Dr Jason Hawrelak on How to Optimise your Gut Microbiome using Stool Testing, Diet, Prebiotics and Probiotics

Hey, guys, this is Criben Governor from the Gut Health Gurus podcast. I'm a food scientist and my colleague here, James Shadrach, is all things psychology with a psychology background. And today we have a very special guest, Dr. Jason Horolak. Jason, certainly in Australia is one of the most, I guess, credentialed speaker educator when it comes to the field of the gut microbiome, probiotics and gut health. Jason, welcome to the show.

Thank you for the invitation to take part. I always enjoy chatting about gut microbiome related topics, so I think we'll have a fun discussion today.

Awesome. Jason, I'm so appreciative for you joining the show. I know we're both crook at the moment, so audience members, please excuse the croaky voices. And maybe a potential break here and there to have a sip of water and a bit of honey tea.

Yes. Yeah, no, I had two days of being very unwell than two days with patients last weekend. My voice is at that breaking point, much more husky than normal.

And that's really interesting, Jason. I guess the two of us who are really focused on, you know, the health space, the wellness, you know, at times when we can get stressed out, maybe it's a lack of streak, lack of sleep, a bit of work stress and, and sometimes, you know, you can get hit by these, these illnesses and it's perfectly normal.

Yeah, yeah, I think it totally is. And I think sometimes it's an enforced break because I tried to sit here and work on Monday and my head was nodding down, my eyes couldn't stay open, like, okay, no, I actually need to take some hours off and go have a nap. And I just generally don't do that. And it's also what I found through my student life and post student life is you go through these periods of very stressful workload. And then when you get to the end of a project, that's often when you fall ill. Often had that at the end of term at university where you cram for exams, you get everything done and then you get over the finish line and then you just fall over and get ill. And that was part of that potential recovery phase. So for me, I've had that sort of year, so it's nice to perhaps see this as the end of the race recovery phase and force time off.

Totally, totally. I could not agree more, Jason. At times we get really busy, we overexert ourselves, you know, and sometimes the body just says, hey, Jason Cribbin, stop, have a break and let me do my job and keep you fit and healthy and going. So sometimes those forced breaks are a very good thing. So, Jason.

Yeah, for some of us that's the only breaks we get because we have a very hard time mandating or creating break spaces.

Yes, agreed, totally. So, Jason, today, just to set the scene for our audience, so we'll have a conversation on I guess the microbiome. We'll delve into general gut health, probiotics, prebiotics and anything that's piquing your interest at the moment in terms of that gut health, probiotics, microbiome space. So just to set the scene for the audience, I've seen some figures recently where it's, and fact check me if I'm wrong, Jason, that approximately 10 million Australians suffer from some form of digestive discomfort. So that's, you know, that's almost half a population. Now, just to kick things off, why do you think that's the case, Jason?

That's good question. And I think inevitably there's going to be, you know, a number of factors that are involved with that. I mean, you'd get, you know, the western diet, typical Australian diet or SAD diet undoubtedly is a contributing factor to that. I think high stress loads and lack of sleep, as we just touched on, I think are contributing factors for that too. And then medication use too. And I think you can take a step back and go, okay, what? All those factors arguably negatively impact the gut microbiota. You know, certain medications do, like antibiotics and proton pump inhibitors and nonstero anti inflammatories, all of which are widely used by Australians at this time point. Most Australians aren't really eating all that well. Sometimes we live in bubbles and you know, all my close colleagues that I, that I see on a daily basis, they eat really well. But then I go down to the local supermarket and I can see what the typical Australians eating and it's quite a different story. Their shopping trailer is filled with cans of Coca Cola and white processed foods and it's just like, ah, that's what they. No wonder their gut isn't going well. No matter. They're not going well more broadly from a metabolic standpoint either. So I think it's a combination of those things and never mind taking even a further step back, going back to the early, early childhood history of, you know, C section birth and formula feeding, early antibody exposure, all of which impacts, you know, gut microbiotic composition and in this early windows, you know, essentially permanently, which I think does preclude to certain digestive and other metabolic diseases for from that time onwards, which is where the research is now teasing out.

So if someone. So you mentioned the word gut microbiota or microbiome. So for someone that's never heard of this concept before, what is the microbiota? What is the microbiome?

Yeah, what's been interesting for me as a researcher who's been in this field for 18 years is that understanding of those terms is now far more widespread than before. You go back 17, 18 years ago, the term microflora was used and very few people were paying much attention to gut bacteria, and very few weren't familiar with the term and familiar with the term probiotics or prebiotics. People just called it acidophilus at that point, had no idea what prebiotics were. So, thankfully, that message has really changed and got out into the community. Now, microbiota is the organisms that make up a certain environment. And obviously we're talking about the gut microbiota, we're talking about the microbes that make up our gastrointestinal tract, but primarily we're talking about the microbes that reside in our colon. It's the colonic microbiota that we're assessing with stool sampling, where the numbers in the colon far, far outweigh numbers of microbes anywhere else in the gut, transit time is far slower. So there's a lot of chance for those microbes and their products and byproducts to interact with the human cells and gut cells and immune cells in a way that sort of alters function of those cells or that organ in terms of the colon, for example. And microbiome tends to incorporate all of those microbes, but also their genetic capacity of what they can actually do as well.

And so in terms of the. The microbiome composition, there was a couple of things I want to dig into. So you mentioned testing as one. So there's options now for people to have tests done. And so.

Which is brilliant. I absolutely love that. As I said, I've been in the field for so long that we had to make do as clinicians and as the general public with suboptimal tools for a long time. You couldn't really get a good feel for what was going on in your gut when we're relying on culturing, for example. So it's been revolutionary as a clinician working with patients over the last five years, where we've actually had access to tools to properly assess the ecosystem and the diversity and the number of species that are present, et cetera.

So someone gets a stool report. So the options are they can discuss it with their clinician who's versed in this field. Or some people are citizen scientists and maybe they want to test themselves and have a look. So how do they interpret these reports?

