Probiotics, Gut Health and Autoimmunity with Dr. Jason Hawrelak

You.

Well, sometimes you have guests on the show that you look forward to for many weeks in advance and today is a great example of that Inside Patterson program support. We've had more than a few people recommend that I get today's guest on the podcast. He's an expert when it comes to the microbiome, probiotics and everything to do with gut health. And his clinic has been set up to treat people with these kind of intestinal disorders. His name is Dr. Jason Horlack and he's the head of research at ProbioticAdvisor.com his passion for gastrointestinal health and the GIT microbiota and probiotics was ignited during the final year of his undergraduate training and subsequently Dr. Horolak did his first class honors degree and PhD degrees in the area of the gastrointestinal microbiota, irritable bowel syndrome and the clinical applications of pre and probiotics. He has written extensively in the medical literature on these topics, including 16 textbook chapters and his research has been cited over 900 times. So thank you Dr. Horolak for joining us today.

Ah, you're very welcome. It's a pleasure to be here. Clint.

This topic is so massive, you know, it's one of these things where I would love to be next to you on an airplane between here and Perth and have five hours to talk about this stuff with you and I could.

Speak about it for five hours straight without much gap. Definitely.

And in fact this is how your suggestions as a guest has come about quite frequently is because my clients have attended your seminars and have gained so much out of your seminars where you present on this topic.

Great. That's lovely to hear actually.

Yes. And the feedback has been wonderful and they've wanted to have you share to to a greater audience. So first of all, how did you become so passionate about gut health?

Good question. And unlike many people, it wasn't because my own personal health issues were gut related. In fact, mine aren't. My gut's one of my strong systems, my lungs are arguably my weakest system. But essentially I had a lecturer in my final year on naturopathy training in fourth year gave a lecture around increased intestinal permeability and dysbiosis, which were constants, widely discussed by Natural paths probably for 15, 20 years even prior to that, but weren't widely discussed in the broader medical community. And the lecture was just inspiring to me of going this is something I want to delve into more because he was just really talking about the fact that we're just at the tip of the iceberg and we need people to delve in a bit deeper. And I was like, yes, please, yes, please, I'll put my hand up. I want to be one of those people. So I approached him right afterwards and said, hey, I'm very keen on doing my honors research in this area. And then that flowed straight onto my PhD as well. So. And it just was like a perfect match from my perspective in terms of once I started delving into the research, this was like, this is what I want to do is what I want to be doing. And 19 years on, 19 years plus on, I still find great enjoyment from reading papers on intestinal permeability and gut microbiota and probiotics and prebiotics and ways we can alter that gut ecosystem. And it's just been phenomenal to watch the rise of this field from being much more fringe going back 20 years ago to now, where it's widely talked about by mainstream media, for example, and on mainstream television networks having shows talking about it. So it's been amazing to see that sort of meteoric rise over that time period.

Yes, just in the time period that I've been paying attention to such things. I got diagnosed with RA in 2006, and in that year I think I saw a bunch of different naturopaths and, and one of them talked about leaky gut and so forth, and, and it was the first sort of, you know, exposure I had to that concept. And then as I read, you know, some scientific papers, certainly not the extent that you do, but just as a, as a layman just reading some of these things, I've noticed that it's become more and more acceptable and mentioned in, in some of the first tier, like the very highest level medical journals that, that is behind autoimmunity. So we've gone beyond the fringe, as you said, and into mainstream.

Yeah, hugely so. But it's still fascinating because you still get patients who. Or I still hear sort of some medical commentators brought out on TV occasionally, like, oh, there's no such thing as leaky gut. Have you not read papers in the last 20 years? Like, you could say that 20 years ago. And I could say, yeah, you'd have to search in the literature to find it. Whereas now, with a link between obesity, type 2 diabetes, autoimmune diseases, to name just a few, and gut increased permeability, the data is so there and so widely published that it's hard to see people now, you see it as putting their heads in the sand and trying not to look for information. Yeah, because you're right, it's there and it's there in mainstream journals and high impact mainstream journals.

How do you implement what you've learned over all this, all these years into your clinical practice? And how do you help people?

Yeah, I mean, it's been. I can think back of how I practice 15, 18, 19 years ago, and it's like things evolve as they should. And I suppose for me though, looking after the microbiota has always been a core concern of my practice and looking after gut integrity. And I think as research has evolved and my clinical experience has broadened and I've gotten a lot more experience, obviously as time progresses and technology that we have access to as clinicians has evolved as well, has meant that the way we treat now is somewhat different than before. But I still see the maintenance of good gut integrity as being pivotal to good health and I see the maintenance of a healthy microbiome as being pivotal to good health. And I think what's really changed is we just have more data on how to achieve that now, particularly in the realms of microbiota alteration. And importantly, I myself as a clinician have access to tools to assess the microbiota in much greater detail than I would have 10 or 15 years ago. The tools that we had were far more crude. We do a stool analysis that would tell you about six different gut species, six out of the 160 or something you might have. But that was the best we had access to back in the day. Whereas now we have tests that can tell us about the entire bacterial composition of that ecosystem. Many of those species, we actually don't know what they do because they've just recently been discovered. And we can say, hey, these things exist. We didn't know they existed before because our technology has improved. It's going to take another 10 years before we tease out what some of them do. Or 15 years. I think whilst we've come a long way, there's still a long way to go. Sure. But because we do have a greater capacity to look at that ecosystem now, it means that we can. Researchers can see the impact of interventions from a dietary perspective, lifestyle perspective, you know, prebiotics, probiotics, et cetera on that ecosystem and even things like her medicines. And then also as a clinician, I can see firsthand, you know, after treating, you know, hundreds of patients, looking at microbiota pre and post, you start seeing patterns and you start seeing what works well, what's been brought from the, you know, clinical trial realm into the clinical practice realm successfully. And what things don't translate that well.

And are the tests though, are the sort of the sample still stools that are being used. And it's just the way the stools are being interpreted that provides the more detailed information.

Yeah, yeah. The old technology that essentially went from the late 1800s to late 1900s was culturing where you would take the poo sample and you'd spread it into a petri dish with some growth media and you'd look to see what would grow. It's essentially it. And you try growing in different types of media and different environments, some with oxygen, some without. And then we'd expose it to different chemicals and we would see what it looked like, what it smelled like, what it did. And then you classify it as a Bacteroides or an E. Coli or something along some sort of species based on those characteristics. It's a very time consuming process for one. But most importantly, from probably the early 2000s onwards, we realized quite clearly that technique was insufficient to see most of what was there. And some research came out suggesting that maybe we can culture 30% of the species that are present somewhat gut, at most 30%. So we're missing it. And some people argue it's even 90% of what species are present in people's guts. We couldn't actually grow using that old technology. So when we started shifting to using a technique called 16S RRNA, essentially using a bit of fragment of DNA that all bacteria share, but it's unique to that genus. So Bacteroides will have a different barcode to Bifidobacteria, which have a different barcode to Escherichia, for example. And we just looked at the amount of that barcode in someone's stool and we can work out, okay, well, bacteroides makes up 30% of that person's ecosystem, bifidobacteria 15%. And then we also see that there's a whole bunch of barcodes that match no known species that we've been able to grow before. So some of these have been named, some haven't been named, but. And we're still teasing out what characteristics they have and what roles they play in the gut. But it was that change of technology that allowed us to really see what was going on in much greater depth, because previous studies, and I can think of a study in hemorrhoid arthritis specifically that I think illustrate this well. And you probably was familiar with the research that was using fasting and raw food vegan diets for improvement of RA. And I think it was in the early 2000s. Some of the research teams up in Nordic nations where this was a common sort of, well, somewhat common way of, of treating ra, decided, okay, maybe they're just changing the microbiota. So let's look. And they use culturing. And they couldn't see a difference from taking people from a typical Western diet to raw food, vegan, with lots of fermented foods. And they said, wow, we can't actually see a difference here using these traditional techniques, culturing. But they did a novel technique which was looking at, I think it was fatty acid profile in the bacterial. Well, and with that technique, they said there was massive differences between them and essentially said that this dietary approach completely changed these people's quality of life and symptom profiles, et cetera. And it looks like it changes the ecosystem, but not with the techniques that are commonly used. We need to develop new techniques to see what was there. And that's really what rolled off from the early 2000s. And now we know that those sort of dietary approaches can make a dramatic shift in someone's ecosystem and that the data from the 1960s and 70s looking at dietary interventions and impacting the microbiota was just too crude. The tools we were using to actually make and see what was going on.

