Hippo Talk with Jason Hawrelak, ND, PhD - IBS Freedom Podcast #113

Hello. Hello, and welcome back to the IBS Freedom Podcast. Omg. I'm so excited for this episode. So we all know and love Amy Hollencamp. Rdex. Hooray, hooray for you. But really, the excitement here is that we have the man that needs no introduction in this space, but I'll introduce him anyway. We have Jason Hobolic, and he's the brains behind ProbioticAdvisor.com, probably a lot of you have used his Probiotic search tool. You've taken some of his courses, you've learned about the microbiome through him, I'm sure. But we have him to sit here and chat with us, and I've got some questions and things to mentally chew on. So welcome, Jason. We are so excited to have you on the podcast. Round of applause.

Thank you. It's lovely to be here. You know, I always love talking gastrointestinal issues and IBS and SIBO and microbiome, so it's always a pleasure talking to other people who are passionate about those things too.

Did I not tell you though, today we're talking about hippos. You got the topic mixed up, dude.

I'm the wrong person for that.

That would be great if we could have a full blown discussion about hippos.

But nay, nay, you're right.

We're going to talk about the gut and the microbiome. Well, let me. Let's start grilling it, baby. What do we start with?

I think you had the questions.

Well, I was gonna start. Do you have any to start us off with? I don't wanna, like, take up all the air.

No, you were chomping at the bit with some. So you start. I defer.

Can I tell you something first? Can I be an awkward and awkward person first? Okay. I have had a term for a long time. Predates me knowing about you. I've had a term for a long time that I have affectionately called a science crush, meaning, like, I don't have crush on the person, but, like, if we could have lunch together, I would absolutely lose my mind. And you have been a science crush of mine for a while, so I'm just like super thrilled that you're here. So, just so you know, now you know the term science crush.

Science crush. I like it.

I wanted to. I want to talk to you. I want to pick your brain.

Yeah, I've got science crushes too.

It's. It's. There you go. Maybe you didn't have the term, but now you know the label to use.

Yeah. Hashtag sciencecrush I will, yes, I will remember that label. It's good, actually.

Good. Well, let's start. If, if I may, let's start with a topic that I think I kind of initially found your work through, which is stool testing. And just like, say like somebody's at home, maybe they just got diagnosed with ibs, they're freaking out, they don't know what to do. Their GI isn't giving them medicine, many answers, if any, and they're thinking about doing a stool test, particularly like a more functional type stool test. So, you know, something that their functional doctor or naturopath could order or something they would order at home. Like, what kind of things might you tell somebody at home if they are considering doing one of these, like, functional stool tests? Like, what type? Do you think that one type is superior? One type of technology? Are there any, like, big grains of salt that we should take when we're looking at data like this?

Oh, Jesus, big questions right out the gate.

And I will say, I think like conventional gastroenterology is still in the space of. No, they're imperfect and they're rubbish. Never use them, right? So like if you took a microbiome test to a GI doctor, they would either roll their eyes or laugh at you or just ignore it and not use it. And I've been. I remember I went to a conference a while back a couple years ago, and they had a whole lecture about like stool testing and clinical practice and it was all ragged on functional medicine and how horrible these tests are and how unusable they are. I think that the truth probably is somewhere in the middle of the extremes of like, their junk never ever used them from the conventional side. And oh my God, these are perfect and infallible and amazing and we can trust the results with 100% certainty. From the functional side, I think the truth is probably somewhere in the middle. So I don't know. With that I will give you the mic.

Yeah, I mean, I think it's partly. I think the issue is it doesn't diagnose a specific disease. I think like conventional gasters are like, we want a test that tells you what disease someone has and these tests don't do that. So I think that's a. They would see that as a limitation. That's kind of the paradigm that they're within is like, this test equals this disease. And it's like we don't having that. We're talking more about digestive functionality, microbiota, ecosystem composition. And I still am surprised at how few gastroenterologists are actually aware of the microbiome and its repercussions and how important it is. Even I gastro my PhD 22 years ago in this area, 21 years ago, and people were talking about it then how important it was in mainstream gastroenterology journals, you know, And I'm still surprised that there's still many clinicians out there in the gastro world who still are fairly ignorant of the gut microbiota, why it's important, how to look at things, what it means. And I think that's sometimes a threatening test to bring in too, because it actually shows they're like, oh my God, I don't know what the hell Bacteroides is. I don't know what a firmicides is, I don't know what a protobacteria is. And they're like, it's useless, I don't.

Know what it is.

I wasn't taught it in my 15 years in training, however many years they do, therefore it must be useless, you know, so there's a degree of. That definitely is with some, and I think that can often be far too common among specialist clinicians in my experience is if it's not something they were taught about, then it mustn't be important, you know, and we can kind of ignore its existence.

Yeah.

But I mean, I think I'm just trying to think of where the best, best place to start. But let's look at different technologies. Maybe that's a good place to start where we've got the old technology, which is culturing. And culturing is where we kind of took a poo sample and we put into some petri dishes and we kind of looked to see what would grow. And that was done from the late 1800s. That's where we first saw E. Coli, pithy bacteria and things like that in poo. So some bugs we've known about for a fair while from that time. And that technology evolved a little bit to late 1900s, but not hugely. It was still the same process of taking poo, putting it and trying to grow it on stuff. But what they worked out in the 60s is if you put it in like a anaerobic chamber that took all the oxygen out, we could grow more bugs. And that kind of blew people's minds. They're like, oh my God, there's not less like 10 species in the gut. There are like 60 species in the gutter. You know, it was like a major leap forward. But what we have found in the last 20 years is that culturing is very Limited in that you can only see a small percentage of what's actually there. That's a huge issue if you're wanting to look at the gut ecosystem and you can't see what's there. Yeah, the test is pretty useless. So I think any test that's using culturing to tell you what species are present in the gut is majorly problematic and immensely limited. And I would not recommend. Culturing will always have a place for how do we assess antimicrobial activity. So you can grow that klebsiella and you can put some herbs or some antibiotics on it and see if it kills that specific one. So culture will always have a bit of a role to play. You'll have a role with. Once we work out what a species is in a fecal from a DNA sample, we can work out if we can grow it, what conditions it might need. We might learn more about that species from growing it. So I think culturing is not dead, but it's not useful to tell us what the ecosystem composition is.

Yeah, and I think I've seen numbers that estimated like 80% of the gut microbiota is not culturable currently. Something like that. Like it's a pretty huge fair whack.

Yeah, it's not like a 5% or something. It's like most. The vast, vast majority of bugs and some of these haven't been named yet either for that matter. Which is another I think some people would see as a broader limitation with using stool tests now is that we're still even the good ones that can tell us what's there with more accuracy. There's still most species, we don't know what they do yet. I do hear that too. But as someone who's been in this field for 20 some years, there's a lot of species, we do know what they do and we do know what roles they play and we can change them and. And that changes people's health. So I think it's still premature to go because we don't know what a lot of them do. We should ignore this entire field. But yeah, so we've got culturing tests, which I think are very limited, and then we've got DNA based tests. And within that broad group, I'd say there's kind of three different technologies that tend to be used that people or clinicians have access to. We've got PCR tests or quantified pcr, which it's accurate, generally considered to be fairly accurate finding things. So it looks for the DNA component for bifidobacteria and it can kind of find that component. Generally, the biggest limitation I'd say with that technology, even when done well, is that it's generally only looking for certain things. And most of the ones that use pcr, what I would call pathogen deep dive tests, it's almost like their sole existence is the to go, how many pathogens can we find? You know, let's look for as many pathogens as possible. And I think even that mindset is problematic because it just means that you're kind of looking for what to kill. What can I kill in here? What can I kill? And every single patient is like, what can I kill? Rather than other other tests that are using 16s RRNA or Shotgun Androbic sequencing. When you look at the entirety of the ecosystem and you're looking at balance. So dysbiosis and when you do those tests is about how balanced is this ecosystem, what can we tweak, what can we change, how can we balance this? And you get quite a different perspective when you order those tests. In my opinion then like, what can I kill in this particular patient? What specific one pathogen or two pathogens can I kill to make this person better? Because I think it's seldom about that. And yes, there are some people where there are things like giardia or, you know, salmonella or something where there is a specific thing that we need to target. But I think for majority of people, and particularly people with UT bowel syndrome, it's not generally that. It's generally a imbalanced ecosystem where even things like, you know, methane producing bacteria, it's not like we want to eliminate and exterminate them. We just want to like lower their levels so they're not producing excess methane, which is a problem. Because having no methane is also a problem, I would argue, but it's just having excess is problematic. So you get a different mindset. And I think the other advantage of 16s and shotgun sequencing is we see the entirety of there and you get to see the balance. You know, I used to find those, those culturing ones where they go, oh, you've got four plus klebsiella. What the hell does that mean?