I think it's actually, it's tricky because it's complex, it's not a simple area. I mean each individual person might have 160 different species present. A number of those species have only been recently discovered and scientists don't know what they do yet or what a normal amount of that population is. So how can non scientists have any interaction with the unknowable at this time point? So I think that really complicates it. And even the stuff that we do know is still complicated too because we might know a number of key genera and some markers that we associate with key microbiota health like diversity. But I still think it can be challenging area for even clinicians with a background of reading scientific studies to navigate. Which I can say from experience of observing people around me, let alone for the, for the general public, it doesn't mean that they should do the tests and engage and start doing it because I think it creates that motivation to learn, motivation to take care and nurture that environment. And I think that's a wonderful thing because it has been a very much neglected ecosystem that people have inadvertently trashed for potentially the 20 odd years of earlier life or their entire life up to the point that they realize that it's important they do a test and then that actually can really change the way they interact with that. I run workshops for the general public for that reason is to help people engage with what we do know about that ecosystem. In five years time those workshops will run far longer because we'll know far more about the different species than what we do now and how to interact and change those things. So we've got, you know, some of the research on the microbotic goes back to 1960s and 70s, but it's really the evolution of technology that really took place in the early 2000s where we moved to using DNA technology to assess what's there that the microbiota researchers just skyrocketed in terms of the amount that's been done and how much detail we can see the changes. Because before that it was pretty hard. When we're using culturing researchers were looking at vegetarian diets versus high meat diets and they couldn't see that it made any difference on the gut bacterial populations. And this was perplexing because it's like it should, but it just didn't Seem to. And researchers are postulating that, hey, I think what we're using is just too crude. These instruments we're using are too crude to actually see the changes that are occurring. And that's exactly what it was. And you fast forward 10 years and using DNA techniques, it's like, oh, now we can see the impact of different dietary approaches, of different medications, chemotherapy, radiotherapy, a whole range of things that we couldn't necessarily easily see before, and also how long lasting they are. We used to think antibiotics impacted the ecosystem health for two weeks or three weeks or four weeks. And it would look like it did before when we use culturing and now we start using DNA tools, it's like, hold on, it doesn't look the same as it did before. Certain species do. They bounce back. Certain species are advantaged by the antibiotic exposure if they have the right genes. Some species are lost and arguably the ecosystem is. Some people are permanently altered in many patients, even after, even when they're healthy. And just a single course of antibiotics. And this has only been teased out when we switch to better technology with the capacity to notice these changes and to deceive species we didn't even know existed before because we couldn't grow them in test tubes.

Let's deep dive into some of the genera, the species, the faula. So if we start at the very top, the two most common ones, Firmicutes and Bacteroides. So are you able to give us a quick bit of information on what these two phyla are all about?

They certainly make up the bulk of the bacterial species within or genera within. Someone's gut will be from within those two phyla. But just because they're in the phyla together, it doesn't mean they have actually much in common. That's perhaps one of the biggest things to point out, because the phyla that humans are in also has lizards and fish. We do have some things in common, but we're actually quite different at the same time. So I think it can be problematic in some ways trying to make too much generalizations or interpretations around phyla level data, except for, in my opinion, when it comes to Proteobacteria, because all Proteobacteria, which is another phyla that most people have in much smaller amounts, thankfully, than Firmicutes and Bacteroides. All protobacteria share a structural component that they're composed of called lipopolysaccharide or endotoxin. All of them, it's just part of their makeup. It's not like. And we call endotoxin because it does have toxic effects. It's not like it secretes it to make us ill, it's just part of its structural makeup. And all of them within that category have got that. And we, there's a bunch of research has come out from 2006 onwards that have highlighted the pro inflammatory role of this endotoxin that's released on a daily basis by your gut bacteria because as they die they sort of that endotoxin gets released into your gut and then some of it gets absorbed. And some people move very, very, very much as to how much proteobacteria they have in their gut. And you could have one person that has 0.5% protein bacteria, which is probably the lowest I've seen in practice. And I've seen other people, there were 25% protein bacteria in their gut and that is huge. And just think of all that. You've got 25% of your gut bacteria, which is, you know, trillions of bacteria are filled with this endotoxin. That's a pro inflammatory compound which we now know that even when your gut is intact and healthy, we're absorbing and getting some in, but when you have more of it, more gets in and it has a capacity to actually damage the gut as well. So I think from a, for a phylo perspective, it's really Proteobacteria to me is the biggest thing I look at there. And yes, Bacteroides I look at too because it also contains all the organisms within that, that phylum do contain endotoxin, but it's not nowhere near as pro inflammatory as prokobacteria endotoxin. So but, but that said, if you have someone who's 25% Proteobacteria and you know, 65% Bacteroides, it's like, whoa, you know, that's a lot of gram negative bacteria, a lot of endotoxin floating around in their gut and which is going to not just stay in their gut but go into their bloodstream and cause a whole range of inflammatory reactions. And I think it just depends on the person as to how that that can manifest. But we know this is a key driver for, you know, metabolic syndrome, type 2 diabetes, fatty liver, even anxiety, depression are being linked with this endotoxin bloating now and Alzheimer's disease, just to name a few.

And say someone comes up with a high level of protobacteria, what steps can they actually take to address this high level to lower those levels?

I mean you would normally that would be the first thing to look at is the file level. Then I look, I dig a bit deeper into the genera, what genera of Proteobacteria you've got. And that can dictate to some degree the best interventions. Because most Proteobacteria as a class of agents are prefer growing at a more sort of neutral ph. And the clonic ph is immensely adjustable with dietary factors and with prebiotics. So through those taking control, and we can control dietary factors, we can ingest prebiotics, and as a consequence we can actually really shift and acidify the colon because essentially we provide food for other microbes that produce short chain fatty acids like propionate and acetate and butyrate, that lowers the ph and that makes it less conducive to the growth of the vast majority of protein, bacteria and those simple things, just eating more plants, food, more fiber, taking the right prebiotics can make an immense difference to Proteobacteria populations. And I see this on a weekly basis in my patients because we test this, we do the interventions, we test afterwards, and those levels go down and generally they feel much better because it is very much a pro inflammatory compound and you don't want that much floating around in your system. You will feel altered from having that much floating around in your system.

So if we delve a little bit deeper into protobacteria, so is it Bilafala and disulfaviburae are the other ones that you're looking at.

Those are two. And those ones are perhaps more significant because yes, they're Proteobacteria, so they contain that pro inflammatory endotoxin. But secondly, they are hydrogen sulfide gas producers. They essentially eat generally sulfur compounds and they convert that through to hydrogen sulfide gas, which is pro inflammatory and is gut damaging at higher levels. A tiny amount your gut can deal with quite fine. But again, you can have this huge variation between having almost no hydrogen sulfide gas producers to being 8, 10% of the ecosystem. And you can just think of how much extra hydrogen sulfide gas is being produced when they're on that higher end of things. So those are certainly two of the genera that I look at. But there'll be other things like E. Coli, Enterobacter, Clyvera, Shigella, Salmonella. You know, some of the ones that we see as gut disease agents are often in that Proteobacteria category. Klebsiella would be another one in the.

Category too, in terms of the, I guess the methane producers. Are you also looking at the Archaea, something like Msmithi.

