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Wellness by Designs - Practitioner Podcast
Understanding Metabolic Endotoxemia with Steven Judge
Metabolic Endotoxemia: The Gut–Gut-Inflammation Link You Can’t Ignore!
Could chronic, low-grade inflammation be rooted in your patient’s gut? In this compelling episode, naturopath Steven Judge unpacks the emerging science of metabolic endotoxemia—where bacterial endotoxins (LPS) escape a compromised gut barrier and trigger systemic immune responses linked to cardiovascular disease, insulin resistance, endometriosis, and more.
You'll gain a deeper understanding of intestinal hyperpermeability, toll-like receptor activation, and how to identify root causes like stress, toxin exposure, and circadian disruption.
Steven also shares evidence-based tools—including omega-3s, polyphenols, PEA, and bovine immunoglobulins—to help reduce the inflammatory load and support long-term gut healing.
This episode is a must-listen for practitioners wanting to connect ancient gut wisdom with today’s cutting-edge clinical practice.
Connect with Steven: Steven Judge Clinical Naturopathy
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DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health
Music. This is Wellness by Designs, and I'm your host, andrew Whitfield-Cook. This is Wellness by Designs, and I'm your host, andrew Whitfield-Cook. And joining us again today is Stephen Judge, a naturopath and nutritionist who specialises in complex, chronic gut issues. Today, we're going to be speaking about metabolic endotoxemia. All diseases have a gut component. Welcome back to Wellness by Designs, stephen. How are you?
Speaker 2:thanks, angela.
Speaker 1:I'm great thanks for having me again absolute pleasure and thank you so much for joining us today. So I think we start off with what is in metabolic endotoxemia and where is it applicable yeah, sure.
Speaker 2:So before defining that, I guess to provide the context as a reminder, you know what is this concept of so-called leaky gut or intestinal hyperpermeability? Right, so the intestinal barrier wall is a gatekeeper, right, physiologically healthy gut. This barrier should selectively be allowing macro and micronutrients and water through the gut wall and into our bloodstreams so that these components can be sent to the organs and tissues that need them. So we could say that the lining of our gut wall should be selectively permeable, right, so it should only be letting through what needs to go through and it should not be letting anything through that shouldn't be found in circulation, so microbial toxins, bacteria, metabolic waste, et cetera. And the structure of the intestinal barrier wall is like this three-layered membrane. So the first layer is the single-celled semi-permeable layer of epithelial cells held together by tight junctions. On top of this is a double layer of mucus on top of these cells and the gut bacteria reside on top of that mucus layer. Due to various factors, what can happen is the tight junctions between those epithelial cells on the first layer can degrade, gaps can form in the lining of this wall, subsequently increase the barrier's permeability, leading to what we call intestinal hyperpermeability, aka leaky gut.
Speaker 2:So the loss of integrity in the health of this barrier, aka leaky gut, has been suggested for decades, you know, if not longer, um to supposedly lead to or be a contributing factor to a variety of symptoms and conditions like not just digestive, but metabolic and neurological and autoimmune. And all these things, and what the research on this area called metabolic endotoxemia is highlighting is that it appears that, okay, it looks like everything really does start in the gut, or is driven by a leaky gut, so to speak, and the mechanisms of metabolic endotoxemia explains this very well at a very specific kind of biochemical level. And, yeah, the research is confirming there's a lot of truth to the concept of so-called leaky gut, which is amazing because, considering that, considering the wisdom of ancient traditions have held this perspective for centuries. Right In Ayurvedaveda, you know, they've always taught that the agni, or digestifies, the key to optimal health in tcm, spleen and stomach, qi are fundamental to overall health and they are a fundamental component of the digestive system, and Hippocrates said that death sits in our bowels and Henry Lindlar said that, you know, um, the accumulated, accumulated morbid matter and systemic poisons that are reabsorbed are what drives disease. So, yeah, it's kind of cool that this field of research on metabolic endotoxemia is starting to confirm all this right.
Speaker 2:So, with all that right so with endotoxemia, the the simple definition of it, which I'll expand upon, is a condition where there are excessive levels of something called lps, short for lipopolysaccharide, in the bloodstream. And so the term endotoxin, which is what lps is referred to. It comes from the greek word endo, meaning within, because lps is a molecule found within the outer membrane of specifically gram negative bacteria. It's what differentiates gram negative bacteria from gram-positive bacteria. It is this LPS that is housed within the outer membrane. And you know, lps inherently shouldn't be an issue. And you know, while a healthy gut wall can handle a small amount of LPS getting into circulation and be appropriately handled by the liver to be cleared from the body, it shouldn't, this LPS, endotoxin should not be getting through that gut wall in large amounts.
Speaker 2:If excessive levels of LPS do get into systemic circulation due to the gut being too permeable, this essentially triggers the innate immune system, leading to this chronic, low-grade subclinical inflammation.
Speaker 2:And, as we know, you know, the chronic inflammatory state is increasingly recognized as a key driver of most chronic diseases.
