A Functional Approach to Crohn's: Prebiotics, Diet & Supplements with Guy Daniels

Welcome to The Perfect Stool: Understanding and Healing the Gut Microbiome. This is your host, Lindsey Parsons. Today I'll be speaking again with Guy Daniels, who was also on episode 156. Guy has a master's degree in nutrition from Florida State University and has been in the functional natural integrated medicine industry for more than 20 years. He served as the director of medical education for the microbiome Home Division at Thorne for 5 of the 13 years he spent there. And he now helps people all over the world with gut health issues, not by focusing on killing microbes, fermented foods, probiotics, or radical diets, but focusing instead on changing the gut environment to favor the health promoters who've been sidelined due to exposures like excessive antibiotic use. He does this in a variety of unique ways, first and foremost being the intelligent use of properly blended prebiotics. But before our conversation, if you haven't yet followed or subscribed to the show, be sure to do so. If you want to get transcripts of the podcast, pop over to my website, HighDesertHealthCoaching.com. And sign up for my newsletter. You'll also get my free ebooklet, Finding Your Root Cause Through Stool and Organic Acids Testing, when you sign up. And if you haven't yet done my quiz on which stool or functional medicine test would get you to your root cause, you can find a link in the show notes and take that. Now on to the show. Welcome back to the podcast, Guy.

Thank you for having me.

Yeah.

So as I mentioned to you over the email, I recently received blood tests back indicating that in addition to post-infectious IBS, I have elevated antibodies indicative of Crohn's disease.

And those are the AMCA antibodies. So I'm interested in learning more about what you discovered about Crohn's disease in your reviews of the research and what you can tell me about these and other antibodies related to Crohn's.

Sure. So, well, these, that's part of a group of a slightly larger family of antibodies, and really what they are, are looking at saccharides and other components of bacteria and fungi. And there's also one, I forget the name of it, but it looks at Saccharomyces cerevisiae, which is also known as baker's yeast, which actually was the first pathogen associated with Crohn's. So, you know, all these bacteria and all these yeasts, they have these different, you know, structures to them and structures to their surface. And they're really— our, our immune system calls what we call them pathogen-associated molecular patterns. Okay, so the immune system just says enemy, enemy, alert, alert. And so these are what are called pattern recognition receptors. So basically, and these things are recognized by different toll-like receptors. There's, I think, 9 or 10 different toll-like receptors in the human body. Toll-like receptor 4 is big for lipopolysaccharide, which is another one. It's, it's the same general family where it says lipopolysaccharide. So it's a lipo component and a saccharide component to the surface of gram-negative bacteria. So basically what's going on here is the immune system is saying, hey, you know what? I'm seeing constant exposure to this particular bacteria or this particular fungi, and we're going to ramp up the immune system and to say, hey, you know, there's more of it over here, there's more of it over there, there's more of it over there, do something about it. And what happens in Crohn's is there is a key defect in antimicrobial defenses. So that's the big thing behind Crohn's, like ulcerative colitis. It's, it's the mucous layer. Crohn's antimicrobial defenses. So there are defects in the, the paneth cells and the crypts of the enterocytes. And so bacteria, bad bacteria, are able to adhere to more efficiently and invade the cells of the Crohn's patient. So yeah, you're gonna have these antibodies to these, you know, different viruses and fungi because there's this constant exposure at the enterocyte, within the enterocyte. When we get to the NOD2 gene and also behind that when you hit the immune system. So all it's really saying is, hey, we have constant pathogen exposure, which is no big shocker because the microbiome of the Crohn's patient is very dysbiotic.

So does it tell me which pathogen I should be trying to target because I had the elevated AMCA antibodies?

Mm-hmm. So my philosophy is I don't target any pathogen in particular. So whether it's E. coli, R. navis, which is a big pathogen in Crohn's, or any species from Klebsiella, Streptococcus, VNL is a big one in Crohn's, Enterococcus is a big one in Crohn's. And oh, by the way, Lactobacillus is almost always high in Crohn's as well. So I don't say here's a bug killer for E. coli, here's a bug killer for R. navis, et cetera, et cetera. The microbiome, it doesn't work that way. And in the experience, you know, we're always giving these antibiotics and all these different uva ursi and berberines and oregano oil and so forth, trying to kill, kill, kill, kill, kill. And the data shows that, yeah, okay, you might dampen down on the bad guys for a while, but the aftermath of all this killing, especially with antibiotics, is the bad guys come back in spades and the good guys are either killed off or they're sidelined. The good guys are like, hey, wait a second, this environment just doesn't favor me. This isn't my pH. My pH is 5.5 to 6.5. Right now we're in a pH of 7.0. Like, I can't operate in this environment. And the bad guys are like, yeah, screw you, we can. This is great for us. You know, there's more oxygen here. You can't tolerate oxygen. We can tolerate a little more than you can. The pH is right for us. And so, and then the, the inflammatory environment then makes the bad guys more pathogenic. It expresses a different— there are genes, but more so kind of genes that are less expressed or not expressed when the environment's proper. So philosophically, what I'm looking at is they're all opportunistic pathogens, whether it's Candida or whether it's E. coli. It doesn't really matter to me. They're all taking advantage and opportunity of an environment which, which they can. In this case, it's an environment that is inflammatory. And this, the good guys, primarily the big thing is the good guys are silent. That's a big thing. It's like when the parents go away and, and all the, you know, the teenagers are allowed, you know, to, to do their thing and go wild and they find like a whole bunch of beer or whatever. It's like they're in charge. Like there's, there's no checks and balances on them. And so that's basically what happens in the gut. Okay.

We'll get to your, your, your philosophy in terms of fiber and such, but couple questions before that. So, I didn't on a previous stool test have an elevation in that ASCA antibody, which is the Saccharomyces cerevisiae one. So would that mean that in my case, S. boulardii is not a problematic probiotic?

So that might be the case. So just to kind of, I, I know what you're asking, so let's, I'll take a step back and kind of do a little background information there. So again, the baker's yeast, that was the first. Big pathogen associated with Crohn's. And then S. boulardii is in the, it's in the same genus, right? Saccharomyces. So in theory, it is a helpful yeast, right? So what does it theoretically do? It theoretically takes up space, right? It occupies space that other potentially more harmful fungi would occupy. But again, if you look at the data, and I have been through all of the Crohn's data, Looking at the fecal microbiome of healthy controls versus Crohn's subjects. All of this, I've seen all of it and I've analyzed, I've compiled all of it. In not one study, in not one study does it say Saccharomyces boulardii is significantly higher in healthy controls as compared to Crohn's subjects. It's not a crucial part of the immune system. So what is a crucial part and what says what happens in all these studies is F. prausnitzii. In every single study where a significant difference was found is significantly higher in healthy controls as compared to Crohn's subjects. What's F. prausnitzii? It's a superhero of the gut. It produces a whole bunch of butyrate. It produces— it cranks out interleukin-10 production, which is an anti-inflammatory interleukin, has other different properties as well. And all of its cousins are consistently significantly higher in healthy controls versus Those are Crohn's, such as species from Ruminococcus, species from Speruria, species from Coprococcus, and the list goes on. So I never ever recommend Saccharomyces boulardii. It's, it doesn't, it makes no sense. The good guys are very clear. The bad guys are clear and nowhere on the, on the board does that pop up.

