Adapted from episode 160 of The Perfect Stool podcast and edited for readability with The Microbiome Expert, Guy Daniels and Lindsey Parsons, EdD.
Lindsey Parsons:
So as I mentioned to you over the email, I’ve recently received a blood test back indicating that, in addition to post-infectious IBS, I have elevated antibodies indicative of Crohn’s disease, and those are the AMCA [Antimannobioside Carbohydrate Antibodies] 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.
Guy Daniels:
So well these, that’s part of a group of a slightly larger family of antibodies. And really what they are looking at are 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, all these bacteria and all these yeasts, they have these different structures to them and structures to their surface. And they’re really what our immune system calls 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, these things are recognized by nine or 10 different toll-like receptors in the human body, toll-like receptor four is big for lipopolysaccharide, which is another one. It’s the same general family where it says lipopolysaccharides, 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, 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. 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. For ulcerative colitis, it’s the mucus layer. Crohn’s is an antimicrobial defense. So there are defects in the pan cells and the crypts of the pterocytes, and so bacteria, bad bacteria, are able to adhere more efficiently and invade the cells of the Crohn’s patient. So yeah, you’re going to have these antibodies to these different viruses and fungi, because there’s this constant exposure at the enterocyte, within the enterocyte, when we get to the NOD-2 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 current patient is very dysbiotic.
Lindsey Parsons:
So does it tell me which pathogen I should be trying to target because I had the elevated AMCA antibodies?
Guy Daniels:
So my philosophy is I don’t target any pathogen in particular. So whether it’s E coli, R. gnavus, which is a big pathogen in Crohn’s, or any species from Klebsiella, Streptococcus, Veillonella 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. gnavus, etc., etc. The microbiome doesn’t work that way. And in my experience 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, this doesn’t favor me. This isn’t my pH. My pH is 5.5 to 6.5; right now we’re at a pH of 7.0, 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 when you’re here. You can’t tolerate oxygen. We can tolerate a little more than you can. The pH is right for us and then the inflammatory environment then makes the bad guys more pathogenic. It expresses a different kind of genes, but more so kind of genes that are less expressed or not expressed when the environment is 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 of an opportunity of an environment 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 all the teenagers are allowed to do their thing and go wild, and they find a whole bunch of beer or whatever, it’s like they’re in charge, there’s no checks and balances on them. And so that’s basically what happens in the gut.
Lindsey Parsons:
We’ll get to your philosophy in terms of fiber and such. But a 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?
Guy Daniels:
So that might be the case. So I know what you asked me. Suppose I’ll take a step back and 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 this. 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 us, I’ve seen all of it, and I’ve analyzed, I’ve compiled all of it, and 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 it 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.
It’s a superhero of the gut. It produces a whole bunch of butyrate. It cranks up interleukin 10 production, which is an anti-inflammatory interleukin and has other different properties as well, and all of its cousins are consistently, significantly higher in healthy controls versus those with Crohn’s, such as species from Ruminococcus, species from Roseburia, species from Coprococcus and it goes on, so I never, ever recommend Saccharomyces boulardii. It doesn’t make sense. The good guys are very clear. The bad guys are clear, and nowhere on the board does that pop up?
Lindsey Parsons:
Yeah, no, I wasn’t thinking of it for the Crohn’s. I was thinking of it more for other purposes, because, for example, sometimes I see people with elevated Candida and I give them S. Boulardi, or maybe they have high levels of Blastocystis hominis, and I use it for that purpose. So, I’m thinking, if somebody simultaneously has Crohn’s and other issues, you know, whether it might be indicated.
