Gut peptides - KPV, GHKCU, BPC157 and more!

Thank you for joining us for another episode of a gut feeling and today we have a part two on our peptide series podcast. Now I don't know how many parts this is going to be. There's still, you know, we've been talking about all the different peptides to talk about and we're going to lump a fair few in today but there's still a lot more for us to talk about. So who knows, this could be a 10 part series, probably not 10, but it could be a multi-part series. We'll see how we go and we'll see how you guys like it as well. So we did Thyrmison Beta or TB 500 last week. If you guys haven't listened to that, we're going to cover a little bit more about TB 500 well, more specifically Thyrmison Beta 4 today but we're not going to cover this stuff we covered last week. So I would recommend listening to that if you haven't. But if you guys are enjoying this content, then let us know. Should I send a message, you know, ask us questions on Instagram, let us know if you've got questions over, you know, more peptide content of this stuff you want us to cover when it comes to peptides, let us know. Dave, how are you doing? Yeah, I'm pretty good. This is a pretty meaty topic that we've decided to sink out teeth into. So we're going to see how it goes. Feeling a little bit nervous about how this is going to go about. We will see there's a lot we want to cover. So today we're going to cover the best peptides for gut healing and we're going to talk about, I'm going to let you guys know which ones we're going to talk about upfront. So we're going to talk about Thames and Beta 4. We're going to talk about BPC 157, which I'm sure you all know. We're going to talk about KPV. We're going to talk about Laras Tide acetate. Am I missing any? I'm going to touch on gel P1s. Yeah, they're just going to be some, do we say like cameos that we might just add in towards the back end of the podcast. Yep. You just want to break down some of the things around like glugon, peptide, one receptor agonist. And then I'm going to mention Vylon. So we'll get into that. Yeah. So they're going to be the key players we're asked to talk about today. Now peptides obviously they've become super popular over the last, I don't know, six months to a year. And part of that's because of the gel P1, I guess popularity, where people started to see how effective peptides can be. Which I think is it's a nice shift that's occurred. You know, over the last few years, it's been obviously a lot of pushback against peptides. It's been a lot of people casting doubt on to where the peptides could be effective, whether they could even have any impact in humans. And then suddenly gel P1s have hit the market and everyone knows someone who's using a gel P1 receptor agonist and has lost, you know, 30 kilos or something. And now people are looking at these compounds and saying, oh my god, they actually do something. So there's a whole stack of people now who are interested in other peptides because they've seen how effective they can be. Now these are things that we've both been using for years. I think probably both of us, we came to peptides because of the effect they have on the gut. And then as we started learning more about peptides, realized actually there's some other cool stuff here as well. And there's stuff from, you know, I guess like an anti-aging perspective in some stuff around body composition. Obviously there's stuff around the gel P1s and weight loss. And there's obviously all these other effects peptides can have and can be used for. But first and foremost, we were diving into these for gut health, weren't we? Yeah. And I want one thing we want to say is that, you know, so well, we see, you know, we would say these are gut peptides. But we also want to make it clear that the peptides that we're talking about here, they've got all these other benefits as well. Yeah. And you know, we have, I'm sure you're going to introduce this ago, but we're sort of going to break it down into a few different topics and we'll get into that. But we want to make it clear as well, okay, that there's also a lot of like crossover and overlap here. Yeah. So even though we're going to, like we're going to break it down to sections, okay, it doesn't mean that, so if we're talking about like IBD for example, and once again, you're going to introduce this, it doesn't mean that some of the other gut peptides that we've talked about, but mainly talked about with a particular category, does it, it doesn't have any benefits around the IBD condition or, and even my boss versa, yeah? And even more than that, that, you know, there's peptides we're going to talk about today from the perspective of gut health, but we might talk about these same peptides in the future when we talk about body composition or when we talk about injuries or healing or anti-acid. I might be treated with the liver. Yeah. Metabolic function, all these other things we might talk about in the future, we might bring up these same peptides again, because some of these peptides, like you mentioned, they're so diverse in the mechanisms of action, there's so many different things that they're doing. It's not just, I guess, concentrated to just one system in the body. So we're going to specifically, even neurological, yeah, like huge neurological benefits as well. So, yeah. But obviously we're going to laser in and focus on, you know, particular gastrointestinal disorders and gastrointestinal diseases. So do you want to introduce it? Yeah. Yeah. So we're absolutely not saying these peptides should or can only be used for these things we're going to talk about. Okay. That's, you know, one key message you want to get across because a lot of these peptides we're using for other things as well. Now, the way we do want to structure this episode is when we look at gut issues, you know, what are sort of some of the key gut dysfunctions that people are dealing with? And then if there were, say, one, maybe two peptides that someone would consider for that particular dysfunction, what might the most effective or almost, I guess, obvious dysby for those particular dysfunctions? Now you've mentioned that, you know, what all these peptides we're going to talk about realistically, they're probably all going to have benefit for all of these conditions. But we want to, I guess, particularly for some degree to some degree. Yeah. To some extent. We'll mention a little bit of that as we go. But just to help locate people into kind of where would you be starting when you're thinking about peptides and particular dysfunctions, we're going to talk about, I guess, the one or two key peptides we would start with for that particular dysfunction. Now in terms of dysfunctions, we're going to talk about celiac disease. We're going to talk about IBD conditions, which obviously is a fairly large umbrella term for, you know, Ulstrich colliders, trans disease. You could kind of put dive particular disease into there. And then we're going to talk about more generally leaky gut or intestinal hyperpamibility. Yes, there's going to be other gut issues that people are going to experience. Yes, forms of discourses that are going to kind of overlap with each of these as well. But I guess these are the broad categories we're going to talk about. All good? Yes. Yeah, let's get into it. Let's do it. So celiac disease? Yeah, let's start there. So I think it's probably important for people to understand what type of damage is taking place. Yeah. Now, I don't think we've done, I've actually done a podcast talking about white celiac hem. We may not have. I don't think we've done a celiac specific. Yeah, not directly on celiac disease. Okay, but obviously it can be a pretty common autoimmune gastrointestinal disease. I mean, 1% of the global population. Yeah, one point. It's something like 1% or 1.4% of the world population. And have you read some stats where they said a number of individuals impacted is doubling like every 15 years or something like that? Interesting. Yeah, so you see all these stats around it. Okay, now obviously I'm not saying that's 100% correct. Yeah, but look, it might be relatively accurate. But and also what I want to make clear is that we're not really going to go into the realms of like gene defects like polymorphisms. I mean, you know, like obviously, you know, talking about the H.O.A. DQ genes, which is like human leukocyte, edgian, H.O.A. complex. So the now obviously the risk of developing celiac is increased by certain variants. But we're not really, we're just talking about the actual. Yeah, this is nice celiac podcast. We might go into that in more detail in a future podcast, but someone who's got celiac hopefully they kind of know what that is and what that entails. Yeah, so we just want to talk about what actual damage has taken place. And then that's the segue into, you know, one of the major peptides when it talked about in regards to how it actually helps with that. Yeah, so so celiac is cryptopipacia and dilliatrophy. So what is dilliatrophy? Okay, this is actually caused by accelerated loss of enturocytes. Enturocytes are in high bunsenus, small intestine. They sit the tip of the, the tip of the bilae or it's decreased production of enturocytes by intestinal stem cells or ISEs, their progenocytes. So one intestinal stem cell repairs an entire patch of the epithelial lining within about seven days. So we're talking about tissue homeostasis, raperoneal, regenerative capacity of the gut lining. So really, and then with some like cryptopipacia, it's where the grooves, they are sort of elongated okay, compared to the normal intestinal lining, which basically have short cribs. So they have blunted or atropic dillitis. So just how you can have, just like you can have atrophy of muscle, you can have like atrophy of the dilline atrophy of the gut lining. So that's really the end one thing. And that's going to lead to things like deficiencies over time. This is why it's such a high percentage of individuals with celiac have things like eye and deficiency, mycognitive deficiency. And you know, obviously the standard treatment for celiac is going to be a gluten free diet. Yeah, we're not taking away from that. Obviously you need to go gluten free. And what you've talked about there in terms of damage to the villae, some of that over time can be reversed. Yeah. And even like they have actually found, and when we talk about the IBD conditions, we'll go into this in a lot more depth. But even with like complicated celiac disease, they actually showed that the number of panacellals was significantly reduced. So then when we're talking about some of