronic fatigue. These guys, the people in academia do not understand chronic.

Kent Holtorf, M.D.

Yeah. Yeah. I’ll wholeheartedly agree with that. Yeah.

Eric Gordon, M.D.

That they could. Phew. I mean, there’s no way you can confuse the depressed person. Okay. With someone with chronic fatigue. Yes. Some people with chronic fatigue get depressed, but you know, when your family abandons you, when you don’t, you can’t function, you can’t, you wouldn’t be depressed. You may get depressed, but that’s not, what’s wrong with you. And anyway, um, so getting back to, so w in our panels, what was so interesting is that, um, what we saw was these group of chemicals called sphingolipids single myelins and Sarah mites, things that I had never heard of. I mean, I had heard of in medical school, basically, actually, when I was in medical, I don’t know if even talked about that.

Kent Holtorf, M.D.

He hasn’t been in fire. Yeah. Okay.

Eric Gordon, M.D.

Right. Pretty much. I mean, you know, I always clapped the, um, uh, the, um, uh, what is it? See I’m getting full. I can’t remember things anyways. It doesn’t matter, but I would just, there, there were, there were, the library was not as big in the 1970s. It really wasn’t a prostate gland. There was, there was maybe three paper thin volumes on prostate gland against when I was in medical school. Okay. Now you could fill a library with things on prostate gland. That’s how far we have come with information. We haven’t learned that much, but we got a lot per patient. So the thing is, is that these liquid, these, um, glycolipids okay. Are a lot, which have a lot to do with exosomes. Interestingly enough. 

Um, you know, the exosomes are made up of these glyco lipid envelopes, a little bit, a few proteins inside. Well, these are, what’s abnormal, significantly abnormal in people with chronic illness, because they’re the, they are the signals that there’s chronic inflammation in the bloodstream. See? Cause that is one of the problems that metabolomics is. We’re looking again at the blood when many times the dysfunction is in an Oregon. And so we’re still looking at just the drainage from the system. And that’s why a lot of signals get lost because if it’s your liver or your kidneys that aren’t doing so well, but the rest of the body is doing okay. If you’re, you know, obviously if you’re measuring the end product of what the liver does, specially or the kidney does, specially you can discriminate. But sometimes you can’t tell when it’s just a little dysfunctional or maybe 20% of your liver is not working well. That’s where the money is someday. We’ll figure out how to really check that. But yeah.

Kent Holtorf, M.D.

Yeah. When you have on the cell signaling on the, on the cell surface, how do you get blood to check that?

Eric Gordon, M.D.

Yeah. Yeah. We’re, we’re, we’re checking the whole system, but we can see patterns. And that’s the important thing, the pattern of inflammation, and what’s interesting is the patterns. So the patterns are similar enough amongst different symptom groups. Like the Gulf war syndrome are significantly different from the line, people from the chronic fatigue people. Okay. But they’re all in that same ballpark, the single lipids are off, but they’re off sometimes in slightly different ways that would make it even more interesting. Okay. Is that amongst the people? 

And I said, we had about 40 metabolites that are abnormal, you know, in the chronic fatigue group and about, you know, 25% work had to do with having chronic fatigue were shared, but 75% of the abnormalities we’re individual we’re based on that person’s biochemistry, genetics, and environmental exposures. Right? All the other things that they have exactly. Can someone order these tests or is this all well, not yet. I mean, there are people selling small panels, but not yet. I mean, there’s a company called metabolome, which you can order your metal, your, your you’re a metabolic panel from, but they’re giving you, I don’t think you get really much information. How do you interpret it without looking at the rest, comparing it to the right. So at this point, metabolomics is, is still in the experimental field. I mean, we had one med tech bio that you had mentioned. We started tech bio with the idea that we were going to measure. We were going to be selling metabolic testing. This was back in 2016. 

When we first met, the first paper came out, we were all like, God, we gotta be doing this. And then we turned around and we discovered something. Is that the information really didn’t give us in chronic Leo people, a lot of treatment help. Yeah. Thanks. I’m sick. I know exactly. We could have been, we would have had to charge $1,500 for the test and it would have just told you, you have chronic fatigue. Now, if we had had a big enough sample size and I could have made an FDA diagnosis, you know, then maybe it’s still a lot of exactly what I had hoped. Okay. Just like, I’m sure you is that if you give me enough numbers, enough chemicals, I’m going to make, I’m going to change things. And this goes back to the big lesson, um, that has a lot to do with the cell danger response. 