Yeah, no, I wasn't thinking of it for the Crohn's. I was thinking of it more as for, for other purposes. 'Cause for example, sometimes I see people with elevated Candida and I give them S. boulardii, or maybe they have high levels of, what's it, Blastocystis hominis, and I use it for that purpose. So, uh, so I'm thinking if somebody has simultaneously has Crohn's and other issues, you know, what, whether it might be indicated.

Yeah. So I have videos on both of those. I have videos on, on yeast, fungi slash Candida, and I'm actually about to launch shortly a video on Blastocystis.

Oh, okay.

So Candida is, again, it's an opportunistic pathogen. Taking advantage of an environment in which it can't. So typically, but not always, it does that because someone took a whole bunch of antibiotics, right? Which kills off both good and bad bacteria. And the Candida's like, woo-hoo, it's party time. We have all this space, we have all these substrates, we're gonna have a good time. With Blastocystis, and I'm fresh off doing all the research for that and brushing up on that because I, that's the parasite I see by far and away number one. When people come to me with their microbiome reports, if they test positive, it appears that it's kind of like a whole bunch of other bugs out there. It's kind of like a mix. But if you have a healthy microbiome, it's not really to be worried about. In fact, it's more abundant in a lot of healthy controls as compared to, you know, those with a certain condition. So, and it actually follows some of the general rules that the good guys do, like it can't tolerate oxygen. Its pH, for example, where it operates. But there's also some not so great data on there. So I think the moral of the story behind Blastocystis is let's make your biome microbiome healthy. And then it's like, yeah, whatever, it's here, but we don't care because, you know, the good guys are in charge because it really kind of is a normal member of the microbiome, kind of like Candida. Candida's a pretty much in a lot of people, a normal member, member of the microbiome as well. So you're not gonna kill it all off. You just have to control it. You have to sideline it.

Mm-hmm.

Okay.

I heard recently in a webinar, actually it was on the Enterostirpes caccae, which they now have a probiotic for, that there was something going on with the lack of conversion of primary to secondary bile acids in Crohn's where the primary bile acids are harming the colonocytes. Is that something that you've seen in the literature? And I'm wondering if TUDCA reverses that process.

Yes. So one of my slides in my Crohn's video I have, I think it's one of the last slides, talks about. Bile acid dysmetabolism. This is not specific to Crohn's. This is a thing that has to do with dysbiosis in the gut. So there's bile acid dysmetabolism in basically anyone who's dysbiotic. So what happens is, is there's typically more primary bile acids and fewer secondary bile acids. That's, that's typically the picture. And I talk about this quite a bit in my video on C. diff infections. And I have, I, I talk about a number of different videos as well. So what's going on in the gut is again, that the bad guys are in charge. There's too many of them, maybe further up the GI tract and, you know, a different quantity and different type as well. And actually was thought a while ago, years ago, that the, the gallbladder and then that duct going down to the pancreas was actually a sterile environment, but it's been recently showed that it's not. And if you have something more like a placebo type of nature, then bacteria can actually work their way up that Tuka. So you can actually have dysbiosis of the gallbladder and getting into the branching of the pancreas as well. So, and yes, in that instance, Tuka would be a benefit. So Tuka is a very helpful secondary bile acid, but Tuka in and of itself is not the solution. What's the root cause? The root cause is dysbiosis, right? You have too many bad guys in different locations and you don't have enough of usually the, the first enzymatic activity is deconjugation. So again, the, the primary acids, they're conjugated with either taurine and glycine, so oftentimes they don't get deconjugated. The second one is, oh, is I, I think it's hydroxylase, so it's be hydroxylation if I recall correctly. So a very, very small number, a very, very small number of the microbiome actually has that. It's a very complicated enzyme to dehydroxylate the primaries into secondaries. And so, and there, those bugs also happen to be rather sensitive to antibiotics.

Mm-hmm.

Which goes in hand in hand with C. diff infections where again, you have the same bile acid dysmetabolism where there's not enough secondaries, there's too many primaries, et cetera. And then you get into torocholate, which is Whole nother story.

Yeah.

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So on my recent— so I did a gut zoomer in July and that was sort of the first indications that something wasn't quite right. There was an elevation in fecal lactoferrin and a couple of the other inflammation markers, but not calprotectin.

Mm-hmm.

But I'm pretty sure that all my bile acids look normal. So could they be within the normal range and there still be like, if you took ratios, you might find that there actually was a problem?

Yeah. I mean, it doesn't mean 100% of the time there's gonna be bile acid dysmetabolism.

Yeah.

It's just a common pattern.

Well, it, it's, it's a significant percentage of the time.

Yeah.

It really is. I mean, if when you look at the clinical data, if you take, you know, if you have 50 people or 100 people in a trial, right? You're, you're averaging these numbers.

Yeah.

So, you know, you're gonna see a significant difference between Group A and Group B. Yeah. But within those groups, you know, there's, you know, 50 individuals, whatever happens to be in each group, you could have someone who's up, upper here and, you know, lower over here in the opposite groups. And so yeah, on an individual level, you may or may not see that. But when we average things out, yes, you do see that.

And how does the TUDCA work in that scenario?

So TUDCA works by various mechanisms, and I have a video on this. It's actually one of my more popular videos. Oh. Which is interesting 'cause I was like, I'm gonna do this obscure supplement that no one talks about and everyone loves it. So everyone loves this video.

Oh yeah. But Cellcore has been touting it for years. I think, I don't know, I feel like I've been seeing videos about it for 6 years from them.