the peptides that are really, they might cover more bases when it comes to the IBD conditions, you can see how they would also cover some of these aspects. And it's cross over again, okay, and cover some of the aspects of what has been damaged with something like celiac. Yeah. So if we could pick one peptide that's going to have the most effect here with celiac, obviously this stuff that you've mentioned with IBD, that could have effect as well. But what would be looking for mechanism wise, what kind of peptide might be most effective? Well, we'll be looking at something and once again, it is cross over, okay, that's normalizing the leaky tight junctions. So the tight junctions between like intestinal cells and sort of like reverse in these leaky gut junctions. Now once again, it is cross over because there's some other peptides, we're going to mention another one, BPC157, that's going to have benefits around that as well. But the peptide that we're going to talk about here is called lyrus tight acetate. And that's a synthetic eight amino acid peptide. Now, is anything you want to say before I give on, go ahead and tell that. About lyrus tight? Yeah. So, yeah, I mean, like it's interesting, if you look at lyrus start acetate, obviously this actually went fairly far as far as the research goes for celiac disease. I don't know when these studies were done exactly about 15 years ago or something like that. And it made it to pass phase two trials for celiac disease. And it was found to be effective in these phase two trials. And then obviously a third phase trial got written up and then it got abandoned. And obviously that's a shame because it was medication that had been made at the furthest as far as potential treatment options up until that point. And ultimately came down to the funding that would be required to fund such a large scale trial. So that doesn't mean the lyrus tight acetate didn't have any benefit. It simply meant that the resources weren't there to fund a large enough trial to potentially show exactly what benefit it does have because you do need a large population or sample in a trial like that. So unfortunately, it didn't make it any further. But there wasn't any, as far as I'm aware, there wasn't any safety issues that were picked up with it. And it certainly did show efficacy in the phase two trial. Well, I mean, if you look at some of the results of the lyrus tight acetate, it restored, distorted tight junctions. And obviously that's what we want. And the other thing just regards to the glider molecule, which is obviously what you find included. So within included, you've got the glider molecule and you've got gluinin. And so the glider molecule is the problematic molecule here. And one thing I do want to mention, like it was research, study, I think it might have been around about 2005, where, and this is not then trying to, they weren't trying to say that the glider molecule was all bad. Okay, they were just trying to understand what reaction it had in the gut lining. And what they found with the glider molecule, whether you were celiac, non-celiac, it actually had the same response within the gastrointestinal track, where it basically stimulated zonulin, which is the gatekeeper to the intercellular tight junctions. And so it basically dictates whether things like fluids and enzymes and proteins, like go through those intercellular tight junctions. So the glider molecule stimulates zonulin and it tells zonulin to open the tight junctions wider. And so the larystite acetate agate is good at preventing the glider molecule from permeating through the intestinal barrier. And so just in regards to the zonulin, the larystite was actually found to decrease the release of the zonulin. And so it's going to get a molecule that can actually lead to increased gut permeability and impaired like because of barrier. Yeah, which is why we selected this is the unparticular peptide we want to talk about. 4 cylactases because it has such a specific action there. Like to actually mitigate the zonulin increase in zonulin and the effect of that on permeability. Like that is so specific to what people with cylactases are experiencing. So that's a pretty cool mechanism of action there for larystite acetate. And larystite acetate. Yeah, yeah. So it's not interupt, yeah. Okay, but just on there because obviously you bought up like you're making it to, you know, what made it to the phase three clinical trials. And you know, that's the furthest in any other cyliac disease treatment, isn't it? Yeah. From my standpoint, I do think that there's some others now as well that have made it that far, but at that point, I believe it was the furthest. Yeah. And it does seem crazy when you would, when you obviously were mentioning, you know, what reasons they gave to obviously, they obviously discontinuing the trials. I mean, obviously they said it was down to the due to the number of new patients that they would require. Okay, well needed to add to be added. Okay, to the existing trials in order to have like significant results. But they're sort of like the results that they were finding. Okay, we're pretty, you know, we're pretty significant. And it just, for my perspective, it sort of just seems that it wasn't the, it just wasn't to the funded really. Okay. So it doesn't really make sense. It doesn't really make sort of like diving into the results. Yeah. You know, I don't know if you've seen these days. I saw some interviews from some of the researchers who were part of that, that team. And you know, these, these interviews were, you know, the best part of a decade ago or whenever these studies were being done. And they were talking really promising about these, about laryzotide. You know, they were talking about, hey, you know, we've, we've potentially found like this treatment for silly eye disease. You know, the data is looking really good. And this was like conventional avenues. And I think, I think maybe even like Mayo Clinic didn't interview or something like that. So it is interesting that this thing that had so much promise did get abandoned. Not because anything bad came out. But just because the, yeah, the funding required was going to be too much. So it is a shame. But, you know, obviously this is a compound that is accessible. People can still use it. And you can actually get this in oral form as well, yeah? So a lot of peptides obviously they need to be injected and you can only get them in injectable form. The laryzotide acetate does appear to be one that might be bioavailable early. Well, it's oral delivery. To my understanding, okay, it's, I mean, you know, it's non-jectable, yeah. So the, I mean, I think I might have said this to you like previously. I think I was reading some stuff when they talked about like trying to create something where there was a bit of a delayed release response to increase the sort of bioavailability. But yeah, oral delivery is going to be the preferred administration when it comes to laryzotide. You know, another thing that's pretty interesting and this is just sort of more, because you would actually look at the mechanisms behind laryzotide acetate and you're definitely going to say it's got also huge benefits around something else that we're going to talk about. Okay, which is hyperpermibility, which is every, like, you know, pig all this in this podcast, go wouldn't know as intestinal permeability or leaky gut. But that's a loosening and a wide need to intercell your tight junctions and a loss of the tight junction protons. And also I would say a loss of e-cat Aaron and we'll get into that maybe a little bit more later on. But the, so you would say just around those aspects go in terms of like decreasing the release of zonulin and, you know, some of the other things I mentioned, like normalizing like leaky tight junctions, get it's going to have, you know, benefits around that as well. And this is why we, this is why we sort of mentioned across over. But even, because if someone's got like more hyperpermibility, okay, they're, you know, the metabolites and the byproducts coming from bacteria, okay, these are sort of not contained within the gut. So there's more BT that's taking place, which is back to translocation, where basically these, you know, things like endotoxin, so things like lipopolyse accharides, LPS, it could obviously be other things as well. They, other metabolites, they basically are passing through those intracellular tight junctions more rapidly and they're getting into the paddock pulltel system, which is like bloodstream liver. And they start to overburden my other organs of the body, okay, like the liver, like the pancreas in the spleen kidneys. So you can actually, it was like a mouse model with the lyrus cytosotate, okay, where they showed that it might have, you know, benefits, like actually benefit like individuals that actually have like non-alcoholic fatty lip disease. So it actually reduced like indicators of like non-alcoholic fatty lip disease. Because of the reduction in the lipopolyse accharides. Well, you would say it's to do with like, yeah, mitigating the back to translocation, okay, so these things, so supporting that sort of like gut delivery access. So in the studies with the mice, lyrus cytosate, is so obviously they're the human trials, they use it early. So in all those animal studies as well as far as your where to the oral as well, they're never used and injectable. Well, you've really made me rack my brain here, okay, but I believe so. I don't want to say confidently, okay, because I'm sure, you know, a little while ago, okay, looking at those, those studies and those research papers, but I believe, I believe so. Because it's interesting, you know, we're looking at peptides here from a gut perspective, and we'll talk about this when we talk about BPC, but arguably if someone's using a peptide for gut health, if that peptide is available to be used orally, arguably that might be a better mode of delivery. And my understanding with lyrusatite acetate was that was partially why they went with oral delivery was because once that peptide enters systemic circulation is going to have less of a direct impact around the gut. And so if you can take it orally, it's going to act a little bit more locally in that area. So you would go in with BPC with some of these other compounds and maybe can be taken orally you might have a similar effect where if you're using it for the gut potentially taking it out of the, might be a better option. Yes, correct. Even like day when it comes to peptides, okay, if it's like neurological conditions, I'm just using this as a bit of an example. They would say