Guy Daniels:
So I have videos on both of those. I have videos on yeast, fungi/Candida. And I’m actually about to launch, shortly, a video on Blastocystis. So Candida is, again, an opportunistic pathogen taking advantage of an environment in which it can, 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 is like, woo hoo. It’s party time. We have all this space, we have all these substrates, we’re going to have a good time with Blastocystis. And I’m fresh off doing all the research for that and brushing up on that, because 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 like a whole bunch of other bugs out there. It’s kind of 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 those with a certain condition. So it actually follows some of the general rules that the good guys do, like it can’t tolerate oxygen. It’s 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 microbiome healthy, and then it’s like, yeah, whatever. It’s here. But we don’t care, because the good guys are in charge, because it really kind of is a normal member of the microbiome, kind of like Candida. Candida is pretty much in a lot of people, a normal member of the microbiome as well. So you’re not going to kill it all off. You just have to control it. You have to sideline it.
Lindsey Parsons:
I heard recently in a webinar, actually it was on Anaerostipes 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.
Guy Daniels:
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 metabolism. 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, there’s typically more primary bile acids and fewer secondary bile acids. That’s typically the picture. And I talk about this quite a bit in my video on C. diff infections, and I have talked about it in 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 different quantities and different types as well. And it actually was thought a while ago, years ago, that the gallbladder, and then that duct going down to the pancreas was actually a sterile environment, but it’s been recently shown that it’s not. And if you have something more like a SIBO type of nature, then bacteria can actually work their way up that duct, so you can actually have dysbiosis of the gallbladder and get into the branching of the pancreas as well. So, and yes, in that instance, TUDCA* would be a benefit. So TUDCA is a very helpful secondary bile acid, but TUDCA, 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 them usually, the first enzymatic activity is deconjugation. So again, the primary acids, they’re conjugated with either taurine or glycine, so oftentimes they don’t get deconjugated. The second one I think is hydroxylate, so it’d be hydroxylation, if I recall correctly. So a very, very small number, very, very small number of the microbiome actually has a very complicated enzyme to dehydroxylate the primaries into secondaries. And so in there, those bugs also have to be rather sensitive to antibiotics, which goes 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, etc. And then you get into taurocholate, which is a whole other story.
Lindsey Parsons:
Recently I did a Gut Zoomer in July, and that was the first indication that something wasn’t quite right. There was an elevation in fecal lactoferrin and a couple of the other inflammation markers, but not calprotectin. But I’m pretty sure that all my bile acids look normal. So could they be within the normal range, and if you took ratios, you might find that there actually was a problem.
Guy Daniels:
I mean, it doesn’t mean 100% of the time there’s going to be bile acid dysmetabolism; just a common pattern. Well, it’s a significant percentage of the time. It really is. I mean, when you look at the clinical data, if you take 50 people or 100 people in a trial, right, you’re averaging these numbers. You’re going to see a significant difference between group A and group B. But within those groups there’s 50 individuals, whatever happens to be in each group, you could have someone who’s up here, and 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.
Lindsey Parsons:
And how does the TUDCA work in that scenario?
Guy Daniels:
So TUDCA works by various mechanisms, and I have a video on this. It’s actually one of my more popular videos, which is interesting because I was like, I’m going to do this obscure supplement that no one talks about, and everyone loves it. So everyone loves this video.
Lindsey Parsons:
Oh yeah, but Cell Core has been touting it for years. I feel like I’ve been seeing videos about it for six years now.
Guy Daniels:
Yeah, and it works great. Like I have a lot of YouTube comments, people saying, oh my god, the TUDCA is the best. So it works. First of all, it’s 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 portal vein, they just get dumped into the liver. So then, the problems start in the gut, then they continue to the liver and the leaky gut and everything else. So it plays a huge role inside the liver. It’s very water soluble. It has a dynamic where it’s very low inflammatory. And then the gallbladder. It actually has historical use, TUDCA and UDCA, which is the drug from historical use for gallstones. And then it works its way to the pancreas, where it can then help with the production of enzymes. So I never recommend enzymes, right? I recommend fixing the system. Like most people who come to me taking enzymes, I’m like, okay, well, it’s fine, but you really should not need them. Well, instead of giving you enzymes, we’re going to fix the reasons why you’re not producing them as well as you should. And then it gets into the upper gut, and it does act as a bit of an antimicrobial, but it also acts as anti-inflammatory there as well. So, 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 on my video, they’re welcome to do so.