Speaker 2:Um, so we have to step back and go, okay.
Speaker 2:Well what's driving chronic inflammation in all of these chronic diseases, and we are repeatedly being brought back to the gut, and specifically this endotoxemic mechanism is a very common explanation linking all these conditions together.
Speaker 2:So you know, we're essentially looking at the downstream effect of specific types of dysbiosis or bacterial imbalances and a hyperpermeable gut wall. So if someone has LPS producing bacteria dominating their microbiome and their gut wall becomes too permeable, this is essentially going to lead to metabolic endotoxemia and so the excessive LPS endotoxin in the bloodstream. It triggers the innate immune system in some very specific ways, which we'll get into, because the immune and kind of subsequent inflammatory chemicals that are triggered as a result of this can interact with and impact such a wide variety of tissues and organs in the body, which is why so many conditions are being linked back to endotoxemia, which is so interesting, and so the term metabolic endotoxemia is simply a term researchers came up with to describe when this successive LPS in the bloodstream was observed to directly kind of be the beginnings of metabolic disorders such as insulin resistance and obesity and that kind of thing.
Speaker 1:So just, there's so many questions floating around about LPS. Firstly, let's talk about that quote-unquote leaky gut. So first things first. It was Brad Leach who basically helped to dismantle that syndrome issue. There's no leaky gut syndrome. It's not a syndrome. That's kind of like saying there's a pain syndrome or a breathing syndrome but there is leaky gut and there is excessive leaky gut, yeah, but it's not a defined syndrome, if you like. So thank you, brad, for doing that, and I've watched Vlad's career blossom over the years, which is great to see. One of my questions, though, is that kids and the elderly have naturally more leaky guts, even leaky brains. How does this tie into function versus dysfunction?
Speaker 2:Yes, love your work, brad. And I agree. You know like I'm very careful when with clients, when discussing these topics of leaky gut, gut dysbiosis, sibo, et cetera. I don't like to refer to them as conditions or diseases, so to speak, even though when you read about things like metabolic endotoxemia in the research it gets referred to as like a condition, um, so to speak, um. But you know the danger there with um, particularly with clients who, um are desperately looking for a, um, a reason for why they're so unwell and what's kind of the quote-unquote root cause of their illness.
Speaker 2:I'm very careful with my language these days to make sure people understand that leaky gut is certainly not a syndrome or a condition. It's just something, that it is the downstream effect of a variety of upstream contributing root causes. I'm very careful to say look, leaky gut, sure it's become a contributing factor to um, perpetuating a disease related to chronic inflammation, but it's that I wouldn't say it's the root cause, because what can happen is people can become a bit too reductionist about it and they're just looking for the next antimicrobial protocol and the next probiotic and it's not to say those interventions are not useful and helpful, but it's like one-tenth of the picture, you know. So while it is helpful to get reductionist about it and get into the mechanics of it, at the end of the day to address all this you kind of actually just have to zoom out and address someone's overall health. Really, you know.
Speaker 1:Yeah, I totally agree with you. I think it was Dr McLion who saliently pointed it out about this kill-kill mentality and he said what happens, particularly with extremely sick people chronic fatigue people, multiple chemical sensitivity, et cetera is you kill everything off in the gut and they've got nothing. So they become what's called the mashed potato and peas brigade and they end up cycling at a lower ebb. They never revitalise their system. So I love what you say about we've got to dig down, or you know, to the root causes. So let's start with those causes.
Speaker 2:Stress, anyone, yeah, yeah, and to your point, like, for example, just recently, you know very recently, in the past number of years, you know there's a lot of awareness around. You know, one of the conditions it's a new study came out, a few weeks ago I think, on an lps producing bacterial overgrowth being commonly associated in women with endometriosis. Um, okay, cool, it's another study looking at this lps endotoxemic link with endometriosis. But then what I see and you know this is just in the online world, but like what I see from the general public and even some practitioners, you know, following from that, which is like cool, this, there's this research here confirming this link with endotoxemia. But then what can happen is people go, okay, cool, the solution, therefore, is going to be how do we kill this bacteria? Um, what are all the things to get this bacteria Like?
Speaker 2:It becomes this almost like conventional medical germ theory kind of discussion. It's like, look, it's absolutely wonderful, there's another link to proving this whole and its relationship to perpetual endometriosis. But I guess, like, the dealing with the bacterial overgrowth is just one piece of this puzzle. You know, it's almost like a damage control kind of style of treatment. Cool, we want to get on top of that. But, like, in the longer term, to get on top of this and educate people about how, to you know, truly reverse LPS kind of endotoxemia and leaky gut we have to zoom out and go and go, cool. But what led to that type of bacterial overgrowth, right and to your point? Yes, stress, nervous system dysregulation, circadian rhythm disruption and poor sleep it was huge, like um a bit more longer term to consider and address. But, like toxicant exposures, the amount of environmental toxicants, um, and medications people being exposed to which you know are perpetuating this on a deeper level, long term, is huge.