Well, that's very enlightening that we have these tools now. And the challenge that we have as patients is once we go to a clinic such as Eubiome, just to mention one that I've used personally, is the interpretation of it. I mean, you get the results and it's just mind blowing. It gives you all of these very difficult to pronounce bacterial strains. And it shows you a comparison between what your stool composition looks like to all the other folks who have a healthy, apparently healthy lifestyle. And it's very hard to interpret what to do with those. So in your clinic, what do you see between a relationship between someone who's, say, has Crohn's disease? And of course, I want everyone to appreciate that when we have a bowel disorder, an intestinal disorder, you know, with rheumatoid arthritis, these are the same sort of internal problems that we suffer. So if we learn from Crohn's, we learn from other similar health challenges, then it can be implemented into a case of rheumatoid arthritis or psoriatic arthritis or so on. So what do you see in terms of the, say, severity of symptoms and the link between people's microbiome? And is there any pattern that's always showing up that you've learned that is a red flag in terms of their bacterial balance.

I would think for many conditions. And in my practice it's very much git based. So I see Crohn's ulcerative colitis, ibs, small intestinal bacterial overgrowth, peptic alter disease. They would celiac disease, fructose intolerance, lactose. So they would make up the bulk, bulk of who I would see in practice. And we know from there is some commonalities that I think would run through a lot of those. And maybe with the odd exception like celiac, where low levels of butyrate producing bacteria is a pattern that tends to run through those disease states and often high levels of hydrogen sulfide gas producers would be another group of bacteria that would, that pattern would run through Crohn's ulcerative colitis, irritable bowel syndrome as well, for example.

Right. Okay, now if we just try and relate that information onto what most of us appreciate on a simple level, which is that we kind of have good bacteria in so verticommas and bad bacteria. So, and we read on probiotic bottles when we buy them that something is a Lactobacillus acidophilus or Lactobacillus X, Y and Z. So how does that footprint of knowledge match with what you've just said? How can we correlate that?

Not so much, because the probiotics that we have access to are generally based on, on two different genera, Lactobacillus and Bifidobacterium. And that's perhaps a bit of a quirk of fate in terms of what we was isolated, you know, fifty hundred years ago from people's guts and in fermented foods, that we sort of stuck with those two genera despite the fact that they are important but relatively small players in the overall gut ecosystem versus something like your butyrate producing bacteria and many people. And it's a healthy population to make up 40, 50, 60% of what's there. Whereas Lactobacilli in a healthy person is 0.01% of what's there.

Which is fascinating if I may jump in, because so many of my clients, including myself on one of my ubiome tests showed that I had no Lactobacillus and it was quite concerning to those individuals and also raised my own eyebrows. So what you're saying is that that's not at all uncommon.

Well, you're right, it's not that uncommon. I mean, I can say that clinically by putting lots of effort back we can general bring that in majority of patients who have apparently no lactobacilli, we can bring it back with targeted feeding, which is different than trying to supplement your way around it, because there are problems with that, which we'll probably get a chance to touch on. But if we focus on feeding up your indigenous populations by selectively using the right prebiotics, for example, and the right sort of dietary approaches, that we can often bring species that are apparently extinct, like Bifidobacter genus, that apparently extinct like Lactobacilli or Bifidobacteria, back up to healthy populations, thankfully. But there would be about 20% of patients I can see clinically from my practice where they are truly extinct from that ecosystem.

And if they're truly extinct, then before I ask you some of these dietary interventions which everyone's desperate to hear now, is it then possible to restore them without that seed of, you know, like if the earth suddenly got flattened by nuclear warfare and there were no humans left, like, how do we then, do we need two humans to then recreate the population?

Well, yeah, so that that person is extinct of Lactobacilli, for example, that taking, eating some sauerkraut or kimchi or yogurt or taking a probiotic supplement won't permanently colonize. And I think we've probably got 40 years of research showing this clearly that in the vast, vast majority of cases, these probiotic strains are very transient visitors. There's the odd exception to that of 1 out of 100 studies that show that one particular strain can colonize for a period of time. Most stick around for a few days at best, or a couple of weeks at best. And you can see their population diminishes every single day. So that is temporary there. So that means we can't do it that way. And there's certainly the capacity potentially reseeding with a fecal transplant, for example. And there are certainly these days the rationale for FMTs or fecal microbial transplants has increased pretty dramatically from where it was 10 or 15 years ago. And there's a lot more patients that I see that have actually done FMTs these days too, as a way of trying to restore diversity back to a very damaged ecosystem, as well as to treat specific disease states like cluster dods difficile infection.

So what if we were to do a combination of eating. Well, you mentioned that the probiotics are transient. So if we, if we take one of these off the counter supplements that we can go and buy from our local health food store and we take this supplement. It's what you're saying is that we know from the studies that over the period of say a week or two, whatever we took is no longer inside our body. It doesn't pollinate, it doesn't stay with us.

Exactly.

The argument I've heard against that just colloquially is that, yes, but it takes up some of the so called real estate or area, therefore helping to minimize the impact of other so called bad bacteria in that space. That's one question. And the other question. So if you could comment on that and also comment on whether or not if doing that and supplementing like we do and then adding foods that are rich in prebiotic, which we'll talk about in a sec, can that maybe provide the spark and also the fuel for it then to colonize? Maybe.

Yeah. So I'll answer that second question first because it's fresh from my mind. No, it's a lovely idea and they've researched it. The particle is called symbiotics, where you combine the right probiotic with the right prebiotic. And there's still very good data showing that when we do this, and we know that this lactose cassii serota, for example, is one particular strain of probiotic bacteria that's commonly found in those Yakult milk drinks all around.

Yeah, the Japanese Yakults.

Yeah, yeah, that's right. So they know that this particular bug likes eating galactoligosaccharides, which is this hyper prebiotic. So they combined the two and said maybe this will mean it will stay around in the gut for longer. It didn't, didn't make any real difference. And there's a couple other studies showing that it didn't really enhance the duration of time at which they colonized. Now it doesn't. I mean, you can still play with that and it may well give it a bit of a boost of population, which is not a bad thing for that first little bit. Maybe you make it stick around for a little bit longer than before, but it's not enough to make it permanently stick, sadly. I wish it was as simple as that.