that like an intranasal delivery, if it comes to standard things like, your crush injuries and traumatic brain injuries and so forth, to actually all put things like the brain barrier and so forth. Well, then the intranasal delivery might be a little bit more effective. Might be, yeah, it might be a preferred administration. So that would also apply to, you know, gastrointestinal disorder and gastrointestinal disorders. So moving on from Lair's tone acetate, unless there's anything else you want to say about it? I think that's some of the major points to be covered. So you've mentioned a few times with some overlap of stuff that maybe one might use your own IBD. So maybe let's jump into IBD now. Yeah, okay. So I mean, if we're talking about IBD conditions, so obviously inflammatory bowel disease. Now, the major ones that people would have heard of, okay, would be, you've got ulcerative clitus, then you've got crones, there's different forms of crones. So crones happens anywhere between, like the mouth to the rectum and people are going to have things like, what are the major ones? I think like 30% of all crones is actually crone zeliitis. So that's crones of the ilium, okay, and that's like the bottom section of the small intestine. But people can have things like perianal crones and then you've got colitis. Now, I would say to a certain extent, like diabetic and diabetic litis, which don't come under the category of like an IBD condition, but some of the damage that is actually taking place is very similar to a particular IBD condition, which would be ulcerative clitus, which we would say is significant goblet cell issues. And so we might, you know, elaborate on that a little bit more. Okay, but if we just talk about the type of damage that is taking place with like IBD disorders, they are characterized by an increase in like epithelial cell death. So that basically means there has to be compromising of intestinal stem cells. I mentioned them before. I see their progeny cells and the other one, okay, would be panacellas because panacellas help with things like, we NT protein, WNT pathway, sickly ADP ribose and in layman's terms, that is cell renewal of intestinal stem cells. So the intestinal stem cells, my point is I've really dependent on the panacellas. Now, if the, with these IBD conditions, I think I mentioned this before, like in when we did a podcast directly on, I said, well, if this is not the type of damage that is actually taking place with like IBD conditions, why when it comes to things like, you know, like obviously what I talked about with the intestinal stem cells, okay, there's such a big factor that they're actually looking at like transplantations, okay, all those cells into the inflamed gut area of people with like, like IBD patients or people with IBD to actually, so it's been considered to sort of reconstruct what the epithelial barrier. So that's really the damage that has taken place. Now, it's a bit of nuances as well. I generally say with individuals with Crohn's, they, and they've actually documented this. They're kind of, they often have like panacellas that have stopped working. Now, panacellas are very unique to the small intestine, only locating the small intestine, and they're the natural defense mechanisms within the gut lining. And for example, if you have a decrease in my A&P's, any microbial peptides from panacellas, then you are more prone to systemic diseases, like fatty liver, non-elcalic fatty liver disease, acute pancreatitis, chronic pancreatitis, just to know me if you. And the one of the big roles of panacellas, they're in charge of a process of sampling, so they're continuously sampling the intestinal microbiota from within the intestinal lumen or the small intestine to basically prevent gut dysbiosis, which is unbalanced gut microbiome. So basically say individuals with Crohn's, often they have panacellas that have just stopped working. Now, even some like ulcerative colitis, which is localized to the colon, and this is like University of Gothenburg in Sweden, okay, that actually showed there was a particular defect in a certain type of goblet cell, there's different types of goblet cells. So ultimately it's a goblet cell issue, and even with some like colitis, that's a goblet cell issue as well. That's an intestinal secretory cell, and without going too much depth with it, goblet cells, they're in charge of a process of sampling as well. They actually do help to keep like regular microbiome and deal with invading pathogens, but they actually help with the sampling of dietary substances, so what does that mean? They actually help to maintain gut tolerance. That's why if you look at things like ulcerative colitis and colitis and diabetic, and diabetic, what can they not maintain? They cannot maintain gut tolerance, and that's why they have the aggravation. Another last sort of thing that I want to mention around the IBD conditions, because it's relevant to what we're going to talk about, is so if you're looking at my Crohn's and ulcerative colitis, there's generally this ramp up, and it's more chronic and prolonged, like an activation of pro-inflammatory proteins. An example behind that, it's quite easy to find this data, that would be things like NF-capathy, which is being linked to accelerated aging, switches on your genetic predisposition for autoimmune disease and cancer, and it in like high amounts of things like interleconcircs, so they're significantly increased, and they drive chronic nucosyl inflammation. So we want to look at peptides, and this is the point that are covering as many of those bases as possible. Once again, we're not saying that there's we're not saying that there's not crossover with some of the other peptides we're mentioning. Yeah, absolutely. I got that. Yes, no, I think that's an important segue because our introduction, because the goal here is not just to use any peptide or hope for the best, even though there might still be some benefit to it. Like you said, how can we be more targeted if we actually identify what is the underlying issue or issues, and a particular thing we're looking at. So in the context here of IBD, obviously, like you said, there's a few different things that fall under IBD, and that might mean that we're looking at potentially a little bit more damage or loss around things like goblet cells or panorcells. We might be looking at an upregulation in information. And so there are the areas we want to be looking at as far as peptides go. What might be some of the peptides one might choose if we're trying to modulate those specific things? Well, one, we've actually dedicated an entire podcast to just talking about this one peptide. And obviously, in this podcast, we're only focusing on the huge benefits around the gut, and that is TB 500. Now, this is thymus and beta 4. Yeah, specifically thymus and beta 4 because usually it will refer to that the fragment. Yeah. So thymus and beta 4, which is made up of 43 amino acids, it's the most frequent thymus in the body, and you do actually find it within my plate loads, white blood cells. But what I want to mention here, they actually did find that thymus and beta 4 was quite prevalent within the intestinal epithelium. They actually did a, I think, called knockout and mice where they knocked out the thymus and beta 4 out of the intestinal epithelium, just to actually see what is the role the thymus and beta 4 within the intestinal epithelium. And that actually impeded on cell-cyclic, cell proliferation. So in layman's terms, that's like a netopology process of the gut lining. Pretty important. Yeah. So now, once again, just to make sure that people understand this, it needs to be TV 543AA, that's what we're talking about here, refers to the full length 43 amino acid. So that's a synthetic peptide that is mimicking them natural thymus and beta 4. That's what we're talking about here. So now, just to make sure to, you know, some of literature around the gut, they actually show thymus and beta 4 was, it showed, it put a significant ability to reduce like inflammatory cell infiltration and even reduce oxab stress in the inflamed colon. Yes, that was obviously performed on mice. Now, so it does have, the other thing is that thymus and beta 4 activates progenisels. And I think I've already mentioned this. Okay, so you've got progenisels in your heart, your progenisels in your lungs. So you've got like cardiac progenisels, like CD9, CD73, CD1, on 7 and thymus and beta 4 actually activates endogenous cardiac progenisels. And as I said, you've got progenisels in your lungs, like basal cells. Now, so thymus and beta 4 actually helps to activate progenisels. And the major progenisel within your gut lining is intestinal stem cells or ISEs, which I've already mentioned them. Now, the, the other thing that thymus and beta 4, because remember, we've already mentioned that if thymus got more significant damage to the gut lining, and I, I think I just bought this up with like, you know, compromisation. So it could be like deficient panacelles, a loss of panacelles, compromised panacelles, what, what, you know, defective panacelles, whatever that might be. Okay, so if that type of damage is taken place, then there's a decrease in the antimicrobial peptides. And so that decrease in the antimicrobial peptides, there's going to be more of these metabolites and bioproducts that are going to start to overburden like other organs in the body. And obviously one of those is, you know, the liver. So if we look at like LPS, which is obviously lipopolysaccharides, and there's different types of LPS and the major form of LPS that we talk about would be hexa acylated or hexacylation. And that's the one that's being linked to the, you know, oxido, nitro, satin stress in the brain, inflammation of the brain, molecular mimicry, molecular mimics, I won't go further than that, but the thing with LPS, it goes from like negative ground bacteria, it can both like directly and also like indirectly, participating in the development of non-alcoholic fatty lip disease. Now, if I'm subbedded for, or could play a role in the treatment of non-alcoholic fatty lip disease, 'cause it actually can help with the guttile of the raxus. Because I think we did cover this in the TB 500 or thompson-batifor podcast, where it does actually have huge benefits around the liver, and that's actually, it does actually help around things like liver fibrosis, or liver fibroids, so it's got like anti-fibotic effects, so in basically inhibits fibrosis. So it's got these benefits, you know, significant benefits around the liver, okay? But also, you know, protective, it's sort of