Speaker 2:Um, yeah, we've got there's so much to consider, so to speak, um but that doesn't mean in the short term we can get very hyper focused on the gut environment and begin to reduce that lps load. That's still important it like, particularly at the beginning. Just start getting that chronic inflammation down just just a point.
Speaker 1:You made that um dysbiosis and endometriosis paper, was that that wouldn't have been written by justin sinkley, would it, I think?
Speaker 1:he's on a paper I think he has, and and and I also take your point there was a, an author, one of my favorite, uh, microbiota authors, katherine lozapone, who years ago now, and she used the analogy of a garden and things like that, which you know some people don't, but in there she spoke about now she mentioned the American spelling, acetaminophen, which in Australia is paracetamol, and paracetamol overuse, leading to increased amounts of P-cresol, which is a metabolic byproduct, which is one of the byproducts which can affect heart function, particularly in those people with kidney disease, when they can't get rid of it. It's just amazing. So you're talking about this whole. It's not just there in the gut, it's the gut things that affect the gut and then the gut obviously flows out into the rest of the body, has to be handled by other tissues, not just the liver, but the kidneys, et cetera.
Speaker 2:has to be handled by other tissues, not just the liver, but the kidneys, etc.
Speaker 2:So you really have to treat the, the patient, in a holistic manner yeah, and like, I love to explain to clients that if you look at the etymology of the word dysbiosis, it's a greek word that means it's a greek word that means wrong living. So it's like yes, it's. You know, dysbiosis.
Speaker 2:Um is the manifestation, or again, the downstream effect, of many different things that do an accumulation of those things over a lifetime. Right, I know some people have this kind of um. There's typically like a um catalyst of an event that you know started everything, so to speak, like an antibiotic or gastro or something. But I don't know, I think I kind of feel like that's usually the straw in the camel's back, so to speak. Um, but yeah, you know, again, it's just, I really, really it can take. If people have never thought about it like this, it can take them a while to kind of get it. But it's just cause and effect like, yeah, dysbiosis is perpetuating and has now been left untreated for so long. It's led to a state of a permeable gut and endotoxemia, but there were things contributing to that dysbiosis over time I, I, you.
Speaker 1:You are so insightful, steven, I've got to say even the word dysbiosis, wrong living. We think wrong living of the bacteria within us.
Speaker 2:It's our wrong living that's caused this yeah, you know, and so poignant, yeah, I mean, when I first heard that I went wow, but that wasn't even explained to me in my training. I just said, oh well, bacteria become imbalanced and it's just something that happens and whatever. When you look more deeply and because you know again, like the medical, conventional medical model is very, um, germ phobic, let's say like um, very hardcore germ phobic. And you know, the opposite of dysbiosis is symbiosis. So we should be living with these organisms, um, we should not be afraid of them and phobic of them. And they're always, you know, even if they're quote unquote, um, imbalanced. They're always trying to serve us.
Speaker 2:So, you know, I think again there's this kind of in terms of supporting people who've got intense degrees of a permeable gut and lps getting into their bloodstream and driving endotoxemia, like, yes, we, we want to as quickly as possible reduce that endotoxic load and heal and seal that gut and reduce the populations of certain organisms in the gut that are perpetuating that. But not in this, you know, kind of black and white warfare mentality of, oh, we've just got to destroy all the bacteria. We have to really step back and try and get people to say cool, but like, why did this happen in the first place, and that's you know. There's a lot to unpack there over time. Yeah.
Speaker 1:So I guess much of your treatment phase, if you like, must be psychology teaching people how to address the psychology that's affecting their stress, that's affecting their physical aspects.
Speaker 2:Yeah, that has become pretty huge for me, like you know, people booking in predominantly for help with the gut issue and I don't't know. But I think a lot of people are expecting a prescription of all this kind of what I would call gut centric supplements, probiotics and robotics, and you know all the supplements for their gut, quote unquote. But I rarely actually do like when I first meet people, um, and you usually send them off for some testing in the meantime. Oh look, I'll usually whack them on some PHGG. But outside of that, I'm pretty much just supporting their nervous system and their stress and their sleep, because that is one of the major contributing factors to dysbiosis and leaky gut and why these imbalances are showing up in the first place. And you know, the gut just won't heal, so to speak, in a state of nervous system dysregulation. So I am, you know, hugely focused on that from the get-go.
Speaker 1:Can I ask, steven, what sort of assessments do you favor to check leaky gut? And I've got a second part to this question, sort of and that is what you mentioned before about working first on these areas that affect the endotoxemia or the leaky gut yeah, and yet people very often want a quick, not bang for buck, but a quick effect, yeah, so how do you balance the longer term issues with getting them feeling a little bit different? And and you know, I think that the term is different not necessarily all well, um, as long as they can feel a change, is that? Do you find that? Or do they need to feel well now?