Lindsey Parsons:
And does it do something to change the composition of the microbiome in that process?
Guy Daniels:
Well, yeah, yeah, because it’s a secondary bile acid, right? So the studies show that when you take TUDCA, you’re increasing your TUDCA, right? It’s a highly beneficial secondary bile acid. So your secondaries go up, right? Your primaries go down. And again, like I said, it’s an antimicrobial. So if you have a SIBO type of condition, where you have too many bugs impacting conjugation and so forth, right? Then you’re going to clean out that upper GI as its antimicrobial effects, and then contribute more to the secondaries, because some of the secondaries do get reabsorbed, right? And then you change the composition from a heavy primary bile acid to more of a secondary.
Lindsey Parsons:
So for someone like me who has post-infectious IBS, where I’m just always going to have recurrent SIBO, would TUDCA be a good idea as a continuous supplement?
Guy Daniels:
It could be, yeah, it could be. I mean, oftentimes 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 going to be on TUDCA for a while, right? That’s, again, a part of a much larger picture. If you have SIBO, that could only be a month that SIBO, a lot of my SIBO people cruise through in about 4-5-6, weeks time. So, you know, once you get past two months, do we really need it? We’ve changed the bile acids metabolism. We changed the microbiome. We’ve rectified the SIBO. You may have had high histamine before. Now you’re no longer high in histamine. You tolerate food. Do we still need it? Maybe, maybe not. So 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, for example, Crohn’s, what we’re talking about, is a great example. So the Crohn’s person usually is going to 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 it. Like I have Crohn’s, for example. Okay, I was diagnosed many years ago, so I’m always taking my one shake a day, most days a week, five, six 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 on this and that and the other thing, I want to get them down to the minimum number of supplements possible to 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’re off and running. They don’t have to take anything again.
Lindsey Parsons:
Yeah, so tell me a little bit about your journey with Crohn’s and how you reversed it.
Guy Daniels:
Yeah. This is a whole podcast in itself. So that’s to be 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 some people, and then I became very thin, and it 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 think. I’m having these unfortunate visits to the toilet. So then it started just getting more and more severe, and at the point where I started looking at food with fear. So I went to see three 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 they don’t know what they’re talking about. And so then the years of research and trial and error started. I did go to one functional medicine practice, but they did the usual yogurt with the probiotics, which didn’t do anything for me and it actually harms a lot of people. That’s a topic in my videos.
Lindsey Parsons:
SCD yogurt, they call it, right?
Guy Daniels:
Yeah, back then, I made my own yogurt with probiotics. So probiotics never seem to make me worse. They make a lot of people worse. They made me worse, but they didn’t make me better, either. So there’s years of trial and error, years of research, years of fine tuning, and then I developed, for a number of years, basically a philosophy, a protocol that worked. And then since about 10 years ago, well it was nine years ago, since I became the Director of Medical Education for a microbiome firm, I just dove into all things microbiome, and I was reading literally 1000s 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 and you start looking at, okay, well, the butyrate producers, they’re clearly good. And this is across the board. Whether you look at Parkinson’s, whether you look at dementia or depression, or whatever it happens to be, these same patterns are across the board. The bugs alter a bit, but the same pattern. So I’m like, okay, 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 doing anymore, so I’m still pretty much bulletproof, after all these many years, and I’m hanging in there. So that’s the story. That’s the short version.
Lindsey Parsons:
So it didn’t, it didn’t get too bad for you?
Guy Daniels:
Oh no, 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 poof, it went right back out again.
Lindsey Parsons:
And did you have pain in a particular location?