Yes. Wouldn't that be great?

Yeah, it would. Going back to the original question, I mean, I prescribe probiotics a lot in my clinical practice, but not because they're permanently colonizing their gut. There's, there's a whole wide range of reasons to take probiotics. And when you start looking into the probiotic science more, you realize that they're not just, you know, placeholders, that, that some specific strains can release compounds that help heal up a damaged gut. You know, that's a, that's a great trait to have. And they don't permanently stay there, but whilst you take them, they will have, they'll secrete that compound which is, which is helpful for speeding up healing. Others will have a direct anti inflammatory effect. Others can, can bind to viral pathogens, for example, and prevent that viral pathogen from causing your gut damage and getting diarrhea. Great reason to take it. And then we have those situations like antibiotics or chemotherapy or radiotherapy where you have a pretty, you're taking agent that causes a pretty great ecological change to that ecosystem in your gut and there's lots of vacant space, in which case when you take a probiotic at that time they will take up those carp. I always use the analogy of the car parking lot that when it's full there's no room for sort of pathogens to grow into or for pathogens to ingest. To find a parking spot, they just have to go out the other end, go in no place to park, they go out. Whereas after antibiotics or chemo you get lots of carp. Parking spots become available and it's easy for those that have survived the onslaught of the chemicals who have resistance to that agent to grow into that space. But it's also possible that you ingest some microbes that normally wouldn't be a problem. But when your ecosystem is that disturbed, there's lots of food and space available for it. And that is a great argument for taking probiotics at, at those, during those sort of interventions and then certainly afterwards to help take up the space and take and compete for food with potential pathogens and certainly use probiotics that way too.

Yeah, that's fascinating. I love that car park analogy. I'll use that one in the future. I'm wondering which way we can go here. I want to talk about foods, of course, and we can spend some time with that. I also want to explore the actual physical mechanics of what these car parks look like and where these gut bacteria actually live inside the body. So why don't we save the food stuff for a little later. Let's talk about the mechanics of taking probiotics and their journey from our mouth to where they're going to end up. So what does that look like?

Yeah, well, it's interesting because I think we now know that even salivary amylase, our digestive enzymes, may actually have the capacity to decrease the growth of some probiotic bacteria that we may have ingested. So that's the first hurdle they have to overcome. And then we have gastric acid or stomach acid, which is probably the biggest hurdle of all. And these days most of the, well, the better probiotic brands, supplements contain strains that can actually tolerate gastric acid. Well, they've been selected on that, they've been trialed and tested. Yeah, they can jump that hurdle. They can survive stomach acid. Well, so they have that aspect and they reach the small intestine and then they have to deal with bile and they have to deal with intestinal digestive secretions. And again, some don't tolerate those well. Some, like most yogurt producing bacteria, for example, explode when they hit the bile in your small intestine. So they're not alive from that point. But again, well thought through and well researched probiotics actually will tolerate those conditions and then potentially have an interaction with other components of the microbiota in the small bowel and large bowel, or with immune cells in your small and large bowel as well.

My, my observation of the literature tells me that most of our bacteria should be in the colon and we have a sort of a, almost a small percentage of our bacteria living in the small intestine. First of all, if you could clarify that and also talk about what happens in the case of small intestinal bacterial overgrowth and why that's such a bad thing.

Yeah, you're pretty spot on that. If you look at the bacterial counts in the stomach are 10 to 100 bacteria per mil of fluid because stomach acid's very good at killing microbes in general. But in the small bowel you're looking at normal levels are 1000 bacteria per mil or less for the first bit of the small bowel. And as we make our way down through, I think it's nine meters in length, that small bowel. It's amazing to think it's all wrapped up in your gut. Towards the end of that, it gets up to about 100 million bacteria per mil. And then you've got that valve which separates the small intestine from the large intestine. You hop over and it's all of sudden 10 to the 11, from 10 to the 8 to 10 to the 11. So it's 1000 fold more bacteria per mil of content. So you're right, the client ecosystem is far more densely populated and a far wider variety of microbe species present. But you do get people where through potentially can be things like surgery where they've removed that valve, for example, or another common cause would be people taking proton pump inhibitors. The class of Medications used to treat reflux disease, where they're essentially stopping the stomach acid from doing its thing, where the small bowel can be overpopulated by bacteria. And then some people having a smaller amount of bugs won't actually make a difference to their quality of life. They won't even notice it. But you'll find other people where, where if, particularly if it's in that first small bit of your small bowel, it can severely disrupt your nutritional status as well because the bacteria are eating your, your food before you do. So you can end up with things like iron deficiency. And I'm sure they, they grab zinc as well, but certainly iron is well noted. And they will eat things like the fructose and lactose and you know, you'll get very obvious symptoms and even glucose in that case too. So if you ate like I wouldn't want you to eat it, but if you had a Danish pastry or something like that, you would get symptoms about half an hour afterwards of bloating, distension, increased gas, for example, and potentially pain and diarrhea. And that can happen in the small intestinal bacteria overgrowth from having cherries and mangoes and healthy foods too because essentially the bacteria are in that bit of your small intestine where you would normally absorb that fructose, for example, that's in those other foods, but it's not being absorbed, it's being eaten by the microbes who produce gas. And then you get a range of, of symptoms as a consequence of that.

I've definitely got some clients who, who suggest that it's. They get a lot of bloating and challenges. That sounds like sibo. And is there some, just some really simple tests they can do? Is there a breath test that I think I've heard of and what should they do about it? Just a couple of sort of no brainer things that they should do about that.

I'm not sure about the no brainer actually. It's a tricky thing. It sounds bacteria growing in your small bowel. It's like not that, not that straightforward. Yeah, I think breath testing is very helpful to help determine. I mean you can get some of this data from good questioning as well surely about looking at timing of things. Okay, when you eat an apple, do you get symptoms in 20 minutes, 40 minutes versus 2 hours, an hour and a half, 2 hours afterwards you can say, clearly say it's colonic or large bowel fermentation, whereas before that time you would argue small bowel. And I think that's a good general rule. But I do think doing breast testing is very worthwhile to definitively see what's going on. And for me, I would do, my typical approach would be a triple sugar test where they would do glucose. These would be at separate times, I should point out too, but they would do glucose, they would do fructose, and then they would do lactulose on different days. And essentially after they ingest those sugars, if your listeners aren't familiar with the technique, but they essentially breathe into these bags every 15 to 20 minutes to collect their gas, gas levels. And what we're looking for is bacterially produced gases, and that would be generally hydrogen or methane currently. And we don't produce hydrogen or methane. Human cells don't, but your gut bacteria do. And we're looking at whether you produce it and at what time point you produce it. So lactulose, for example, is a good control sugar in that nearly everybody will produce hydrogen or methane from taking lactulose. But for most of us, it would be you. To give it to 50 healthy general people, it would be from the 90 minute mark onwards, whereas in the colon, but if it happens at the 40 minute mark or 60 minute mark, then you're like, okay, that small bowel, and certainly with fructose, you shouldn't be producing any gas at all for ingestion of fructose or glucose, they should be well absorbed into your system. And if you produce gases, that generally tells you that there's a problem there. Although with fructose it can be either a small bowel issue where you get this big spike in gases at the early minutes, 20 or 40, 60 minutes, for example, or in the more classic case of fructose intolerance, it would actually happen in the colon, which wouldn't be sibo, but if it happens in the early time points, it would be sibo. And same with glucose. You should always absorb glucose, fine, you should not have any increase in gas. But if you get a bit spike, then you know it's actually bacteria eating it in the small intestine to blame.