Yeah, yeah. So Methanobrevobacter smithii would certainly be on my radar, too, and we'd be looking at whether it shows up in the test and what percentage it shows up in the test. And to be honest, as a clinician, I actually find breath testing is a more accurate way of assessing for methane status, because you do get some people, I mean, everyone in my patient where they've shown up with high methanobirivacter have shown up as a high methane producer on gas testing, too. But I've had patients that have showed up on a gas test but didn't show up with detectable levels of Methenoba bacteria on stools. So it was relatively small amount in that stool sample. So I think breath testing is a more reliable way of ascertaining someone's status. But when it's high, then that is usually correlated with slower gut transit time and or constipation.

Great. And we'll talk about pre and probiotics in depth down the track. But in terms of intervention with a prebiotic for specifically these, I guess these negative species or pathobiant species that you're talking about, is there any recommended prebiotics that people might want to consider if they have high levels of these bacteria?

Yeah, certainly. When it comes to Methenobacter smithii, that the ingestion of partially hydrolyzed guar gum, which is a prebiotic fiber, usually results in a decrease in methane output, and it results in a normalization of stool form. So those people who are on the constipated end of things, it tends to soften the stool, allow for easier passage.

And in terms of a dose level.

Most clinical trials using phdg, which I'll say for sure it's far easier to say, is about 1 metric tablespoon. So 5, 6, 7 grams per day would be a typical sort of dose. Now, I do work with some very sensitive patients, so sometimes we've got to start with a quarter teaspoon a day for a while and build up. But most people can start with just that therapy dose, assuming they're not in that extreme sensitivity region.

And this is also applicable for the protobacteria that you're talking about?

Yeah, it does. Partial hydrolyzed gargon doesn't seem to shift the overall ph dramatically. It does up the production of butyrate specifically. And I think the butyrate and Methinobrobacter are often negatively correlated, so that higher butyrate is lower methynobibacter and vice versa. So I think that butyrate itself seems to inhibit the growth of methynobracter. Now when it comes to other like hydrogen sulfide gas producers, it can be, I think the change in ph has to be a bit more dramatic than just upping the B joy production. So I don't think PHDG on its own seems to do much for those populations. But I have found that inulin phos, fructoligosaccharides or galactyl oligosaccharides, both from a research perspective, can decrease numbers of those hydrogen sulfide gas producers. But also clinically, I found it to do so with my patients. Too often you've got, we do dietary stuff too, so we don't say just take this and keep eating the same diet because we've got to take, ideally take away some of that food source. So with Bilophila it's often bile, It's a bile acid eater, that's what name Bilophylla comes from bile loving microbe. And its population is generally very much dependent on how much fat you eat, but also what sorts of fat too. Because certain types of fat, dairy fat in particular, when we ingest it, we have to create a different sort of bile that's much higher in sulfur and Bilophylla loves that sulfur rich bile and their populations can bloom as a consequence. So often you'll see people with higher Bilophila on a high fat dairy diets. Also you'll see it as a consequence of bile acid supplementation. So there'll be people out there who don't think they tolerate fats well when they eat it. So they say, oh, I'm going to take some bile ox bile as a supplement or bile acid supplement. And they, what they don't know is they're often feeding the Bilophylla and you can have patients go, I haven't seen this with patients where it's gone from, you know, 0.05% up to 5% of the ecosystem within just, you know, six, eight weeks on a bio acid supplement. So it just works as a preferential food source. So I would consider bio acid supplements, a bit like an anti prebiotic and selectively feeds microbes that cause you harm. That's not to say there isn't a time and place for them, but I think when they're overprescribed and someone that doesn't need extra bile, they're harmful.

Absolutely. And what I love about what you do, Jason, is that you're not only looking at the research studies, but you've also got practical experience when dealing with clients. So you're looking at, I guess, stool samples and the resulting DNA microbiome testing. You're making the adjustments required using prebiotic supplementation and then potentially retesting the client and seeing if there is an impact on these prebiotic supplementation. So that.

That's awesome.

And how about we segue now to some of the positive ones? So ones like Lactobacilli, Bifidobacter akamansia. So what, what's, what's the story there, Jason?

Yeah, well, I think most people are familiar with Lactobacilli and bifidobacteria. Those are the two classic ones that people tend to be familiar with. And there's probably a couple reasons for that. One is they were isolated from the human guts a long time ago, over 100 years ago. So we've known about them for a long time. Lactobacilli are also the predominant fermentative organism in most fermented foods. So that would be from yogurt, sauerkraut, kimchi. So a range of other indigenous ferments will generally have lactoacillis as dominant end species. And then many of our yogurts contain bifidobacteria, too, or people just call it bifidis, for example. So I think that's partly why we're so familiar with those ones. And despite the fact that looking at lactobacilli, they actually play a very small role in the gas in terms of the colonic ecosystem, you know, they're immensely important for vaginal ecosystem health. They're like the dominant species in the vagina ecosystem, but when it comes to the gut, they're often there at like, you know, between 0.01. Up to 1% would be totally normal, you know, but people expect it to be there in large amounts because it's the bug they know about. It's one that's all the supplements contains. So therefore it should be really high. And then it's like, no, it's actually a relatively small player. It doesn't mean it's not playing an important role, but it is a relatively small player. And then we've got bifidobacteria, which is a bigger player in that you'll see it in healthier ecosystems between like 2 and 5% of that, that sort of ecosystem composition. And because it's there much higher amounts, hundreds of four times bigger than active silite, it has a capacity to interact with you in a Far, far bigger way. And we know that one's very. The genus in general is important for gut integrity. You know, and I often see people, because I do, you know, intestinal permeability testing for a lot of pat that those who have leaky gut have often will have low Akkermansia and low bifidobacteria, or none show up on their testing. And it's like, okay, they're lacking two of the species or they're in such small amounts that their body has evolved in relationship with as part of their functioning role was to help heal up a damaged gut. And you can see it's gonna be much harder for that healing process to progress forward if the key cells whose role it is to do so aren't there or they're in 100th the amount of what they should be. So for me, I've often seen that relationship and on the other side of that is when we actually nourish Akkermansia, we nourish gifacteria, we bring those populations back up to a healthier state, then we get an improvement in gut integrity as well.

So how do we.

So it's always a core focus. Absolutely.

And how do we increase levels of these beneficial types of bacteria in the gut?