But the big teaching for me is that what we saw is that just because something was high or something was low correcting, that didn’t change the system, sort of like we talked about in the beginning, the right supplement. Doesn’t always change the system when somebody is chronically ill, because what we’re dealing with is compensation because it’s a result. Yeah, exactly. And, you know, being a doctor, we got so used to, if you bleed, you know, if you’re low in blood, we give you blood, you know, their blood pressure talking to be lower. Everything’s a cycle. And

Kent Holtorf, M.D.

You know, where, what caused what, you know, the genes great days. And then they affect the genes. So what you know, where, where do you go? And everything, every system seems to be effective in these patients and, and where do you start? You know, one causes the other cause the other, and kind of doesn’t matter what the initial thing is now it’s this big vicious cycle. But, um, with like the cell dangerous bunches we’ll talk about, but mitochondria are key.

Eric Gordon, M.D.

Right. And actually, let me just one of, one of, um, another, another dr. Bob aphorism, um, is, you know, like the, the path to health is, is not the reverse. It’s not reversing the path to disease, you know, again, cause that is the way we often approach medicine because we are, our medicine is based on, uh, uh, uh, uh, trauma, uh, the story of trauma, you know, we’re, we really good. If you broken traumatically, we put you back together because the instigating event was the trigger and we just have to repair it, you know, just remove it and let the body heal. Unfortunately, with chronic illness, that doesn’t happen because the instigate, the thing that’s making you sick is your body’s response to the trauma. Just like we see with our line patients, you know, there’s a, I don’t know a significant number of people you’ll kill the bug. They’re better, but there’s even more that we get stuck with. You kill the bug. They’re still there. So anyway, so then they’ll sort you that mitochondria of how to think differently about disease and that is the mitochondria is, um, mitochondria have different forms. I mean, obviously we know you have like different mitochondria in your heart than in your fiberglass.

Kent Holtorf, M.D.

And let me just mention that, you know, mitochondria in the cell top early medical school, um, they’re basically an evolution they organism that was probably separate and came into the cells, but they were taught. They make the energy for the cell. That’s kind of what they do. That’s what we’re taught in medical school. And that’s what the ask, you know, 99% of doctors. That’s what they’re gonna say. So I just want them to explain what that is.

Eric Gordon, M.D.

Yeah. Right. And that type of mitochondria, that form is Bob has labeled M two and you can ignore the, the numbering. Um, I usually get them confused anyway, but he did. So, um, but this mitochondria, this is the mitochondria that’s functioning. You normally in your body and its job is to produce ATP efficiently. Okay. Um, energy, right. Energy, energy. And, um, and, and it makes some of the raw materials that allow you, that your body needs for, for growth. Um, but its main function is to take the energy that’s produced by burning glucose and make that efficiently into a lot of energy. Okay. By passing the electrons down the electron transport chain. Now that’s the [inaudible]. Now what happens is that if that, if that mitochondria starts to sense that it’s not getting its share which normal amount of raw materials it Browns out, my analogy is that it’s like the old days when you knew, um, you know, the vandals were coming, the, you know, the barbarians were invading. 

You would like burn the fields retreat into the castle and seal the walls. And so hopefully they would, they would, they wouldn’t be able to survive long enough to Lacy each and they move on. And so we do the same thing that mitochondria, when it senses that it’s not getting enough energy, it stops making as much ATP. And by doing that, it increases the, since mitochondria, when you make ATP is when you use oxygen, that’s when your body’s using oxygen. Okay. Um, you can burn, you can burn sugar without using oxygen, but, and we call that anaerobic glycolysis. But, um, what we, when the mitochondria are involved, it’s a aerobic, it’s using oxygen. So when that stops oxygen, concentration goes up in the cell and that creates a very oxidative, um, a rich environment. And so you have to, your nucleus then starts to pour out your antioxidants as a response. Okay. 