Really?

What does it mean? Because, you know, normal level of klebsiel are like 0.05%. Okay, so or less. And let's say you've got a 0.1% that might show up as four plus. But I've had patients where 65% claim Klebsiella on a stool test that would show up as 4 Plus. And are they different? Yeah, they're different. Do you treat them differently? Yeah. Do you have to worry about side effects and die off reactions differently? Yeah, like I'm actually quite shocked at the degree of die off I've had from my patients who are like 60% Klebsiella when we use herbal antimicrobials is like the severity of die off symptoms in that situation versus a 0.1% Klebsiella is quite different. And you would treat that differently. And you also get to know the context of what that's in, you know, what's the number, total number of species present, what's the spread of those species and that you only get from using 16s or shotgun. And for me that's why they're my major favorites when we're wanting to look at the ecosystem because I want to see the entirety, I want to see diversity, I want to see ecosystem richness, I want to see how things are could compare the proportion of different species I think is super important. Now sometimes those tests often won't necessarily have the functional markers though, like digestive markers and protein, fatty acids and things like that. So sometimes if I want to know those things, you have to do two tests. That's kind of the limitation currently it's like, okay, well if I want to get the best idea of gut function, inflammatory markers and microbiotic composition at the when, to me that requires two different tests to do that. Yeah, because I think for some people I do want to look at calprotectin, lactoferrin, short levels of fecal fat, you know, malabsorption type things, pancreatic elastase, shorted fatty acid ratios. So I think there are a time and place for those sort of more comprehensive stool analysis, stool ph that I do find useful. But I'd say for majority of my patients I'm more interested in ecosystem composition.

And.

So I would use 16s and shotgun far more commonly in my practice without the additional CDSA type ones. And I think the other aspect with the CSA1 CDSA or CSA ones is I kind of have to tell my patients to we'll ignore the cultural culture section because that culture picking isn't particularly accurate at telling us what's there from ecosystem perspective. And we'll rely on the other tests to tell us what's there from microbiology perspective.

Well, and I always wonder too, like when I see those culture tests because sometimes people will bring them in to me and I take a look, see. But you know what if you had a normal amount of E. Coli or Klebsiella. But you're growing this on a petri dish, presumably in an oxygen rich environment. And what if it's just we're favoring the growth of oxygen tolerant bacteria.

Yes.

You know, so it's like maybe that's.

Normal and to be expected that Klebsiella and E. Coli are like blooming like crazy on virtually every CDSA and CSA test. Like maybe that's actually not atypical. I'd be kind of curious to see like 100 samples from healthy normal people and see if they had like four plus klebsiella. I think that might.

I share that concern totally. And times where I've done like a split poo and sent that person's poo to a lab doing DNA technology and when we're using culturing and then it's like, oh look, it's four plus Klebsiella. But that's a 0.001%. Bacteroides was four plus and it was like 20%. You know, it's like, well is it 20? You know. Yeah, it was pretty useless. And I do agree that what we might be just growing is we just have a medium that the bacteria really love and that petri dish media may be something that powers them. On bionic growth factor you get this very exaggerated response and unrepresented what's actually there in the ecosystem. What I like about DNA based ones is they're killing everything once the poo is out and we get this lovely representation of actual populations that are there in the gut.

Yeah, yeah.

One thing too, and I want to circle back and just. I love everything you're saying. I think that, you know, you're really exemplifying that the gut microbiome so complex and I feel like there is this mentality with our clients like you were harping on a little bit. It's like, oh, we just need to kill something. That's it. Like we just need to find that one. It factor in the gut boogeyman to kill, to kill. And it's like, no, that that's probably again, there are some boogeymen that you probably do want to kill and ruling those out can be a good thing. But I think for the majority of people, if you're going into a stool test with the mentality of finding something to kill, it's probably not the best mentality to go into a stool test. It's probably a better mentality to think like, you know, I want to see you Know if there what the proportionality and the complexity of my microbiome, and maybe I don't get all the answers from it, but you can. You can gather some decent insights to help you move forward. But I think always just having a humbling mentality that, like, okay, the microbiome is complex, and it's like, we can't just target one thing without it affecting a bunch of other things. Um, yeah, and I think the more we kind of oversimplify the microbiome, the more we can get into trouble.

Um, yeah, I'd agree with that, too. Well, yeah, and it's. There's so many problems with this world, too. Like, I. I've seen a lot of patients, and I think probably practitioners who, like, they look for the boogeyman, and when the boogeyman is not there, like, they almost. They get disappointed, oddly. And, like, I do get it on some level, but I think this will sound overly harsh, but I think there's some truth to it. It's easier to take a month of an antimicrobial and, like, fight a battle, do a strict diet. You know, you just have to suffer through this one month, and then you're going to be cured and everyone's going to be, like, farting rainbows with the unicorns and frolicking off into the sunset, versus talking to people about what we harp on in this podcast a lot, which is stress, sleep, mental health, nutrition. Are you eating enough? Are you getting vitamins and minerals and fiber and stuff? Are you actually eating vegetables? Like, just the really basic, unglamorous, unsexy stuff that takes so much more effort, and it's harder to really motivate yourself to make those changes for the rest of your life. Versus, oh, I could just take a magic pill for a month and then all my problems are magically solved. Like, that's very tempting for both the patient and the practitioner, because then also as the practitioner, if you identify a boogeyman and then you treat the boogeyman, like, you kind of look like a hero. Like, da, da, da, da, I saved you from E. Coli. Oh, my God. And, like, it's not to say that being the hero is unappealing to me, but it's just we've got to be careful with these, like, kind of common human brain lesions. Shall we call them? Can I ask something else about stool testing while we're on this topic, by the way? Yeah, I've noticed, and I'm sure you've read more articles than I have. I'm sure. So maybe I can get your perception on this. I've noticed when I read research about the microbiome, it feels like the vast, vast, vast, vast majority is 16s testing. Like, I don't know if I could put a number to it, but like 80 or 90% of the articles I see is about is 16s. And then more and more we're starting to see some whole genome, you know, sequencing kind of stuff, but it's still not ultra common. Like, that's definitely a lesser player. And then it's at the point where, like, if I see somebody talking about the microbiome and it's based off of a PCR test or culture, it's weird. Almost like I kind of, I. I kind of like pause and almost like, was that an illusion? Oh, yeah. It really is a PCR test that they're using. So why do you think that is? Do you think it's, do you think it's because 16s has been around longer? Do you think it's because it's cheap? Because, like a 16s test, the commercially available ones are pretty cheap. They're like 100, 120 US dollars. Do you think it's because it's been around for a while because it's cheap? Or do you think that there's another reason that I'm just not familiar with because I've never done research?

I reckon it's because. Partly because it's been around for a while and partly because they're inexpensive to do relatively. Yeah. And whereas shotgun is newer and the biggest issue is just cost, you know, like, if we do research studies and it's like, okay, we can get a 16s test done from the lab for $100 a shot, you'd argue, hopefully less, but let's say it's that. And then we contact a lab for using shotgun, and it's $350 or $400 per person per test. Yeah. Pharmaceutical companies have got lots of money. They can afford to pay for such things. But for other researchers, like, that's huge. You're paying four or five times as much for getting. Will you get probably more accurate data down to, like, species and strain? Yes. And you can look at, you know, genetic pathways, which are interesting and might learn more. You know, I do like aspects of shotgun, but I think the reason why it's, it's the cost differential is the biggest reason why we're using mostly 16s and we get to see that entirety. Because I think the issue with PCR is you can see what you want to see. But you don't get to see the entirety. And I think most researchers are wanting to look more broadly and to try to find things and look at, you know, invest, find new things that they may not have seen before because we, you know, but if you're only looking at, okay, bifidobacteria high or low in IBS patients and that's all you'll see versus what does the ecosystem look like in IBS patients? Yeah, yeah, but, but you're very much spot on. So I think even, even the disease associations we see, like, you know, dysbiotic patterns we see are often much more at the genus level because we've been using CCNS to really discover things a lot more. Will that change? Yeah, I reckon it will. Another 20 years we'll probably be looking at, okay, rather than just Bacteroides and having overgrowth, you know, too much Bacteroides, we're looking at, okay, Bacteroides fragilis versus Bacteroides satamacron or whatever it might be, or Vulgaris. And, and we won't even have the tools to. We have the research done to tell us how to deal with that. Because at the moment we're like, I know how to deal with broader Bacteroides overgrowth, but do we have the tools to go, okay, well we want to leave Bacteroides vulgatis but treat Bacteroides fragilis. We don't know currently how to do that because that requires lots of investigation using shotgun sequencing. So as a 20 years from now we'll have that kind of data. But at the moment we're seeing much more genius level associations. And that's partly why I'm quite happy using that kind of data to help inform see what my patients ecosystems look like and how to move forward. Because that's kind of the best research that we've got is based on that.