like, once again, it's covering both aspects, it's covering the gut, and it's also covering the liver, so then it's supported around that guttile of raxus. The, there was, like an even like, I think they administered, I was a bit of a loop with this one, okay? They actually had like a lethal dose of LPS, like a endotoxin, and that created a significant reduction in blood thompson-batifor, but then they administered thompson-batifor, following the LPS dose in the mice, so once again, it was mice, and at lower levels of like inflammatory cytokines, even reduce our spectra-mortality, okay? Which is like death, like death rates, you know, significant protective, you know, benefits. The other, the last point that I sort of wanted to get across is a little bit different, what I'm talking about here, but I've mentioned this to you before, is just in regards to the, there's just an example around like a thing called suboric dermatitis, for people who don't know what I'm talking about, like just like dandruff, and they've actually used a, what's called like a recombinant human thompson-batifor, like it's like a bioengineered lab product version, like a gel basically, and they're using that topically, and they actually compared that to ketoconazole, which is what they use in anti-dandruff shampoos, but the problem with some of my ketoconazole, they actually suspended that in France, and ketoconazole is, basically has like a padatoxic side effect, so it actually can cause high levels of light in the injury, but they did a comparison between the thompson-batifor, like the gel, and the ketoconazole lotion for the scalp. Now, the thompson-batifor actually provided greater efficacy and sustained effect, okay? In the treatment of the scalp, so it was greater than the ketoconazole, but this is not really what it's about, it's more around the fact that the thompson-batifor dramatically improved microbiome homostasis on the scalp, so they actually shifted the scalp, like the scalp bacteria towards a healthier composition. The only reason I'm being this up, okay, because that would actually reiterate by getting the actual structure of, in this instance, the scalp, okay? But also the structure of the gut lining, if you get that right, and then you help with these, if I go to the gut lining, if you help with these, your particular epithelium in cells, great example would be like panna cells, which actually help to maintain microbiome homostasis and intestinal tract homostasis, then you're actually helping with this microbiome balance. That's what would be my point. - This is a really bad analogy, but I'm gonna give it anyway. I remember seeing this study on, it was kinda like how people interacted with place, okay, like with their local community. And they had areas where there was more litter and there was more graffiti, and I guess I planted the litter or whatever, I don't know how they did this. And individuals in those situations, they were less likely to do things like pick up litter, they were less likely to do sort of proactive behaviors in that environment when it was all messed up. And when they had environments that were cleaner, that there wasn't graffiti or whatever, and then there was a piece of litter that people were exposed to, they were more likely to actually pick it up. And so the environment actually influenced people's behavior, not a great analogy, but in a similar sense. - I'm not in there. - Yeah, it's some overlap. So when the gut environment or the skin environment or whatever microbiome we're looking at, when that's intact, then the inhabitants, they play along better. - Exactly right. - So what you've just said there, the skin with the skin, you're gonna see the same thing from a gut perspective as well. When the gut lining is, that it isn't damaged, it isn't compromised, you're gonna see microbiome, ratios improve, you're gonna see a better outcome there. - And this is the thing, so obviously I'm just using that as an example around the scalp, yeah, okay? Yeah, yeah, but obviously, I'm really making this about the actual structure of the gut lining itself. And so a lot of people were like, if you ask people, okay, what prevents gut disposes, which is like unbalanced gut microbiome, what's really gonna help with microbiome homeostasis. If you're asking your naturopaths and functional medicine practitioners, I don't wanna sound like I'm having a gold people here, maybe I am, but most of the time, what are they probably gonna say? They're gonna say things like pre-botics and probiotics and kimchi and sour crowd. Now, I'm not saying those things have no benefits, by the way, okay? They'll probably mention fiber and so forth. I'm not, once again, I'm not saying that those things don't have benefits, but if you look at it like, some way, panacellas, I mentioned them all the time, okay? But, you know, one of their major roles is to prevent gut disposes. It's one of their major roles, okay? Because I've talked about process of sampling, where they continuously sampling the intestinal microbiota from within the intestinal lumen and the small intestine to basically prevent gut disposes. Hard to put a percentage on it, okay? But there's such a key play around that, okay? If I was to take a guess, I'd say probably 65 to 70% of your ability to prevent that gut dispose is really coming down to them. That's how important they are. And so, I always say to people, do we really think that we would have been reliant on an external factor to really do that for us like all the time? Once again, it's not me saying that those things don't have benefits. I just want to make that clear. Now, when it comes to IBD, there's probably more so than the other conditions we're gonna talk about today, there is a high prevalence of disposes. And you've touched on that a little bit. So, you do tend to see things like increase amounts of EG coli, which is a negative gram bacteria producing LPS, which you've talked about. You do tend to see some literature showing a high prevalence of Candida, so yeast. And we're not gonna go too deep into like antimicrobial peptides, but there is another peptide which has some benefit around some of the inflammatory stuff you've touched on, but also could have a bit of an impact around some of the disposes that people might be experiencing with IBD as well, isn't it? - Yeah, so I'm assuming, okay, we're talking about KPV. - Yes, exactly. - So, for people who don't know what KPV is, it's classified as a tripeptide, so it's made up of like lysine, proline, dalline. So it comes under the, what is it, the alpha, melanocytes, stimulating hormone, sort of like, it's what, it's the melanocordon derived peptides. I think that's the kind of thing. - Same way we've talked about like, thymus and beta-4, and then TV 500 being like a small part of that thymus and beta-4 molecule, then KPV is a smaller part of this larger amino acid. And so like PT-1 for one or melanotan-2, these are even more than melanotan-1, these would be like, what would you say? Sort of larger sequences, I guess, of this amino acid profile we're talking about here with KPV. - Yes. And so, - Tymus I-BD conditions, you've already mentioned in K-Bad, are gonna be a lot more prone to gut disposis, which is unbalanced gum microbibes, and they're gonna have a lot of co-infection. They're gonna have multi-lay back-to-wishers. And this is where, if you're looking at the research around KPV, it's very interesting, and it seems pretty good. So the KPV can actually have anti-microbeur effects, and if you actually look at the literature, that was against like, staphocobusaurus. Now, there's more virulent forms of staphocobusaurus, and the thing with staphocobusaurus, which can also make up a small intestine back to overgrowth, it is very anti-bore resistance, very drug-resistant. So that's why you got like, you know, MRSI, okay, you got a multi-drug-resistant staphocobusaurus. It's just really hard to deal with. And so that's one, okay, that was actually shown to be effective against, and the other one was candidate-elbecence. Now, we're not obviously talking about the commensal forms of candidate-elbecence, which have actually been shown to help with like, mutual dissimilation, mutual absorption, and aspects around your MRSI, so obviously talking about the more virulent forms of candidate-elbecence, which actually have been linked to things like systemic diseases, that includes like cancer, fatty liver, non-alcoholic, fatty liver disease. So we're talking about the more virulent forms. So that would make it KDV, you know, relatively effective around what we're talking about here, which is like co-intextional multilayback to issues, because the other thing is that, you know, people with like IBD conditions, a lot of time they're gonna be used like, you know, drugs and medications to try and reduce the information. And when they're using those types of drugs and medications, a lot of time it can reduce the sort of like, the killing of the pathogens, okay, your ability to, you know, break down the bacteria or cell wall and like, realign the bacteria basically. But if you're taking something like KPV, not only would it actually help in regards to like, you know, reducing the information. But, It's not going to reduce the sort of like your ability to kill the pathogens. In fact, it's actually going to enhance it. That would be the big thing. And just around that inflammatory load, which you can actually find, I mean, KPV was actually shown to inhibit the activation of NFKB. We spoke about that. I think there was another one called MAP canace as well. These are just like inflammatory signaling pathways. And you obviously mentioned colliders, which is IBD condition and I've fixed the large intestine. Well, there was research where they looked at, where they basically induced colliders. A lot of time, you know, some of the compounds they use, there's one called DSS. It's called Dectrine, Soul Factsodium. So they actually showed that the KPV reduced the instances of the DSS induced colliders. So that's like, well, that's now getting down the realms of what's still, you could actually use that as potential treatment of IBD. I think they sort of concluded that within that research. So yeah, I don't know if there's anything you want to add around that. No, I think that's it. I mean, it's probably worth mentioning that as a very small peptide, it probably is bioavailable early as well. Yes, you could potentially take that. Well, I would say excellent oral bioavailability from what I've looked at. Some people talk about the delivery, who might elaborate on this a little bit more like like a cymo technology. I'm not