Guy Daniels:
I had some pain. I had anal fissures. So it was not fun. It was not fun. Yeah, and I have three of the top genes in Crohn’s. Now the gene thing 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 who have Crohn’s but don’t have the genes. The big gene is the NOD2 which is the intracellular antimicrobial fence. But when you have a whole bunch of these genes, and you take a few antibiotics and this and that, then, you know, it kind of stacks up on you.
Lindsey Parsons:
Yeah, I thought that I had no family history of any of this. And then I found out that my aunt had had Crohn’s and had to have a temporary ileostomy, and it was reversed not long ago. And then my dad just had some serious gut stuff happen. But anyway, so in terms of diagnosis of Crohn’s, I imagine it’s one of these things that probably gets missed a lot, because, 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. I mean, how are most people getting diagnosed?
Guy Daniels:
Well, I think a lot of the colonoscopies do reach the ileum. I think especially if they’re suspecting Crohn’s right.
Lindsey Parsons:
I just had a regular colonoscopy two years ago, and there was nothing. It was clean.
Guy Daniels:
Yeah, yeah, no. I mean, if there’s suspicion of Crohn’s, I have photos, I think I don’t know where. But, you know, here’s a look at this, this is from my ileum. It’s probably distal ileum, right? And then I had a colonoscopy about six years ago, which is perfectly clean, so, you know, something’s going right there. But, yeah, I think that’s the gold standard. I think there’s another way they could do imaging and so forth. But I mean, most people I talk to come to me with having done at least one colonoscopy, and usually there’s often 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, other times it’s like a firm you have Crohn’s.
Lindsey Parsons:
Yeah, no, I thought, because I just had this colonoscopy. I was clear, but, obviously, I mean, they specifically say on my colonoscopy, then we stopped at the ileocecal valve, so it’s
quite clear. I mean, and it may not have been present then, because this is all relatively new, because I’ve had pretty frequent stool tests, I don’t know, for various reasons, because of the podcast, 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 Ruminococcus gnavus, and E. coli?
Guy Daniels:
Yeah. E coli species, species from Enterococcus, species of Fusobacterium are in there as well, species from Streptococcus, species from Veillonella. Yeah, I think that pretty much does it.
Lindsey Parsons:
So Fusobacterium, I have this issue with the stool tests, all of them list Fusobacterium, as if there’s a normal range, but there’s, I looked it up.There’s no good Fusobacteria.
Guy Daniels:
No, they’re bad guys.
Lindsey Parsons:
Should we have any of them?
Guy Daniels:
Well, yeah.
Lindsey Parsons:
They’re all bad guys. So, like, why is there a normal range?
Guy Daniels:
Yeah, well, because they could be down there. So, Fusobacterium, that’s just for 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, they are part of the oral microbiome. And so if they’re kind of nasty in the mouth, think of how nasty they are in a whole different location where they’re not supposed to be, where they’re not supposed to be in abundance. So as a part of the oral microbiome, you can see them in a stool analysis, right? 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 there’s two theories on F. nucleatum. One is this makes its way down the GI tract. So especially if you take in 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, 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, etc., 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 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 pretty pro-inflammatory. So again, what’s the key? The key is, we’re all going to brush our teeth, we’re all going to eat. We’re all going to have dental cleanings, right? We’re all going to whatever it happens to be. We’re all going to swallow food. The key is to make sure the good guys are in charge. They’re going to produce antimicrobials, 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 going to be down there. We’re all going to have E. coli. We’re all going to have a number of the bad guys. We’re not all going to have the same percentages and the same exact ones, but we’re all going to 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 going to do is, first of all, you’re not going to kill them all off. They’re going to hide out in their reservoirs, and they’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 the genes in the bugs. You go, well, we killed it off in the GI, 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 the feces, right? It’s hanging out in the gut. So again, 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, because we’re not going to outthink millions of years of evolution. Let the good bacteria figure it out. Okay, you know, they’re going to do their thing and just let them do their thing. Feed them and let them take charge.