I love it.

And from that we get to look at hydrogen, whether you're a hydrogen producer or methane producer. And just those two simple things can actually change how we treat. And this is where doing the breath testing is, versus just basing on symptoms can give us more useful data. And for me, whether you react to lactulose, fructose or glucose tells me data that actually impact my prescribing of generally herbal antimicrobials as well. So I Find I get useful data from that.

Okay, beautiful. First of all, I love the. In some ways, the practical nature of it is that we have a finite period of time that it takes for our food to move from A to B. And using that as a guideline, we're able to find out where on the path the problem is at based on how long it takes for the gas to come breathing into this bag. Does that bag then get sealed and given to your laboratory and then the tests are run on the gas?

Exactly. So that they will then look for the amount of parts per million of hydrogen or methane or hydrogen and methane in the best labs at those points. And you also want to make sure they do that at the 15 or 20 minute time marks, not 30 or 45 minutes. You see some labs that do 60 minute time points and it's just too big, have a gap, you can't see what's going on. You could have total normal zero, then a rise and normal 60 minute, but then at 120 it's a spike up and you're like, well, yeah, what's happening between? So the best Labs will do 15 or 20 minute time points and they will allow you to do those three sugars on patients and potentially more, but at least those three.

Yeah. Okay. And then you said you treat those with antimicrobials and then what sort of expectation of success do you have once you start the patient on those?

Yeah, well, it would usually be for me a combination of things. So I would use, you know, choose the right probiotic to suit the patient in the presentation. I would use the right prebiotic in that situation and then I would use herbal antimicrobials too. And that would be tailored on whether it's methane or hydrogen dominant and whether the their bugs could eat lactulose or not. So I'd fine tune it based on those and same with some other prebiotic recommendations, might be fine tuned based on the breast test results as well. Now typically, I suppose I should say there's a few ways of approaching SIBO that perhaps there's more hardcore ways which could include antibiotics or antibiotic combinations through to more hardcore herbal agents which high potency enteric coated essential oils through to what I would, what I would see is a next level down of using herbal tinctures that have antimicrobial effects but are less likely to cause collateral damage to the colon ecosystem. So I'm wanting to be selective and it goes back to what I said before about really caring about that colonic ecosystem and doing My utmost with every intervention I'm prescribing to take into account the health of that ecosystem when I'm prescribing. So I try to choose my herbs to work more selectively, at least for my first few iterations before I pull out the bigger guns in terms of treatment. And generally they work, which is good. But it may take a little bit longer to work than taking hardcore essential oils that are enteric coated. That might work within a couple of weeks. In my experience, we usually start seeing some shifts. Sometimes it is within a week or two, which is always great for me and the patient. But I can see the median time with my approach is around the four weeks where something. The knob gets turned on. I'm not sure why it takes that long, but it's pretty consistent. That's the median time, you know, sometimes sooner, but that's the most common.

Do you think that. And now I'm pulling out my big guns of knowledge that there's some quorum sensing going on with regards to the shift of the microbiome because. Or the shift of what goes on even in the SIBO situation. And for my audience, what I'm talking about is there was a study by a lady, I can't remember, but she talked about how it took a certain amount of bacteria, I think, in a sea creature before it shifted from a certain color to another or something. Anyway, I'm not putting together much of a factual statement here, but this concept of where the bacteria are somewhat aware of their numbers around them and at some point they can then make a collective decision about a takeover or a return and so forth.

Interesting idea. Interesting concepts. Yeah. I mean, I'm not fully sure. And we're often using, as I said, it's a multi pronged approach where you have a prebiotic compound that's nourishing certain species, you've got a who then start changing the environment to one that's less conducive to the growth of potential pathogens is often the way I'm looking at it. I'm potentially using a probiotic strain that can also have selective antimicrobial activities to reduce levels of bugs we don't want present. And then the herbs are helping that too. And whether it's just. It just takes a time to get through that resistance. And certainly we know that some of the hero medicines clearly can degrade biofilm, for example, which is sort of that protective layer that pathogens may actually have or the SIBO bugs may actually have in that sort of gut layer that will Initially protect them from the antimicrobial compounds, but then as that may slowly get stripped away over time, then may allow the herbs to penetrate through and actually kill the bugs at the more core aspect of it. So that's certainly a potential scenario of what's occurring. That explains the time difference.

Okay, thank you. Now, I have a couple of clients who have been in a state of wellness, and this is not so much a question, but just to add to what you're saying as a warning who have taken for things like sibo or just for some other milder health conditions than rheumatoid arthritis symptoms. They have taken some antimicrobial anti parasitic herbals and have had consequently, symptoms of their rheumatoid arthritis come back. And so I think that you're warning about how cautious you are about the treatment of the sibo is very apt because I've had, as I said, some clients who were fairly freely taking these herbal treatments and had a negative impact on their symptoms. So just a word of caution there. You want to be getting these kind of prescriptions from someone like yourself, rather than just buying them over the counter or taking them irrationally.

Yeah, definitely. And I concur. I've certainly seen patients who's got integrity has deteriorated from taking discriminate herbal antimicrobials.

Yeah, they're powerful, aren't they?

So these days, with some of the concentration techniques we have, they are the amount of oregano, for example, that goes into making a little drop of essential oil is actually quite substantial. And if you had to grow your own oregano, distill it yourself, you would use it like gold because you'd realize how much you'd have to grow to get that small amount. And all of a sudden now we've got these intericoded capsules with tremendous amount of herbal components. And it's also a selective extract that only pulls out certain constituents. And I think I gave a talk about this just a few weeks back at a herbal medicine conference, was looking at. Okay, because we've got lots of different ways of giving a herb, from a powder to a tea, to a decoction, to tincture, to a tablet extract, to entericoted essential oil type combo. And when we only pull out the high notes were sort of leaving behind lots of other compounds that may have balanced out that impact. And we can see that like clove is a good example. Clove is a herb that does have antimicrobial activity that's in the volatile components, so the essential oil components. But it's Also extremely potent in polyphenols. And polyphenols tend to have selectively nourishing effect that they nourish sort of the more beneficial bugs in the gut, the anti inflammatory ones, but can also be antimicrobial in their own right. So when you give it as a tincture or just sort of ground up clove, you're actually getting the complete combination of compounds where if just the essential oil, you're just getting these sort of the antimicrobial bits without the other notes alongside. And I think there's greater potential of causing harm in that situation than if you're giving it as a tincture or as a powder, for example. I do enough pre and post testing with my patients to know that giving some of these same antimicrobial herbs as a tincture doesn't result in the same microbial ecosystem disruption as it does from taking the more concentrated tableted extract.

Yeah, definitely. Gotcha. Let's talk about the where these bacteria live within the colon, if you don't mind. My teachings around this in my presentations involve what I have read in the literature, which is that our mucus on the epithelium increases as we move throughout the small intestine and into the bowel, or should I say it's a single layer or there's a small amount of mucus in the small intestine, but there is a double layer and much thicker mucus inside the colon. And that that's where our bacteria live. And I'd like you to comment on that. And if that is indeed what goes on. And also I've got a theory that the drugs like prednisone, the steroids that are taken in some instances for some people with inflammatory arthritis, tend to deplete the mucus that exists on the bowel wall in the same way that when asthma patients take steroid treatments as inhalers for their asthma, it gets rid of the mucus and helps them breathe better. I believe that those drugs also deplete the mucus on our intestinal wall, thereby reducing the available space and home for bacteria to live in.