Yeah, it's, but, and it works great. Like I have a lot of YouTube comments, people saying, oh my God, the Tug is the best. So it works. First of all, it's an anti-inflammatory. So typically when you have dysbiosis in the gut, you have this dumping of all these pro-inflammatory compounds. It could be whole bacteria, parts of bacteria through the, via the portal vein. They just get dumped into the liver. So then, so all these, these problems, the problems start in the gut, then they, I mean, they kind of continue to the liver and you got leaky gut and everything else. So Tutka plays a huge role inside the liver. It's very water soluble. It has a dynamic where it's very low inflammatory. And then in the gallbladder, it actually has, has historic use, Tutka and Udka, which is the drug form, historical use for gallbladder, for stones, for gallstones. And then it works its way to the pancreas where it can then help with production of enzymes. So I, like, I never recommend enzymes, right? I, I recommend fixing the system. Like most people come to me taking enzymes. I'm like, okay, well it's fine, but you really should not need them. We're got, what, instead of giving you enzymes, we're gonna fix the reasons why you're not producing them as well as you should. Right? And then it gets into the upper gut and it acts, does act as a bit of an antimicrobial, but it also acts as anti-inflammatory there as well. So, and it crosses the blood-brain barrier where it has anti-inflammatory benefits there as well. So it's a really interesting compound and if anyone wants to check out my video, they're welcome to do so.

And does it do something to change the composition of the microbiome then in that, in that process?

Well, yeah, yeah. Be it because it's a secondary bile acid, right?

Yeah.

So the stu— the studies show that when you take Tutka, you're increasing your Tutka, right? It, it's a highly beneficial secondary bile acid. So your secondaries kind of go up, right? Your primaries kind of go down. And again, like I said, it's an antimicrobial. So if you have like a SIBO type of condition where you have, you know, too many bugs throughout the GI tract impacting conjugation and so forth, right? Then you're gonna, you know, you, you kind of clean out that upper GI as it's antimicrobial effects and then contribute more to the secondaries. 'Cause the, some of the secondaries do get reabsorbed, right? And then you change the composition from a heavy primary bile acids to more, more of a secondary.

Mm-hmm. So for someone like me who has post-infectious IBS, where I'm just always gonna have like recurrent SIBO, should I, would, would TUDCA be a good idea as like a continuous supplement for me?

It could be. Yeah, it could be. I mean, oftentimes it's, it's a temporary thing. It depends on the person. If you have fatty liver, right? Non-alcoholic fatty liver disease, then you're probably gonna be on TUDCA for a while, right? That's again, a part of a much larger picture. If you have SIBO, that actually only be a month. That SIBO, you know, a lot of my SIBO people cruise through in about 4, 5, 6 weeks' time. So, you know, once you get past 2 months, do we really need it? We've changed the bile acid dysmetabolism, we changed the microbiome, you know, we've rectified the SIBO. You maybe you're high histamine before, now you're no longer high histamine, you can tolerate foods. Do we still need it? Maybe, maybe not. So, and oftentimes probably not. The goal So my goal is not to have people on a lifetime of supplements and a lot of them, right? It depends on the individual. Some people come to me and they have a broken microbiome. Like for example, Crohn's, what we're talking about is a great example. So the Crohn's person usually is gonna have to be on something probably for the rest of their life because you have to compensate for what got broken, compensate for the exposure of faulty genes, and you have to manage that. Like for, I, I have Crohn's for example. Okay. I was diagnosed many years ago, so I'm always taking my, I take about one shake a day, most days of the week, 5, 6 days a week. So that again, just to maintain that, because even to this day, after managing things for so long, I still know I can't do certain things, right? So I need to control that environment down there. But again, if someone's taking turmeric and this and that and the other thing, I want to get them down to the minimum number of supplements possible. To, to kind of get over that hump, get them feeling better, and then just let them go. Let them, you know, fly away from the nest and hopefully they really, you know, they're, they're off and running. Don't have to take anything again.

Yeah. So tell me a little bit about your journey with Crohn's and how you reversed it.

Yeah, this is a whole podcast in itself, so we'll have to get the short version. I was apparently very susceptible to antibiotics because I only had a couple rounds and from those couple rounds I got a horrific case of thrush. So, which happens with, you know, with some people. And then that kind of, and I, I become very thin and that kind of like murmured for a while, for a few years. And then I started building up food allergies. I'm like, all of a sudden I can't eat this thing. I can't, I'm having these, you know, these unfortunate visits to the toilet. So, and that then it started just getting more and more severe. And at the point where I'm like, I just started looking at food with fear. So I went to, I went to saw, I saw 3 different GI docs. One said, there's nothing I can do for you. One said, it's in your head, even though there's clearly blood in the toilet. And one said, you have to take prednisone for the rest of your life. So I rejected these clowns because, you know, they just, they don't know what they're talking about. And as I, this, then, well, the years of research and trial and error started. So I did go to one functional medicine practice, but they you know, it was the usual do the yogurt with the probiotics, which didn't do anything for me. And it, it actually harms a lot of people. That's a topic in one of my videos.

SCD yogurt, they call it, right?

Yeah. That back then it was a, it was just like I made my own yogurt with probiotics. So like probiotics never seemed to make me worse. They make a lot of people worse. Never made me worse, but they didn't make me better either. So there was like years of trial and error, years of research, years of fine tuning. And then I, I developed, you know, for a number of years, a basically a philosophy, a pro protocol that worked. And then that since about 10 years ago, well, it was 9 years ago since I became the director of medical education for Microbiome Firm. I just dove into all things microbiome and I was reading literally thousands of papers and I was taking meticulous notes and going, okay, hey, lactobacillus really is not that great. In fact, more often than not, it's significantly higher in Crohn's subjects. Than it is in healthy controls. So, you know, and you start looking at, okay, well the butyrate producers, they're clearly good. And, and, and this is across the board. You look, whether you look at Parkinson's, whether you look at depen— dementia or, or, or depression or whatever it happens to be, these same patterns are across the board. The bugs alter a little bit, but the same pattern. So I'm like, okay, I'm, so then I refine the protocol to where I am definitely feeding the good guys. I want them to be in charge. And then these other supplements I'm not, I'm not doing anymore. So I'm still pretty much bulletproof, you know, after all these many years and I'm hanging in there. So that, that's the story. That's the short version.

So it didn't, it didn't get too bad for you. It sounds like it didn't get to—

it did. Oh no, I, I had, I had terrible diarrhea. I was about 30 pounds lighter than I am now, 25 pounds lighter. I was anemic. I couldn't, I mean, I ate, but then it was, boom, it'd go right back out again. I would have—

And did you have pain in a particular location or?

I had some pain. I had, I had, I had anal fissures, you know, so it was, it was not fun. It was not fun.

Yeah.