Lindsey Parsons:
Okay, so what kind of symptoms do people feel in Crohn’s disease that are distinct from other conditions like IBS or even ulcerative colitis?
Guy Daniels:
Well, then you get into the other confusion, like you mentioned before, 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 have diarrhea, but also colitis. Most people have diarrhea as well. And then you have IBS, people with diarrhea. So how do you distinguish those right? So within the absence of, say, a colonoscopy, that’s a little hard to tell, you kind of like throw unintended 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, there’s a lot of room for confusion. This is not a symptom, it’s an unfortunate outcome. You can have different things, like fistulas. Basically a fistula is where cells just go wild and they start boring through and just like, I’m going to make a channel this way. And you wouldn’t know if you had a fistula connecting your small intestine, but you would know if you had, for example, a perianal fistula, where all of a sudden you’re starting to leak feces. Because, 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 woman, I think it is, will get a recto-vaginal 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 I have a video on ulcerative colitis. I have videos on IBS, again, the players are generally the same. You know, the good guys like F. prausnitzii are significantly lower in IBS and Crohn’s and also colitis. You know, the bad guys like E. coli are significantly higher in all three of those conditions as well. So the common denominator is they’re driving inflammation. And the whole spin the wheel and see what disease we get, that just comes down to genes, like uncovering which genes you particularly you have, so 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.
Lindsey Parsons:
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, using diets like specific carbohydrate diet or low FODMAPs or IBD-AID. I’m assuming that’s not the approach you use. Do you feed fiber to a flaring gut?
Guy Daniels:
Yes, yes.
Lindsey Parsons:
So gradually or suddenly?
Guy Daniels:
No, I go in guns blazing. So with those diets, like some of them, not the FODMAPs, I think. I do not recommend fermented foods. Low FODMAPs don’t recommend dairy because of the lactose. I don’t recommend dairy because of the proteins. 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, also, if colitis is a big one here, the dysbiotic gut has a hyper vigilant 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’ve already seen those before. They already have an immune system that’s ramped up to fight more inflammation. We don’t need dairy anyway, so I’m a no dairy guy with probiotics, the fermented foods. I do not recommend them again.
And I’ve done a meta analysis, Crohn’s, also 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, the 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, because 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 [those diets] have their differences. But generally speaking, they take away carbohydrates that can ferment. I’m like, “no, don’t do that.” Give them carbohydrates to ferment. Like, for example, the low FODMAPs 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 a huge meta analysis 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. prausnitzii, species from Roseburia, Ruminococcus etc., 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, 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 going to be less of use because there’s less fuel to feed us. Right? 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 some success with symptoms? Yes, it does. The data is 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 it, what they wind up doing in the long term is reducing the good guys because 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.
Lindsey Parsons:
But at the end of the day, you’re pushing the good guys in the colon. So for people like in my scenario, I’ve got antibodies to my migrating motor complex, essentially. So I’m always going to accumulate bacteria in my small intestine. So I, in an effort not to wipe out the good guys, I’ve avoided things like berberine and oregano oil, and 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 also sometimes use the pomegranate peel.
Guy Daniels:
So the small intestine does have its own microbiome, for starters. And then, like in SIBO, there are too many bad guys in too much abundance, crawling 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 going to 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 eat your way out of this. I’ve seen it a million times. It’s just not going to happen now.
Lindsey Parsons:
Now I’m talking about additional fibers. I’m not just talking about diet.