Speaker 2:yeah, look, I guess that's as a clinician. Like you know, we obviously have this overarching theme if we want to treat the underlying causes, right. But you know, some people are in significant pain and distress and we absolutely want to give them symptom relief too, right, it's a bit of a um. So you know, when I first meet people and you know we're discussing testing, if we are getting testing. While we're waiting for that testing, you know, like I said, we do want some symptom relief and so, if appropriate, I try not to impose strict elimination diets on people unless they're pretty debilitated with symptoms, you know, and I see a need for them to establish a bit of a baseline. Like we need to calm all of your symptoms down, to establish a baseline of you know what it can feel like, like how is your body functioning when you remove the variable of all these foods coming in and perpetuating your symptoms, so that people aren't just chasing the next supplement when you know, because of their state of chronic inflammation and leaky gut, their diet is unfortunately making them very systematic. So, look, I will get into the elimination style diet area if appropriate, but some people, just based on what else might be going on, I may not see a need to take them that far and I will just, you know, give them some supplements to improve their sleep and support their nervous system or some, you know, just some herbal medicines to improve their gut function, like bitters or liver support. Yeah, it's kind of dependent on the person, um, but while I'm trying to get them some symptom relief and give them some foundational support at the beginning, um, with test, with the testing question, um, look, on paper, so there's two areas to this. Right, it's like if you have a dysbiotic gut with a dominance of lps producing bacteria, combined with a very leaky gut wall, that is going to lead to significant endotoxemia. So you know, on paper it's like okay, well, to see if someone truly does have a leaky gut, I'd go to the lactulose monotone test now in clinical reality just to save people some time and money.
Speaker 2:If we need to prioritize testing, I will go with microbiome testing as a big priority, just because I say to them look, whether or not it turns out, you truly have a very permeable gut wall. All the style of treatments we need to do anyway are going to treat a leaky gut. It's going to improve that. So I'm happy to safely assume because it's not going to treat a leaky gut. It's going to improve that. So I'm happy to safely assume because it's not going to change what I need to do for you.
Speaker 2:To begin with, if you want to check, cool, we can check. But at a minimum let's check that in six months, make sure it's, you know, actually gone, so to speak. And so the reason I want to prioritize the microbiome testing is like, cool, if our treatment's going to take care of a leaky gut anyway, I'd rather see what the entire microbial environment looks like and what your type of dysbiosis is, so to speak. You know, are there significant LPS bacterial overgrowths and or hydrogen sulfide overgrowths? I'd rather have the information that will help direct their treatment, if that makes sense. But if people want all the data, cool, we'll get it all. If that makes sense. But if people want all the data, cool, we'll get it all.
Speaker 2:Um, and you know I'm always, yeah, outside of gut testing, I'm again zooming out and looking at someone's overall health. So I'm always getting the appropriate pathology done, so to speak. And you know because, again, well, what contribute? What contributes to dysbiosis and leaky gut? Well, nutritional deficiencies and, you know, maybe some undiagnosed conditions that haven't been found, like gilbert syndrome and all that kind of thing, but that, yeah, that's generally my approach with testing yeah, um, you've just turned what I used to do on a ted.
Speaker 1:I used to favor the lactulose mannitol test and I totally get you. Yeah, I totally get you. So I used to favour the lactulose mannitol test because it's relatively inexpensive versus the microbiome testing. But I totally understand what you're saying, so thank you for that. That's great. That's actually really good. It gives you a lot more information about what's going on, because the other stuff is going to improve the lactulose management test anyway.
Speaker 2:so it's like yeah, yeah, because some I know it's like tests, don't guess, quote, unquote, it's like, but again it's not going to. It's not going to change my treatment too dramatically, at least to be, yeah, let's just get into it yeah you know, yeah, love it, love it.
Speaker 1:Um. So can we dive into a few conditions at all? You mentioned, for instance, you know your metabolic, neuro, autoimmune. Can we start with those? I know that this is, this is more than a broad brushstroke, but um, can we start with maybe those sorts of types of conditions?
Speaker 2:patients that come and see you with those For sure. So I guess to preface that, what I'll just briefly explain is like what happens once the LPS endotoxin is in circulation in excessive amounts, because this is honestly when you understand this.
Speaker 2:It's like okay, well, how does endo endo, how does pcos, how does insulin resistance relate to metabolic endotoxemia? It's like the same pathway, it's the same chain of events and then will just manifest in a different way depending on the person. So if lps endotoxin is in the circulation in excessive amounts, there's this very specific cascade of events where and this can get super dry and complicated. But if people want to um, this is awesome paper 2021 paper in frontiers of immunology, called the role of metabolic endotoxemia in systemic inflammation. Um, you know, that's the paper you'd give to anyone, especially like a health care, especially a health care practitioner, who's like still living under a rock and is skeptical about all this. Um, that explains it so well. But essentially, um, you know, lps gets in the bloodstream and binds to something called lbp. There's this lps lbp complex. It attracts the attention of CD14, so protein made of macrophages. It's part of the innate immune response and so the LPS-LBP complex gets transferred by CD14 to something called toll-like receptor 4.