And, and I have, I have several, I have 3 of the top genes in Crohn's. Now the gene thing, the gene thing is, is kind of hit or miss too, because you have a whole bunch of people who have the genes but don't have Crohn's. And you have a whole bunch of people have Crohn's but don't have the genes. The big gene is the NOD2, which is the intracellular antimicrobial defense. So, but when you have like a whole bunch of these genes and you take a few antibiotics and this and that, then, you know, kind of, it kind of stacks up on you.

Yeah. I thought that there, I had no family history of any of this. And then I found out that my aunt had had Crohn's and, and had to have a temporary ileostomy and it was reversed. Not, not long ago. And then my, my dad just had some serious gut stuff happen. But anyway, so in terms of diagnosis with Crohn's, I imagine it's one of these things that probably gets missed a lot because like you do a colonoscopy, you're not going up into the ileum and you do an endoscopy, you're not going down that far either. Is that, I mean, how are most people getting diagnosed? Because they have severe symptoms.

Well, I think a lot of the colonoscopies do reach the ileum. I think especially if they're suspecting Crohn's, right?

So, right. No, if they weren't, like I just had a regular colonoscopy, not, you know, I don't know, 2 years ago and there was nothing. It was clean.

Yeah. Yeah. No, I mean, if there, if there's suspicion of Crohn's, like I have photos, I think, I don't know where they are, but of, you know, of, you know, here's, look at this. This is from my ileum. It's probably distal ileum, right? And then I had a colonoscopy about 6 years ago, which is perfectly clean. So, you know, something, something's going right there. But yeah, I think, I mean, that's the gold standard. I think, you know, there's other, they could do imaging and so forth, but I, I mean, most people I talk to come to me with having done at least one colonoscopy. And usually there's oftentimes an endoscopy with that as well. Oftentimes they're told they have a suspicion of Crohn's, but it's really just kind of like a wishy-washy diagnosis. So, and other times it's like a firm, you know, yes, you have Crohn's.

Yeah, no, I thought because I just had this colonoscopy I was in the clear, but obviously, but I mean, I, they specifically say on my colonoscopy, then we stopped at the ileocecal valve. So it's quite clear they did not go. Oh, okay.

They did stop. Yeah, yeah, yeah.

Yeah. They didn't go far enough. I mean, and it may not have been present then because this is, this is all relatively new because I've had pretty frequent stool tests. I don't know, for various reasons, cuz of the podcast, I've been, I've been keeping up on this stuff. So you've mentioned the bacteria that tend to be dominant in Crohn's, right? So you said it was, uh, Ruminococcus navis and E. coli.

Mm-hmm. Yep. Yep. You have species E. coli, species from Enterococcus, species of Fusobacterium is in there as well. Uh, species from Streptococcus.

Yeah.

Species from Veillonella. Yeah. Um, I think that pretty much does it.

So Fusobacterium, I have this issue with the stool test, like all of them list Fusobacterium like as if there's a normal range. But there's, I looked it up, I like, there's no good Fusobacteria.

No, they're bad guys.

Should we have any of them? Yeah.

Well, so yeah, they're all bad guys.

So like, why is there a normal range?

Yeah. Well, because they could be down there. So, so Fusobacterium, that's just for the, the audience here. That's the genus. So within the genus you have a whole bunch of different species. So you have like Fusobacterium nucleatum and a whole bunch of others.

Yeah.

They're bad. Right. So where do they come from? Actually, they come mostly from the mouth. Mouth, right?

Yeah. Right.

It's part of the, they are part of the oral microbiome. And so if they're kind of nasty in the mouth, think of how kind of nasty they are in a whole different location where they're not supposed to be, or not supposed to be in abundance. So as a part of the oral microbiome, you can see them in a stool analysis, right? So, so the big thing with Fusobacterium nucleatum is it's highly correlated with colorectal cancer.

Right.

And I have a video on that as well. So, so there's two theories on F. nucleatum. One is it just makes its way down the GI tract. So especially if you're taking PPIs, proton pump inhibitors, which block stomach acid production, you have lost that protective area, that protective barrier keeping bugs from the upper GI from getting to the lower GI. So it passes on through down the GI tract and takes up residence in the lower gut. Where it causes big problems, pro— very pro-inflammatory. The other theory with it showing up in the stools is actually just simply from brushing your teeth, eating, flossing, dental cleanings, the list goes on. So there's a whole bunch of data that shows that, you know, dental procedures, et cetera, flossing result in the different bacteria from the oral microbiome making its way to the blood. So the theory is somehow from the blood it works its way down to the lower GI and then populates itself in the lower GI. So either way, there's a large— there can be an abundance of F. nucleatum in the lower GI driving inflammation. The other interesting thing about that too is when the cancerous cells metastasize, oftentimes they have F. nucleatum within them and you can track it to the site that they metastasize to, and the F. nucleatum is still inside the cancer cells. So it's, it's, it's pretty pro-inflammatory. So again, what's the key? The key is we're all gonna brush our teeth, we're all gonna eat, we're all gonna have dental cleanings, right? We're all gonna, whatever it happens to be, we're all gonna swallow food. The key is make sure the good guys are in charge. They're gonna produce antimicrobial, you know, peptides and so forth, help with the mucus lining, help with the immune system, butyrate production, the list goes on to keep these bad actors in check. You're not going to kill off all of the bad guys. They're gonna be down there. We're all gonna have E. coli. We're all gonna have, yeah, a number of the bad guys. We're not all gonna have the same percentages and the same exact ones, but we're all gonna have bad guys. So we have to keep them in check by nourishing the good guys instead of being like, oh, berberine kills off this bug and oregano oil kills off this bug and amoxicillin kills off this bug. All you're gonna do is, you know, first of all, you're not gonna kill 'em all off. They're gonna hide out in their reservoirs. And we'll come back at a later date, which is actually very true for, say, for example, for UTIs. So the data shows for UTIs, the number one source for UTIs is the gut microbiome, right? Even you can go back and look at, you look at the genes in the, in the bugs and you go, well, we killed it off in the GI, in the, in the urinary tract, but the same bug is back with the same genes in the urinary tract a year later. Well, where was it? It wasn't the urinary tract. Well, guess what? We found it in, in the, in the feces, in a feces sample, right? It's in, it's hanging out in the gut. So again, you, you have to look at the overall picture and everyone says kill, kill, kill. They want to just kill, kill, kill. And I have these people all the time, but really you need to nourish the good guys cuz we're not gonna outthink millions of years of evolution. Let the good bacteria figure out, okay, you know, they're gonna do their thing and just let them do their thing, feed them and let them take charge.

Okay. So what kinds of symptoms do people feel in Crohn's disease that are distinct from other conditions like IBS or even ulcerative colitis?