Guy Daniels:
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 had 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 seven 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 of 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 as a general rule, the bad guys love to ferment things like protein. So the bad guys love the carnivore diet, but some of them came from prebiotics. So if you’re going to throw seven grams of pick your prebiotic into the gut, and the pH is favoring the bad guys, where a pH of seven, 7.1 whatever happens to be, then the bad guys were like, hey, this is fine. Like the bad guys are going to 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 four prebiotics, I know that the Crohn’s profile is – so we flipped the numbers before we talked about low good guys, high bad guys – I know Crohn’s profile for the healthy controls. The opposite end is high. F. prausnitzii, okay, what prebiotics does F. prausnitzii consume? Pectin and inulin, okay. What else are the healthy controls high and the Crohn’s people low in? Okay. Roseburia, and you go down the list, what does roseburia like? Well, roseburia likes to ferment arabinoxylans, where do arabinoxylans come from? They come from bran, right?
Some of these diets say no grains, right, don’t do grains. Well, the husk of say, rice for example, or wheat for example, that’s full of arabinoxylans. The good bacteria love arabinoxylans. So I go, okay, so it’s low on this, and it’s low on this. So I’m like, we’re going to feed these different prebiotics across the board to make sure we feed the full spectrum of the good guys. 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, and inulin is really not a good choice 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 other ancillary agents in there as well, right? Because, again, we have to look at what are the deficiencies in Crohn’s. We have a deficiency in antimicrobial defense and so forth.
Lindsey Parsons:
I know you like PEA* as an anti-inflammatory, 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 it’s immune stimulatory. I think there’s andrographis. There’s a number of other things that I’ve seen.
Guy Daniels:
So fish oil, the data is terrible, and really, I never recommend fish oil. I don’t think for anyone. PEA is actually meant to be a temporary solution. So what I’m trying to do is, in PEA, I think, the data is more robust than, say curcumin and say Boswellia, right? So those are kind of direct anti-inflammatories. When you use those, you’re using the allopathic drug mentality, we’re going to give anti inflammatories, right? So, okay, why are we doing that? Well, because something’s driving inflammation. Well, let’s get to something that’s driving inflammation, right?
So I don’t recommend boswellia, although it has some decent data. I recommend PEA really, for a few different reasons. Because, one, it acts as a mast cell stabilizer, and mast cells are a big problem in Crohn’s. Another thing, it helps with sleep, so people who have dysbiosis are chewing their tryptophan because they’re making a bunch of serotonin in the gut. So mast cells don’t produce just histamine. Mast cells produce like 30+ chemical compounds, one of them serotonin. So if you’re constantly inflamed, constantly with diarrhea, you’re eating your proteins, right? But tryptophan is the least occurring amino acid, so you’re cruising through your tryptophan stores to make serotonin, to deal with the serotonin, in this case, is pro inflammatory, and you have no tryptophan leftover to enter the brain, and now you’re not sleeping well. So PEA 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, and maybe dementia, 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, that’s meant to be a short term thing, until you can start producing your own butyrate, right?
Lindsey Parsons:
So I didn’t understand the connection between the tryptophan. How does, how do they interact?
Guy Daniels:
Well, they don’t really interact. It was an analogy. So, the tryptophan is not making its way to the brain because it is getting chewed up in the gut. So if you’re not getting tryptophan to the brain, you’re not getting serotonin in the brain, because 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. And someone who’s high histamine, with mast cells who are unstable, and someone with diarrhea, right- I can’t do that, right?
Lindsey Parsons:
Oh, okay, so you’re giving them PEA too, right?
Guy Daniels:
So I give them PEA to help them sleep, right? That’s one of the angles of PEA, to help stabilize the mast cells, because they’re very unstable in Crohn’s patients. And then to 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, my consultation on days one until day 30 or day 40, whatever it is, until you’re much more stable. You’re sleeping better, your anxiety has gone down, you don’t have diarrhea. Well, we don’t need the PEA anymore. You’re producing your own butyrate. What do we need it for?
Lindsey Parsons:
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.