Yeah, so, so essentially it's feeding them. That's the core aspect. So it's working out what foods these particular species eat. When it comes to, to bifida bacteria, that's been, excuse me, it's been pretty well researched over the last, you know, 20, 30 years. But prebiotics, so we're looking at inulin, phos, inulin being a long chain, fructooligosaccharide, which means it's very long, whereas oligo fructose is probably the best term for a shorter chain fructoseaccharide. And what a lot of research does this day is it combines them together because you have some bifid bacteria that like the long chain and some that like the short chain. So if you have a combination, it means you got the best chance of feeding your individual bifidobacteria. So I think that that combination of oligarch enriched inulin, to use this proper terminology, which is very important wordy, but I'll use it, is a fantastic prebiotic that works very well for picking up bifidobacteria quite broadly and Akkermansia as well. The other sort of key prebiotics are lactulose. And lactulose is a indigestible disaccharide that was Originally used in infant formula ages ago to try to make it more like breast milk. So it was the first sort of prebiotic induced inoculated infant formula which never followed up well until very recently. Once again now it tends to be using conventional medicine as a laxative because in large doses you can't break it down and digest it. And if there's too much for your bacteria to eat in your gut, then it has an osmotic drawing effect, draws fluid into there and softens your stool and eases the passage of sense stool. But at the doses we tend to use, which would be minimum therapeutic dose is 1 teaspoon per day, 5 mils contains 300 grams of lactulose itself and that's the minimum therapeutic dose. At that dose you tend not to get a laxative effect, but what you do to get is a prebiotic effect. So it works very well for feeding up bifidobacteria. Quite broadly. Higher doses I find can bring up lactobacilli and they also work. It also works as a food source for Akkermansia in most patients, but not all. And for faecalobacterium in the vast majority of patients do it. Faecalobacterium is another of those species that people would be less familiar with for good reason because we've only realized it existed about 10 years ago or something like that, yet it actually can make up 25% of what's there in your gut. We just couldn't see it before. We didn't have the technology and tools to see that it existed. Where now we see it's a pivotal health promoting species. That's a key butyrate producing bacteria.

Yep, that's, that's a good works on.

That and serves inland floss I should say too can also bring up fecalobacterium. And the last prebiotic is that I'll touch out in this category is galactooligosaccharides, which we can find in some food sources like legumes. They'll contain stachyose, oraphanose, beet beetroot can also contain that compound too. And if you're eating a cup of legumes a day, for example, or more, you'll meet that sort of minimal therapeutic dose of galactyligosaccharides. Otherwise it's pretty hard to get from your diet if you're not having legumes. But you can get supplemental sources that works very well for feeding up bifidobacteria and faecalobacterium. But generally doesn't impact Akkermansia or in my experience, lactozilli.

So Aston, you mentioned short chain fatty acids and some of these short chain fatty acid producers like the Carlobacterium prenatal. So firstly, just for someone that's never heard of short chain fatty acids like butyrate, what are these compounds? What do they actually do? And maybe talk about some of the other species that are involved in production of short chain fatty acids.

Yeah, well, there's three main ones that bacteria produce in your gut and they do this essentially when they're fermenting fibers, oligosaccharides, resistant starches, even sugars, they're producing short chain fatty acids and gas as a byproduct. And the three main ones that I did briefly mention before were acetate or acetic acid. Same thing you find in vinegar. You're just allowing bacteria and you sort of create that in their own little bottle before you get by. The same thing's happening in your gut. Propionate and then butyra and butyrate is generally one of the smaller percentages in terms of output, particularly in people eating a typical western diet, because they're generally not eating much to feed those butyrate producing bacteria. So the top of that list is the Callobacterium, but then we've got other ones like Blotia, Roseburia, Subdola, Granulum, Anerostypes, Anaerotrunchus, Intestinibacter, or other species or genera, sorry, in the gut that our key butyrate producers do. And when we feed them, or we feed them resistant starches, we feed them partially hydrolyzed guar gum, we increase the output of butyrate because we're nourishing those species who produce that as a byproduct. And butyrate is an amazing substance. And I was heartened to see an article published in a mainstream neurology journal, you know, two years ago that said, you know, the best thing we can do for brain health essentially is eat more fiber. They would not have published this, you know, 10, 20 years ago, but it's amazing to see that there. And it's because of this production of butyrate and butyrate has gut healing properties which are, are really important. And maybe we'll, we'll segue there first because you're, you're colon, your, your large intestine, essentially we've evolved this relationship with, this relationship with these butyrate producing bacteria, so much so that 70% of our energy needs for our colon cells is reliant on this butyrate that's produced. If we don't produce that butyrate, we don't have the energy for those colon cells. We get inflammation and they don't function quite right. That's huge when you think about it, is that we've totally reliant upon butyrate production by these bacteria to nourish cells to function properly. And if you don't have that, you don't have cells functioning properly and a whole organ in your body, I think that's, that's pretty massive to consider. So most, when you only produce a little bit of B2, a lot of that will get sucked up by those colonocytes. Colon cells, they'll use every single drop that's produced because they need it. But when you produce more than that, you produce more than the minimum amount required for their functionality. That's when it can reach your circulation. That's when you start getting the other body wide benefits of butyrate. And those things include improving blood sugar regulation, improving insulin sensitivity, improving mitochondrial function, decreasing brain inflammation, you know, having a whole body wide sort of anti inflammatory effect. It's an amazing, amazing substance. And so I think it's pivotal that we look after those little butyrate producing factories in our gut and feed them and nourish them because they're there, happy to make butyrate for you if you feed them. And it's just an issue for most people is they're just not feeding them. And I see this time and time again when I'm doing microbiota analysis is that there's many patients that really are following dietary approaches that provide insufficient food source for those B tree producing microbes. And that means that they might be there at 5 or 10% of the overall population, whereas in other people they'll be at 50 or 60% of the population. And thinking about that again, that's huge, huge difference, huge variation in how much butyrate is produced and how much butyrate is then absorbed. Where you get all of its medicinal benefits.

So what's your thoughts? And so clearly there's a food, there's a food intervention that you use to, to increase butyrate production. What about exogenous butyrate as a supplement?

I do use it in a supplement in, in certain patients, but I usually use it as a complement to fixing up the indigenous producers. That's always in my, my core aspect is you've got them there, feed them and they'll make it for you. It's a much cheaper process. It's how we evolved. It's like, it makes more sense. But you do get patients. Do you see some of these that, that have their gut is so damaged, so inflamed that they can't tolerate even the tiniest amount of intestinal gas being produced, which means that they can't really go much more in terms of fiber or resistant starches or even with a generally well tolerated prebiotic fiber like partially hydrolyzed Gargo. And thankfully, this is a small percentage of people, but I do have some of them. And that's where endogenous or exogenous butyrate as a supplement, I think comes to play. And even potentially using. I've had patients with very severe visceral hypersensitivity in their rectum. So, you know, some patients severe enough that they had to do an enema every single night before they could go to sleep because just the sensation of fecal matter in their rectum was enough to cause pain and prevent them from falling asleep. So they have to like, empty out the rectum every night, just like in sleep, because of the nerves were so inflamed in that area that even the tiniest amount of pressure was enough to cause pain. And then you could use butyrate as an enema in that situation to try to decrease that inflation. And that's been used as a therapy tool in ulcerative colitis research too. Where, where again, that rectum area was very inflamed from the ulcera colitis. And then topical butyrate can actually help decrease that inflammation, promote healing.