Well, then, then, then you get into, yeah, the, the confusion like you mentioned before, like what the hell do I have? Yeah. IBS can look a lot like Crohn's. So the big thing in Crohn's is most people gonna have diarrhea, but ulcerative colitis, most people gonna have diarrhea as well. And then you have IBS people with diarrhea. So how do you distinguish those, right? So with, within the absence of, say, a colonoscopy, that's a little hard to tell, right? You kind of like just throwing, pun intended, you know, crap against the wall to see what sticks, right? So you can have pain in the lower right quadrant. So the classic Crohn's presentation is in the distal ileum, which happens to be in the lower right quadrant. The appendix is down there too. So like, it's, you know, there's, there's, there's a lot of room for confusion. You could, I mean, this is not a symptom, it's, it's, it's unfortunate outcome. You can have different things like fistulas where you basically, a fistula is where cells just go wild and they start boring through and just, they just like, I'm gonna make a channel this way. And you wouldn't know if you had a, a fistula within connecting your small intestine But she would know if you had, like, for example, a perianal fistula where all of a sudden you're starting to leak feces because, you know, it's, it's not like a second anus, but it's not. And so you're like, wait a second, what's going on down there? About 9% of the women, I think it is, will get a rectovaginal fistula. In other words, there's a boring of the cells from the rectum to the vagina. So that would be, you know, an obvious thing. Well, hey, wait a second, what's going on here? But I mean, there's a lot of room for confusion as well when it comes down to Crohn's and is it ulcerative colitis? Is it IBS? But again, they're all tied together with significant bacterial dysbiosis in the gut. So yeah, I have a video on ulcerative colitis. I have videos on IBS. Again, it, the, the players are generally the same. You know, the good guys like F. prausnitzii are significantly lower in IBS, in Crohn's, and also colitis. You know, the bad guys like E. coli are significantly higher in all 3 of those conditions as well. So the common denominator is they're driving inflammation and the, the, the whole, you know, spin the wheel and see what disease we get. That just comes down to really genes, like uncovering which genes are, you know, you particularly, you have. So, mm-hmm, the bugs, the methodology isn't that drastically different. It's just the genes. But still the bottom line is to me, basically the same.

Yeah. So in the typical approach to IBD, Crohn's or colitis, that's flaring, meaning there's diarrhea, there's loose stool, or sometimes constipation, there's pain, blood, mucus in the stool, that kind of thing, is to completely reduce fiber intake until the flare calms, like using diets like specific carbohydrate diet or low FODMAPs or IBD-AID. I'm assuming that's not the approach you use. Do you, do you feed fiber to a flaring gut?

Yes. Yes.

So gradually or suddenly?

No, I, I, I go in guns a-blazing.

Do you? Okay.

So, so with those diets, like some of them not well, the FODMAPs, I think does, I can't remember the FODMAPs does, but the others recommend, for example, fermented foods. I do not recommend fermented foods. Low FODMAPs doesn't recommend dairy because of the lactose. I don't recommend dairy because of the proteins. So, and some of the other ones recommend dairy. So there's no dairy because, and again, this across the board for people, especially with autoimmune disease, constipation, ulcerative colitis is a big one here. The dysbiotic gut has a hypervigilant immune system. It's always looking for a fight. Dairy proteins are the number one offender. So if you throw dairy proteins in down there, they're like, hey, wait a second. They, they, they, they've already seen those before. They have already have immune system that's It's ramped up to fight them, more inflammation. We don't need dairy anyway. So I'm a no-dairy guy. With the probiotics, the fermented foods, I do not recommend them again. And I've done meta-analyses, Crohn's, ulcerative colitis, dementia, Parkinson's, the list goes on and on and on and on. Anxiety, on and on. Kidney disease. Lactobacillus is basically always significantly higher in those who are sick versus the healthy controls. Typically dysbiotic gut is a high lactate environment and it's a high Lactobacillus environment and Lactobacillus species. Now we're talking the former genus Lactobacillus, 'cause it's been reclassified. They make a whole bunch of lactate. So why would you want more Lactobacillus and more lactate in what's already a high Lactobacillus and high lactate environment? So I disagree with them there. So, and then, then they have their differences, but generally speaking, they say take away Carbohydrates that can ferment. I'm like, no, don't do that. Give them carbohydrates that can ferment. Like, for example, the low FODMAP diet takes away things like garlic and asparagus and onions and apples and carrots and all these things. These are the preferred fuels of the good bugs. That's their fuel. I've also done huge meta-analyses on all different prebiotics administered in trials. And to see in human in vivo and also humanized in vitro trials to see which prebiotics move which bacteria. In other words, will promote them. And again, it's clear there as well. So it's very clear in the literature that the good guys like F. prausii, species from Roseburia, Ruminococcus, Coprococcus, et cetera, their preferred fuels are the locked up sugars in these carbohydrates, things like pectin from apples and pectin from carrots and inulin from onions and inulin from asparagus, And the list goes on. Those are their fuels. So if you take the fuels away from the good guys, what are they going to do? They're like, well, hey, wait a second. There's less fuel here. I'm— this is going to now be less of us because there's less fuel to feed us. Right. And then the bad guys are like, hey, this is great. They just took away all these fuels for the good guys. And now there's more protein coming down the chute. We love to ferment protein. And so you've changed the balance. Now in the short term, the low FODMAPs diet, does it yield, you know, some success with, with symptoms? Yes, it does. The data's pretty clear on that. So for 2, 3, 4 weeks, whatever it happens to be, your gas and bloating will go down. Okay. Granted, that's the case. But if you look at the studies using the low FODMAPs diet, and I have, in the, what they wind up doing in the long term is reducing the good guys cuz their fuels have been taken away. What I'm saying is let's bring those fuels, a lot of them into the system. To change the balance, to drive the abundance of the good guys. So now they're in charge.

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Mm-hmm. But at the end of the day, you're pushing the good guys in the colon. So for people who have, like in my scenario, I've got antibodies to my migrating motor complex essentially. So I'm always gonna accumulate bacteria in my small intestine. So I, so, you know, in, in an effort not to wipe out the good guys, I've avoided things like berberine and oregano oil. And I, I've, I've been using MSM to just periodically kill some bacteria as my bloating increases. This is simultaneous with feeding them good fibers. So I mean, where in that scenario, what else can you do? I mean, is there a least harmful antimicrobial? Like I'm, I, I also sometimes use a the pomegranate peel.