Yeah, that's a good point. There's almost some element of like, why bother getting more detailed? Because we don't have the research to really inform us on our decision making anyway. Even if we did have the more detailed information for that patient on some level, like maybe there's a time and a place for some detail. Certainly.

Yeah, I agree. Like sometimes I've got a colleague who specializes in infant microbiome and for her looking at the exact species of Bifidobacteria that is present is immensely important because there's enough research in that area looking at that and even targeting interventions that you can actually work in that species level data more.

So, yeah, makes sense. Again, I don't want to, like, take up all the airspace. I know that Amy's sitting there quietly for so much of the podcast.

No, I'm. I'm enjoying my. I'm thoroughly enjoying myself. Um, you know, I think, again, like, another thing that's so interesting when you are just specifically kind of going after the bad guys is there's really not tons of discussion, I think, in the functional medicine space about the good guys. Like, I think there's some, but it's majorly outweighed by the bad. You know, looking for the, you know, klebsiella or pseudomonas or, you know, some of these, quote unquote, like, opportunistic baddies.

I don't know.

I don't know if that's the best way, the best term. But, you know, I think that there's so much discussion of these bad guys that there's so much less focus on getting the good guys up and running again and supporting the good guys and trying to support growth of the good guys. And I find that it's a harder sell to patients too, because, again, they just want to go. Because all the focus is on the bad, so they want to go back to the bad guys. But, yeah, I do find that too, just in this space, that there's just less focus on kind of growing the good guys. And I think, you know, with some of the work that you've done with your own patients, how supporting the good, how important supporting the good is in the whole context of the. Of the ecosystem, like, does that almost become more important than pruning out the bad? I feel like I've kind of found that more so in my practice. Working with people is, you know, really just trying to foster the good. There are times when you do have to prune a little bit and you might have to do some antimicrobials just to kind of like help. Help manipulate a little bit. But I do think, you know, it's pretty amazing how much supporting the good can have a pretty great effect.

But, yeah, totally, totally agree. And even just supporting the good can reduce levels of support potential pathogens too, right?

That's.

To me, that. That is definitely not discussed as much of the functional medicine field as it should is like, you use prebiotics and you can reduce levels of pathogenic bacteria pretty, pretty quickly and effectively without killing, without the collateral damage you might get with killing agents. You know, I tend to be as selective as I can with the herbal agents that I use for killing anyway. And I think there, there is if you have that as an a goal in mind, you can choose to more carefully to limit the damage you're causing, which I don't think is done enough, to be frank. But I think also it's like you do use prebiotics and you do see levels of pathogenic bacteria go down and pathobions go down. So you don't always have to go in there with that. I must kill this. It's like, let's actually just enrich the ecosystem and the good guys will deal with it. You know, it's like that's generally what occurs when we're talking about colonic ecosystem changes anyway. Small bowels look a little bit different. And I think I'm much more prone to using, you know, antimicrobial agents for sibo, for example, than colonic dysbiosis. Again, it depends on the ecosystem, but geez, I do a lot more work with prebiotics and dietary change in colonic dysbiosis, for example. And you see dramatic shifts in ecosystem composition.

Yeah, well, I, I find just in our work with clients too, I sort of take, okay, what's the most conservative approach we can take? And we can always go more aggressive too. But I think clients want to start at the aggressive. Like, I want to just punch this. And it's like, no, let's just try something that's going to be naturally more ecosystem friendly as a whole. Um, and again, we can always go more clearance based if we need to. But if, again, if you can lower methane producers with Ph.D. g or you can like start, you know, lowering some of these bad guys with a, with something gentle, why wouldn't we start there? So yeah, it's always an interesting conversation with clients though, because it's, it's still like, let's punch it. And it's like, I don't know, we might not need to punch it. Let's just do something gentle and supportive in the totality of the microbiome versus trying to be so aggressive. So again, I, again, I think that that's such an important point is you don't have to start out aggressive. You can start out kind of with these strategies that can still be pretty powerful, but they're, but they're going to be supportive of the microbiome as a whole.

Yeah, well, it's like you can't take away antibiotics. Like once you've administered an antibiotic or an antimicrobial, you can't take that away. So you might as well do something that's largely not going to harm the person or harm the ecosystem and start gentle and then work your way in. But I think it's. People are really desperate and they want fast relief. I think that's why.

And that bit I totally get to, but it's also, for me, it's about informed consent to people being aware of the repercussions. Because, I mean, I think when people are. Because antibiotics are often I. I would say overused in the functional medicine world.

Yeah.

For indications that are, I would say, are questionable from the evidence perspective. You know, where it's like, oh, let's try it. Let's try these antibiotic combinations, see if it makes a difference. But they're not. The patients aren't necessarily told that by doing that, that. You know, there's a study published in Gut a couple years ago that nine species of bacteria went extinct from a single course of, you know, antibiotics administered into the arm. You know, it wasn't even oral. Nine species from that. And it's like, okay, well what. There is no return from that extinction bar. Fecal transplants. You know, there are, you know, more extreme ways of getting microbes back. But patients aren't necessarily told that. They're like, okay, we might, we'll do this. May work, may make a difference. You might lose 12 species of bacteria forever. We don't really know what that means yet. Maybe 15 species will lose as well as cause these major sort of disruptions. And it's not to say we all know there's a time and place for antibiotics are immensely useful in safe lives. And absolutely, there's no discussion about that. But it's times where they're in between, where you've got choices. It's okay, we can use the prebiotic to modify the ecosystem. You can use herbs or you can use an antibiotic, you know, and again, there's a different range efficacy of degree of collateral damage within that field of antibiotics. But I think sometimes people grab the. In functional medicine will grab the antibiotic path far too quickly. And I think it's partly it's all this idea that you can just reseed by eating some sauerkraut or.

Yeah, yeah.

Or taking a probiotic supplement, a multi strain probiotic will permanently stay in your gut forever from that point. I think it's always been a bit of a ludicrous idea because when you start looking at the composition of the ecosystem and you know, the 150 or 200 different genera, if you're lucky, that are there, and you're like, okay, well, if you do kill off your Anaero stipes or subdural granule. And these bead ray producing species, like you can't just shove some bifidobacteria in there and go. Even if it did stay, it's like it doesn't do the same thing. It's like it's not the functioning of the. I think it's. Even if you have 10 different types of iftobacteria and eight different types of lactozili, they can't replace these like butyrate producers, other sort of fiber fermenters. I think it's just never kind of made much sense, let alone the fact that they don't stick. I mean we've got so much research showing that the bugs that we're getting from fermented foods or from probiotic supplements, the vast majority of them are just temporary visitors that persist for short durations of time.

Well now this brings up another question and this could be a hot topic within the field of functional medicine. You're just not using the right probiotics, Jason. You need spore forming probiotics, spore formers for everyone. They stick around in your gut forever, right?

I mean let's evaluate that stool testing pre imposed and see that for yourself. Myself, Yeah, I suggest you try that to see that.

Luckily our viewers know that that was dripping with sarcasm. So they know me well enough by this point. But, but seriously, like the companies that make the spore forming probiotics and the people who sell them online and write the blog posts and the YouTube videos, they make it sound like God's greatest gift to probiotics. And this is like the only thing you need. Nobody should ever take lactobacillus because it's useless. But the spore formers will really reseed the gut and hooray. These are the best ever. And like they could be helpful. But I don't think it's the be all end all of all probiotics ever.

No. And the thing issue I've always had is how dismissive they are of all like lactobacilli or bifidobacteria based probiotics just by default. And it's just, well, you can't ignore all this, hundreds of clinical trials because, because it's inconvenient for you going, oh, they don't survive transit to stomach and small intestine, therefore they don't work well when they often do. Their strains are chosen because they do survive stomach and transit and bile salt exposure, et cetera. And three, we've got clinical trials showing that they actually work. And I think if you're promoting a product that doesn't have clinical trials showing it works and saying it's superior to those that do have clinical trials showing it works, there's something wrong there. And I think that was certainly an issue in this. That's, that's for sort of when they first came out. There's a lot of hype without the research that is changing thing, thankfully. And there's some companies that are putting research money into research, which is fantastic and I love to see. And that means we get to see what these things actually can do in and then potentially compare them to other bifidobacteria strains or lactobacillus strains. But I think this dismissing the entire area of lactobacillus bifidobacteria based probiotics has just been nonsensical and it's just a system, you know, I think it's a bad way of selling product, you know.

Well, and it always just struck me as like, ah, this is clearly just marketing to you.