So, but the other thing that’s happening at that time is that mitochondria also start to take some of the ATP that it’s still making and put it onto the cell surface. And it becomes a signaling molecule and ATP adenosine triphosphate and, uh, and all of its derivatives, especially things like things that we think about like adenosine, our cell signaling molecules, these work like, um, Peregrine hormones. They’re giving information to the immune system at this nearby cells that there’s danger here. There’s a problem. And think this happens on an ongoing basis. I mean, this is kind of how we learn when ourselves actually put a little more ATP on the outside. If it’s a nerve cell, you learn faster. Okay. Cause you, you focus. I mean, you can’t focus on every, every input that comes into your body. So you have to know which ones to focus and danger focuses you at all levels, because this is a very conserved. This has been happening since we were amoebas, okay, this is the first thing and what happened and it creates what we call sickness behavior. You’re fatigued. You withdraw socially, you lose your appetite. You know, I mean, all these things are happening because you’re making less energy.

Kent Holtorf, M.D.

Yeah. And it’s like, I tell people to get the flu. It’s not the virus. Cause it’s your body’s response.

Eric Gordon, M.D.

Exactly. And what happens is that the mitochondria are directly involved in creating what they eat, the increasing the inter uh, interferon one group, which has made intracellularly and you know, starts to make the inflammatory home. And the thing that makes you feel sick. Okay. So that’s the, that’s the normal, um, well that, that that’s, that’s what happens when, so you have the, the normal mitochondria or making energy acute, then it goes to this [inaudible], which is like this battleship form of the mitochondria. Okay. And it also causes changes in the cell membrane, the cell membrane thickens, it starts getting less permeable. Cause it’s defending itself. It’s less, you, you stop communicating when the cell is really injured, like an injury, it stops communicating to the cells next to it because it’s got a heel. 

So this is, this is what’s happening when it’s healing. And then the next state is what we call the M zero stage is, and this is, this is what happens when you’re making energy by burning sugar. But the mitochondria have turned on again and are now using oxygen. So there’s no longer oxidative stress, but you are now using that ATP to make, you know, you’re not making ATP, you’re using the electron transport chain to make intermediate chemicals, um, things that make all your perimeters, which is part of your DNA and RNA, you know, and also chemicals that will help make hemoglobin and acid to Kuwait to help burn your fat. So you’re making all kinds of things that help the cell grow. This is what happens in a cancer cell. Okay. But this is also what’s happening in your normal cells when they are rebuilding after injury. 

Okay. And at that point they’re not communicating well with each other. And this is, this is one of the things if cells and then the next step is they go back in, the mitochondria are now operating normally, but now you’re in what we call the third stage of the cell danger response. And the cells are just beginning to begin to communicate with each other. And if they don’t fully go back to normal communication, we now have senescent cells, which is one of the dangers of aging. It’s not the dangerous, that’s probably how we do a lot of this aging process slowly falling apart is that we have more and more, um, cells that haven’t been able to come fully back online, they’re working. They just don’t have enough energy and they’re not communicating. You see, this is the thing is communicate, you know, remember that cooler. You’re old enough cool hand, Luke. You know, what we have here is a failure to communicate.

Kent Holtorf, M.D.

It’s interesting. And you know, with the mitochondria, I think, yes, almost every person who’s chronically ill, what’s their body temperature. You know, it’s low, we’ll check, everyone’s basal metabolic rate to come in the sick patients. They’re usually 25% lower, you know, so they’re burning less oxygen, making less heat, you know, you’re making energy or creating heat and they’re all low and they don’t eat anything and kind of, you know, they’ll gain weight unless they have, you know, terrible gut issues who can’t eat anything. But, um, it’s, it’s interesting. So yeah, we see that commonly, I think more and more, even on a subtle level where people don’t feel horrible, but very low metabolism or they’re kind of that early phase. Yeah.

Eric Gordon, M.D.

It, it, it’s, it’s, it’s where you get stuck, you know, that’s the thing, different diseases, get you stuck in different places and, and it can be happening in different. See what’s confusing is that we always want to make blanket statements, but it can be happening. You can have cells in your body that are stuck in the CDR one, you know, and then you might have slot of scarring and hypertrophy of tissue, or especially if it’s CDR dumps are CDR two, you’ll get a lot of scarring, you know, in CDR one you’ll have a lot of inflammation cause there’s usually, you’re still signaling the neutrophils to come cause problems in CDR. 