Yeah. So I mean, the, the small intestine does have its own microbiome for starters. And then like in SIBO, it's too many bad guys in too much abundance crawling up too far up the GI tract. But when you're addressing it with prebiotics, okay, so I'll take a step back. So a lot of people tell me, Guy, I eat healthy, but I can't get better. And I go, yes, I know. I've heard that a million times. And I say, you're not gonna fix this with diet alone. Because things have become broken in your microbiome and you really have to drive it with significant change. You can't just, you can't eat your way out of this. I've seen it a million times. It's not going to happen now.

Right, right. No, I'm talking about additional fibers. I'm not talking about just diet. Right, right.

So, right. So now I'm getting to that. So in a lot of people, then there's a lot of trials on this as well. They use one fiber. So you might have inulin, or you might have partially hydrolyzed guar gum, you might have something else. So you throw in one prebiotic in there at a dose of maybe 7 grams, 10 grams, 12 grams, something like that per day. So what does that do? Well, again, if the bad guys are in charge of your gut microbiome, some of them can use those for fuels, which is why the definition of prebiotics is incorrect, right? Prebiotics are basically, the definition is basically a fuel that feeds the good guys, right? And that's an incorrect definition because a number of the bad guys can use those prebiotics for fuel. Now, when the bad guys— now, gen— as a general rule, the bad guys love to ferment things like protein. So they, the bad guys love the carnivore diet, but some of them can ferment prebiotics. So if you're gonna throw 7 grams of pick your prebiotic into the gut and the pH is favoring the bad guys with a pH of 7, 7.1, whatever it happens to be, Then the bad guys were like, hey, this is fine. Like the bad guys are gonna get more of that prebiotic than the good guys will. Plus you're only putting in one prebiotic. So now you're only feeding a certain section of the good guys if they're even getting the fuel at all. Right. So is that a recipe for success? So what I do is I use multiple prebiotics at significantly higher doses. So now if I'm using 4 prebiotics, I know that the Crohn's profile is, you know, so we flipped the numbers before we were talking about low good guys, high bad guys. I know that Crohn's profile for the healthy controls, right? The opposite end is high F. prausnitzii. Okay. What prebiotics does F. prausnitzii consume? Pectin and inulin. Okay. What else is the healthy controls high in and the Crohn's people low in? Okay. Roseburia. And you go down the list. What does roseburia like? Well, Rosemary likes to ferment arabinose islands. Where do arabinose islands come with, come from? They come from bran, right? Some of these diets say no grains, right? No, don't do grains. Well, the husk of say rice, for example, or wheat, for example, that's full of arabinose islands. The good bacteria love arabinose islands. So I go, okay, so it's low on this and it's low on this. So I'm like, we're gonna feed, you know, we're gonna use these different prebiotics across the board to make sure we feed the full spectrum of the good guy. Am I using my hands too much? 'Cause I'm half Italian, so, so am I. I can't talk without using my hands.

Paisano.

So, so anyway, I'm trying to feed all the good guys who I know are low on the average microbial fingerprint, right? So then they can go ahead and crowd out the bad guys. So it's very plausible that you're throwing in 10 grams of inulin or, and inulin's really not a good prebiotic anyway for someone with diarrhea. 10 grams of inulin or 10 grams of partially hydrolyzed guar gum, but that's not enough to change the environment. On top of that, I'm throwing another ancillary agents in there as well, right? Because again, we have to look, what are the deficiencies in Crohn's? We have a deficiency in antimicrobial defense and so on.

There, I know you like PEA as an anti-inflammatory, as a, as a gut healing supplement. There's others that are frequently recommended in IBD. I'm curious what you think, like curcumin, fish oil. I've heard of chaga, but I also know that's immune stimulatory. I think paswelia, Andrographis. There's a, there's a number of other things that I've seen.

So fish oil, the data's terrible and really I, I never recommend fish oil, I don't think for Anyone. Mm-hmm. PEA is actually meant to be a temporary solution. So what I'm trying to do is, and PEA I think is more robust than say curcumin and say Boswellia, right? So those are kind of direct anti-inflammatories. When you use those, you kind of like, you're using the allopathic drug mentality. We're gonna give anti-inflammatories, right? So, okay, so why are we doing that? Well, because something's driving inflammation. Well, let's get to the something that's driving inflammation, right? So I don't recommend curcumin. I don't recommend Boswellia, although they have some decent data. I recommend PEA really for a few different reasons. Mm-hmm. Because one, it acts as a mast cell stabilizer, and mast cells are a big problem in Crohn's. Okay. Another thing, it helps with sleep. So people who have gut dysbiosis are chewing through their tryptophan and cuz they're making a bunch of serotonin in the gut. So mast cells don't produce just histamine. Mast cells produce like 30+ chem compounds. One of them's serotonin. So if you're constantly inflamed, constantly with diarrhea, you, you, you're eating your proteins, right? But tryptophan's the least occurring amino acid. So you're cruising through your tryptophan stores to make serotonin to deal with the in— the serotonin in this case is pro-inflammatory and you have no tryptophan left over to enter the brain and now you're not sleeping well. So PA helps with that for example, but it's meant to be just a temporary help until I can address the root cause, which is a dysbiotic microbiome. My intention for anyone except for maybe autism is, you know, and maybe say dementia or Parkinson's, is no long-term use of PEA. That's meant to be a short-term thing. It's like when I give butyrate, when I give butyrate, that's meant to be a short-term thing until you can start producing your own butyrate.

Right, right. So I didn't understand the connection between the PEA and the tryptophan. How does, how do they interact?

Well, they, they don't really interact. It was, it was an analogy. So, so the PEA I use, the tryptophan is not making its way to the brain because it's getting chewed up in the gut. So if you're not getting tryptophan to the brain, you're not getting serotonin in the brain cuz serotonin doesn't cross the blood-brain barrier. If you're not getting serotonin in the brain, you're probably not sleeping. You might have some anxiety and/or depression. Okay. I can't give tryptophan in someone who's high histamine with mast cells who are unstable and someone who has di— and with diarrhea, right? Someone with diarrhea. I can't, I can't do that.

Right. Oh, okay. So you're giving the PEA to Right.

So I give 'em PEA to help them sleep, right? That's one of the angles. PEA to help stabilize the mast cells because they're very unstable in the Crohn's patient, right? And then help with overall inflammation. But again, it's a temporary bridge to get us from the mess you're in now when I see you on, you know, my consultation on days, day 1 until day 30 or day 40, whatever it is, until you're much more stable, you're sleeping better. You know, your anxiety's gone down, you don't have diarrhea. Well, we don't need the PA anymore. You're producing your own butyrate. What do we need it for now?

There's a lot of good data around PEA and pain as well. And I imagine that's also very handy for someone who's in pain in the gut. Right, right.