Yeah.

Like this isn't about the truth. It isn't about like what's clinically relevant or what's, what's like documented in the research. It's just if you, if you fool enough people with these statements, you're going to sell a few more bottles of your product.

Yeah, exactly.

And so not a good way to go.

We should be doing this. No, no, it should be okay. My product is superior. We've got clinical studies showing it works better at doing or does something unique. Totally on board with that. But, but just saying ignore all this other research. It's rubbish. Panda doesn't exist and our products are better, even though there's no research saying it is. That's not good. Not good science.

They're. They're silly billies. How about that? They're silly billies. What about. Can we talk about. Okay, so I, this is again my perception. You've been in this field longer than me. I feel like the hot topic. And maybe I got this idea from you initially in one of your courses. Like the Hot Topic, the It girl boogeyman from like the 90s and early 2000s was Candida. Everybody had Candida. Everyone's talking about Candida. Everybody's doing a Candida cleanse. And now, you know, like 2015 onward, now the it girl is more so Sibo. But do you want to. What are, do you have any little nuggets of wisdom to share about Candida other than feeding the good guys and changing The PH of the ecosystem is going to inhibit a lot of Candida for you.

Yeah, which is how I usually approach it and try to use selectively acting antifungals when it's there. I mean, I do think we're kind of at a challenging point with looking at the fungal ecosystem. I don't think we have any tests available to us as clinicians or the general public that tell us a comprehensive overview of what's there. This is the issue in that we know from research studies that the microbiome is complex and there's a bunch of different fungal new species that are normal for us to have and what levels are probably normal. And that's kind of only, I'd say come out the last five years or six years, that kind of research. It's very early yet, but it's not available to us. So for us we can do a stool test where we culture and go, okay, can we, we cult grow this thing? But we know there's a bunch of stuff we won't be able to grow already. And I don't think anybody does a really good DNA based assessment of what that fungal ecosystem looks like so we can get a better idea of what's normal, what's abnormal and how it responds to different treatments too. There's some interesting research, a bit of a tangent, but I can't help but think of this study done on fluconazole in rats. And they gave these rats these fluconazole and some fungi went down totally, but other fungi went up and the net result was the same amount of overall fungi was there. It's just you had different fungi there and the bacterial ecosystem changed too because it turns out the different fungi were cross feeding with different bacteria. And we completely changed the fungal ecosystem, we completely changed the bacterial ecosystem. It's just like, ah, gosh, you know, that was not on anybody's radar before that kind of study was done. And I think we're so early into the piece yet that we're often have no idea, in my opinion what we're actually working with the fungal ecosystem yet because we don't have right tools and sometimes we're stuck using urine markers to try to tell us what's going on from a fungal gut perspective. Yeah, just not ideal.

Yeah, I was going to ask about the urine markers because that's another one that I'm inherently quite skeptical of personally. Like I have used it, I've played with it, but when I've used the one popular test in particular, I'll have to have you know, my system go back through the data kind of like I did with the other test. I feel like my memory of it is that literally every single person is diagnosed with some sort of fungal overgrowth on that popular urine test.

So it does seem common for people.

To show positive on that test. And I get their selection bias because I work with people with gut problems. So I know that more of my people would have fungal overgrowth as opposed to the general population, probably. But, like, close to 100% is just real fishy in my mind.

Yeah. Oh, yeah. I know. My brain kind of flags that too. And I think, because we just don't have a great way, because it won't necessarily correlate with culturing or PCR tests won't show anything wrong, but it could still mean that there's some other fungi there we just don't have the proper testing for. But it may mean it's not. It might mean that they ate some food that contained arabinose that's showing up in their pee. Because a lot of food to do. Yeah. You know, so I'm cautious around making diagnostic decisions based on that.

And I wonder, too, a little bit about some of the urine tests too, because, like, I think I was telling Nikki this when I was younger, I had my eardrum burst and I had a whole bunch of yeast in my ear. And again, like, women. Women have yeast infections. Again, like, it's. There's yeast other places in the body too. Like when you have a urine. Right. When you have a urine test, like, can you really isolate where the yeast is? It could still be a microbiome issue. It's just not necessarily necessarily the GI microbiome.

Yeah.

But, yeah, I always wondered a little bit about that. Like, if someone just was really prone to vaginal yeast infections, like, did they necessarily have a GI yeast issue? Maybe, again, but maybe not.

Great. Great line of thought, actually.

Yeah.

Wondering if that. The test actually controlled for that with, you know, the healthy controls. Males, females, vagina microbita. That's. Yeah, it's very interesting.

I think I have seen some research that suggested, and I don't remember, like, how old it was or what the methods were, but I do think I've seen some data that suggested that, like, women with chronic vaginal yeast infections, I want to say it was like 80% of them also had some manner of fungal overgrowth in the gut. And I don't remember what the numbers or, like, what the testing methodology was, but I feel like I remember seeing that at some point. I probably made a YouTube video and just forgot about it now on that topic. But. Right, yeah, it. I think that honestly, this could be said for blood and urine, Right? Like, if you do a test with blood or urine, you're kind of speculating on where that metabolite came from. Right? So like, okay, when you measure C reactive protein in blood, you know, you have influence inflammation, but like, where's the inflammation? Yeah, you don't know based off of that? Well, you kind of do. Like, CRP is made in liver, but. But you get the idea. Like, you could have that for any number of reasons. Or if you find fungal metabolites in your urine, it could be coming from your vagina, your sinuses, your funky weirdo ear. Side note, horrifying little nugget of wisdom from the E nose, throat area of practice. There's a thing called a fungal ball. It's literally just a ball of fungus lodged in your sinus. It's a real thing. Don't Google it, but that is a thing. And sometimes you have to get a fungal ball removed from your dang sinus and it's about enough to make you want to hurl. I had a very persistent sinus infection a couple years ago, and I was moderately convinced that it was a fungal ball. And I went to my ENT and he was like, oh, yeah, I have a colleague in California who treats those all the time. But it's not fungal ball. No.

Okay. Yeah. And one would think that would produce some sort of fungal markers too, in that case.

Right, Right.

Because it's going in the blood and then you're filtering your blood to create urine and then you're peeing it out. So it's all the same juice. Yes. Oh, goodness gracious. Well, now, could we actively doodle on something like a real world application of some of this stuff for a moment? And I'm selfishly going to ask you this because it's a question I have. So I started doing this fun little experiment on my YouTube channel where I basically doing like three or four 16s tests and kind of taking the average of those, and that's my baseline. Then doing two weeks of an intervention of some sort of prebiotic. Right. So like I did. I did phdgg, glucomannan, I did 2 FL. But I ended up trashing the data because my diet was different. I was on vacation around the same time. Okay. So I ended up trashing the data on that, but. And then after the two weeks of supplementation, I redo another like three or four 16s stor stool tests again take the average from all of those as my like pre and post intervention data points. Yeah. What I noticed with two, the two that I've done, glucomannan and phgg. The data at the two week like after two weeks of taking that prebiotic, I'm still taking it, but it's at the end of the two week period.

Yep.

My bifido did not go up at all. But two weeks later, at the end of the washout period, before I did the next intervention, my bifida went crazy. Like I'm talking like less than 1% up to 9 and 15% respectively, which is absurd for me especially because I've had craploads of antibiotics in my life. So my bifido are consistently low. But do you, do you think that it's. That it took two weeks for my bifido to like get the memo and really go up or was there something else? I couldn't find anything else in my diet or like supplement routine. I couldn't find anything else about my life in that time period that would have explained it. The first time it happened with phgg, I was like, I said this in the video, I was like, well I had red wine like one night six days prior and like maybe the polyphenols really did something for the bifido, I don't know. And I just kind of shrugged it off as like, oh, this is weird and surprising. But then the same thing happened with oh no, it was glucomannan was the first one. And then the same thing happened with PHDGG, but even more exaggerated. It went up to 15%. And I was like, what the what?

Wow. I mean that's a big increase with bifida with phdg. To be, to be honest, I generally don't do follow up microbiome assessment less than four weeks. Yeah. And I think it probably takes in my mind and whether this is based, I've been doing this for years. Whether it was based on clinical observation before that two weeks was inadequate and took four weeks time to see the sort of bigger shift from it. And again sometimes after eight weeks you see another bigger shift move on from the, that, that point too. So I think there is a bit of delay even though we've got, you know those studies where you, the David study in 2014 where they, they took people on like an all meat diet and yeah, Even within like 48 hours there's like a massive change around an ecosystem. So you know, we need, the ecosystem can change relatively rapidly at certain Situations. But my experience with prebiotics is as an add on is, I'd usually give it four weeks to do its thing to see the impact.