Okay.

And furthermore thereby making it hard for nutrient uptake. Because as I have become, as I understand the mucosal linings where a lot of our nutrient uptake occurs. So I just like your feedback on my understanding of these kind of concepts.

I think in terms of the broader concept of mucosal thickness, et cetera, I think that's pretty spot on. And I think you're right that for the most part bacteria are where they should be living is in that mucus or on the outer side of that mucus, ideally. And there are some species that tend to live a little bit more deeper in there. But what we don't really want is a bacteria directly interacting with, with gut cells. And that is something we see in inflammatory bowel disease like Crohn's or ulcerative colitis, is you often do have bacteria interacting directly with gut epithelial cells. And people are arguing that's part of the issue here is that you have some of these species and in those cases it might be something like E. Coli or Bacteroides that are interacting in a way that causes that sort of inflammation and causes that disrupted integrity in that localized area. There are certainly medications, and I'm not sure about prednisone specifically because I haven't specifically looked. And whether they've researched, it's another question. But there are meds that do damage the mucosal layer. And I do have some caution around. I mean, obviously there's times and places for a whole wide range of medications where they save lives and they alter completely what's going on in a beneficial way in terms of quality of life and pain, et cetera. So we have to keep that in mind too. But there are some cautions of omid that do strip away that protective lining, particularly with long term use, in terms of potentially increasing risk of a relapse of certain conditions in that case, or certainly change in the ecosystem composition as well. Because if you're altering that sort of thickness or you're actually altering the amount of food that's available for microbes and that will result in a change ecosystem.

Yes. Okay. You touched upon the Crohn's situation where the bacteria are getting in contact with the, the epithelium and interacting with the, the cells there of the gut wall. Let's now talk about leaky gut, just the mechanisms behind it where it occurs. Small intestine, large intestine or both.

Yeah, well, arguably both. But. But I would say that generally when we use the term leaky gut or increased permeability, we are talking about the small intestine. Yeah, but, but there, I think there is certainly the case of large bowel leakiness. So we need to keep that in mind. But generally when we're talking about that, that's what we're referring to.

And what are the mechanics behind it? If you could just give us a refresher. We've got some bacteria and food particles maybe passing through into our bloodstream.

Yeah, yeah. Because normally Your gut cells have this lovely intact barrier there and it just lets in certain things in certain amounts. So it's quite tightly regulated. But what can happen is if we take a medication like non steroidal anti inflammatory like ibuprofen or something like that, even continuously for a week or two is enough to cause disruptions to the gut integrity. Alcohol in more than four standard drinks is enough to cause gut gut leakiness as more acute examples. And certainly an imbalance of microbes in the gut can also result in increased gut permeability and that can be through the production of, I mentioned before, hydrogen sulfide. Hydrogen sulfide gas can cause increased gut leakiness. And another bacterial component called endotoxin or lipopolysaccharide that is found in all gram negative bacteria but but a very pro inflammatory sort of endotoxins found in a group of bacteria called Proteobacteria which can be very much overgrown in many westerners for example, and that itself can cause damage to that gut. And that leads to a couple things and you're right, it means we can start absorbing food proteins that we wouldn't otherwise do and food chemicals and that can be things like cislates and amines that weren't a problem before. And all of a sudden your gut's leaky, these things get in and all of a sudden you start reacting to these different foods, lots of healthy foods that you didn't react to before. But you're also getting bacterial compounds too, like even more lipopolysaccharide. And lipopolysaccharide is very much a driver of body wide inflammation that's now been implicated with obesity, type 2 diabetes, metabolic syndrome, Alzheimer's disease, depression, anxiety. And so essentially when the gut's leaky we get more of that compound into the bloodstream. Your liver can deal with a bit of it and then when it's constantly coming through, it can't deal with all of it, it reaches your broader circulation, then it causes inflammation and it can manifest in different ways in different people. And that's where I think genes comes into the picture as well. But certainly it's very, very pro inflammatory compound. So it's pretty common for my patients to present with a whole when I've seen people with anxiety, depression through to ulceraculitis and Crohn's and those more and celiac disease where leaky guts are definitely part of what's going on, but also that dysbiotic environment where there's too much endotoxin in the gut lumen is a common scenario in practice for what range.

Of conditions lipopolysaturitis is that? Sorry, I think you mentioned it, but just to clarify, is it a byproduct or a toxin or is it part of the bacteria itself?

It's part of the bacteria. So just like we grow fingernails and we grow hair, they grow this stuff called lipopolysaccharide. So it's not like it's secreting this compound to make us ill, but it's just that it's composed of it. And when they die, that just releases that bit into your gut. And when your gut cells are really intact, only a tiny amount that gets through and your liver will deal with it generally. But when you get your gut cells aren't so intact, you have increased permeability and, and, or you have a much higher level of endotoxin containing bacteria in your gut. A lot more gets through.

Right, yeah. Okay.

Yeah.

You mentioned before in talking about the hydrogen sulfide gas producing bacteria, but also the butyrate producing bacteria. Yeah, butyrate is a, a product that is produced by bacteria also. And we want a lot of that, don't we? Can you speak about that for us?

We sure do. We sure do. And it's one of the most marvelous substances that bacteria produce for us. We're so dependent upon it that our colon cells, our large intestinal cells, are reliant on it as a food source. Like we've evolved this complete reliance on bacterial creation of butyrate because that makes up about 70% of their energy needs are met from this. And if we don't produce enough, our colon cells don't get fed. Essentially that's a big issue. And there are people arguing that this is certainly a driver for a lot of western diseases where people tend not to feed their butyrate producing bacteria very well on a standard western diet. But certainly cases like ulcerative colitis as well, which we see being associated with western diet and lifestyle. So butyrate is, as I alluded to, the main food source or fuel source for your colonocytes, large bowel cells. And then when we produce more than they can use, then it goes into your circulation. And this is the most amazing thing because when it's in your circulation, it has a body wide anti inflammatory effect. It heals up like a damaged blood brain barrier. It actually changes how neurotransmitters are created in your brain because it decreases inflammation there, improves blood sugar control and insulin sensitivity. It's an amazing substance. The more research we do on it the more amazing we actually find it is. And here we've got these little factories in our gut, happy to make it for us if we feed them. And this is the issue because a lot of people aren't feeding these species and that means that our gut cells don't even have enough, let alone our whole body has enough of this substance that we've evolved with and we are reliant on for physiological activity.

Okay, so the million dollar question then is how do we feed them? And if that's really beneficial for our large intestine, are these butyrate producing bacteria also helping the leaky gut scenario in our small intestine?

Okay, yes. Yeah. And this is a cool thing too and is when we actually increase butyrate production in the colon, we actually speed up healing regeneration in the small intestine too. So for me, this is a big part of my leaky gut treatment is looking at, yeah, I might supplement some glutamine, other things that are the main food source for the small intestinal cells. But I have to nourish the butyrate producing bacteria because if they can increase their production of butyrate, it's going to heal up the entire small and large bowel.

It's amazing, isn't it? I mean, I can see why you're passionate about it. I don't quite get goosebumps because we haven't really touched upon something that's a life changing example where it's very emotional, but it's intellectually exciting, this stuff.