sure around that. That's just me personally. I know you can use that injectable as well. Now, maybe for some of the mechanisms that I've been talking about, you could say like injectable could still be considered to be more effective. Once again, it just comes down to what you were talking about, whether you wanted to act more directly on the gut. But the injectable might still be considered to be more effective than by the oral forms, because for some of these mechanisms, it can bypass the digestive system, basically. So there would be an interesting combination. Someone didn't want to be injecting peptides, which I get a lot of people don't want to. Then from an IBD perspective, KPV, and I mean, obviously we've talked about that as a day to day, being bioavailable early as well, you could combine those two things. Yeah. You've talked about thomas in beta 4. Do we just want to inject it? Sorry, sorry to interrupt because I don't know if we mentioned this, but I just want to make sure we did. We did say obviously with the thomas in beta 4, obviously TB 543AA, but then I don't know if we said, well, it obviously has to be injectable. Yeah. Yeah. Yeah. Yeah. What else from an IBD perspective? If there was other peptides, one would want to consider? Well, I mean, obviously what I mentioned, Akale, was just around that, the aspects around that inflammatory load. I can't remember I mentioned this stuff. I mean, it's more prime-fumistry proteins than this, but I mentioned NFKAPAB and interleukin CX. So, then we really want to look at a peptide, Akale, that is really effective, that sort of like you're bringing down that inflammatory load. Now, one peptide, I think, is just one of the best around this, Akale, is GHKCU. Now, I'm sure we're just going to do want to go straight into some of the aspects around GHKCU, or do you want me to cover some of the aspects that might be. Now, people will know GHKCU as a topical peptide, that people might use for skin health, maybe they'll use it for hair-regrowth, and obviously it's got those benefits as well. Some people know it as helping with injuries, and connective tissue, and collagen synthesis, and again, those are amazing benefits as well. But it's not talked about all that much from a gut perspective. So, why are you listing it here for IBD? Well, once again, Akale, just around the. It's the ability to reduce the inflammatory load, I think it's. And you can definitely find some pretty good research around this. I think this was actually. They were doing this research in terms of like it possessing. Obviously, I mentioned LPS a go, but it possessing protective effects against. It might have been LPS induced acute lung injury. So, what they actually showed within that research is sort of like. It actually held with like inhibiting like problem-planetary processes. It also actually held with like acute respiratory distress syndrome as well. But basically in that research, it's suppressed like into lukinsix. It also de-activated like inflammatory genes, and there's actually. So it actually inhibited the synthesis of fibudogen. So fibudogen is a complex glycoprotein that is basically synthesis like bodily bath. But that's also involved in production of things like CRP, like C-reactive protein, SAA, which is like serum amyloid alpha. And even GHK, like within that same research, was shown to actually suppress like NFKB. I talked about that. Akale has been linked to like accelerating aging. And also I think like NFKB might be linked to things like rheumatoid arthritis and lupus and type 1 diabetes and multiple sclerosis and demionation. So there's actually shown to suppress like the NFKB. So really quite amazing for like bringing down the inflammatory load. I mean that's only one aspect. But I think even there was. Once again, I think it was to do with like LPS, to do with the lungs. And they looked like obviously LPS can activate like airway, epithelial cells and neutrophils and resulting in like a release of like pro-emptumatory medias, such as like reactive oxygen species and TNF alpha and interlecon sex, interlecon sex. And basically in the research they show that GHKB is pretty effective at inhibiting those pro-emptumatory processes. So yeah, from a lung perspective, this is not related to the gut, but it just made me think about it. Have you seen the stuff there around asthma and GHK? Now I mean, that's a great point because there's even a stuff around like restoration of like COPD, which is. So this is around like you know, lung disease and infancy, urine asthma. Okay, so I've definitely seen that. One thing I'll say because GHK is sort of like it's really like stem cell therapy because like GHK increases the expression of the thing called the P63 protein or the P63 gene. So basically stimulates the levels of this gene and the P63 protein, that metabolism plays an important role in like epithelial stem cell regeneration. Now so you know how I was talking about like intestinal stem cells, okay, their progenital cells go with this light stem cell therapy. Okay, it's like the replenishment and rejuvenation of like the other epithelium within the gusher and testicle trap. Now GHKCU is probably helping with most likely with this different types of progenital cells within lungs. The major type of progenital cell within the lungs is basal cells. And so the basal cells actually help to replenish and rejuvenate all the other epithelium within the airways like tuberolous cells and squamous cells and cobalt cells. So if it's doing that within the lungs, okay, you would say well, most likely, okay, going to have those benefits within the gut lining as well, that would be my point. Now one of the other functions or mechanisms around GHKCU was it's effect around up to your glating, situ and one activity. Now that obviously has benefit from an anti-aging perspective and some people know about like NAD and so that involvement in the situ and one involvement with NAD. But for me gut perspective, why would this stuff matter? Why would GHKCU help when we're looking at something like Clietus models or Ulstrich Clietus? Like what's it doing more there? Well, it probably would be down. I mean, if you look at, it probably would be down to obviously some of the things that I've already mentioned, especially around like, you know, regeneral cells like intestinal stem cells, in case of the ability to replace and rejuvenate like other damaged epithelium within the gastrointestinal tract. If you actually look at it, there was, I think they, I don't know if you mentioned this already, okay, but there was like a, so with Ulstrich Clietus, which is obviously localized to the colon, that's really a goblet cell issue. And so then goblet cells, there's a thing called Mug2, okay, which is their Mucin. And so Mucin is like a protective jaw-wired substance. It actually helps it like our spectra-ampathogen removal, but it's like protective layer for the gut lining, lubrication of the gut lining. And so Mug2 is produced and expressed from goblet cells, basically. And so if it's able, someone had, let's say I had a decrease in Muc2 or they had no Muc2, they, or they, okay, let's say they just had a decrease in the Muc2, they basically have like no Mucas. And now the bacteria is in direct contact with the epithelium and that would trigger information, okay, or that would trigger a response that you, similar to what you would see with Ulstrich Clietus, basically, okay. And so GHKCU demonstrated they have like, once you end that DSS sort of like, induced ulcerated glitis. That was in mice and it demonstrated like a therapeutic effect around that. And so it promoted like mucosal healing. It also enhanced like tight junction progeny expressions that basically means that even, you know, like GHKCU is still going to have benefits around things like hyperpermibility, leaky gut and testal permeability as well. But also reduced the number of like, GH17 cells. With GH17 in the case of obviously they talk about that in regards to like problem disorder, but GH17 increases interleukin-17. And interleukin-17 creates increases neutral recruitment. Now, neutrophils are a type of white butt cell. It doesn't mean they're bad, far from it, okay. But they make up anywhere between 50, 60, 70, 80% of your total white butt cell supply. But if there's too much neutral recruitment, okay, that can actually lead to a thing called on neutral gastrointestinal mediated injury, where your own immune system can end up damaging the gut lining. So my point is that GHKCU can reduce the number of things like TH7T, having that impact on interleukin-7T and even things like neutral recruitment. Now if someone's using GHKC topically, they're like, "Oh, that's my skin care routine or I'm using it from a hair." It's not going to enter, well, some of it might enter systemic circulation, but in probably some small amounts, it's not going to have these effects we're talking about here. So the question would be, how does one need to take GHKCU to do all these things you've just mentioned from your gut perspective? If it's not going to do that if you're using it, using it topically, can use it early? Or does it need to be injected? Yeah, so I would say there's a bit of merconous, a bit of gray. We're going to get into that. I mean, GHK is a matric ion, so it's basically classified as a small molecule peptide. Now it's basically how he's doing, how he's doing, how he's doing, how he's doing. I guess the, well, because, like, if you actually look at it when it comes to the skin, for a compound to be absorbed more efficiently into the skin, it needs to be, this is to do the molecular weight, it needs to be under 500 Dalton. So it looks on my GHKCU, I think it's just under the like 400 Dalton. I guess that's why it gets absorbed well into the skin. Now, when it comes to, so I guess one of the arguments that gets used around the, the all-by availability when it comes to GHKCU is they say that it's highly susceptible to the breakdown by digestive enzymes, especially this one called carboxypeptodase, which actually helps you to breakdown, you know, pro-tetanes, amino acids, and also the stomach acid. Now, so that's why they say you might need to look at, you know, certain things to improve the uptake of the GHKCU, you know, within the gastrointestinal tract, and that's why a lot of people talk about like liposomes or liposimal administration, which is like nanosyze liposomes. And the idea behind that is the liposomes that act like a tiny base bubbles, okay, that basically shield the peptide, like from the stomach acid. Now, the thing around that is that it's very, it's very hard to find literature that actually