Wow, that's amazing. I've never actually heard of that before. That is gold. So in terms, let's, let's segue now on. You mentioned about people suffering from digestive issues. Firstly, let's talk about. This is actually I should mention to the audience there was numerous questions put forward by our community that we're so excited to ask Jason. So I wrote a list of them down. We'll try and get through as many as we can. But someone asked about the relationship of gut dysbiosis and brain function or I guess, mental health.

Yeah, I mean, I think I've got a whole lecture on the connection between, you know, depression and, and gut dysbiosis. There's a lot of literature there. So. So even some, you know, pivotal animal experiments have shown very clearly where you can take, you know, poo from a depressed person, give it to, to a mouse and rat, and that rat will become depressed despite no change. Anything else? Just from inoculate and you can take poo from a healthy, not depressed person, give it to a rat, they don't come depressed, they're quite happy still. It's not just getting poo, you know, human bacteria that's a problem. It's that depressed person's bacteria. And it actually changed neurochemistry in the rat after getting that poo transplant. So we know there's this direct relationship there. And I do personally see that the building data set around endotoxins with anxiety and depression and Alzheimer's as being people here to keep an eye on, because it just fits ticks so many boxes. Because we're living in a day and age where our interventions like proton pump inhibitors, for example, and antibiotics often increase the relative proportion of proteobacteria in our gut breeding and dietary approach. For many people, that there's a decent amount of proteobacteria populations that are there and there's a lack of gut integrity, allowing more of this compound to get through and enter. Toxins do cause brain inflammation. They do change how your brain neurochemistry works. We shunt more of the tryptophan down a different pathway. It's not made into serotonin. We can give healthy person like you or me, give you a shot of endotoxin in our arm, we get depressed. It lasts for about six hours afterwards. This is very, very clear. So we know this occurs. And what's probably been teased out since 2006 onwards is that we actually are getting little doses of endotoxin all day, every day, and some people getting more than little. And if you're eating a dietary pattern that is one, conducive to the growth of proteobacteria and two, inhibits growth of gut healing species, you end up with this leaky gut, lots of proteobacter, lots of endotoxin, lots getting through. And that is arguably one of the drivers for these sort of depression anxiety epidemics that we're seeing.

So James is. He's got a psychology background. So James is. Any questions you want to ask around this mental health connection between gut health.

Sure, Jason, thanks. I think that's fascinating. I always had an inkling that eating certain foods would kind of create like a dip in mood or just negatively impact how I felt. But it's fascinating to hear all the science that's backing it up. So I was just wondering for our listeners, are there any types of diets in particular foods you would recommend to avoid so they don't experience these negative effects? Yeah, yeah, that's A good question, Big question. It's such a challenging area to navigate diet these days because there's so much information out there and so much conflicting information out there. So for me it's a matter of going back to what the research is saying. So you know, we know that saturated fats, whether that comes from, from dairy or from a, you know, steak or from coconut oil, we know that saturated fats increase the absorption of endotoxins. You know, they will bind to them and create a bit of a raft that facilitates their transmission through the gut into your circulation. You know that, that's clear. So I'm very cautious around the use of, of saturated fat sources and, and essentially dietary approaches that, that have a low amounts of fiber. I think those are perhaps the, the key things for me is like the amount of saturated fat you're having and the amount of fiber you're not having that are potentially very problematic because there's a few aspects of that because some of the fibers can actually bind to some of the endotoxins and help prevent them getting absorbed. But importantly, when you're eating a fiber rich diet, you're nourishing the species that actually are conducive to good gut integrity as well. And that again is going to have a sort of indirect way of limiting absorption of those compounds. And there's some fascinating research where they can give people like a McDonald's meal and look at the amount of endotoxin that hits their bloodstream before and after. And it's like, wow, there's a massive increase in endotoxin after that McDonald's meal. But if they have some high, high fiber foods with that McDonald's meal, it nearly blocks all the endotoxin from being absorbed. Even though they're still eating the crap thing. If it is lots of fiber alongside of it, that actually prevented it from occurring. So not that I'm suggesting we do that approach, I'm suggesting we do both. We avoid the crap food and eat of lots, lots of fiber and avoid things that are obvious triggers like the saturated fat. That's amazing.

So Jason, the next question we had from our community is that how does light and sleep affect the microbiome?

Yeah. So light is. I'm not that familiar with the research around light microbiota. So there's probably other people can answer question better than myself and I'll leave it to them. But certainly I'm familiar with some. The information around sleep and sleep does seem to have a lack of sleep seems to be problematic for a diversity perspective. I Think it was less than 7 hours sleep tended to diminish your microbiotic diversity. And we know that diversity is one of the key markers of a healthier ecosystem. And there's a number of animal studies I think, showing too, that chronic sweet deprivation. So less than that disrupts that ecosystem and I think leads to an increase of, you know, protein bacteria once again, which is what you don't. Don't really want. What was fascinating, one of the animal studies is they did a, you know, a crappy western diet and sleep deprivation versus a healthy diet and sleep deprivation. And the culmination was atrocious, you know, because the lack of sleep wasn't as bad as a typical western diet was. But you combine the two together, the changes were huge, substantial shifts in that ecosystem. So I think we have to consider good sleep as part of our gut management. Good gut management strategy too, undoubtedly.

I couldn't agree more. It seems like that seems to be the norm in, I guess, our western culture. Bad diet and bad sleep and too much stress.

Yeah, people get stressed, they often sleep less and eat more crap food and you get this horrible negative cycle that goes on.

It is horrible. So another buzzword that we hear a lot about is sibo. Now, Jason, what is sibo?