Admittedly, with the experiment I was impatient because I was like, fair enough, if I do this, like, okay, if I do it this way, then I could churn out one video a month and I could get this, you know, like, just go through it. But also it was very weird, slash awful for my gut. Like, my gut has been rock solid for years. I have not had IBS in a lot of years. My gut was very perturbed doing that, where I was like two weeks on, two weeks off. Two weeks on, two weeks off. So that's also. I stopped the experiment for right now and I'm going to pick it up again in 2023. But I did decide, like, I'm going to have to do a full month with a little bit of a ramp up and then a full month off with like a little bit of a ramp down and I'm going to have to like elongate the experiment. So I'm already, I'm already getting impatient thinking I can only do six of these videos in 2023. Damn it. But it's.

Yeah, I love the idea of it. I do. But I think you're right because, I mean, even working with most people that we would work with in the, in the gut placebo, IBS world is that prebiotics you. We'd never started the therapeutic dose. It'd always be this like low dose and slowly build up.

I would give myself a day, you know, like with the phgg. I started off with one scoop per day for one day and then I just went right up to the two scoops a day. Come on, Jason.

Yeah, to be totally fine with that. Like, I still, you know, recall working with, with people who don't have major gut issues but just want to make their ecosystem healthier. Geez, yeah. They could start with the therapeutic doses and they'll fart a bit more, you know, big deal. For most of us, it's not such a big deal. But for other people who are getting pain, discomfort, bloating, distension, change in bowel pattern, it's like you've got to incrementally increase up to get to that dose and may well take. Yeah, you're right, like three or four weeks to get to the actual therapeutic dose. And then you want to test that dose for about four weeks and then sort of do a test to see what you can look like. And your gut may not need that much for ramping up. But, you know, it's just reality with people that we work with with is often it's slow and cautiously increasing the dose.

Yeah, yeah. And I would never do that to a patient, what I did to myself. But again, I was like, I'm totally fine. I'm good, man.

Yeah. No, I remember I did a workshop and these people were just generally healthy people for the most part, who wanted to get healthier ecosystems. And I was talking about prebiotics. And then he does lactulose and inland fos and gauss at the standard dose. All at once from out of the blue? Never. And he said he was farting like a tremendous, tremendous amount of farting. But his bifidobacteria went from 0.1 up to 30% of his ecosystem. I still recall that was one of the earliest high bifidos I'd seen. And he's like, damn. Yeah. But that's four weeks of doing three different prebiotics at the high dose. But he could handle that. He, Scott could handle that. His work life, he was outside carpenter. So, you know, letting off a lot of flatus was okay in that situation.

Yep, yep. Well, I'll keep you Posted on the 2023 version of the experiment.

But curious.

Like I said, it's, it's, it's going to be slower for sure.

Yeah.

Got to be nicer to my gut.

Yeah. What are. Do you have any tips in terms of like, dietary fiber you like people to incorporate or even the prebiotics that you typically use? Like, are there any tips that you have your clients do? I know you said the titration up, which we've talked a lot about. It's always hard because there is some adjustment period, you know, and with the IBS space, there's always fear of like, oh, you're telling me to take prebiotics? What, I've been low fodmap for three years and you're telling me to take a prebiotic. So I think it's always a good conversation because you'll be working with someone who isn't getting any better on these low fiber diets. And it's like, let's try something new. But of course your gut's gonna be a little shocked having a prebiotic fiber in there if you haven't had much fiber in three years. But yeah, like, do you have any general tips, like both from dietary sources and then just like prebiotics ones that would be good starters that you like? I'm sure every, every microbiome is different.

But yeah, yeah, I do think that for like someone who had like IBS type signs and symptoms and let's say that we ruled out SIBO and fructose intolerance and lactose intolerance and a bunch of other things that might be causing those IBS like signs and symptoms. I think partially hydrolyzed guar gum would be my go to. And I think I used it when I first came across it in 2015 or something like that. I was like, why have I never heard this before? And I sort of did a systematic review trying to pull all the research together about phdg in ibs. And it's like all these, you know, I think it's eight positive studies that were done and you know, it's like, oh God, it's very consistent. And probably the first 30 people I used it on with IBS worked beautifully. No one had a side effect. It was like the dream prebiotic fiber. Then I had one person that got some bloating with and like, okay, well it doesn't work since, you know, it's not side effect free for everybody. But it geez, it goes well with this population. So I still think that's probably my, my go to. But also galactol oligosaccharides is probably my second favorite sort of supplementary fiber in that population. But I also think it's like, okay, we have to look at, you've got transit time, you've got to look at whether it's slow or not. Because if it's slow, there's a greater chance you're going to react to any fiber and certainly potentially phdg, certainly more likely gauss. And look at the role of visceral hypersensitivity and that phrase patient too, you know, so if they're got statin flame that like tiny amounts of increased gas is going to cause excruciating pain and discomfort, which is can be the case with some patients with ibs. I think I'd actually before I necessarily did much with phdg or dietary fibers from a diet perspective either I would do work on the, on the trying to decrease episodal hybrid sensitivity. And that work might go for two or three months. Before we go right now, let's introduce that quarter teaspoon of PHDG a day and then half a teaspoon and three quarters of a teaspoon. And so we start to build up and other people, it's a motility that you've got to kind of get going better. So that gas that does get built up doesn't get stuck behind sort of all that fecal matter and cause bloating and distension too. So you might do some work along that. And luckily, I mean we know that things like partially hydrolyzed gargoyum tends to speed up transit time in people who have slow transit time. We know we can use the right probiotic strains to help facilitate that too. You know, the biogaia strain or the. If that's from lactose HN019 we know and often speed up transit time quite effectively. So they can be useful tools to help facilitate better tolerance to prebiotic fibers as well.

Yeah, that's great. Just one, I just was gonna highlight one thing that you said that I think is important sometimes focusing on that some of the functional breakdowns are super important. Um, even. Well, you can do em simultaneously but you know, if the microbiomes awry. But your motility is really poor. Like you might wanna focus on the motility first. Or again, if you're not breaking stuff down up top because you have low stomach acid or you know, you have low pancreatic enzymes or something like that, you probably want to focus on those things first because they're going to affect what bugs grow and what bugs don't and how you tolerate treatment and different strategies going forward. So I like that you point that out. I think that's a really important point for people to. When they're experimenting with some of this stuff. If it didn't work at first, maybe there was a motility issue. Maybe try it again once. That's running a little smoother for sure.

And I think the visceral hypersensitivity thing is often. We know it's very common in IBS patients.

Right.

And it can be extremely severe. Like you know, patients who can feel every little gas bubble. I've had patients who had to do an enema before bed to wash out the fecal matter so they could sleep because the feces that remaining in the colon and the rectum area was causing so much pain they couldn't go to sleep. You know, that's more extreme. End of just like that's. That area was so nerves were so inflamed in that area. But it just means that any sort of gas production is notable. And it's like I can look at the ecosystem, it's like oh, you know, I remember having one patient, it was like 2% butyrate producing species. 2% was all there was. And lots of hydrogen sulfide gas producers. And it's like we really need to change this for you to get better. But visceral hybrids was so severe that we couldn't just go, yeah, eat more fiber, take this prebiotic. It's like, will that change the ecosystem? Yeah, it will, but it's going to cause excruciating pain and discomfort and horrific quality of life for a while, maybe for a long while. So it's like, no, we've got to do these little baby steps. Okay. Now we need to treat that before we can actually do too much. And some of the patients are really tricky when the ecosystem is that deranged because you know that the ecosystem is causing the visceral hypersensitivity. So it's like, yeah. And so that can be really challenging patient to work with that. That subset that's that severe. And they've been on. On a. This person was just eating two chickens a day. That's it, you know, nothing else. And. And practitioners were like, ah, let's cut out the potatoes. Then she goes, oh, no, I got worse when I cut out the last remaining fiber foods than what there was before. Yeah, I reckon you do. You have because your butyrate producers are all gone, almost all gone now. And your hydrogen sulfide producers are even higher. And hydrogen sulfide gas causes visceral hypersensitivity. So you're kind of stuck in this tricky situation. But, yeah, sometimes you've got to do a lot of prep work before you can do major microbiota modification.

Yeah.

And a, you probably made Amy cry on the inside talking about the person eating, like, one food or two food. The dietitian's gonna weep over here right now.

But I think that what the. The saddest thing though, too. And we talk about this all the time. You know, if practitioners are moving so many foods and, you know, nutrition is important for gut function and for the, you know, intestinal lining to be healthy. Like, there's so many reasons why you need optimal nutrition for gut to function. And just there seems to be no discussion of nutrition at all. Like in the fundamental, like, oh, I need enough B12 or I need enough thiamine, or I need enough of this. Like, there's no nuanced discussion around that. Which is very frustrating, I think, because it's just like, oh, just keep removing. Like, you can survive off those two chickens, even though there's like, you know, no vitamin C. No, like, you're super deficient in all tons of different things. Like, there's so many gaps. It's like, how do you overcome that?