And when I read more papers about butyrate, as I said, I get even more passionate about it. And it, it's doing lots of stool assessments with microbiota assessments with patients. Some patients have got 10% butyrate producing bacteria, other people 60%, 16 or 60, they have six times as much butyrate producing bacteria in their gut. And that obviously flows on in terms of what consequences there is, because if you only have 10% of what's there, it means you're not feeding them well, they're not producing much butyrate and there's going to be flow on consequences from that which we're seeing all around us. Us in terms of the conditions associated with metabolic dysfunction, I think are very much related to this area. So how do we feed up our butyrate producing bacteria in our microbiota? It's really soluble fibers and resistant starches are probably the core aspects of things. So fiber more broadly, having as a wide variety of fiber as possible I think is certainly one of the recommendations. I do give to my patients across the board, but it's soluble fibers and resistant starches that are perhaps the biggest drivers of B production.

So can you give us examples? Obviously, we're all pretty across this, being on a plant based diet with most people who are following my program. Yeah. So soluble fiber. Yes. But I would like you just to talk about fiber a little bit more in some basic terms and give us the differences and then some examples of some resistant starches as well.

Okay. We can start with resistant starch. You'll find that resistant starches are widely found in whole grains and legumes and root vegetables as well. To give you an idea, as well as some things, like unripe bananas might be one of these sort of fruit selections that you can consume. It's made it all that pleasant. But you can take powdered green banana flour these days as a way of trying to get resistant starch in without the unpleasantness of eating the unripe banana itself. Yes, but I think it's those two groups that are sometimes avoided by people that are actually trying to look after their gut and trying to do the right thing, but inadvertently end up starving off their butyrate producing bacteria because they're not feeding them. And so we find that particularly bigger chunks of grain rather than finely milled and obviously whole grains rather than refined white will have more resistant starch. We'll also find that if it's heated and cool. So if we have cooked some, I might cook some black and brown rice. Black, brown and red rice, actually I might cook for dinner and then I'll eat it cold the next day as part of a salad. And it's going to have more resistant starch when it's cold. So the starch changes shape when it's cooked and it changes shape again. And this is called retrograde starch. And then it's resistant to our digestive enzymes, reaches the colon where it feeds the microbes that produce butyrate.

Sometimes I have listeners who take things very literally. For example, we had a guest who wrote a book called the symbiont factor. Dr. Richard Matthews, who's in the United States, who's got a great deal of knowledge around similar topic that we're talking about today. And he talked about fermenting his oats. And I still get questions all the time about how do I ferment my oats because he talked about fermenting my oats. And so just to. Just to kind of get ahead of the game here, should we be waiting on our food or should we occasionally be allowing some of our cooked foods to cool down and eat the next day or is the level of improvement only small in terms of its butyrate potential?

I would say it's pretty marked, actually. So I certainly recommend that patients do this. With pasta. It's the same if you're using whole grain, gluten free sort of pasta, the next day it's going to have more resistant starch and legumes. It's the same scenario. As well as chunky grains like rice, which probably would be similar with quinoa, but I don't think there's quite as much in quinoa. But rice is certainly a good example.

Wow. Okay. So you say whack it on a salad the next day and you're in business for your lunch.

Yeah, so I might have like a vegetable stir fry one night and then the next day I would have, I just add lots of leafy greens and some sliced up tomato and cucumber, et cetera, to make that rice in a salad dressing to make that a rice salad and have the next day. And that way I'm getting that resistant starch.

Fantastic. And in terms of quantity of resistant starch are the green bananas or the powdered green banana. So, yeah, the green banana powder. Are we going to have as much impact if we try and go down that path, if we put the green bananas in smoothies or something? Or is the biggest impact going to come from just eating our whole grains and so forth and having legumes?

Yeah, I mean, I think that's the best way of doing it. And I think it's. I'm quite fine with blending up some green banana into your smoothie too. I prefer using food as a basis when I can. And that's not to say I don't use prebiotic supplements, because I do. And frequently when I'm trying to shift that ecosystem very quickly to a healthier state and trying to revive species that are at the edge of extinction. I totally use prebiotics in that case as supplemental powders as well as they're doing the dietary work. But we're trying to maintain that healthy ecosystem with the dietary work long term.

Okay, love it. And then soluble fiber versus insoluble fiber. Little lessons.

And some people are wanting to toss out this concept because I'm not sure how, you know, but essentially soluble fiber means it mixes with water versus insulin fiber. It doesn't. That's really where the term comes from. But we know that those fibers that do sort of mix in with water that are more viscous tend to be fermented better, Whereas cellulose would be an insoluble fiber, at least in westerners these days, isn't widely fermented. It's a little bit, but not that much. Now if we gave a bolus of cellulose to some rural African tribe that hasn't had antibiotics and C sections and eaten a fiber diet for all their entire existence, they still have their cellulose degrading bacteria, so they'll still get some nutrients out of that or some clonic energy out of that, whereas we don't so much. But soluble fiber generally is fermented well and that's why it's feeding some of the butyrate producing bacteria. So the soluble fiber that we find in legumes, tofu, tempeh, for example, would be clear examples of the type that's been shown to increase P2A production in the colon.

It's interesting you mentioned legumes both in the soluble fiber category and also in the resistant starch category. Is there therefore very little surprise that legumes are the sort of the blue zones hero of longevity?

It's not that surprising when you're looking at that from a gut perspective. I know people and this always blows my mind that the vehemence against legumes in certain parts of the blogosphere currently. But when you're looking back at guns, these things have got polyphenols, so they're often like black beans and they've got the beautiful red color for adzuki beans, for example. And polyphenols feed our good gut bacteria. They contain resistant starches, they contain soluble fibers, and they contain oligosaccharides which feed our beneficial bacteria. So they might contain four or five different compounds that are nourishing the sort of beneficial anti inflammatory bacteria in our gut. So no, I'm not surprised that you're.

Saying, is there any common mistakes with, for example, legumes that people make when they eat them? Is there a problem, for example, because they're high in protein to combine them with another food source that doesn't get digested well as a combination? I guess my question is if people have beans and rice, or if they have say lentils and rice in a yellow dahl or something, are we talking about a really healthy meal there or are we making some kind of of mistake?

Really healthy meat? I would say I don't think that we have to strict about separating out proteins and starches, et cetera. It's very, very small proportion of people that makes Any differences to their quality of life? Yeah. So no, I think those are lovely so far. My Mexican beans with lots of black beans, lots of onions and garlic in there. And then I have that on my black and brown rice combo. It's like I'm nourishing my microbot in numerous ways with a meal like that.

You mentioned garlic and onion. All good.