Well, it's small intestinal bacterial overgrowth sibo. And if you would have asked that question in the early 2000s or late 1990s, it would have been seen as a rare condition typically observed in people with Crohn's disease or some people that had part of their small bowel removed because they had chunk of their small intestine removed. It meant that there was a bit of dysfunction. There's often a bit of pocket that would form there which a bacteria would sit in and stagnate because it just wouldn't flow as per usual. But in the early to mid-2000s, an American researcher put forth this idea that, hey, this is actually more common. It may be the key driver of irritable bowel syndrome, which is, you know, quite a common gut condition. You might argue that, you know, 10 to 20% of Australians at any time point will suffer from IBS. So, you know, that was a pretty astonishing statement at that time point. And I think we find down. It's. It's probably not quite like that, but, you know, I think you suggest that 84% of people with IBS had SIBO. And I think more conservative estimates when they do more, more broad studies around the world might be 30% of people with IBS actually suffer from overgrowth of Bacteria in the small bowel. And these bacteria can come from one of two areas. One is from the oral cavity down SIBO as a consequence of proton pump inhibitor use. So those people who are taking medications for gastric reflux, for reflux disease, getting SIBO is quite common for them. I think there's a meta analysis done in, I think it's 2013, suggesting that people taking proton pump inhibitors, that whole class, had a sevenfold increased risk of developing Sibo. And essentially you think about that. You've got, I think it's 100 million bacteria per mil of saliva. You're swallowing a liter of saliva per day. So you're getting about 100 billion bacteria you're swallowing on a daily basis from your oral cavity. And normally your stomach acid is there to that kills the vast majority of those bacteria. But you take that away, you're having like, you know, that's often equivalent of like 10 probiotic capsules per day just from swallowing saliva of microbes that are, that are getting down there. So it's not surprising that SIBO has become far more common because the rate at which proton pop neighbors are being used has expanded dramatically over the last 20 years.

I'll just pause there for a sec. So I did get a question. I'll just pause you there for a sec. I did get a question from one of our community members regarding exactly the same thing you're talking about. With the large amount of bacteria in the mouth, is there a place for a mouth probiotic?

There totally is. And there are research teams developing that now and there's a few in the marketplace, mostly in North America and probably Europe. Australia's a bit behind in certain areas and this would be one of them. And most of it's been looking at gum disease and dental caries so far, which are good areas to research. But they might expand a bit more on that. I mean, I think for someone that's trying, that needs to be on a proton palm inhibitor. And I, you know, and research tells us that actually a decent proportion of people who are taking them actually don't need to be on them. So it's always worthwhile they have to check in with their provider of whether they need to still be on that medication. Maybe it was appropriate two years ago or two months ago, but it's not need it now. But those who do need to be on it, that the ingestion of a particular probiotic strain, The Lactose Reuteri DSM17938, very catchy name, also known as the Bio Gaia strain. There's a very cool study published, I think it was last year, showing that maybe even this year, but very recently anyway, in the big scheme of things, that, you know, when people took this instead of a placebo, it reduced the rate of sibo occurrence dramatically. When they had to take proton pump inhibitors, it was a dramatic decrease from taking 10 drops per day of this particular probiotic. So whereas we have research with other probiotics showing that they didn't work. So it's not like all probiotics will be helpful, but that one in particular does seem to be effective to prevent the development of sibo. So for someone that has to be in a ppi, I think that's a bit of a must.

Alongside that, we do jump around a lot in this podcast, but before we segue.

Yeah, fair enough. It's one of the, you know. Yeah, they all flow on different areas. That's fair enough.

Exactly. And before we jump into probiotics, which you perfectly segued into, I wanted to talk about something in that I find interesting that's popping onto my radar, which is helmintic therapy. So the use of whens to treat gut dysfunction. Now, what's your thoughts on that, Jason?

I think it's an interesting idea, and to be frank, I'm not totally familiar with the overall area. I'm familiar with some of the research that was done on helminths for celiac disease, for example, and the results, I think, were quite disappointing. So there might be some indications where the theoretical evidence or theoretical rationale manifests with good clinical trials as a useful treatment approach. I mean, I kind of like the thinking that we evolved. We've normally had parasites there, so maybe something is dysfunctional in our system. We don't have them anymore. I mean, I can relate to that underlying theoretical rationale for the use, but certainly when I read the research of using the American oakworm, Necator americanus, in celiac disease, it was. It was quite disappointing. It's like it caused a lot of pain and discomfort, and it slightly decreased inflammatory load after a dose of gluten. It's like, well, that's not all that helpful. Thanks very much. If it totally prevented the damage caused by gluten, then maybe it's worth it for those people who really miss their croissant or their danishes or their slice of sourdough bread. But in this case, it was just slightly limited, the damage that was caused. But certainly. But you still got a week's worth of horrible symptoms from ingesting the worms in the first place. So I don't think it was worth it. But there might be other areas where the research has, has evolved beyond that.

That I'm not familiar with and continuing on that train of thought. So let's, let's talk about parasites. Are they a real problem? Something like blasto? You know, a lot of people focus heavily on parasite elimination. What's your thoughts on that?

I think it really depends on the, the microbe in question and you know, something like giardia. Yeah, like if someone presents to my clinic with giardia, I do use these herbs and prologics, et cetera, to eradicate the bug because it does cause massive malabsorption in the small bowel, potential nutritional deficiency longer term, but certainly a lot of symptoms in the short term. And you know, so yes, I think giardia is one that you, yeah, you would get rid of, but I think you have a range of others and, and I think this is an area where clinicians are behind the times in some areas versus what the research is saying when it comes to what's like we normally have protozoa organisms in our gut. They're normal, you know, and it's only because we're using DNA that we can now see that they're there. And we're still trying to find what the normal amounts are normal species. And that's ongoing now. But I think there's a lot of those clinicians out there that go in really heavy handed to try to kill off these things that there are the research scientists out there saying this is actually normal species. And I would include things like Dientamoeba fragilis and Blastocystis hominis in those categories. So there's been a number of recent research studies that come out of Europe showing that these things are normal and they probably play pivotal roles in the healthy ecosystem. You know, some people are arguing that there are the apex predator, that they eat bacteria and if you take that apex predator out of an ecosystem there's consequences which is overgrowth of certain bacterial species, you know, and I think this is fascinating and from a research perspective and looking at an ecology perspective, it's like taking the wolves out of Yellowstone national park or taking sharks of ecosystems there are consequences and people are arguing the same thing with gut too. So I just feel, I think for those people that went way out of their way taking quadruple antibiotic cocktails inter colonically and orally to try to kill off these things that often have limited evidence of causing harm in the first place and called irrevocable damage to their bacterial components of their ecosystem as a consequence of that approach. To kill off something that may have actually been playing out a role that's keeping them healthy, which I think very few clinicians are familiar with that. More research that's come over the last couple of years looking at the role of commensal protozo organisms in the gut. Same with the microbiome too. It's like I'm not that familiar with microbiome. It's relatively new area of research. But we're supposed to have fungi in our gut. Yes, this is normal. And if you just go killing it all off, there are consequences to that. Do we know them all yet? No, just teasing out what these species are and these sort of web like effects of their interaction with other bacterial species there. So there's some, I think it was an animal study, but they gave them one of those antifungal agents and yes, it killed off and damaged and changed the microbiome quite dramatically. Some species went up, some species went down depending on what they were susceptible to. But also they'd actually change the bacterial composition indirectly because of all those sort of interactions between different species. And that was like unexpected consequence that wasn't, wasn't beneficial for these particular animal models. It would sort of cause this sort of dysbotic bacterial ecosystem to develop after taking this sort of oral antifungal. So it's, it's in a similar category in my mind of going, okay, we're in early days. We need to be aware or try to think more about the consequences of treatment to kill off all the fungi in the gut or kill off all the protozoa in our gut because we don't know whether this is a good move or not, and the long term consequences of that at this point and.