Guy Daniels:
Most of the data is for PEA is for pain, and I bet people have seen my video on PEA. And they just come back with these miracles comments on YouTube saying, “Oh, my God, this was the greatest thing,” 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. 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, right? So Streptococcus, you have these amino acid sequences, and Streptococcus that looks like some of the connective tissue in our body, and then the immune system 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 is like, I don’t know if that’s connective tissue or not, but I’m going to attack it anyway. So again, for autoimmune like rheumatoid arthritis, let’s not do a lifetime of PEA, which may eventually stop working for you, let’s address the root cause.
Lindsey Parsons:
So yeah, I downloaded your Crohn’s protocol, and I’ve been trying to get up to the level of fiber in your shakes. So I’m curious, because it’s really challenging. I mean, I’m a slim person, and two shakes a day of 40 grams of fiber or something.
Guy Daniels:
Yep, yep.
Lindsey Parsons:
I can hardly eat anything else. Just kind of wondering, like, first, can I reduce it a little bit given my size? Can you accommodate for smaller people? 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 egg?
Guy Daniels:
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, and things like butter are easy calories, and, honey, can be easy calories and just eat. I need you to eat and to focus on eating because, yes, it can’t be filling. The other thing is, because it cranks up so much, butyrate increases the satiety hormones, so sometimes people just don’t feel hungry, right? And I tell them again and again.
So like, when I sell the protocols, it’s $25. It’s like, here’s a package deal for the average microbial fingerprint in my consultations. That’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. But eventually what happens is, 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 they basically get to the point where, “hey Guy, I don’t like you so much in this first month because I’m pretty uncomfortable”. And I tell them that in the consultations, I’m like, listen, you’re probably going to hate me in week two, week three, or something like that. You’re bloated, if you had like psoriasis before, I may 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 ones can be a challenge. 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? And yet, it was a blend. And this is what I formulated years and years ago. It was a blend between understanding that individual prebiotics would fail a lot in trials. And I read those trials we talked about already, 10 grams of this or seven grams of that, it’s a lot of failures. And so I go well, single probiotics at lower doses aren’t working. The data just doesn’t support that. Then you look at the data, well, Roseburia species like this one and F prausnitzii likes this one, and Coprococcus like this one. I go, okay, well, we want to have a healthy diversity. So we want to feed the good guys across the board. We don’t want to focus on just one. So that made having multiple prebiotics necessary as well. So I eventually got to the point where I actually ran out. When I was the director, I ran a trial, an IBS trial, and I had a 100% success rate. So I’m like, okay, well, 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 continued with. And it depends on the person. When I do this again, with the canned protocols, I build it for the average microbial fingerprint. But if I’m doing a consultation with you, and you’re saying 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’s a two-way street. The information you give me is invaluable, and I’m going to take it.
Lindsey Parsons:
So, like, if I have good amounts of Roseburia, you might say you can cut back on the prebiotic that needs that?
Guy Daniels:
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 a game changer. Like, I have to change that protocol that’s built for the average microbial fingerprint which may not work for you. Okay, so because you have problems with constipation, that’s not the rule. The rule is diarrhea. So the consultations, I can take the deep dive, and it’s something geared specifically for you.
Lindsey Parsons:
So I know there’s concrete research showing the negative impact of gums and emulsifiers like Carboxymethylcellulose, Polysorbate 80, Carrageenan, Sodium stearoyl-2-lactylate, Diacetyl tartaric acid esters and Maltodextrin and a few more in IBD. But I’m wondering your thoughts on some of the ones that are used in the nicer, organic, gluten-free foods like guar gum and xanthan gum. Are those things that you think should be avoided by people with Crohn’s?
Guy Daniels:
Well, I mean guar gum, 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 worked with guar gum before, it just forms a giant lump. 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 those. So, yeah, those are to be avoided. But guar gum, I don’t see a problem with that.
Lindsey Parsons:
And again, what about xanthan gum?
Guy Daniels:
Xanthan gum, I have to say, I’ve never taken a deep dive into that.