Very good. Yeah. Because they contain oligosaccharides and they can be called inland or fructooligosaccharides, or in some terminology they call fruitans and galactans for the other sort of oligosaccharides we find in legumes, for example, or galactooligosaccharides. Yeah. So I think the biggest issue people have is when you're not used to eating them, you start eating them, you produce more gas. Yeah. And if your gut is working the way it should, you just fart more. That's it, no problem. And then that usually peaks out by day 7 or 10. Now the problem comes is if you have sibo, for example, then you get more gas, you get more pain, discomfort, bloating, distension. It's not very pleasant if you have very slow transit time in that year. What I would see, I mean, some patients I have, if they eat something and it comes out 16 hours later, other patients, it's 10 days later before it comes out, how much gas gets build up and how little of it gets expelled. If it takes 10 days for stuff to move across. So you introduce legumes into that situation, they again might bloat and distend rather than just getting more farting. So sometimes you have to do some preliminary work to make the gut capable of dealing with the increased gas production in people whose guts are very damaged, because you know they're going to be very much part of the process to keep them in good shape and to heal the gut. But they're going to cause symptoms in the. In a short here and now. So we would often, if it's on with sibo, we deal with the sibo first and then they often have colonic inflammation that we have to decrease first. That makes their gut hypersensitive to intestinal gas due to the level of inflammation that's present in the gut. So those are sometimes pre work we have to do before they can introduce more legumes. And we do. It's like take a tablespoon every second day for a few weeks and then try to open it up. The mistake you can also make is just eating a huge bullet Once a week, your gut's not going to adapt so well as if you eat a relatively small amount every couple of days and then slowly work your way up. But if you're one of those people that just gets more gassy, more farts more with legumes, then you can go in pretty quickly and just know that your system will adapt quite readily over a period of week to two weeks.

Yeah, I love that really, really slow reintroduction concept and something that I recommend as well. I'm just very pleased to hear that that's also something that you find works for your patients.

Yeah, well, these days I'm seeing some very people with very, very inflamed guts compared to where I was at five or 10 years ago. So we have to go very slow with that. And strange enough, it's not always like I often find in conditions like ulcerative colitis, people can go straight on legumes and the sort of coating cooled whole grains, for example, and it's totally fine. But then I've got patients with irritable bowel syndrome and SIBO, where it's actually really slow going. And even if when the SIBO treated, we often will have to do six months of colonic work before they can introduce much in the way of legumes.

Right, okay. I know we're sort of at our time here, but if you didn't just indulge me just for another few minutes if that would be okay. Vegetable oils, I have a particular passion against them for their pro inflammatory effect. The literature seems to be a little bit in two camps about this. One is it's high in omega 6 fatty acids, which is the inflammation pathway that gets triggered. Another is that I have a lot of studies that I've pulled together that shows that fat, in general, high fat, tends to increase intestinal permeability. Could I get you to give me your views on this? Which one is it or is it both?

Yeah, I've come across those studies to Clint that linked the high fat diet with increased gut permeability. And as we know, the current vogue is high fat. So those studies are being stuffed down and we can actually see them and not talked about much. So it's nice to have someone else actually bring them up. So I think it's a bit of both that you have. Certainly the Omega 6 content is the precursor of arachnoic acid, which is a pro inflammatory compound that our body produces under some sort of stressful scenario. So having less of that in the system's obviously good, but I Do think there's the potential of just the higher fat content, particularly, I think for me, where it's isolated away from whole foods. So I've got less issues with people eating olives, nuts, and eating avocados. No concerns there. But I do have concerns with people just dumping tablespoons of coconut oil on their. Their foods, for example, or heaps of ghee or butter or lard on their foods. I've got far more concerns around that. And there's a whole bunch of data around the impact of saturated fat in particular facilitating the absorption of endotoxins that we talked about before. And saturated fats, whether they be from dairy or even from coconut, seem to be able to bind to lipopolysaccharides or endotoxin and facilitate their absorption into the bloodstream in a way that olive oil didn't, for example, or fish oil didn't.

Wow, okay. Yeah, I'd love to see that study as well. I'd include that one in my study. That's cool. That's cool. Because I'm always looking at ways to justify the effects that we see in practice, which is that if someone goes and eats a bowl of hot chips, I mean, it's game over tomorrow. It is game over. And it's not the potatoes, it's the oil that they're cooked in. So thank you for that. I just want to wrap up with some quick questions for you. Just so these commonly frequently asked questions that we get and sort of just some brief answers from yourself.

I'll do my best, but brevity is not always my strong point.

Look, the time restraints only to respect your time. So if you're happy to give us longer answers, that's wonderful for us. I don't think there's anyone watching or listening right now saying, come on, wrap this up.

Okay, good to hear.

Can fermented foods you mentioned sauerkraut, pickles and so on. Two questions around them. Are they healthful for us to eat? And do they provide us with potentially bacteria that can become part of our own ecosystem? And is the salt an issue in them? Do you think the salt has an impact on our health negatively?

Ah, interesting that last, last point. I mean, I think it would depend on how much salt was used because I've been a fermenter for nearly 20 years, actually. So I do think that I've often made very low salt varieties, which is a pinch of salt for a big vat. So I don't always think salt is hugely essential. It depends on the takings you're using, et cetera. It just happens to be that lactobacilli that are the main origins left in most of these traditional ferments handle high salt and a lot of competing bugs don't. So you're selectively creating an environment that or you're creating an environment that selectively benefits lactobacilli because they can tolerate it and competing bugs don't. So that's part of the reason why, as well as just the food processing aspect, that salt pulls the moisture out. So when you're just chopping cabbage by hand, then the salt will do that additional job of pulling some of the moisture out. Whereas for me, I would use a one of those twin gear juicers when I used to make my version of petrol ferments and that would pull the juice and fiber, separate it out and then you put it back together and you wouldn't need much salt added to that because there's nothing new to pull out. You don't need to pull out the water. And there's always enough native lactobacilli to dominate the ecosystem anyway, because it always sour quite beautifully. So I've made some low salt ferments, so I think it's not always essential. So just keep that in mind, I suppose, with ones you buy and how much salt might be added to that. Because there's lots that I have that are not usually salty and I've had others that are add way too much salt. I'm like, oh, I'll be in a teaspoon of this. Seems like it's way too much. Whereas others I can eat half a cup and doesn't taste that salty at all. So there's that. And I think we touched on this concept before about being able to colonize your gut with bacteria from fermented foods. And it just doesn't happen. And that doesn't mean that you shouldn't eat them, enjoy them. I had lovely bits of kimchi on my breakfast this morning, for example, and it wasn't because the kimchi bugs were going to live in my gut forever after. The reason why, because I like the taste mostly more than anything else. But you also get that glycemic index when you actually have the something with the lactic acid and acetic acid we tend to find in these ferments actually lower the glycemic loading of that meal. So your blood sugar will stay far more stable after you eat a fermented food like that, or add that to your normal meal, for example. It also has a range of gut healing compounds called polyamines in sauerkraut and kimchi that speed up sort of healing and regeneration of damaged stomach cells and small intestinal cells. Another reason why. And potentially antifungal compounds, too, because the main competition for that nutrient in that ferment vessel is often yeast and molds. The lacto sili will often produce some sort of antifungal compound to keep them at bay, essentially. So we might be getting small amounts of this, which you could argue would have a beneficial effect on your gut. Just keeping, perhaps. Although I should point out that we know so little about the microbiome in terms of what's healthy, what's not, when looking at the fungal components of that ecosystem. But I think the trace amounts we find in there are probably not. Not I've always considered beneficial anyway.

Okay. Fascinating. Okay, thank you. Shelf stable probiotics are now really popular versus the more sort of original style, which is everything needed to be refrigerated. I've come to understand that it's just the technology that's used, and the manufacturer guarantees the numbers on the bottle right till the expiration date. Do you have any? Well, I'm sure you do. What's the official take on the shelf stable versus refrigerated?