Speaker 2:So when you start looking at all the research on metabolic endotoxemia and oh, what's going on with endotoxemia and endo and endoxemia and parkinson's, it's talks about many things, but particularly particularly this tlr4. So, um, with toll-like receptors. They are the principal inducers of innate immunity, and it's why sometimes you'll see what is endotoxemia. They define it as a chronic state of innate immune activation due to toll receptor activation, because the job of toll receptors is to detect the presence of microbes in circulation or their components, and so different types of TLR receptors are responsible for detecting specific types of microbes and components. Tlr4's job is to recognize lps, and so when it finds lps in circulation, it binds to this and there is this subsequent release of a myriad of inflammatory cytokines, um. So tlr4 activation activates nfcaptop, nfkb, which then leads to production of, you know, tnfa and toluquin one and toluquin six, etc. Um.
Speaker 2:So you know a cool way to think about it is like tlr4 detection of microbial components is considered the first line of defense against bacteria, the most extreme example of this being sepsis. Right, it's the same thing. It's just a much more end stage version of endotoxemia, if it gets bad enough. So when bacteria translocate into the gut and it overwhelms our immune system to the point that the inflammatory cytokines triggered by TLR4 lead to tissue damage and organ failure, right? So I think I was reading in that paper. The LPS levels observed in sepsis are about 15 times higher than those seen in individuals with what we call metabolic endotoxemia. This lower-grade endotoxemia, but it's the same thing happening on a lower-grade, subclinical level, but obviously people aren't, you know, having organ failure.
Speaker 1:But it's the same mechanism in the heart, gland.
Speaker 1:That's huge what you're saying there, stephen, because with sepsis it gallops along. You know, the early signs are so weird like they're more delirium and things like that that you would not associate with quote-unquote an infection. Yes, and yet just imagine, forgive me, sorry and their treatments for sepsis are not, let's say, optimal. You know, there was Paul Marrick trying to use his tap therapy. That's the. What is it? Thiamine, ascorbic acid and prednisolone, or prednisone, knocked on the head, if you like, by Monash University or poo-pooed by it. But nobody is looking, certainly in the orthodox world, about changing or treating the gut. Imagine, just imagine, if people presenting early enough with sepsis were treated with quite innocuous things given orally, like, I'm going to say, this serum bovine immunoglobulin complex, which I love, or probiotics like Saccharomyces boulardii or, you know, lactobacillus coagulans, whatever, rhamnosus LGG, whatever. Yeah, imagine if orthodox therapists started to embrace this in a hospital situation. Yeah, oh my God.
Speaker 2:Yeah, and you know, and again, to the lay person, or maybe even practitioners and people in healthcare, again, it's just a subtle use of language. For me I think it's important. But it's like, you know, sepsis isn't just an overnight random event of a bacterial invasion. It's like there was a sequence of events leading up to that. You know it's um, yes, once they got in in that to that degree, cool, you're going to need the damage control level of, you know, acute emergency treatment. Um, but, yeah, it's, this is huge in between gap. And but you know, even like I was reading a paper 2024 paper this year, august in onco target, a cancer journal, talking about how, in post-operative patients treated for colorectal cancer, it discussed the importance of gut barrier integrity in preventing bacterial lps endotoxin translocation into circulation after surgery. Because they're acknowledging that, due to the damage to the gut barrier post-surgery, if that gut wall is still quite permeable, it's the translocation of LPS compounds which increases their risk of local bowel and systemic cancers post-surgically in the future. So I thought that was really cool to read that they're looking at that and to note LPS trans because of this TLR4 activation pathway and the subsequent immune and inflammatory events. I mean, if you just pop google, pop med, a type of cancer, lps, endotoxemia all of them are being connected to this, like it's starting to be acknowledged. Um, you know, whether it's prostate or colorectal, um, you know, like helicobacter, and the risk of gastric tumors is a classic example as well. But, yeah, so once we understand that pathway, it's like, okay, cool.
Speaker 2:How does this relate to metabolic issues? You know, with atherosclerosis, obesity, type 2 diabetes, you know, the atherosclerosis one is a really interesting one because you know when LPS is essentially transported from the lumen into circulation via hyalomicrons, right? So, and there are different sizes of all these lipoproteins, right, you've got LDL, vldl, small, dense LDL, and LPS can bind to all of them, and you know. So the ability of the lipoproteins to bind to LPS, it's again, the body does everything very intentionally that binding of LDL to LPS is considered protective. You know the ldls are trying to prevent sepsis. They're like, oh shit, there's lps in the system. Bind to that, get it, recycle it through the liver and get it out.