One because that’s, that’s that, that, that, that acute phase of inflammation that in some people doesn’t tone down. Um, so it helps us think a little bit about this. Um, what I’m hoping is going to do eventually is help us treat people as we, as we can measure metabolic comics and enough people, and eventually even be predictive. I mean, to me, the really hot thing is if I can measure your Metalogix at age 30 and see where you’re headed, especially through the lens of the genetics, you know, we’ve all been frustrated by the genetics. Cause remember, 20 years ago we thought, Oh boy, we’re going to open that book of genetics and get all the answers. And low and behold, we opened the book of genetics and we mostly get confusion,

Kent Holtorf, M.D.

You know, and that is, that is a problem. And like all, especially all these genetic tests going out, which I do like them is that really correlating them with, you know, with metabolomics and, you know, are, if you’re seeing the results, like I have people have, you know, myself, I have like every gene that’s terrible, I should have high homocysteine, but I don’t, you know? And, uh, so it’s, yeah, it’s interesting. I think yeah. Using it in correlating it with WhatsApp, WhatsApp

Eric Gordon, M.D.

With what’s happening because we, we, yeah, I’m genetics. Genetics is, is a mess because we didn’t realize how much is, um, uh, is variable. Ha ha. You know, we, we thought it was a binary system on off, and it’s not at all. And, but, but if we combine it with the metal below mix and the history of what we see, we can see where things are important and then treat appropriately, instead of putting people on 35 supplement, you know, it might my, my whole thing in life. Cause I said, I went through too many years with the, with the shopping bags. People would literally walk in with two shopping bags, full of supplements. And I hate that, you know, I made a lot of money with that for awhile, but I didn’t like it.

Kent Holtorf, M.D.

It kind of goes into treating a healthy person versus a chronically ill where I’d say treating the mitochondria that you can give them all these things, cookie 10. And, but if it’s not working, it’s not going to help or healthy person may get a little boost if, if they’re low, right. But chronically ill and you gotta look at it a little differently.

Eric Gordon, M.D.

Absolutely. You know, it was just some of the things we were talking about. There, there are, you know, there are some of those, the peptides that seem to work just in a very, um, benign manner, they always help almost everybody or they don’t hurt. And there are some of the peptides that seem to have some double edged sword to them. And that’s because I think they’re the ones that will work, um, powerfully in that CDR to mode when the body is in that place where it is acting actually like a cancer cell. But we want, you know, that that’s a time when using some of the, some of the interventions that will help the cell not kill itself is really good because you don’t want to lose a lot of brain cells or a lot of heart cells, you know, until you’re waiting for the, um, for the, for the basketball church to rebuild, you know, you’d rather not lose them cause they think they grow back, but not really well. 

So, so you would like to prolong their life. And so we, there are some peptides that will help do that, which is really great if you have a stroke or a heart attack, but if you’ve got a tumor, it might feed the tumor because it’s that same metabolism. The tumor is in that same metabolic phase of burning sugar to grow and using the mitochondria only to make raw materials, not using it for energy production, because it’s, that’s the important thing of, of, of, of where I think, um, understanding metabolic and this one was understanding med belongs, but thinking about the cell danger response, thinking about the cycles of what’s happening in the body now, it’s not easy. 

Cause, um, it’s just, we’re just, we’re making it up, learning it all at the same time, you know, getting that thought process going of like, am I dealing with a person who is going through just a, um, a normal healing process okay. After an injury, you know, there’s that six month, it could be a normal human process. Or am I dealing with somebody who was stuck in the early phase of inflammation and we can’t get them out of there, you know? And that would be, that would be a time. Um, you know, I think something like the BPC one 57 is because I think that’s what it helps do is help mobilize and get you to continue the healing phase.

Kent Holtorf, M.D.

Right, right. Yeah. And it, uh, he had so many, uh, things that does, it helps you to basically, um, heal and rejuvenate lower inflammation is what, what the peptides do you like?

Eric Gordon, M.D.