says what the oral biobailability of GHKCU is. Well, when I say it's very hard, I mean, I, you can't actually find anything, okay, that actually states what the oral biobailability is. So a lot of time it is based on, well, it's a proposed mechanism. And I'm, once again, I'm not saying that we might find out in, you know, two years time or three years time or five years, five years time that the oral biobailability of GHKCU without using my liposimal, like, well, maybe the oral biobailability might not be that great, okay, maybe the percentage might not be that great, okay. But my big point is we don't actually know. It is, don't know that information, yeah. We don't have that information, okay. And the other issue is we don't, so a lot of time when you're looking at the research around GHKCU when they're talking about the administration of that, they just suggest they don't actually state what the oral biobailability is, okay, if it's basically encapsulated into liposim, they just state that it could be administered orally when encapsulated into the liposim. But they don't say what the oral biobailability is. Does that make sense what I'm saying? Yeah, yeah. I mean, they're not comparing it to, they've got no baseline for what it's, it's standard biobailability is. So how can we know, how much is it in a hand, so we don't even know what we're starting with. So it is definitely, there's definitely a limitation then in the information that's available. And you know, it's, ultimately, you just can't really make claims and you can't possibly say this is how much more effective it's going to be if it's liposim, all of this is, you know, how much, you know, it's going to be, you know, usable in an oral form at all compared to injectable. We just don't know. I mean, like I've not seen anything that even really gives us anywhere to start with understanding that the best I've seen is that's my point. Yeah, yeah, yeah, this is no study point. I mean, there's, there's animal studies. It's my studies where they do use it orally. They use it in drinking water. And you know, there's one study I'm sure there's a few, but there's one where they use it for again, it's induced colliders or ulcerative colliders. And using it orally, they note the improvements in goblet cell numbers, reduction in information, the colonic tissues improved. Like it's effective, essentially, as a treatment for colliders in that study and they're using orally. Now, obviously there's a difference between, you know, the stomach of a mouse and the stomach of a human and there's changes differences in, you know, the transitor time and the stomach and the acidity, a human stomach is a bit more acidic than a mouse stomach. So, you know, that doesn't tell us that therefore it will definitely be effective orally if you humans, but at least, you know, that would be a good, it would be a worst study point if it didn't work orally for mice. You know, I can understand if we had that information, I can, the okay, it's probably not going to work for a human. But all we've got so far says, hey, it works for mice and I'm not aware of anything saying that it definitively doesn't work for humans. So there's a bit of, what would you say, hopefulness. You know, we don't know, we can hope for the best. There's not enough evidence that this point is suggested it doesn't work. I guess would be the way I would look at it. Yeah. And then you've, like obviously people have gone down the path where they say, well, you've got to use things like PEs, yeah, like intestinal permeation enhances. The example behind that would be like stack, yeah, which I think I've asked you this before, like, but to snack, do they drive that from like industrial soaps? Like I'm not 100% sure around that. Okay. But, you know, yeah, does that, I mean, obviously, I think you've told, you've said this before, okay, it's probably going to come down to, I mean, if they're using a snack, is the dosage high enough where it's going to create massive problems around that? But is it leading to like, you know, alterations, like intestinal epithetial type junction, or ten expression, is it like, you know, maybe that's has to be a more significant dosage for a tap, but it really problematic around that. Okay. But then is that something that we really want to use that would be the, yeah, if it's not necessary, do we want to be using something that's inducing permeability, potentially not? I mean, obviously it is used. It's used with a lot of gel P1s, but again, if we, if we don't know that it's needed, do it is want to be using it just for the sake of it. And that could be like, you know, I'm not against Lypa Sama as well, okay? And who knows? We might find out, okay, yes, the oral bi-valibility, like when we have the data, okay, it might be more significant. But I guess our big point, okay, within this podcast is, well, the reality is we don't, you've got nothing to compare it against, because we don't even know what the oral bi-valibility of just the GHK CU is in the first place. So, but and then might not be, because once again, okay, when you, when you use the administration of Lypa Sama or Lypa Sama, it's just, it's obviously a little bit more expensive as well, okay? And the, the big point around that would be, is it how much of a variance is there, okay? Because it might not be that significant either, yeah? But our big point would be, we don't really know, yeah? Yeah, yeah, yeah. Now, so obviously, like you said, oral, we don't know for sure, injectable, yes, you can use it as an injectable, do we want to give any sort of framework or reference point as to kind of how long one might use it for or dosing? I mean, obviously being a copper-based peptide, people are concerned about copatoxicity. Now, in the dosing, we'd be talking about from a gut perspective that the likelihood or the risk of copatoxicity is so low, right? You have to go extremely high. I mean, there's some documentation about GHK CU, like people going the realms of, you know, I think I mentioned this too before, you know, 50 milligrams, that's actually in relation to certain types of cancers and so forth, you go, but even a little bit higher than that, okay? I'm not saying I'm not telling people to do that either, yeah? Is any noted copatoxicity in those doses? Well, look, you really, I really have to rack my brain around that, okay? But I think, like, you would have to really push up the dosage, okay? I think it's like in the realms of going, you know, beyond like 100, yeah, 100 milligrams or 100 milligrams, 100 to go. I looked at it a while ago. My recollection is you would probably have to take about 30 times the dose of what we would normally use and you'd normally be talking about maybe two milligrams. So again, it was a while ago that I was trying to do the numbers, but when I was looking at it, I was thinking like, anyone taking below 60 milligrams, I can't see how this could possibly have an issue around copat. And the other thing to note is, you know, we're not obviously massive proponents of using high doses of copat, but there is, I mentioned like the asthma thing before, you know, there is data, for example, like people with asthma who have worse symptoms have lower levels of GHK and there's data using copat with people with asthma and improving symptoms. So, you know, to then fear monger about a little bit of copat probably, unless you've got like Wilson's Z's or something, is it going to be a concern? And it's also important to state that, you know, obviously, you know, we obviously produce we produce GHK, exactly. And yeah, and the thing with like, you know, GHK, the amount that we're producing sort of like diminishes as we age, yeah, what they say at the age of like 20, like the placement levels of like GHK, something on thing was like something around like 200 NGML, okay, and then by the age of 60, okay, it declines to 60 or like 80, I think it might be, yeah, like 80 NGML. So it's, you know, decreasing as we age. 60% reduction or something like that. Yeah, yeah, it's a bit. Which is an interesting point in of itself, because it makes me wonder, well, if we're naturally declining in GHK levels, and I get that this, the top of part is a question like, yeah, but does that mean potentially one could do more regular cycles of it? Could one maybe use for longer periods of time? Because essentially, if we could, we probably want to maintain levels of 20 year old. So should we be taking huge amount of time off from it? I don't know, like maybe maybe it is one of those ones that you want to run, you know, more often than not, maybe. Well, I think like, you know, what we were talking about the oral bi-validability, it's, it's obviously not that helpful, okay, that we don't really have to add it to say what that oral bi-validability is, okay, because if we knew, yeah, okay, well, you know, if we were just taking like a certain oral amount, could we actually have the potential to run that for quite a while, okay, before we would actually have the cycle of it, yeah, okay? I mean, look, if I, if, you know, if I was, if I'm using injectable with people, I would generally go in the realms of like, you know, two milligrams and probably do that for like 30 straight days. Sometimes I can do a split dosage and that can be due to the factor. And this is not that common. I just want to reiterate that, okay, is that some people can experience like a bit of, you know, maybe a bit of bruising around the point of injection, okay, but I think we're spoken about this. Doesn't tend to happen. Well, you know what Dave, ironically, we have just spoken about this and I was saying, you know what, I've only had like one client with this has been an issue. I had a client message me today and they've actually just had that issue where they say, I'm, I'm going to be bruising. It's hurting quite bad. Well, I mean, injecting the GHK for there you go. That's the universe after I've just told Dave that I hardly ever, if anyone can plan about I've had someone today. But like you said, you can split those, you know, one thing I said to this client was, I know that she's really constituted it in a small amount of liquid and potentially you can't do it in a little bit more that I mean, I'm speculating here to be honest, but my suspicion is that would potentially help with some of that burning or pain sensation that one gets one can get when they inject it. But yeah, as far as peptides go, the GHKC use is one that's more likely to give you potentially some pain. It is comfort when you're injecting it. Well, they say, you know, sometimes you might just have to change the point of injection, like obviously, you