Speaker 2:Um, the issue, and you know, in studies, this is partly how statins appear to work too um, because statins increase LDL receptors, which increases recycling of LDL and LPS from circulation. The issue, though, is that, you know, not all lipoproteins get recycled. The smaller, denser LDL particles don't get recycled, so LPS remains in circulation, and so it's like well, what happens then? Again? We go back to this kind of tlr for activation, so the lps triggers the innate immune system, um, and that forms a foam cell like soft plaque at the endophilium, and that is the beginning of atherosclerosis. This is so interesting.
Speaker 1:Oh, it's a. Look, there's a huge topic, look, it's a massive topic. Can I ask, though, at some stage we're talking about interventions, right? So when do you intervene with? You mentioned it partially hydrogenated guar gum, phtg, probiotics. We've spoken about the bovine serum. Immunoglobulins yes, when do you institute those things that heal the gut versus other things, like you know, nac, calcium deglucorate, other detox reg regimens, liver, gallbladder, herbs that might clear toxins? Do you work on, obviously, stress and psychology in that first diet and then what comes in Soothe the gut? When do you start clearing?
Speaker 2:Yeah, look, I do begin immediately. Um, the main, I mean pretty much these days, assuming against this, safely, assuming there's a degree of this permeability to deal with. And everyone's got a bit of despise is going on the end, from all the testing I do, everyone gets a very high dose of a, you know, purified third party um tested omega-3. That's really important. Um, there's research on the omega-3 for, you know, reducing LPS translocation and a dampening of TLR4 signaling and it's, you know, crucial to the nervous system. So the omega 3 is up there. The? Um, the bovine derived immunoglobulins is a really nice one I'll use at the beginning for some people and or once that results, about confirming things, it's really nice to again come in with that. You know, initial damage control, like okay, we've got to get this inflammatory load down as soon as possible by trying to neutralize and clear lps, like to start that process. So the immunoglobulins are really good for that, as is the fish oil. Um, as is, um, you know, prebiotics, you know prebiotics right, particularly um, the polyphenol variety, let's call it right. Oh, so I mean, yeah, they act as prebiotics, so to speak. So, um, yes, you know, like dietary, all our kind of like rich colored plants, so to speak.
Speaker 2:Um, pomegranate is a pretty incredible one. Um, may sneak that into someone initially, but if not always like pretty much everyone gets pomegranate for a variety of reasons. But in the context of um lps endotoxemia, um, you know there was, for example, there is a really cool human trial. It's a randomized trial pomegranate polyphenols given to overweight and obese people with hyperlipidemia over three weeks and it showed a significant decrease in plasma LPS binding protein, crp, while increasing butyrate-producing bacteria and decreasing pro-inflammatory organisms like methanobrevibacter. Decreasing pro-inflammatory organisms like methanobrevibacter. So polyphenols, particularly pomegranate, are kind of like the ultimate intervention for reducing LPS load, likely via feeding bacteria that reduce gut inflammation and heal a leaky gut and decreasing the bacteria that are perpetuating that issue.
Speaker 2:Yeah, honey oil, the immunoglobulins, um look some people, I will get them straight onto a curcumin just because it's um. The research on that for reducing gut inflammation and for permeable gut is just um, yeah, pretty awesome too yeah, cool and sorry.
Speaker 1:I mentioned things like you know, your calcium decalucrates, your nacs, your clearers, your phase yes yes um, can you give us a dose guesstimate, a dosing range that you might use and perhaps, if you might um you know, start off a little bit sheepishly in some people?
Speaker 2:yeah, yeah. So yeah, to your point there. Like something I haven't mentioned I should have is when we're getting a bunch of testing done. I make everyone do um an at-home transit test, right. So they consume um corn or sesame seeds first thing in the morning. Write down what time they did that and what time they first see it in their toilet bowl, because bowel movements this observation of bowel movements are notoriously not reliable to tell for someone to say whether or not they're constipated, so to speak. And having optimal transit time between 16 and 24 hours um is crucial because otherwise you're reabsorbing compounds right and that dramatically perpetuates and worsens a leaky gut lps issue um. So in that context hence it's kind of another win for phgg.
Speaker 2:But in that context, particularly in a female who has super obvious relative estrogen excess issues, I will very regularly put them on calcium deglucorate um to help the liver and the gut along um. That I'm usually doing like it's about a thousand milligram dose, kind of higher end dose, but that works so well. Um and nac does have some very cool um research on reducing kind of lps endotoxin load um and helping with um tight junction protein regulation. That, and we know it has. Again that what I might pull out, particularly if, on top of the gut issues, um, I've got a client who has got some pretty intense nervous system dysregulation and, you know, anxiousness and because of its kind of glutamate modulating kind of properties, um, you only need about 600 milligrams a day of that, I find. Um, it seems to do the job and it's super cheap. Um, yeah, so so many options, options to support all this.
Speaker 1:Right, this really depends on the person oh yeah, um diabetes, let's move on to that. Disorders, um, I mean, diabetes is so huge. You, you were talking about somebody, um I think with, was it? You were talking about somebody with polycystic ovarian syndrome. I know you were talking about women with estrogen problems. That was it. That was oh wording yeah, so can. Can we talk about that hormonal regulation then?