Well, and I would say Maybe the problem is because we've hammered the snot out of this over the years and we'll continue to do so. But maybe the way to phrase it is that there's so much emphasis on nutrition for pathology that there's no room for a discussion of like nutrition for healthy human beings. Right. So like the idea of like you need healthy, optimal nutrition just to be like a healthy person and to heal your tissues and to function, like there's no conversation of that in the functional space. Even though they'll say from the rooftops food is medicine. But there's all this, this idea of like, well, you have to starve the one bad guy or the boogeyman and they use food as medicine. But it's like you have to cut out oxalates now, you have to cut out histamine now, you have to cut out fodmaps, cut out fiber carbs, all of it. So it's, that's, that's my story and I'm sticking to it. Yeah. Focusing on nutrition for pathology instead of nutrition for healthy human beings.

I hear you.

Yep. I was going to ask too. So going back to. So you had mentioned visceral hypersensitivity and working on that first. And I'm glad you pointed out that hydrogen sulfide can cause visceral hypersensitivity. So like doing things to target those microbes could be helpful. Is there anything else that you want to say about visceral hypersensitivity or like things that you have found really helpful for people who struggle with that?

And this is where I think heral medicines are fantastic because we do have some data, mostly animal data, but that's the best data we've kind of got on their capacity to decrease visceral hybrid sensitivity. And it works in my experience with humans for that matter. But the herbal combination iberogast is commonly used in IBS circles because there's clinical studies showing it helps reduce IBS symptoms in the short term. And it does for some people, does release reduce bloating and distension and cramping and pain. But for others it doesn't have that impact. So sometimes they might try it for two weeks. Ah, it didn't work for me not knowing that with long term use it diminishes visceral hypersensitivity. So that's not after a week, that's not after two weeks, it's after three months of daily consistent use. I find a well absorbed turmeric extract. I tend to use the curcumin phytosome Meriva because it's really well absorbed and it clinically seems to work with well in concert with Iberogast. And to me that's my dream team for decreasing visceral hypersensitivity. And there's some research on melatonin in this field too. But melatonin can potentially slow down gut transit time. So there might be again a time and place for it. For people with really quick transit time. You'll go ah, melatonin might do both things here, work on that and slow down that really rapid gap Constipated. You might be more cautious around melatonin usage.

I feel like I've seen stuff that suggests melatonin is a prokinetic though.

Yes. But in the low dose there's some really funky animal studies where they're like yeah, it's a very dose of hinder response at a low dose of melatonin is appropriate. In a high dose there's some human studies showing it slows down transit time. So I think it's. And I'm still experimenting trying to find find what dose does what. To be honest, it's like I don't. If I had some lovely skin to probes or something, we can do this really systematically but I don't have that access. So we just have patience. Let's try this dose of melatonin and see if it works as a prokinetic. But it doesn't seem to slow things down anyway at a low dose, whether it's working as the proconic as I'd like, I'm not sure necessarily. But it does help with disorder hypersensitivity as well.

Kind of almost like low dose eulerthromycin or low dose naltrexone. Like the low doses of the medication do completely different things. Yeah, both of those are prokinetics versus being an antibiotic or I forget what naltrexone is used for. Normally I think.

Yes, as do I actually. And there's also some research on pepper and caraway combined to decrease invisible high resistivity. This is an interesting study because they peppermint oil on its own didn't do this. Caraway oil on its own didn't do that. But when they combined the two together there was synergy and the decreased visceral hyper hypersensitivity and I've used that successfully even as a herbal tea of peppermint caraway for example for remember I had one patient with who had had closing difficile infection, she'd taken antibiotics to deal with that which in this case was thankfully successful. But she had this lingering visceral hyper sensitivity afterwards. And this persisted for months. Months. And then she responded amazingly well to because she was a tea drinker. So okay, well let's just do this. And I just recall that she responded, responded really, really well to that combination.

Interesting. Well, I feel like TCM practitioners have kind of understood herbal synergy for a really long time and it's taking a while for the western world to catch on to that idea. But the idea that herbs can be synergistic or like enhance the effectiveness of each other has been known for thousands of years. Just not in the western world perhaps.

True enough. And western herb was certainly believe that too. We tend to combine formulas more individually for patients. Unlike TCM where you've got these thousands of year old formulas that you might go this from the mat, this pattern disharmony. And sometimes I've had the, I think hubris is the word of going, I reckon I can make that TCM formula better by changing this herb, which I don't think should be in there and I'll replace it with something else. And the mix did not work. No, I recognize people formulating 2000 years ago did a better job than me. I shouldn't question that.

Yeah, they did it their way for a reason.

Yeah. Or maybe over generations of clinical observation going no, this combination is ideal in this situation.

Yeah, yeah, that makes sense I think to share too. Like look, you brought something to the table. I'll share this for what it's worth. A couple of other things maybe for visceral hypersensitivity. Well one I learned from you. There's the probiotic. What is the strain? The 299V lactobacillus. Was it plantarum? I think that's been shown to reduce visceral hypersensitivity too. I'm pretty sure I got that from your stuff. Look, I've schooled the teacher on his own material. Who knew? I told you, you've been a science crush for a long time. But also I wonder, I've played a little bit with like vagus nerve stim here or there, like putting an ear clip on the tragus of the ear and doing that sort of stuff. I had one patient who thought that a device called the alpha stim was really helpful and it was a similar idea. Like he had had C diff. Teenage kid, 17 year old kid. He had been on doxycycline for three years for acne. Just why the fuck not? And then he had to take an antibiotic for like a sinus infection and bam. C. Diff. At 17 or 16 they had gotten rid of the C. Diff, but he had had lingering visceral hypersensitivity and just a lot of pain. And it was actually. I can't even take credit for this. I didn't really know about this, but his acupuncturist recommended the alpha stem to him and he thought it was really tremendously helpful. I've been kind of playing with. I got one myself to kind of fiddle with it a bit. But yeah, at least I have a couple of people who have since tried the alpha stim and thought that that was helpful.

Interesting.

And then like I said the like vagus nerve stim with the ear clip on the left tragus and doing that seems to have helped too. And then right now I've got a couple of people experimenting with castor oil on the abdomen and then leaving it on maybe with some heat.

Okay.

And then seeing how that works. Some people have said that it's helpful. Some people have been like, eh. But I figure a lot of women use castor oil for period cramps.

Yeah, interesting.

It felt like vaguely related enough that it's like, yeah, just slather it on your belly instead of down near your pelvis. Same diff, Crampy, irritated muscles and nerves. Right. Like it's kind of the same thing in a different location.

So cool. Well, yeah, well, it's nice hearing that. There's more tools that I'm unfamiliar with. And butyrate. I think butyrate helps too. It's just that sometimes you can't feed those butyrate producing bacteria that well in those people that have extreme visceral hypersensitivity. And that's where the few incidents where I will use preformed butyrate. Whereas most people, I prefer nurturing their own butyrate producing factories because they're there. Let's feed them and get a lot more beady being produced that way than what we're generally getting in to form. But in those people who have extreme levels and can't tolerate any sort of increase in fibrous material because of gas bubble causing extreme pain, then I think butyrate preformed is actually helpful.

Have you ever used butyrate in an enema with patients?

Yeah, I have.

And could you just like break open the capsules and put that in the enema solution and use that? I mean that's. I have suggested this to several patients, but zero of them have taken me up on the offer because enemas just, they're not as glamorous as the orally administered.

They're not. I tend to reserve like what I call retention enemas for listen, sometimes with extreme rectal visceral hypersensitivity. I've used them and, and often more often for ulcerative colitis as well, where that particular part, lower part of their colon is in rectum area is really inflamed. And because essentially things we're taking orally, curcumin, et cetera, is going to be more diluted by the time it gets down to that last bit of the colon. So I do think, and I've had some people where it's been immensely helpful and I think the trick there is having a small volume. That's been my experience is like with a retention enemy, you don't want like a big bloody enema kit. You want like, you know, 20 mils, you know, like a tablespoon's worth of material that you put in there at night and then it could sit in there all night and then come out the next morning. So I might use a combination of, you know, Rhea curcumin and aloe vera juice, for example, and maybe some phdg in that, you know, that will be individual to be per person. But I do find those potential enemas can be really helpful for the end inflammation in that area.

Well, yeah, that's a valid point. Like if you get one of these big honkin enemas. Side note, weirdest series I ever did for my YouTube channel was the coffee enema series, because I did them for a few days because, like, I can't talk about them if I've never done them. Right? Yeah. So weirdest experience probably of my life was when I did coffee enemas for like a week. So I could do that YouTube series. It was bizarre. But. But what was I saying with that? I got sidetracked by my own little story.