Lindsey Parsons:
That’s in a lot of products. I’m trying hard here. That’s like, in coconut milks, it’s in almond milks, it’s in any kind of bread. I just got some where the pot stickers like, I mean, anything gluten-free, because I’m gluten sensitive in this scenario. I don’t know if that’s a general problem with Crohn’s or not.
Guy Daniels:
Well, I generally tell people to try to just eat whole foods. And some people do that, and some people don’t, but, for example, myself, I just cook 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, 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 hyper reactivity to a whole lot of things.
So for example, and I just 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, 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 three foods. The food is not the problem, right? You get into all this, oh, oxalates and this and that. You know, I have an oxalate video coming out soon, too. The food’s not the enemy, okay? Which is why these people go carnivore, like, oh, I went carnivore, and I felt great my first month or year. Then I went downhill. But, yeah, you can avoid the foods. You can avoid the vegetables, you can avoid 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 is it why I 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, or 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?
Lindsey Parsons:
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.
Guy Daniels:
So no, they don’t, no, they don’t, no.
Lindsey Parsons:
So how come, when we fix our microbiomes, we still have to keep doing that?
Guy Daniels:
I don’t know. I can’t answer that question. So, I mean, yes, I’ve had people who are perfectly healthy. They screw themselves up with going on radical diets, paleo or fermented foods. I eat a whole bunch of fermented yogurt, the whole nine yards. And probiotics, 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. They’re on their merry way and going back to their life.
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 the people who have been on 100 rounds of antibiotics. Yeah, we’re a different group of people, right? We got broken along the way, and it’s never going to be the same again. And I don’t know why, for the life of me, I can’t figure that out. I’m like, okay, this person is doing great. We’re feeding the good bugs. The immune system is now more tolerant. It’s not hyper reactive. Why can’t this person go back to doing this 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, to this day, I still can’t do them, after years and years doing this, you know. Okay, well, Guy, 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. 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 two, three years later saying, well, I was feeling so great, I stopped doing everything, and now I’m a mess again. I’m like, did you take like 100 rounds of antibiotics before in your life? You’re like, yeah, because I’m reading in the notes you did. Yeah, I did. Didn’t I tell you your gut was broken? You had to do this the rest of your life? Yeah, you did. But, you know, they don’t want to do this stuff. Yeah, so they come back.
Lindsey Parsons:
Okay, one quick question left, people who are constipated with this quantity of fiber. Do you ever get people who get totally backed up, like they just cannot eliminate it?
Guy Daniels:
I mean again, it’s them. I have a constipation protocol that’s successful about 90% of the time, within one week’s time.
Lindsey Parsons:
So even with the quantities of fiber barreling down at the beginning…
Guy Daniels:
You have to realize the vast majority, the only thing 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, the activity in the gut, the propulsive activity in the gut. But again, I’m also offering up my IBS constipation protocol, other ancillary products in there as well, to help get things moving a lot. So you could say, okay, Guy, if you could give an example. And this happens sometimes in people, someone’s constipated, they take a whole bunch of psyllium, 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. I have a number of both video and written testimonials for people who were constipated for many years and are doing great.
Lindsey Parsons:
Okay, I’ll take your word for it. 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.
Guy Daniels:
Well, thanks for having me back on. I appreciate that.
If you’re dealing with gut health issues of any type (diarrhea, constipation, bloating, SIBO, IMO, H2S SIBO/ISO, IBS, IBD, gastritis, GERD, H pylori, diverticulitis, candida, etc.) or have an autoimmune disease and need some help, I see individual clients to help them resolve their digestive issues or reverse autoimmune disease naturally, You’re welcome to set up a free, 30-minute breakthrough session to see if you’d like to work with me. I also have my own two products, Tributyrin-Max, which is particularly helpful for loose stool and diarrhea as it slows your motility and firms up your stool, and SBI powder, which is an all around gut pathogen binder, which is super safe and won’t harm beneficial bacteria, and is usually the first line of treatment I educate my clients about in order to avoid stronger antimicrobial herbs.
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