Speaker 2:yeah, so um with um. You know, addressing insulin resistance, I mean, like anything, there's many factors to consider, right, like sleep, diet, macronutrient, stress deficiencies, etc. Um, but you know I do see a lot of women with pcos and people on a weight loss journey and many things um, and you know, typically I wouldn't say most of those people have a chronic gut issue at the same time. So they're not thinking about linking up. But the research is pretty um strong on this point that you know, metabolic endotoxemia may actually be the primary insult, beginning the pathogenesis of something like type 2 diabetes due to its effects on insulin resistance, right, wow. So I think it's like the American Diabetic Association have been researching this since like 2007. American Diabetic Association have been researching this since like 2007. And you know, in this paper, you know, first of all they showed if you took that CD14 innate immune system protein out mice with it, you know, injected with LPS didn't have any immune activation, right. So just kind of clarifies one of the mechanisms. But again, this um tlr4 activation occurs due to excessive lps. There's there's so many mechanisms to back up that lps may be the primary insult. Like you know, the tl of tlr4 activation um reduces insulin sensitivity um by inhibiting insulin receptor activities and the inflammatory cytokines increase liver glucose production and subsequent chronic inflammation. It decreases glut4 translocation which prevents proper glucose uptake um. So this idea that the metabolic endotoxemia piece is what begins to make someone not so resistant sorry, not so sensitive to insulin is compelling, you know, because there's this big question when we talk about all this, like well, was it chicken or the egg? Right, who knows, maybe it's different depending on the person. But I think at the end of the day, because of the tlr4 activation induced by lps endotoxicity um, it needs to be considered. I think it's a really smart approach to say reducing insulin sensitivity um in people who, whether it's pcos or obesity and or right um, it does. You know it's not really going to change my approach and you know, with obesity as well, you know there's interesting research on that. You know Many people I know association isn't causation but in studies they do observe people with obesity have much, significantly higher populations of the LPS producing bacteria, gram-negative bacteria.
Speaker 2:And once there is, what the research shows, like, particularly on, like the effects of diet on LPS endotoxemia, is that if you give a quote-unquote normal weight versus an overweight individual a very endotoxic meal. It's a very high in, say, processed saturated fats and refined sugars. They both have a very similar endotoxic response but if you give that same meal to an obese person, their endotoxic response is significantly more toxic. Their endotoxic response is significantly more toxic. So it's kind of like once someone is obese and because the TLR4 activation that's on overdrives, kind of perpetuates fat storage and increases inflammatory cytokines, an obese person's endotoxic response to food is a lot stronger. Obese person's endotoxic response to food is a lot stronger. So taking an approach of investigating and addressing metabolic endotoxemia in that patient group is really important. And yeah, like really educating people on how to reduce and you know a strong endotoxic response in their diet.
Speaker 2:And again there's this question of what came first. You know a strong endotoxic response in their diet. And again there's this question of what came first. You know a higher endotoxic response to food due to being obese, or was it? You know weight gain due to high metabolic endotoxic responses to food, and you know, I mean you could argue on both sides. But there's some interesting research suggesting the metabolic metabolic endotoxemia preceded the obesity um, just based on studies showing that people who had more potent endotoxic responses to food um had a significantly increased risk of developing diabetes and obesity down the track. So you know, are some individuals pre-programmed with a certain microbiome to have more significantly endotoxic responses to food and therefore be at higher risk of developing metabolic issues? Is the argument?
Speaker 1:Stephen, can I ask just to give us an overview of I mean, this would be an overview of your mind, obviously, but give us an overview of what sort of journey these patients have. You know, if you can just try and think about a few patients that you've treated recently, recently around this concept of metabolic endotoxemia, can you give us a an example of of how they improve over time, what sort of conditions you've treated?
Speaker 2:yeah, look, I do see a lot of endometriosis, um, and so, for example, if I can think of some people recently and you know these clients particularly they're not well, you know, they're in a lot of pain and distress. They're desperately seeking solutions, right, and so they're absolutely a group who, while I'm begging on about treating the cause, I want to get them some symptom relief ASAP. Right, that's right. With these people, I love me some PEA and yeah, I guess, similar to the story what I was trying to say earlier, it's like, because people are so unwell and really want a solution and find out about this link with the gut. You know, again, a lot of these clients come in very focused on the gut and it, you know, I make sure I explain to people really well, yes, we're going to treat your gut, but, um, requiring that actually sorry, treating that actually requires us to zoom out and really support your overall health too. It's not just going to be a gut protocol of probiotics and it's a mix. You know some people that really hits home and they get it, um, and they're they're up for it. I'm looking at their overall kind of life and health and the sleep and the stress and all the things um, and others not so much Um, but I'd say the overwhelming majority of people, once you get that point across, they get it and you know their treatments are similar in some ways and different in others, just depending.