The virome as well. What's your thoughts on the virome?

I know almost nothing. It's hard keeping up to date with the bacterial ecosystem. Changes in the amount of research coming out and keeping a little bit of an eye on the microbiome and the protozoa composition are not keeping up to.

Date with the virus and the metabolite. That's the other hot area I'd say as well.

Yeah.

So, Jason, let's talk about probiotics now. This is a quite a controversial topic at the moment with the study coming out about the, from the Weisman Institute around antibiotics and also probiotics. So what's your take on, I guess, the effectiveness of probiotics? And especially after a course of antibiotics.

Yeah. And I think there's a few things to, to tease out here. And, and one, it's on my agenda to really properly critique that study because I haven't had a chance to look at every little depth of it because I, you know, see patients and teach things, take my priorities critiquing and study on something I might do in the summer on a day off. But, but I think there's a few things to be teased up. One is, is extrapolation of, of the research findings so, you know, you can look more broadly at that research field and you'll find there's a number of animal studies and finding the probiotics were helpful. Yeah. Did they get published in the same journal? Did they get worldwide media attention? No. So we're like taking one study out of context going, hey, look at this, this is what all probiotics must cause harm to the gut and it slows down normal redevelopment of the ecosystem post antibiotics. And what you can't do is say anything, bar the fact that this particular preparation used in their study is not appropriate for this task. That's all. You could not extrapolate that. You should not be able to beyond that because they only looked at one probiotic preparation. It turns out that the lactoi in there, in that specific preparation secreted compounds that inhibited growth of a number of other beneficial bacteria in the gut. Is that something all activists will do? No. So you can say this particular product should not be used post antibiotic. I would totally agree with that. You know, we know from looking at the antibiotics and probiotic literature that there's some that seem to be effective and some that don't seem to do anything. And it looks like there might be some that might be harmful to take at that time. And again, it goes into using the ones with clinical trials of efficacy for that condition. And I'm a firm, a mover or pusher for evidence based prescribing of probiotics. So use the ones with evidence showing that they work. You don't experiment on things that may not work. And this, I think, if anything is a clear example of the potential negative consequence of using one. That's no research showing it works that might actually cause harm and slow down the regeneration process because we have other studies showing that actually probiotics can speed up regeneration process post antibiotics or importantly reduce side effects and reduce overgrowth of nasty potential pathogens like Clostridge fissile. So I think it was just the conclusions were, I think far Too strong for the type of evidence that was created and how it was blown up everywhere. It was like on news sites. It was not even just people we talked about gut health. It was all these people that normally don't even know know that gut health exists. Talking about this study that all probiotics are bad who are not familiar with the area at all. It was, it was immensely frustrating.

Absolutely. And I appreciate your, your take on that on that study and hopefully we'll hear back when you do the, the full critique of the study. But what, what I wanted to delve into is there seems to be some group like broad groups of probiotics. So there seems to be your bifido lacta type probiotics, then your soil based organisms, then the yeast one. I think it's S. Puadi, you can never say it properly and E. Coli. So maybe if you could quickly talk about the difference between these different types of probiotics. In what situations would we use these probiotics? And finally, should probiotic probiotics be used symptomatically or can they be used prophylactically?

I think for certain conditions we know the use is definitely prophylactic. So I mentioned that Reuteri DSM17938 for the prevention of SIBO and someone who takes a PPI inhibitor, great clinical data on that. We know if you take it, you know L Rhypnosis gg, a specific probiotic. When you're being exposed to people who've got viral gastro, your reduce developing viral gastric will go down. So I think there's very specific instances where the right probiotic will make a big difference from preventive perspective as well as for treating certain disease conditions too. I'm just a proponent of using the right strain with the right action for the right condition. And I think that means that it's pretty hard to make. In fact it's impossible to make class specific recommendations of all Lactobacilli are good for this. All bacteria is good for this. All soil based probiotics. So I mean what does that mean? I've got soil in my yard that has a whole bunch of different species in the soil that's from Byron Bay or the soil that's from Cambodia. They have different species in it and it doesn't mean that they have anything in common besides the fact they like growing in soil in different environments. So I think we can't make broad generalizations around that either. So we can make therapeutic claims when we have trials showing that they work and have a Specific action and I think before that time, particularly with things like the soil waste providers claims and health debut. Claims and health claims came out well before there was any research or they did anything. And I think that's quite problematic. I hear you about eating more dirt and then we don't eat as much dirt as we used to. I hear that I have kids and they're out in the garden. I have an organic garden. I don't necessarily wash my veg and stuff, so I get dirt too. That's fine. But that's quite different from concentrating up and making all these claims around it before. There's good science showing that they actually have those claims just because they come from dirt. So I think we've got to be careful of making broad generalizations around categories of probiotics. I think the reality is the research tells us that these things aren't even species. It's not genera specific, it's not species specific, it's strain specific. For many applications, perhaps not all, but for many it is.

So strain. 100% agree. So strain specifically. And what's your thoughts on doses? It seems to be dose being an important factor as well.

Yeah, well, I mean I think there's been, there's a bit of pushback from prologue researchers on this because they're, they're frustrated by the commercial interests who are saying the higher the better, the higher the better. It needs to be 500 billion. Look at the research. The research tells us that most of the time a billion CFU is adequate. Look at what was used in that exact study. For that indication, I may have used a billion CFU colony forming units. So a billion organisms may have used 100 million and it worked, you know. Yes, sometimes. The research used 450 billion for VSL number three. Yes, that works. Would I use that one in lower dose and expect the same effects? No, but if our Mercif GG works at 1 billion, then all will use 1 billion. You don't have to use more than what we shown to actually work. There is some research showing that for some indications there is arguably a dose dependent effect. So let's look at Bifidaturium lactus HN019, which is a microbe that speeds up gut transit time. And there's one big study where I think they gave 1 billion versus 15 billion. And sorry, I might be a little bit off by my numbers. And the 1 billion sped up gut transit time significantly, but 15 billion sped up even more. So in that case I'd be like, yes, for my Patient to present with slow gut transit tonic constipation. I'll generally use 15 billion because that will work better. But for most strains we don't have that dose comparative data. And some strains it's been shown that there's no difference at higher doses for certain applications. So I think we have to go beyond this higher dose is better thing. And just using the right dose, the right strain and the right dose trumps any theoretical considerations around the wrong strain and high amounts.