know, generally the administration is subcutaneous in the midline. But you know, I might do sometimes a split dosage around that, but it is fine to do the two milligrams as well. Yeah. And you might run that for like 30 days and you're sort of cycling it. Some people say you sort of might need to drop off for, you know, two months, three months. Look, and also you could potentially, based on the severity of the, you know, obviously what we're talking about here, the severity of the damage to the cut line, okay? You could run it longer than that 30 days as well. And maybe you wouldn't have to have such an extended break. Like I'll just give you some parameters around this. Yeah. But you know, they generally say, you know, two milligrams, 30 days and you might take about, you know, two or three months off and then cycle it on again. Okay. But there's a bit of nuance with that as well. Yeah. I mean, again, wouldn't you say that a lot of those cycle lengths are kind of speculative as well? Exactly. Exactly. Dada or Nat. And to be honest, I kind of question where a lot of those ideas come from. Like I know, I don't know if you've sort of looked much into like Dr. William C's and know for myself, I based some of the cycle length off of what William C's talks about. But even then I wonder like, where are these coming from? Like someone ultimately, if we don't have the research in it, someone along the way is making an educated guess. And you know, that's all well and good. We need a starting point. But I think we just don't have enough research to actually definitively say, this is how long we want to cycle these things. Like it's sort of best guess at this point in time. Yeah. One thing is important to probably state, just so people know that you can, there is just actually just GHK as well. So using the GHK as a use sort of like has the advantage of using just the GHK because you can alleviate things like copper deficiency and yeah. And so obviously like all the benefits that we're talking about here, okay, is really based on the GHK. GHK is a you, okay. But obviously there is, you know, benefits around even just like the GHK. I think they might, there might be some of these like neurological benefits. I think it might have been in regards to like fragmented memory and issues around the brain with like sleep deprivation and short sleep tone frames. I think it might have been from a neurological perspective, but that's sort of me. Yeah, they're seeing neurological stuff. I think there's stuff around like the juiced anger or aggressiveness even. Yeah, I mean, it might have been the same research, quite by the way. Yeah, potentially. Yeah, yeah. Okay, moving on from GHK. See you. Now just before we jump into permeability, I do want to flag our gelp ones. So obviously a lot of people wear gelp ones and they're using these for weight loss and fat loss. But there is some interesting stuff about gelp ones when it comes to in particular, I'd say IBD, but I guess more broadly, you could look at it from a gut perspective. Now we've touched on I think in a past, some potential concerns about gelp ones when it does come to the gut and just briefly that the main concern there is that gelp ones do reduce gastric motility. So they are slowing down the trans time from stuff leaving a stomach. Part of that effect means that there's going to be just a bit. Sorry to wrap, dear. Okay, because obviously, I know I think we've spoken about this like in another podcast that we've done around the world. Wait, let's compare some of that again. I mean, there's obviously just some of this, you know, potential stuff around like promoting like BT, we obviously have been speaking about that like back to a tens location. Wasn't there some stuff like in, like in due, seem like an increase in like intestinal equal life? So I'm just going to flag you now to go. You probably been into that research a lot more than myself. Yeah, I'd have to go back and look at that. I know that there is, there has been some favorable changes in microbiome observed. So there's been like increases in acumencia. Biorecollection, at least in one study was reduction in some negative ground bacteria actually. But I guess, you know, the issue there is going to come largely down to that sort of effect around the stomach function. And then what we also tend to see around that reduction or that I guess increase in that delay of stuff leaving the stomach is also tends to be a bit of an impact around gallbladder function as well. And that's partly why you see an increased risk around things like the gallbladder disease, gallstones potentially. And if there's reduction in gallbladder function or in bile output, obviously that could predispose someone to dispose as well. Yeah. So there are those concerns. So again, I don't want to sort of make it out like this is the peptide to use for IBD because there's some potential concern. And we do some data showing an increase in SIBO as well and JLP one uses. Well, it's interesting what you say just just around the stuff that I'm commenting with Cinect filler without going too far down that rabbit hole because obviously, you know, you'd be talking about benefits of things like improving like insulin sensitivity and helping around my insulin resistance and so forth. And interestingly in Africa, like they generally do show that a lot of people see by their tend to have a bit of a lack of a bit of a lowering or lack of like acumencinocilia, which is quite interesting. Okay. And the other thing is with the acumencinocilia, it actually does promote a process called differentiation. The differentiation in the case is when an unspecialized cell becomes specialized. And so this was actually to do with like, patisels. So I'm just putting that out there. And you know, you're talking about that benefit around the acumencinocilia, which is that's a similar benefit to what they saw with like net foreman. Yeah. Yeah. Yeah, yeah, exactly right. Yeah. So potentially there could be some benefit of your microbiome. Like we just said, there's also some potential concern over microbiome. So that could be a bit of a wildcard in some ways. But if you look at the outcome data we've got in human users of GLP ones, there's actually really good outcomes or fairly good outcomes around IBD. So there's reductions, for example, in medication use in people who have IBD who use in GLP ones, so like Kodogoseroid use goes down. There's reduction in hospitalizations. There's a reduction in flares in disease flares and increase in quality of life. And if you look at the animal studies we've got on it, I'm not familiar with any of any human studies that have then assessed some of these endpoints. But if you look at animal studies, we do see that there's actually an increase in goblets cell number and that there's an improvement in goblets cell function in my studies when using GLP ones. Now there does seem to be more of an impact at least when we look at the human outcome studies on improvements in people who are obese. Right. We know that there's a correlation with IBD and obesity and obesity, and it does worse than the IBD outcomes. So part of the confounding variable here is going to be, well, how much of these improvements just due to the reduction in body weight because obviously these drugs work very well from an obesity standpoint. some of the data we do have in it. And my is suggesting, hey, this actually, you know, improvements here as far as you gobblet cells. So that would suggest potential improvements when it comes to things like osteovalidous, especially you talked about, you know, mousse production, mousse production from the gobblet cells. So I think it's an interesting one to watch, I guess, this space on some of the data that might come out around GLP ones. I think it's something that, you know, people have been so preoccupied with their benefit around fat loss that maybe some of these other potential benefits it could be there. Maybe you've been overlooked a little bit. - Yeah, so we should we, should we move to. - Yeah, let's conclude. - Yeah, I mean, obviously we, we're probably, you know, another podcast we're actually going, we're obviously going to go into the aspects of like, glue gun, like peptide, one receptor agonist and semi-glute tide in, I would say, a lot more depth. - Yeah, yeah, yeah, absolutely. Pemibility, that's the last one in the list. So leaky guard, hyperpermibility, permeability. Obviously this is, you know, there's going to be overlap here with what we've talked about in both cellar disease and IBD. And this is a, you know, in some ways, this is a little bit more of an umbrella term. But there's, there's a couple of, well, one in particular, peptide that we've left until now. And it would probably be the one where we'll look out for leaky guard, wouldn't it? - Yeah, so obviously the one we're talking about is BP-71-57, which I think is like, sort of been, like the post-achonable peptides. You know, yeah, yeah, and, you know, obviously, derived from like human gastric juices. It's, you know, 15 amino acid chain. And I mean, I think I would mention, like, you know, what's really taking place with hyperpermibility. And I like it in terms of the loosening and the widening of the intracellular type junctions and the loss of the type junction proteins. But there's also like a loss of e-cat error in there as well, which basically initiates and stabilizes self-cellednesia, which is basically keep the intracellular type junctions nice and tight against each other. And actually, there's a loss of e-cat error because actually e-cat error actually helps the maturation, maturation in the positioning of panacellas, but it also actually helps with the positioning of God but cells as well. And, you know, the one thing is, we're some like, you know, we might say BP-C is really good around it. There's too much like transcellular activity and parasitic activity, but we do want to stay as well. It's also really good if you have actually too much like transcellular activity. So obviously, if people have like IBD conditions, okay, then there's obviously going to be issues around both, ultimately. But if you look at some of the stuff around BP-C-157, and I mean, there's actually stuff around, you know, having the potential to help with IBD conditions and find two power disease. I think I was actually in condition, that was actually in condition, such as ulcerative colitis. We obviously, there's simply damage to the epithelium in the large intestine and obviously like God but cells. But it actually helped with things like intestinal swelling and it preserved like colon health as well. You know, so