No, that most of the data is for, for PEA is, is for pain. And I've had people have seen my video on PEA and they just come back with these like miracles comments and, and YouTube saying, oh my God, this was the greatest thing. So, but again, they're taking one supplement to address, say, rheumatoid arthritis, for example, right? Okay. Well, there may come a time where that supplement stops working for you, right? Or, you know, why don't we get to the root cause? Which, if we look at rheumatoid arthritis, there's a huge connection to species from the genus Streptococcus. All right? So Streptococcus, you have these, these amino acid sequences in Streptococcus that look like some of the connective tissue in our body. And then the immune system kind of says, doesn't really know the difference between the two. It says, well, I've seen that before in Streptococcus and I see it over here. And, but the immune system's like, I'm not sure, I don't know if that's connective tissue or not, but I'm gonna attack it anyway. Right? So again, for autoimmune, like, you know, rheumatoid arthritis, let's not do a lifetime of PEA, which may eventually stop working for you. Let's address the root cause.

Mm-hmm.

So yeah, I, I mean, I, I downloaded your Crohn's protocol and, and I've been trying to get up to the level of fiber in your shakes. So I'm curious cuz it's really challenging. I mean, I'm a slim person and 2 shakes a day. Yeah. Of 40 grams of fiber or something.

I mean, it's in about that. Yep. Yep.

General range. Like I can hardly eat anything else. So I was just kind of wondering, like, for, can I, can I reduce it a little bit given my size? Is there, can you accommodate for smaller people?

Yeah. So. As I say, my consultations.

And also, how did you get to that high level? Is this all trial and error until you're just like, now I'm finally cracking this, this egg?

Yeah. So it's, it's, um, okay. So try to do one after then to the other. So it can be a challenge. And for people who are more slender, I tell them, listen, it's going to be an effort, but I need you to eat food. I need you to take in calories in the first month. You know, and things like butter are easy calories and, you know, honey can be easy calories and just eat. I need you to eat and you focus on eating because yes, it can be filling. The other thing is because it cranks up so much butyrate is we increase the satiety hormones. So sometimes people just don't feel hungry, right? And, and I tell them, and again, so like when I sell the protocols, it's $25. It's kind of like a, here's a package deal for the average microbial fingerprint. My consultations, that's, you know, it's $500 for the hour, but I get to dive into everything as something specific to you and your needs. There's email follow-up. So, you know, so part of that consultation is I want you to eat food, food, you know, but eventually what happens is your, your digestion improves so much that you're able to absorb your nutrients so much better that you actually do put on weight. So my people who do start out being light because they have diarrhea from Crohn's or ulcerative colitis or something else, They eventually do gain weight with me because they're absorbing their nutrients better. But yes, the first month can be challenging. Plus I can make people bloated and, you know, they basically to the point where, hey, you know, Guy, I don't like you so much in this first month because I'm pretty uncomfortable. And I tell 'em that in the consultations. I'm like, listen, you're probably gonna hate me in week 2, week 3, or something like that. You're gonna be bloated. If you, you know, if you had like psoriasis before, I might make it worse before I make it better. Or if you had brain fog before, I may make it worse before I make it better, but some things might get better quickly too. So the first one's gonna be a challenging, I make, you know, I don't deceive anyone on that one. I make that very clear, but it's necessary to do that, which is your second question, why so much? So, and yet it's, it's a, it was a blend and this is, I formulated this years and years ago. It was a blend between understanding that individual prebiotics would fail a lot in trials. And I read those trials, 10, we talked about this already, 10 grams of this or 7 grams of that, just a lot of failures. And so go, okay, well, single probiotics at lower doses aren't working. The data just doesn't support that. Then you look at the data, you go, well, Roseburia species or Roseburia like this one and F. prausnitzii likes this one and Coprococcus likes this one. You go, okay, well, we want to We want to have a healthy diversity, right? So we want to feed the good guys across the board. We don't wanna focus on just one. So that made having multiple prebiotics necessary as well. So I eventually got to the point where I actually ran a, when I was the director, I ran a trial, an IBS trial, and it had 100% success rate. So I'm like, okay, well, you don't, you don't see that every day. And that was with the dosing schedule that I had built over time. And so that's just something I've continued with. And, but it depends on the person. When I do the, again, with the CAN protocols, I build it for the average microbial fingerprint. But if I'm doing a consultation with you and you're telling me these different things, then in my head I'm going, okay, let's take out this and let's add this and let's reduce the dose of this because it, it's a two-way street. Mm-hmm. The information you give me is invaluable and I'm gonna take it. I'm gonna—

Yeah. So like if I have, good amounts of Rosa Buria, you might say you can cut back on the prebiotic that needs that, or—

Right, right. Or for example, even bigger one, if you're one of those rare people who has Crohn's but has constipation, right? That's, that's a game changer. Like I have to change that protocol that's built for the average microbial fingerprint may not work for you. Okay. So, cause you have Crohn's with constipation, that's, that's not the rule. The rule is diarrhea. So the consultations, I, I can, you know, take the deep dive and it's, it's something geared specifically for you.

So I know there's concrete research showing that negative impact of gums and emulsifiers like carby methyl cellulose, polysorbate 80, carrageenan, sodium stearoyl 2-lactylate, diacetyl tartaric acid esters, maltodextrin, and, and a few more in IBD. But I'm wondering your thoughts on some of the ones that are used in the more like nice organic gluten-free foods like guar gum and xanthan gum. Are those things that you think should be avoided by people with Crohn's?

Well, I mean, guar gum, that's, that's a prebiotic supplement, right? So there's the partially hydrolyzed guar gum. So the reason they hydrolyze it is because if you ever work with guar gum before, it just forms a giant lump, right? It doesn't, it doesn't disperse, but the principle is still the same, right? It's just something that's more tolerable in your shake. So, there's a fair bit of data that shows that guar gum, AKA partially hydrolyzed guar gum, feeds a whole bunch of good bacteria. I tend to avoid the ingredients that I can't pronounce. I have a tough enough time with all the bacterial names. I have to pronounce all of those. So yeah, those to be avoided, but guar gum, I don't, I don't see a problem with that. And again, that—

what about xanthan gum?

Xanthan gum, I have to say I've never taken a deep dive into that.

'Cause that's in a lot of products. Like I'm trying, I'm trying hard here and that's like in coconut milks, it's in almond milks, it's in any kind of bread. It's in, I just got some, were they potstickers? Like, I mean anything gluten-free. 'Cause I, and I, and I'm gluten sensitive.

Yeah.

In this scenario. I don't know if that's, that's a general problem when Crohn's or not, but I am.