Absolutely. Jason. I think the takeaway for me is that even for the public, they need to be working with someone that's versed in probiotics, that understands what the strains are actually doing, what sort of dosage, what sort of research study are they basing these recommendations from, rather than willy nilly buying probiotics off the shelf and, and hoping because perhaps they're not.

Yeah, because the claims on the labels don't always match what the research says. Absolutely. And it goes both ways. Even those that have great research on them don't always show that research on the label. And those that have no research on them will often make lots of claims on the label. So you can't go by what's on the label, you know, and I totally agree that working with a probiotic literate practitioner is essential if you want to get the most out of that tool. And same with prebiotics too. There's some people out there who think that prebiotics are fiber. It's just like, no, not all fibers are prebiotics. Prebiotics are selectively fermented and feed specifically on certain bacterial species. And that's immensely helpful when you're looking at an ecosystem that has a certain type of dysphotic pattern. You want to increase Faecali bacterium and Akkermansia, then you can use the right tool to do that. But it's not to say, hey, eat more fiber. And I agree they need eat more fiber probably too, but it's knowing the specifics. So I think working with people, clinicians that are, that are probiotic literate and prebiotic literate and microbiotoliterate will actually make a big difference to your gut health outcomes and broadly health outcomes. What's not being connected to a dysbiotic gut disease wise at this point in time, there's very few conditions that aren't linked to dysbiosis in the gut. So I think that you'll be well served to have someone working on that component of your overall health.

Absolutely. And Jason, I know your time is precious and we're definitely going over time, but just if you wouldn't mind, just a couple more questions and we'll wrap it up. So, just to finish off the whole prebiotic loop, we spoke in detail during the previous discussion, but is there any other prebiotics potentially aside from food sources that people could potentially consider?

The ones I highlighted were the cholat oligosaccharides or fructaligosaccharides, lactulose partially hydrolyzed gorgon. I mean, I think those would make the bulk that I use in my practice and have the best data set for definitely meeting the criteria. You do get other things like acacia fiber for example, that's got a couple of studies showing a bifidogenic quality, which means capacity to enhance bifidobacteria populations. And I think there's a room for that particular supplement because it tends to be well tolerated by by those subjects who can't tolerate much gas production. Whereas inulin false lactoids tend to be pretty gassy. Gauss less so, but acacia tummy fiber less so again, but it only feeds bifidobacteria. So I haven't seen it make any changes either from a research perspective or in patients from a Faecalobacterium or Akkermania perspective. Whereas something like Neal and Phos will do all three of those ones, which is very cool. So that would be also in my list of therapeutic prebiotics to use. And then the rest is working with dietary components of things like polyphenol rich foods and foods that contain those prebiotic compounds. And then resistant starch containing foods would be the core tools I would use to shift someone's ecosystem. And you can shift it hugely, dramatically within a short period of time by cutting out certain foods, increasing intake of certain foods, increasing prebiotics, and you can make massive shifts quickly.

How about digestive enzymes? Is that something you use in your practice?

I use them mostly in celiac disease patients actually, and not that much outside that occasionally, but celiac disease patients, because even when their small intestine is normal, quotation marks after, you know, the CELAC is mostly cleared up, seems to be healed up, looks normal on an endoscopy, they still will have lower brush border enzyme function. So digestive enzymes on those little, you know, villi in the small bowel will always be hampered in celiac patients. So having extra digestive support I think is essential for that population. And that would be long term, like forever. But I don't use them hugely in.

Practice outside that Hydrochloric acid.

I think it is over prescribed and I think it's to do with a extremely unsubstantiated theory. When you look at the research data that reflux disease is caused by hypochondria and this is a project, I have my group of students in the US do a research search on the data around low hydrochloric acid being common in GERD patients. So reflux of these patients and their task is to find any research study that actually finds that's the case. And every single year they come back saying we couldn't find anything. The medical literature says that people with GERD have normal levels of gastric acid or relatively higher than healthy control, not less. So I think there's a, in that functional medicine community, there's a lot of misunderstanding around the prevalence of hypocardia, which means it's often over overused as a tool. And I have had occasions where it's actually caused not only just worsening pain, but actually ulcerations of people esophagus as well, when they were taking it, when they did not need to be taking it because I read on a blog that they should be taking it. So I'm cautious around its use because you can't rely on the fact it doesn't cause you burning pain, that it's not causing you damage. That's one thing is clear from the reflux literature that you can have severely ulcerated esophageal mucosa but no pain. And you have people that have pain and have, have very little damage. They're not, no apparent damage to their esophageal mucosa. So we can't just rely on the lack of pain that is not causing you tissue damage. So that doesn't mean I never use them, but I almost never use hydrochloric acid.

So a couple of final rapid fire questions for you, Jason. What's exciting you at the moment in terms of the research gut health? What's the first thing that comes to mind?

I just think the link between the microbiota and everything, it's a very broad, exciting area, but I do find it, it just, it goes back to, you know, I'm a naturopathic clinician and we've talked about the importance of gut health and there's naturopaths talking about, you know, optimizing gut bacteria back in the early 1900s, you know, so that's an older concept for us. And speaking of naturopaths who were trained in the 80s, that was part of their training talking about dysbiosis and gut bacteria. And we didn't necessarily have the right, the best knowledge of what tools to use as we do now, but it's always been part of that thinking of that gut is the root of ill health. And if that's functioning right and the ecosystem is not that healthy, there are consequences. And I think, I just love the fact that that's being shown so clearly in the research that's come out of the last 15, 20 years and continuing to code every single day.

Absolutely. It's such an exciting time for people, people in the space with an interest in gut health. Yeah. And if you could, you know, for our listeners, if there's one thing that they could do to improve their gut health, if you could just pick the one thing, what would it be?

Eat more colorful plant foods.

Great. I love that. I love that. That's a great way to, to end this amazing discussion. Jason, I am so, so grateful for you giving up your time to spend this morning with us to record the podcast. And I will link to you in the show notes if people want to connect with you. Do you want to quickly maybe let people know how to connect if they want to connect?

Yeah. So I've got a website called the Probiotic Advisor that is all about evidence based prescribing of probiotics. It's geared mostly for clinicians, but I do have a teaching course online course portal too that's connected to that, that we've got courses for the general public about microbiome health and for. For practitioners to. To upskill in the. The ever expanding, challenging area to navigate that is gut microbiota health.

Absolutely. Jason, thank you so much and you have yourself a great day.

Ah, you're welcome. It's great chatting actually. I got totally into it in now feeling a bit sick. It was all good. Awesome.

Thanks Jason.

Thank you.