Well, at the BPC BPC [inaudible] is one of my favorites because, um, I, a lot of them, a lot of the patients, I don’t see a lot of patients anymore. Okay. And the patients, a lot of the ones that I have are people who have failed, um, not just what everybody else does, but also what I do. I send them out and they come back and, you know, and try and everything mentally, you know, 10% better here, 20% better there, I, I don’t live in the world of home runs anymore. Um, I missed that. But, um, the, but anyways, with those folks often, so many things are inflammatory. So the BPC going 57, I’ve been amazed that even people with major mass cell issues had been able to tolerate it.

Kent Holtorf, M.D.

Yeah. And that’s more and more becoming a big issue with these patients with pots, but really, I think it has to do with so many of these chronic infections, you know, basically mass cells are the allergic cell, but they we’ve learned that the basics create tons of inflammatory products, not necessarily just histamine cause allergic reaction. So, um, yeah, calming those down actually on part, a lot of mass cell mass white groups, they’re still stuck on directly inhibiting mass cell, but really looking upstream and affecting the immune system, which affects the mass cells. I think as much more effective means

Eric Gordon, M.D.

I’m, I’m I’m with you. I mean, that, that was something, um, when dr. Afrin first started writing about it, like, I, I had dinner with him in the first he’s he has changed the first dinner I had with him. He, he didn’t quite get how important it was to deal with the infections, but now he does. It’s really, I mean, I’m really impressed with that, man, because not many people learn. Okay. You know, especially when they, when, when they think they have the answer, you know, and he, you know, he really,

Kent Holtorf, M.D.

Yeah. I posted a, um, on that girl, but I said, you can kick me out of the group, but this is what I’ve found that works, you know, against what even these amaz guys consider really smart, dedicated people in there too. And I’ve seen you post a lot too. Yeah.

Eric Gordon, M.D.

Yeah. It, it, it it’s, it’s, it’s just, it’s nice to see, but it would put the mass cell. So that’s the other thing, that’s fun thing that, you know, Bob pointed out to me, the mass cell is the original immune cell. The first in the Mo when you have a multiorgan system, no system, the first immune cell that popped up long before T cells and B cells and macrophytes, this was the mass cell. So that’s why it is. So it seems to be everywhere and do everything to our patients cause it’s primitive, but it makes like 200 different chemicals. And, um, you know, it’s, it’s so again, and treating it, I love your idea. You have to go a level one or two levels up to really help. So fix the immune system and probably the most important thing, the hardest, but sometimes the hardest thing is, is get that sympathetic nervous system off the roof because that’s what, you know, when you, when you stay ill, you can’t help it. You you’re, you’re, you’re activated, you’re you’re, you know, is that it gets turned down and simply it gets up. But if we can turn that down, we can often really ameliorate the mass cell issue as well. It’s just

Kent Holtorf, M.D.

In a little Pearl I, uh, lecture on is that one major stimulator to mass cells is corticotropin releasing hormone. So, you know, basically the sympathetic nervous system, you’re going to stimulate cortisol, which Prototron release hormone, stimulates ACTE H then secretes cortisol. So these patients will have even high, normal cortisol, but their ACE gauge is very high. So they’re just, you know, in fight or flight. But if you give a little more cortisol lower that ACGH, that lowers that CRH, oftentimes the symptoms get better.

Eric Gordon, M.D.

Yes. And that that’s the wise use of low dose cortisol is it is a true art.

Kent Holtorf, M.D.

Yeah. You got to in some people, you know, it’s, uh,

Eric Gordon, M.D.

Yeah. In a way, when you think of it, that really is, you know, um, and then Steve, you know, you know, cortisol is really not an amino acid peptide therapy say much places.

Kent Holtorf, M.D.

Yeah. And it actually, BPC will actually lower that CRH or lower the ActX we can check see. Right. Um, and when they’re high cortisol and you, I don’t want to give them cortisol, but their ACH is even higher. A BBC will actually, uh,

Eric Gordon, M.D.

Oh, thank you. That’s a really interesting Pearl. Yeah. I like that. I, you know, like many people I started off using BPC, you know, focused on the gut.

Kent Holtorf, M.D.