Maybe it's the volume of enemies.

Yeah, the volume. It was like. I don't even know. It was like quarts of water. It was, it was a lot of liquid. It's all I'll say.

And that's what you don't want to do with someone who's got rectal hypersensitivity, rectal inflammation in that area, or resurrection. If you put a huge volume of something in there to stress out those stretch sensors, you don't want that. You just want a small volume that can stay in there. So the principle is different. And you have to use some of those little like rectal bulbs rather than. Yeah, because I've got an kit too. It's like, it's this huge. Fits like a couple years of water. Like you can't do a small volume in that either. It's just not useful tool for that.

Yeah, yeah, yeah. I'm kind of picturing one of those like nose Frida squishy balls. Almost like something like that. I would imagine would be more appropriate here.

Totally.

Yeah.

Sorry.

Disappeared for the dose. Frida.

Oh, yeah, I missed it. Sorry. My. My computer was about to die, so I was like, I gotta plug it in. I think that would have been bad. Yeah. My husband, I think he unplugged my computer blast and so I had to sneak off and plug it back in.

He's tried to sabotage it.

He didn't sneak off that will.

Because we all savage turns out. And I was stumbling over there, the. The little low energy thing popped up and I was like, oh, gosh.

Well, you did it. We're proud of you.

Thank you.

And you're still here. I know, I forget honestly, where we were before I got on my tangent about coffee enemas. Oh, I think visceral hypersensitivity. Um, do you have anything that you want to weigh in on for that matter? Amy, again, try to be mindful to give you a turd. So I don't just.

Yeah, no, I. Again, I. This has all been really interesting just to hear kind of some different things that could help there. I. I know that there is like some research and again, like this would be like not my.

The first go to.

Like, I'd much rather try some of the. Some of the stuff that you guys are suggesting. But like low fodmap I think has been shown to help a little bit with hypersensitive visceral hypersensitivity too. But again, would not be my first choice. You know, if you were kind of trying to manipulate the diet and again, your best bet is trying to figure out if there's foods that might trigger it more so than others and working on the mechanisms that might be breaking down that are causing some of the visceral sensitivity would be way more effective in my opinion. Again, taking some butyrate to support your microbiome if you're not producing butyrate would. Would be a much better option than probably starving butyrate producers. Even more with the low fodmap diet. But like, if you were in a pinch and wanted to do something for a week or two, you know, it's something you could potentially do. But again not, not the, the other things that you mentioned are much I think better and more productive for the ecosystem and the gut as a whole.

But yeah, well, and even if you want to experiment with like low fodmap like you said, you could do like a modified version of it. Right, right. So you don't have to do the full diet. You could just experiment with. I'm going to not eat beans, wheat, garlic and onion for like a week or two and just see what happens. You know, take out the biggest offenders and just. Right. Kind of play it by ear. You don't have to cut out all the things.

Right.

Yeah. I mean I think it's interesting looking at that even the pre. Low FODMAP diet stuff we were teaching about treating IBS pre low fodmap there was still knowing that legumes and onions and garlic and stuff cause problems and increase gas. It just was like the codification that happened with, with Dr. Sue Shepard that was great in the, in the, in the name and the research that was sort of done on that sort of system. But the idea is that people don't necessarily going to react to all those things, you know.

Right.

One of those categories. But you cut them all out, you'd see the benefit, then you kind of introduce them back in. And that was certainly my take when I saw spoke to Dr. Shepherd was more about short term diet. Let's bring the back in as quickly as we can. But it doesn't often manifest that way in clinical practice where people are on these diets for years and not necessarily treating the underlying issue. I mean I think that's the thing because for me it's like it is a diet that reduces symptoms immensely. Well, you know, no doubt, no argument there.

Right.

But we know it caused detrimental shifts to the ecosystem and I would argue that for most people it doesn't fix the underlying.

Right.

Visceral hypersensitivity issue. You know, because I've had patients that have been low FOMO for years and yeah, their symptoms are manageable while they're on it, but it never. They go back to eating something and the symptoms come back. It's three years on. It's like. And that's not what we want. Ideally, let's see if we can sort this so that you don't have this visorum acidity and then you can eat these foods again and not have to be on such a restrictive diet. And I think for most people we can get there. You know, there are some people that are obviously exceptions in more challenging treatment paths. But I'd say for most people with ibs, we can get there by doing, I think, appropriate testing to work what's going on, and appropriate individualized treatment to address what their issues are. Because for me, IBS is just such a. I always tell my students an umbrella term. It just means you got these symptoms, but it's like your job as a clinician is to work out why this person has the symptoms, at least what their contributing factors are. You know, for some people, it will be sibo, but not everybody. Some people will be visceral hypersensitivity, but not everybody. Some people stress be the main driver, but not every. Like, a patient I had yesterday was, like, pooed consistently daily except for when she got highly stressed, and then bowels stop, and then bloating distension occurs. Okay, but not everyone gets that impact on that, but it's okay. Well, stress is obviously one of the axes that we have to leverage in this particular therapy relationship to get certain things moving. Better transit time, high methane. You know, a bunch of stuff that we'd have to kind of look at for this IBS patient. People who come with that label of IBS to work out what are these. What factors are their triggers or their causes, essentially, you know, and then how can we best address that for that person?

I feel like patients would almost be better served if we just drop the s altogether. Like, if we said you have an irritable bowel Instead of you have, like, saying you have ibs like you have a cat or you have this. It's like we're using this label and kind of handing this thing to them, and then they're like, oh, this is my precious, and this is my answer. And it doesn't really tell you anything. But again, if we could tell people your bowels are irritable. Now let's find out why. That kind of phrasing, I think, opens the door more for, like, the workup and the conversation and the curiosity of, like, what led me down this path and why am I here, and what are my triggers and what aren't my triggers?

Yeah, no, I think I like that, actually, because I think we tend to get a bit attached to that. It's okay. I find out what's wrong. It's like, no, you have a certain symptom cluster that meets our current definition of what we call IBS Rome 4. But it's like, why have you got. The symptoms might be quite different than someone else who's got. Meets the Rome four criteria, you know, and if you haven't been worked up, like, the number of people who actually, in my opinion, have ibs when I've actually diagnostically worked them up properly is really small. If we actually do a proper workout, we work out, there's generally something there. And that's not just. There are people who would have classic ibs, but I'd say it's actually relatively small proportion when. When people are, Are. Are appropriately worked out.

Yeah, yeah, I'll throw this out there too. I think it's applicable for IBS in general and certainly for SIBO and visceral hypersensitivity. Like, a lot of the stuff that goes hangwire with these conditions, you can kind of trace it back a few steps to the nervous system on some level, right? So like the gut brain axis and the vagus nerve and the enteric nervous system, like those nerves stimulate the muscles in the gut to contract and then that's what we end up calling like motility or peristalsis or the MMC or stomach emptying. Like, it's just. It's muscles contracting and muscles contract because a nerve told them to contract. So it's. We're kind of looking at a neurological pathway where like, with visceral hypersensitivity, we have nerves that are really hypersensitive to any stimuli or any stretch sensation. And they're freaking out for reasons that they probably shouldn't freak out about. And like, even things like low stomach acid, like, the stomach doesn't make acid for funsies, it makes stomach acid because the nervous system and the gut brain axis told it to. You close and open sphincters because your nervous system told them to close and open. So I almost feel like too, a lot of the IBS and SIBO kind of space could benefit from tracing back and thinking, okay, what does the nervous system need to be happy and healthy, right? Like adequate fuel delivery, adequate oxygen delivery. Like, if you're iron deficient or anemic or B12 deficient, good luck. Because nerves like oxygen a lot. Like, you need enough building blocks to make neurotransmitters. If you don't have like, you know, the tryptophan or the vitamin B6 or the whatever or the choline to make your neurotransmitters, like neurons don't work for free. They kind of need all that stuff to make all their juice and do their things. So I feel like we could kind of trace things back and think about it as nervous system related. In a lot of cases, so that might be one of several missing links in this world.

I like that. Thank you.

I do too. Oh my goodness gracious. Well, I want to be mindful of your time so that we don't hog your day. I know it's the end of the day for us and the beginning of the day for you.

Beginning for me? Yes.

Yes. I'm curious just. Just because I'm Snoopy. Have you been up to anything fun or cool recently or do you have any like recent projects or upcoming projects or revelations or anything like can we get an IBS Freedom podcast exclusive from Jason Parvolak is basically what I'm asking.