Speaker 2:But yeah, look, endo, I have really good results. I don't know why. It's just once you and they all. For example, endo has this big link with histamine as well, right, they're all. It's like cool, he's low histamine diet, it'll give you some relief, but it's not a solution. Um, so with the histamine conversation, everyone's like oh, I want to find it if I've got histamine bacteria in my gut. Honestly, 90% of them don't um, but 90 of them do have, like in my experience, significant overgrowth of e-coli, right, kind of classic lps, um, producing microorganisms. So I, I don't know, with endo, I find if you really get on top of that endotoxemia and you know, get gut centric and cool, reducing coli populations and all that kind of thing like they get significantly better um can I ask what dose of pea do you?
Speaker 1:what do you use?
Speaker 2:I'll go pretty high for the first month, like about 600 milligrams twice a day for a month, and then ideally reduce that back to a three to six hundred maintenance dose. But awesome, awesome for pain relief, right, because right, and when someone's in that degree of pain, it's like they don't care about the multiple variables of dysbiosis that they need to address over you know years. Just like, yes, but we need to get people symptom relief. So the the PEA is pretty incredible for that, like yeah and and do you take?
Speaker 1:do they take the PEA every day through their cycle or just when they're experiencing pain?
Speaker 2:no, I get them every day, every day, yeah, yeah, most people, it's such a huge issue, so under treated, poorly managed, poorly diagnosed. Yeah, it's a travesty, yeah, I mean you know when we talk about medications and okay, what contributes to leaky gut, dysphosis and lps? Okay, what medications? If the anti-inflammatories are shocking, you know they are very well known to perpetuate okay, well, what actually leads to these bacterial population? Um balances and yet some people are surviving on those meds and it's like cool, yes, that's some good alternatives.
Speaker 1:Um yeah, in in desperation. I've seen one woman, uh, taking the high dose ibuprofen, that's the 400 milligram tablets, just popping them, yeah, all day, trying to get relief because there was. She couldn't get relief from, uh, a doctor who was hesitant about using opioids and um, and so she was popping these ibuprofen during the day and had a gastric bleed. Yeah, so she was done either way.
Speaker 2:She, you know, yeah yeah, yeah, and you know again, a lot of this comes down to lifestyle and diet. And you know what's the saying Outcomes are generated by habits, but most you know people in chronic pain. They know what they need to do, but they can't deal with it you know.
Speaker 2:So the symptom relief is really important at the beginning. Right, that's what's the challenge about being a clinician. It's like cool, we want to treat the cause, but we also want to get you feeling better as soon as possible, without ignoring the root cause, you know.
Speaker 1:So pea is just a total winner for that and also I have to ask about omega-3 fish oil. You said that you you know you put a decent dose in. What dose do you use?
Speaker 2:uh usually about. I mean, I'm using uh fish oil with a very high ratio of EPA to DHA. So if someone's pretty inflamed, some pretty serious gut nervous system issues, I'll go about two to three grams total omega-3 with about a three to one ratio of EPA DHA. Yeah, I go pretty high dose with that. They may not need to take that much forever but again just to get as much impact on that inflammation and endotoxic stuff ASAP. Yeah, really high dose fish oil to begin with is very helpful Beautiful.
Speaker 1:We've learned so much from you, stephen. Just one last quick question where can we learn more now? You've? You've given us some great papers throughout this. I hope we're going to be putting these up on the website, um, and in the show notes, um. We'll definitely do that. Not, I hope, anything else. Any other seminal works? Have you got any courses, for instance?
Speaker 2:no, they're in the works. Um, you know, because I've been talking a lot um in this chat about, you know, symptom relief and damage control treatments for lps, and but there's a much bigger picture to um consider, right? Um, that's kind of what I'm in the process of developing a course on, because it's just it's not sustainable for me or clients like legit time or money to get through all of like, okay, what are the things I have to consider to get figure that all out in appointments. It's just not sustainable for anyone. Um, so and I'm a bit all or nothing, like I don't want to I well, I'm gonna make something which kind of covers everything, all these variables, and you know, here's the phases to go through and that isn't the work, so it'll be out eventually I look forward to that mind map.
Speaker 2:Oh my gosh. Yeah, it's been a process, but yeah. So until that is out, you can just find me rambling on my Instagram.
Speaker 1:Stephen Dutch, that's your path on my website.
Speaker 1:Yeah, I love your work, Stephen. I love your mind and I love that you don't just focus on the problem at hand but look at what's causing the problem. You can see it's pretty evident that you've got a lot of love and care that you give to your patients and it's not just in about a little bit of poking it with a symptom relief. You really want to get them well, you want to get them vital. I really applaud you and what you do. Thank you so much for your work.
Speaker 2:No worries, andrew, it's a really cool chat.
Speaker 1:Thank you everyone for joining us today. We're going to be putting up a heap of information for you in the show notes and remember you can catch up on all the other podcasts on the Designs for Health website. I'm Andrew Whitfield-Cook. This is Wellness by Designs.