Yeah. And, and as the gut is very, you know, we’re finding more and more the gut brain gut, everything access. And it’s really, again, that epigenetics, um, you know, goes along with that. Um, and you just, I’m kind of getting close to ending here, uh, like the famous thins, the,

Eric Gordon, M.D.

Oh, I love the thought that the time it sends and again, in my population, I’ll often start off with assignments in beta for before I’ll use the alpha, you know, I just find that, you know, it’s, it’s often in people who are really have very reactive systems, I need to mellow the immune response

Kent Holtorf, M.D.

A bit. Yeah. And then just kind of, for everyone watching that, Sophie, if you look at it as over-simplification, you have kind of T H one, um, uh, which is the intercellular, uh, immunity in T to which it goes to age 17, but, um, and usually everyone’s out of balance. So this is kind of the inflammatory auto-immunity, uh, BPC lowers this T before kind of is a modulator both by MIS and alpha one really increases, uh, T H, which is good, but it also is growing kill infectious, and you can have more reaction, um, to that. So it’s often good to start with the BBC that the lowers that, that T H two and lowers that, that inflammation that people can tolerate. Um, and just a little side note to find Mulan, probably it’s much more anti-inflammatory than all the other pharmacists and for herps is that we use that. 

So just a side note And is that, that is always important because it’s, it’s, it’s balanced. I mean, and you know, when, when somebody is staying ill for a long time, um, you know, occasionally, you know, there’s no rules, you always want to make rules, but there aren’t any you do. Cause you have to same thing with like the LL 37 stuff, you know, which is a really nice immune just goes out there and like gives information immune system, you know, kind of kill, you know, in a lot of people it’s, it’s, it’s really easy, but in, in my patients, I go very, very, very, very gently and unfortunate. I don’t think we can get that anymore.

Eric Gordon, M.D.

Yeah, you can. But, uh, it’s hard to get harder and harder, but L 37 just sobered knows it’s a antimicrobial peptide. So it’s very broad spectrum viruses, bacteria. Um, but also like BPC, you don’t think of it as the antimicrobial peptide, but it kills viruses, candida. Um, and you know, one study showed that it, uh, killed the herpes virus and one, 100 at the dose of a cycle of IR, um, we will have BPC with KPV, which is alpha monocyte stimulating hormone, uh, which is like, Malana tan makes you tan lose weight, Barbie doll, uh, peptide. Um, it’s a small fragment that, which doesn’t cause the pigmentation, but amazingly anti-inflammatory and antimicrobial, I would love that because you see old days we used and I still occasionally used, you know, when we could get, we put, now we have to use the Malana toy, but used to get MSH, you know, along with VIP, those are, I mean, this is another contribution of, of shoemakers, you know? I mean, like those, again, they really help reset the imbalanced immune response. You know, I was very, very, very impressed with those. So, I mean, I think that’s the, those are really, those are really important ones.

Kent Holtorf, M.D.

Yeah. It’s nice for that. That should be out, um, probably the next month, but yeah. Great studies on planetary bowel disease and, uh, uh auto-immune um, so you know, a lot of literature on it, which is nice.

Eric Gordon, M.D.

Yeah, no, no, that, that is, that is, is fascinating. It’s fascinating stuff. And you know, the microbiome just to say is that, that’s the other thing we can see a reflection in the microbiome we can end up there’s about 30 and probably more, um, chemicals that we can measure in the mid, in the metabolome and the, in [inaudible] in your blood that are clearly from your body, doesn’t make them, it was, it was the bugs in your gut. And a lot of them are,

Kent Holtorf, M.D.

And it’s interesting with this gut brain access that it goes both ways that the gut, you know, based fluids, the brain and the rest of the body, but also the rest of the body, the brain influence the gut. So it’s like you give all these probiotics, but then all of a sudden it’s back to the way it was, you know, because the influence the other way of what’s going on in the system. So it’s, it’s interesting. Yeah. Everything’s at

Eric Gordon, M.D.

Chicken, everything, you know that my, my, my favorite thing to say is, um, yeah, I have two favorites quotes. One of them is everything works. Sometimes I’ve used your line, actually lecture name that I just have to say. I mean, like I love, I I’ve worked with some brilliant practitioners over the years who, who have, uh, much more patience than I do and are able to like stick to one therapy for a while and you really get to see the full beauty of what it can do. I, on the other hand tend to be up, you know,

Kent Holtorf, M.D.