This year has been like. I feel like I've barely left. Between working with patients and working with doing research stuff, I don't think I'll feel like I've left my head eyes above the parapet. So this thing to do anything too creative? One thing, a paper was just published yesterday on that research team I was working with did that was looking at antibiotic usage and instances of depression. So we're doing a systematic review looking at essentially do and does taking course antibiotics increase your risk of getting depression? And to date every single study has shown that it does. Yeah. And that's obviously the gut microphone brain microbada link. So that was kind of exciting to finally get that one published. It's always nice to get something published.

Yeah.

So that's kind of new. And I am working on new, new, new course content because as we're coming up to the summer break, which is not for you guys like depths of winter, but a time where my marking load and teaching load decrease so I have a chance of like not just doing paperwork and marking. I can actually look up and. And go, what?

Yeah.

What new can be created? What new? What needs to be gap needs to be filled. What information needs to get out there? Yeah. So I'm looking forward to having some time to do that.

Well, and hopefully you're doing a lot of self care and just taking care of yourself too, because you can't teach us fans anything if you burn your adrenals to a crisp and burn yourself out into nothing. So like take some vacation. Also don't feel pressured to do stuff for our sake. Like just take care of yourself also. And I definitely got to look up that study. That's wicked fun.

Yeah, we always have to like be very circumspect with our conclusions. So just keep that in mind for us to get it published. Like you can't say that it does something. It's like you have to say it looks as though it might do this. Even though every single study says this, we can't actually say it is a connection. It's like, there may be connection. More research is needed. So go, go deeper than that because that's probably what the abstract will say. Look at the studies. Every study shows that there's connection there and sometimes lasting for 10 years. After course antibiotics, your risk of depression was actually increased. And that PhD student I'm working with now, we're doing a study looking at antibiotic use during pregnancy, like during labor, for example, and seeing if you. It leads to increased risk of prenatal depression as well. So that's exciting. And we're kind of just got to the end of enrollment with that one, so we'll probably know, get the data over the next six to 12 months.

Yeah, cool. Very cool. See, and look, this is why maybe I was a researcher in another lifetime, but not this one. I think I just need to stick with YouTube research because, like, I don't know if. I don't know if I saw that compelling evidence. I don't know if I could put in the abstract anything other than this clearly causes depression, guys. So, like, I give you credit for doing, like, what you needed to do to get it published and not using overly strong language because I don't know if I have the restraint to do that.

But it's a tricky thing with academia, actually. Like, you're never allowed to say anything strongly, you know, And I think there can be benefits to that. But I think also with a situation. I remember my first ever systematic review was looking at lactose rhamnosis. GG doesn't prevent antibiotic associated diarrhea.

All right?

Every single study said it did. And my original write up was like, here's the low cost thing we can do to prevent this side effect. In many countries, that's available to yogurt. You can just eat the yogurt while using the antibiotics and look at the better outcomes we'll get. And the peer review is like, no, you can't. You can't say that. Even if every study says it, you can't recommend they actually do it where let's say it's something positive. It's just like, whoa. That was my first, like, major taste into the peer review process, was that you have to calm everything down and go that it looks like it might work. And you might think about taking this alongside that maybe, but do a lot more research first before you do anything. It's just like, yeah, it's all.

I'm feeling raging listening to this, and I'm not like, a naturally ragey person, but I'm feeling, like, my blood pressure go up. Hearing that I would need to take up kickboxing or something and just, like, punch stuff. After dealing with something like that, that's just. That's frustrating.

Yeah.

Because people want it in plain language. Like, what should I do? Is this. Oh, and I saw a kitty or. No, a dog.

A dog, I think. Yeah.

I got excited. I love both. So had to make mention of that. The people on the audio version of this podcast are like, what? What?

No, they want to see my little, little cavalier King Charles. One to the frame. She's quite lovely. Yeah.

Cute. Well, I appreciate the cameo. I'm sure Amy does, too.

Truly love dogs.

Yes. Well, Amy, my darling, do you have any further questions for our guest of honor?

No, I think this has been great. I've. I've loved every second of it.

Yeah. Every moment.

Every moment.

Yes.

Yeah, we'll.

We'll keep an eye on your stuff. Stuff.

I know.

Can't wait. You. You could find the man himself on Facebook, kind of. He does have a Probiotic Advisor page. We were laughing about this earlier. He does have a pro. A Facebook page for Probiotic Advisor, and he occasionally will post stuff, actually. Okay, can I. I know we're wrapping up. Yeah, I know we're wrapping up for the most part, but can I just weigh in on one more thing or comment on one more thing? Do you want to comment at all on the study with the SIBO breath testing and the mouthwash? Because I found that on your Facebook page when you posted it there. So kind of fill people in if they don't know about that study and then, well, comment.

Well, I'm slightly. Probably rusty on some of the details of it myself, but the biggest takeaway was One of my PhD students is actually delving into this. It's a great band of researchers. What's coming out of here. But it's like doing a mouth rinse actually changes the breath test results. Yeah. So different labs will recommend. Some recommend doing a mouth rinse, and some don't. But if you do mouth rinse, you can get the. We're getting all these false positives results. If you do mouth rinse before the first breath test only, maybe that's probably the biggest takeaway. There's a bit more in that paper, but, jeez, it's just like. Okay, so if you do a mouth rinse before baseline, you're Even if you have all These major jump ups at the 20 minute mark, enough to be positive. Who would not have been positive. We didn't do the mouthwinds beforehand.

Yeah, and that, and that makes sense because. Right. Like the way that the tests are usually interpreted is a difference in the gases from baseline. So again, if you artificially tank your baseline and then you have, you know, the next couple of samples go up, it is going to give the illusion of a peak when there really wasn't a peak necessarily that early on in the test. But what I actually found even more fascinating maybe is that the study was beautifully designed too. But I thought it was cool that you had some data where people only did the mouth rinse for the first one and then you compared whether they did that or not and they got a bunch more false positives with that. But then there was also the difference between people who did an antimicrobial mouth rinse before every single sample versus people who did not. Or versus the same people, I think, who did not. And even that, like, you got far fewer SIBO diagnoses. Hello. But you got far fewer SIBO diagnoses when the people used a mouthwash consistently before every single sample. And it makes you wonder, is some of, again, is some of the stuff that we're diagnosing as SIBO actually funky, funky dysbiosis in the mouth and it has nothing to do with the small bowel?

Yeah, it did bring up some of those questions and we delved into it and there are methane producing bacteria in the oral cavity too. So like. Oh, yeah, it does bring up some questions around breath testing reliability and pre breath testing procedures and what might impact results. And we. Part of Sharon, whose PhD is in, is we're delving a bit more into that with further studies that have not been published yet. But looking at, okay, what's the impact of water rinsing and other things? We don't really know because it's like, does it have the impact or not? And we're trying to tease out some of those things now to hopefully improve kind of the process that will go on with breast testing. So we do get more accurate results and have less chances of false positives. Essentially.

Yeah. Because we don't need people getting false positives and then obliterating their microbiome with antimicrobials out the wazoo and doing low FODMAP for the rest of their days.

Exactly.

Because they think they have SIBO and they actually don't.

Yeah, concur. I think false positives have a lot of negative outcomes associated with them potentially. You know, obviously it depends on what path they choose, but generally it'll be something that damages their, their microbiota as a component of that treatment that they don't need.

Yeah, yeah, yeah. Oh, I'm glad I, I remember to make mention of that study because I thought that was again, just beautifully designed. Kudos to the team and also just deeply, deeply fascinating. You're asking really good questions.

So.

So yeah, we'll keep your eye open on more research that comes out of Sharon's PhD because we're kind of delving into doing work with people with fibromyalgia. We've done like glucose fructose and lactic breath testing and different sort of pre breath testing procedures looking at microbiota composition people with fibro. So it'll be interesting findings when it all comes together.

Yeah. Cool. Well, keep up the good fight and don't forget to share findings like this on your Facebook page because some of us old timers still use Facebook and you are one of, you're one of the few people I follow on Facebook. So that's how I got the news on that last article. Thank you.

Well, I might post something with that decision. I could be article with the antibiotics too.

Hey, there you go. There you go. Look. Yep, keep it going. But yeah guys. So like I said, you can find the man himself on Facebook. The the page is called the Probiotic advisor and website probiotic advisor.com his courses are awesome. Very reasonably priced I might add also and the Probiotic like database tool is just so good and very reasonably priced too. Like it's totally worth worth having that and yeah, just thank you so much for coming on. It was a blast and hopefully we'll see you on the Internet real soon and otherwise. You guys know my shtick. If you're on YouTube, do the like subscribe, comment, etc. And if you're on a podcasting app, leave us a five star review if you feel so inclined. But we will see you right back here for the next episode of the IBS Freedom podcast. Toodaloo.

See everybody.