Well, I, I mean, I generally tell people to try to just eat whole foods.

Yeah.

Right. So. And some people do that and some people don't. But like, for example, myself, like I just, it's just cooked from scratch. So it's good. I got the organic oats and I got the free-range eggs and the list goes on. But I understand, you know, everyone can't do that, but it kind of falls in the same basket of food avoidance, right? When you correct the microbiome and you correct the hyper-inflammatory immune system, then you correct the hyperreactivity to a whole lot of things. So for example, and I just, I had another consultation, we talked about this in the consultation earlier today where this person kept blaming foods like, oh, this food and this food and this food. I'm like, you have to stop blaming the food. The food is not the problem. I can eat that food. Most of the people out there can eat that food. It's not the food, it's your immune system. Your system is reacting to this, that, and the other thing. And which is why a lot of people get painted into a nutritional corner because they react to everything under the sun and now they can only eat 3 foods. The food is not the problem, right? You get into all this, oh, oxalates and this and that. And you know, I have an oxalate video coming out soon too. The food's not the enemy. Okay. Which is these people go carnivore, like, oh, I went carnivore and I felt great my first month or year and then I went downhill. But yeah, You can avoid the foods, you can avoid the vegetables, you can avoid the whatever it happens to be, but it's not the food's fault, it's your immune system. Okay? So ask yourself, why is my immune system so hyper-inflammatory? Why does it want to pick a fight with everything I throw down my gut? Well, because it's constantly on alert mode. Why is that? Oh, because we have this constant ongoing attempt at an invasion in our gut, which is, you know, in most of our immune system, 80% of our immune system is in and around our gut. And then this stuff goes systemically with gut permeability. So again, we have to get to the root cause. The root cause is why is my immune system— why are my mast cells degranulating, blah, blah, blah. Why do I react to everything? Well, what's the root cause?

So for people who didn't ever have one of these conditions, who had a healthy microbiome all along, they don't have to eat a gut shake for the rest of their life.

So No, they don't. No, they don't. No.

So how come when we fix our microbiomes, we still have to keep doing that?

I don't know. I don't, I can't answer that question.

Okay.

So I mean, yes, I've had people who are perfectly healthy, they screw themselves up with going radical diets, paleo or fermented foods, or eating a whole bunch of fermented yogurt, the whole nine yards and, you know, probiotics. And they come to me like, Guy, I was perfectly healthy up until I started trying to get more healthy. And I'm a bloated mess and blah, blah, blah. And I fix them in a month and they're off their merry way and doing, you know, back to their life. That's not us. That's not us.

Yeah.

That's not a whole bunch of ulcerative colitis and it's not a bunch of other people. It's not people who've been on 50, 75, 100 rounds of antibiotics.

Yeah.

We're a different group of people, right? We're the, the gut, gut broken along the way and it's never gonna be the same again.

Yeah. Yeah.

And I, I don't know why for the life of me, I can't figure that out. I'm like, okay, this person's doing great. We're feeding the good bugs. The immune system is now more tolerant. It's not hyperreactive. Why can't this person go back to doing this, that, and the other thing? Like for me, okay, if I go to a Chinese restaurant and I have soy sauce with MSG in it, forget about it. I'm done. I'm in the bathroom the rest of the night. I cannot do preservatives. I, I, to this day, I still can't do them after years and years of doing this. You know, okay, well, well, God, your mast cells should be stabilized by now. Yeah. As a general rule, they are. I can drink alcohol. I can do other things, but I can't do preservatives. Why that one thing?

I don't know.

I don't know. And why can't someone— I don't want to do a shake anymore. Okay, fine. You can stop doing a shake. Once I fix you, you might be fine for a month. You might be fine for a year, you know, but I've had people come back to me 2, 3 years later saying, Well, I was feeling so great, I stopped doing everything and now I'm a mess again. And I'm like, weren't you, didn't you take like 100 rounds of antibiotics before in your life? You're like, yeah, 'cause I'm, I'm reading in the notes like you did. Yeah, I did. Didn't I tell you like your gut was broken? You had to do this first your life. Yeah, yeah, you did. But you know, they don't wanna do this stuff. Yeah. And so they come, they come back.

Okay. One quick question left. People who are constipated, this quantity of fiber Do you ever get people who get totally backed up? Like they just cannot eliminate it?

I mean, again, it's a, I have a constipation protocol that's successful about 90% of the time within one week's time. So even with the quantities of fiber barreling down at the beginning, because you have to realize the vast majority, the only thing I, I recommend that's not completely fermentable is psyllium, right? Psyllium is about 25% fermentable. Everything else is 100% fermentable. Inulin, pectin, partially hydrolyzed guar gum. So you're not building bulk. And on top of that, you're increasing butyrate production, you're increasing serotonin, you're, you know, the activity in the gut, the propulsive activity in the gut. But again, I'm also offering up in my IBS Constipation Protocol other ancillary products in there as well to help get things moving along. So you could say, okay, God, if, if, if you, you can have an example, and this happens sometimes in people, someone's constipated, they take a whole bunch of psyllium.

Yeah.

And they're all backed up, right? That happens. But I don't give psyllium by itself. It comes with a number of other prebiotics, a number of ancillary supplements. I correct the microbiome and these people are off and running. And I have a number, a number of both video and written testimonials for people who were constipated for many years and are doing great.

Okay. I'll take your word for it. Well, actually, I guess I could just look at it anyway. Well, thank you so much for coming back on and talking about Crohn's with me. This is very timely for me and I'm sure for many other people. So I appreciate it.

Well, thanks for having me back on. I appreciate that.

So I'm very thankful to have had Guy on again because I interview a lot of people and not many people have as good a background on the research on the microbiome as Guy. So I've really been learning a lot from him and implementing his methods with my clients. Since I first interviewed him months ago. So this was a great chance to dig deeper on his protocols and how he came to them and how they play out with his clients. You can support the podcast by buying supplements at a discount from my Fullscript dispensary, ordering tests at a discount from my Rupa Health Lab store, or using my affiliate links to iHerb, which is available worldwide, or Amazon. And just to note that you can use my Amazon link to buy anything, not just supplements, and support the podcast.

And I see there's definitely some of you doing that now, and I really appreciate it.

If you'd like to connect with me online, you can follow my High Desert Health Facebook page, join my Gut Healing Facebook group, or join my newsletter list at highdeserthealthcoach.com. Www.meredithroddy.com, as well as follow me on Instagram, TikTok, Pinterest, and X. Links for those are in the show notes. Thanks for joining me today, and here's wishing you all the perfect stool.