I’ve, I’m Mikey, I’m Andy D I’m moving on.

Eric Gordon, M.D.

Yeah. Moving on. Okay. That didn’t work, you know, I mean, and which is a shame, cause I have learned, thankfully I had these people around me, so I watched, and I learned through them that many times, if you wait three months, it does work.

Kent Holtorf, M.D.

Yeah. That’s about the max I give, but, and that’s the problem too. It gets very complicated. If you do treat Vinay works, that it doesn’t work, uh, that you treat and B doesn’t work and do, try to see it doesn’t work, but they do it together at work, you know? And so there’s so much to it yet.

Eric Gordon, M.D.

I was going to say, at some point I was going to make, is that when we’re, when people are stuck, I just, it’s not be, I just fully, I really believe that so much of chronic disease can be ameliorated, maybe not cured, but ameliorated and helped if people pay more attention to the fascia and the connective tissue and the musculoskeletal system, because that is often where you’re getting that, where the glitch is in the feedback from the central nervous system to the Oregon and vice versa is because those nerves are often very sensitive to, um, fascial tension. And to be honest, just like, you know, the acupuncture meridians are probably flowing through the fascia and if that’s all tight, that’s when you acupuncture just, you know, it doesn’t do much.

Kent Holtorf, M.D.

Yeah. And it’s interesting. I know dr. Neil has talked a lot about the fascia and go along with that, with just the practical, we have a STEM cell doctor and he comes, let’s say you have rotator cuff, right. Normally to inject in there, right. Next deal road, the STEM cells, right into where the, uh, you know, where all the problem is, he just does it sub kind of sub Q into the fascia. Right. And you’re like, how is that going to work? And 10 minutes later, the people who have full range of motion, um, it’s, it’s incredible. We’re thinking like, okay, this, this is, this is ridiculous.

Eric Gordon, M.D.

Yeah. It’s certainly, you know, I mean basically neural therapy, you know, is where we, we put information right below the skin that feeds into the sympathetics and they’re going right to the brain. I mean, it’s, this body is just so amazing. I mean, like, you know, it doesn’t matter. I mean, that’s, my, my dream is to have, is to have the team of, of, um, of people who can dance, who can treat different ways, but who can actually work together. One of the difficult things where you have seen over the many years that you’ve had your clinic is how hard it is to get the 18 Louie to work together.

Kent Holtorf, M.D.

Yeah. It’s hurting cats. Yes, yes, yes, yes. Yeah. So, yeah, you’re, you’re good at doing that. We, so I think we’re running out of time here. Um, and just want to say, uh, yeah,

Eric Gordon, M.D.

I hope, I hope, I hope people learned something. I, you know, it’s often hard to convey new complicated ideas, uh, in, um, yeah, in a short time, but I think the main message is that there are more forms of mitochondria than we knew then when you’ve thought about before and, uh, one. Yeah. And they do actually change shape in the mitochondria while they’re changing the, when they’re in the normal form, the [inaudible] they’re long strings, they kind of connect to each other. When you go into that game zone, they break apart, they stop connecting.

Kent Holtorf, M.D.

And yeah, I think there was a study, very old study where they did muscle biopsies in chronic fatigue syndrome patients and their mitochondria were very different.

Eric Gordon, M.D.

Oh yeah. Another conversation one day that isn’t directly related to peptide is a riff on a recent study of showing that serum from chronic fatigue. Patients actually has some interesting effects on normal people. But anyways, there’s so much to talk about, can you, you are make them sick, but you actually make them healthy, not healthy. You make them resistant to viral inspection.

Kent Holtorf, M.D.

Interesting. So, yeah, it’s all set up to fight. Yup. Yup. It’s price at a price. Yeah. Yeah. Nothing’s free. Well, always wonderful to talk to you. Um, always a new things. Uh, so really appreciate you being on with us and, uh, thanks so much.

Eric Gordon, M.D.

Okay. My pleasure. Okay. Bye. Bye. Bye. Looking. Where’s the button.