I just want to say that it's not just limited, okay, to the, the, the, the intracellular type junctions and the damage that has occurred within that area. - Yeah, yeah, yeah. I mean, even stuff around like end-set injury damage, you know, stomach ulcers. So, I guess one of the mechanisms behind BP-C-157 is going to be the increase in angiogenesis and the increase in nutric oxide. Yeah, so basically it's helping with, what would you say, like supply, like blood supply, nutrient supply to essentially like anywhere there's damage. So, you know, this is why, what I call it a smart peptide, I don't know, that it's ultimately able to locate areas of damage and information and essentially just provide some of these building blocks to actually help resolve that, that information and that damage. - Yeah, I mean, you know, I mean, you know, like I think you've, I don't know if you've already mentioned this, go off as like, you know, gashary protection as well. You know, it proves like GI, because of integrity and, you know, obviously mentioned around improving the nutric, the nutric oxide and even it's a pretty good at decreased in the side effects, all the negative impacts that you get from things like insa, like non-steroidal antianfumidic drugs, but also alcohol, because like alcohol can actually cause like alter, you know, ulcerations and erotions and loss of epithelium. And I mean, even if you look at some of the stuff around, like BPC157, it can actually alleviate symptoms of, even like alcohol intoxication and, isn't there stuff around as well, yeah? Like BPC157 helping with like alcohol dependence and sort of like, isn't that sort of classifying? Like, like, like alcohol and taginers and, um, so, you know, it's like, a lot of this damage that's actually been caused by the alcohol and we actually know that alcohol actually can create long-term damage in the gut lining. There was actually research they did on mice with actually did research on acute feeding and chronic and prolonged feeding of alcohol, to rats and mice. Um, and that actually damaged intestinal stem cells or ISEs, I mentioned them, okay, but not only did it damage the intestinal stem cells, but actually impeded on their replacement process, okay? Um, and the replacement process is really dependent on panacellas because of things like sickly ADP ribose and, uh, WNT protein, WNT pathway, this is like self-renewal of intestinal stem cells. So that obviously means the alcohols, even having like a negative impact on, and obviously the panacellas as well. And, uh, you know, obviously BPC has been shown to have, you know, really protective, um, protective mechanisms around that. Now BPC is one that is bioavailable early. And so like we know it's advised gastrojuices is to actually got studies in that, which is really nice because we don't have that for other things. So you could argue we take this early or injectable, you could decide, you know, we've talked about this in the past about, you know, do clients seem to experience better results when they're using an early or injectable? And I think we would both say that doesn't seem to be a clear pattern there. It certainly does seem to have good benefit from a gut perspective when it is being used early. So I, you know, generally we would look at most peptides and say, well, if you can inject it, it's probably worth injecting it. But BPC is one where I don't feel like we're leaving much on the table if we do use it early, actually thinking in some people, they are going to notice that's working better, most likely from a gut perspective, then injecting it. And the one thing you, one thing around that would be also the form is really important when it comes to the old bioavailability. Okay. So it's got to be an arginate salt and a lot of time, a lot of the BPC157s that you might be getting. Okay. They're not actually that form. So you just want to make sure around that. And when it comes to the dosaging, you know, I generally say, all of the, I'm sure you're probably very similar. Anywhere between like 500 to 1000 MCG, like micro-milligrams, like, I really. But obviously you can, you can do that injectable and you can do that injectable subcutators in the midline to actually help with like gastrointestinal disturbances and gastrointestinal problems as well. I would generally say, especially with like BPC157, and you're, we're talking about thumps and baddafore, or the TB543AA, generally with those ones, they're generally better to administer, close to a point of issue or point of pain. So for example, if you have like a torn middle co, middle co-lactual ligament, okay, then you would want to inject, okay, the BPC157 close to that point of issue. And you know, you know, when it comes to the dosaging from that perspective for like an injury, it can be in the realms of like 200 to 300 MCG, you know, some people might do that twice in a day and that's doing it injected around the injury site. You know, I think like, you know, some people talk about going as low as like 400 to 600 MCG for oral, oral administration, okay, but I'm generally sort of between that five and two thousand MCG. I would still cycle BPC157, even though once you've quite rightly pointed out, it's just really hard to find definitive. Yeah, I think the best we can usually do is are there things that are getting de-centitized if we're using this long term? And for some compounds that are, and then for some like GHK, I look at that and I'm like, well, what's actually getting de-centitized? I'm not aware of anything. So BPC, again, is there a huge change? Well, obviously there's a heavy amount of factory on GABA, don't mean. So maybe from that perspective, it might be something you'd want to cycle a little bit. You know, how long? You know, four weeks, eight weeks. How long do you have off? All that is a little bit speculative. Yeah, I mean, sometimes I keep even with the oral, I get people to do sort of like eight weeks on and then four weeks off. But I mean, is there any major problem that's going to occur from someone extending out a little bit longer? Yeah, okay, I'd go on like 10 weeks, I'm like down to go, but I still would say it is better to cycle it. But you know, there's obviously been people who've been running something like an oral BPC-157 for quite a long period of time. But I still think, okay, it should be cycled. Yeah. Probably more ran of efficacy would be my concern rather than will it be bad for you? Yeah, correct. Correct. Correct. And once again, we do want to say that it doesn't mean that the BPC-157 is not going to have benefits around the other conditions that we talked about. It's definitely still going to have benefits for especially some way, complicated celiac disease and celiac and definitely light the IBD conditions. That's one of the major points that we want to bring up. And you can stack these as well. You don't need to just take one. You can actually take everything we just said You could take everything we just said, you could do that, or you could stack in a two or three of these together. You know, it's not like, oh, you just need a pick one. That's only one you can use. No, these things are going to work synergistically. And you know, that's actually worth mentioning with the BBC, is that there's a lot of people online talking about peptides, and then there's kind of like two mixed messages. One will be like, peptides will solve all of your problems you know, and they're doing it on the else. And then the other messages is no point doing peptides, unless you do everything else. Peptides aren't going to do anything. Obviously, they do something. You know, we're looking at these, yes, a lot of these animal studies, but you look at these animal studies in mice, and it's reversed the condition they've got. Did the mice go and start journaling each morning, and were they meditating, and were they, you know, only eating organic grass-fed beef? No, like they were just normal mice, doing normal mice things, living in a cage. And this peptides still fix that issue. So to me, it's a little bit ludicrous to say that it's not going to do anything without the basics, but don't overlook the basics, 'cause the basics still do a lot. So, you know, I wouldn't say, hey, just use BPC by itself. Stack it with these other gut healing compounds. We've done whole episodes on this kind of stuff. You know, eat well when you're doing this, sleep well when you're doing this. It's all going to enhance efficacy, but peptides do work. - Yeah, one, I just wanted, this is almost like an honorable mention. There is just real quickly on this, maybe, you know, further down the line in another podcast, we might mention a little bit more, but there is another one that sings relatively interesting, when it comes to the gut. It's called Biolong, and that's basically a dipeptide. So it's the shortest peptide, and it's lysine and glutamic acid. So it's actually a thymus derived peptide, and it sort of seems to have like this editumac activity. It's actually uptaken, uptaken more by the intestines, and it actually does help with things like tissue regeneration, in areas like obviously the intestinal lining, but also it can be like liver, thymus, lean. A lot of the research really has actually been done within Russia, I think that there's like 40 years of research in Russia, and it's also pretty good for modulating like prime thymj proteins. I think we've shown a modulate like NFKPB as well, so modulates like cytokine production, and even modulating like a immune cell activation, and also like epitalin, which is sort of like a longevity peptide, and actually can normalize like talamiar length as well. So some of these benefits, but I'm not gonna go, you know, to use my one, I'm not actually aware of it beyond what you said about it. Is it injectable or oral? Oh, oh God. That's, you haven't used it with any of that. I haven't used it, yeah, I've just been doing a little bit of research around it, and it's sort of like, you know, and it's a new one sort of like on my radar. Yeah, okay, interesting. I haven't even seen it available anywhere, so I'm sure it's one that presumably people start talking about, or we'll see you hit the market, maybe. Anyway, that's it for our gut healing peptides. Thank you so much for joining us. If there's more you wanna know about peptides, shoot us a message, ask us a question. If you want more episodes like this, let us know, 'cause there's a whole stack more peptides out there to talk about, but ultimately we want this to be helpful for you guys. So let us know your feedback, and we do hope you'll join us again in two weeks for another episode. Thanks guys.