Yeah, and it very much depends on the strain, the bacteria that were used. And I mentioned that obstacle course with probiotics that was used, and one of the obstacles or hurdles they have to jump is shelf stability at room temperature. So newer ones often will tick the boxes because they were chosen to be developed into a commercial product because it has shelf stability.

Right. Which isn't the best motivator?

Well, typically. Well, it's usually not the only one, thankfully. So these days, they would look at gastric acid stability, bile salt stability, whether it adheres temporarily, how it adheres, whether it produces a compound that is selectively antimicrobial to kill off potential pathogens or pathobions, but leave the good guys intact. And shelf stability, those would be sort of the basic criteria. And it's safe when ingested. So those would be the basic criteria. So they tick those boxes and it's like, okay, so what companies will often do is take that strain, do some animal research with it, then do human trials with it, and they go from that isolation through to a finished product. And in which case we know it's shelf stable, and we know it may well have therapeutic effects beyond just taking up car spots in the gut. But it actually may be useful for. We can look at a strain called Bifidobacterium lactase HN019 that speeds up colon transit time time significantly. So this is one that's very good for people with slow gut transit time or constipation. So that's an additional attribute it has besides just ticking all those basic boxes. It actually has therapeutic effects. And I think for me, this is one of the key things about probiotics is you choose the one that displays the actions or characteristics that you want to take or the physiology you want to change. So if I've got someone with slow gut transit time, I can give the strain that speeds that up. If I have someone with damaged small intestines or increased permeability, I can give the strain that can speed up healing of that. That, yeah, if I have someone with Helicobacter pylori causing stomach ulcers, I can give a strain that helps reduce levels of Helicobacter pylori. And not all strains do, but some certainly do. So it's really trying to match what you're trying to do with the strain that has the action at hand. And this is what 40 years of probiotic research has really told us. The best way of using probiotics is very in a targeted way. Rather than just throw, let's throw 150 billion CFU of 10 different strains at something with another strain shown to do anything. I think that's a poor way of using probiotics and you'll get poor results comparatively then if you use them selectively, going, okay, well this strain has got the exact actions that I'm after. I'll give it to you in the dose. That's got human clinical trials showing it works. And you know what, it usually works rather than guessing and experimenting with unknown.

Agents, essentially, which really explains why your clinic is doing so well, because this is hard to do as a patient if you really, you know, first of all working out what your actually situation is. And second of all, knowing how on earth you can then know what, what bacterial strain is suitable to helping that. And then how on earth are you going to find it? I mean, you go to your local, you know, Whole Foods in the US or health food store here and say, hey, I want this strain and someone's going to look at you blankly.

So sadly, yes, and that's why I developed some online, some tools to try to make this easier because for that exact scenario. So if you look at something like rheumatoid arthritis, like I think the strain with a positive study with bacillus qu Wagulan's GBI 3068 6, which is a really catchy name and easy to memorize. Not. And it has been shown to help reduce pain levels in patients with rheumatoid arthritis, for example. Yet there are other strains that there's a combination of laxmis prohibnosis GR1 and laxmusilous fermentum RC14 given to RA patients didn't improve things at all. So I think RA, like any other condition, is there's strains that. That to date have shown efficacy and those strains that have shown not to be useful. And there's a bunch of strains that have never been researched and we have no idea what they do. So for me would generally go with the ones that have clinical trials showing that they're helpful. And the challenge is, as a patient is going through the literature and working out what strain it is and where to find it. And this is also a challenge for practitioners, too. I should call that multitude of products in the market that it can be hard to take the time to adequately assess before prescribing.

Okay, when should we take our probiotics? I've read on an empty stomach and I've read right before meals and interestingly, right before meals that happen to have somewhat of a fat content in them.

Yeah, I think the data is pretty clear that we get better survival with meals with the. Right after. Yeah, your stomach acidity is far stronger. It's more acid on an empty stomach. People forget this, that the PH might be two, two and a half when it's designed just to kill any microbes that go in there. And that's what you're doing. If you just take your probiotic on an empty stomach, very strong acidity.

Suicide missions straight in.

Yeah, exactly. Whereas when your ph, when you're having a big meal, you're looking at three and a half, four or four and a half. And you have much better survival at that PH range, which is closer towards. It's not neutral, but it's more in that area than a much more acidic physical. So data is very clear. And data has shown that a bigger meal in terms of, I would say carbohydrate content is probably a whole grainy sort of thing, or legumes would actually enhance survival. And there's certainly research on dairy enhancing survival too, and something about its capacity to buffer the PH in the stomach. That means you can give a lot less bacteria in a dairy form than you could in a capsule to get the same number of bacteria, as I call it.

I keep thinking of more questions. Sorry. But I guess. Well, the comment on that is it always seems to come back to common sense. I mean if the body's not eating anything then the body would think, well at the moment I'm walking around and I'm just, I'm outside, I'm doing whatever I've been doing from a evolutionary point of view for thousands of years, millions of years. It's not likely that I right now want to take in a whole bunch of bacteria. Right. It just doesn't make sense. But then when I'm eating my food again, if we look at more primitive kind of ways of eating, we probably got some bacteria from the soil, we probably picked up, you know, bacteria from the plants that we're eating that aren't washed and so forth and most likely.

Fecal, fecal exposure from.

Right.

Because we haven't washed fertilize plants and yeah, we didn't wash our hands and we're drinking the water downstream from people that are upstream maybe wash their hands or wash the bottoms in that stream, you know. So I think yeah, there's that aspect.

So it does make sense. And do you think that as the food moves through the, through the digestive tract with that bacteria that that bacteria begins to immediately start to consume some of those resistant starches and some of that fiber on its own?

I would suggest that would be the case too is that you're actually providing some food, food for it too. And some of that's obviously going to be digested in a small, small bowel for example and absorbed. But this could still even with, with a dose of, of like glucose, which is a well absorbed sugar, a trace amount will always be malabsorbed in everybody for example, or sucrose. So in that case if there's any bacteria with that, they would have a little bit of to go along. So yes, I think that's another way of looking at it that you're providing a bit of a food package with drop off of bugs to help us.

Get through childless image of these bugs as they're going moving down like a slippery slide through the intestine, just feeding as they go, eating away. Can we overdose on probiotics?

I think based on current data we'd say that they're an immensely safe class of agent. Really reviewing some of the data for a textbook chapter I did recently, it was like looking at all the studies today looking at kids. The placebo had more side effects than the probiotic did. So I'd say for the vast majority of people, probiotics are safe. And the range that we would typically use, clinical trial perspective, is between 100 million bacteria up to probably 450 billion. So giving way above that amount? Well, we don't know, I suppose, arguably because we haven't done the research on it and certainly beyond what we would find in traditional fermented foods. So there might be a point at which there is a problem because we just don't have data. But certainly up to that point, they're mentally safe in the vast majority of people. And it doesn't mean that there aren't the occasional person that you have to be more careful with. Definitely. And be more selective with what probiotic you use. Definitely. But I think in general they're very safe class of agents.

I now want to close by finding out how people can contact you and so forth. Before we do that, do you think that this is something we've overlooked? Is there something that you find is really important to convey in these interviews you've done with other people or in your presentations?

I think we've covered most of the important aspects, I believe, and you're always limited by time. But I think just love your microbes. Microbes, nourish those microbes. Because I think that greater understanding that's coming out is that we're not just a human body with microbes there, that we actually are a superorganism that's composed of human cells and microbe cells and that makes you you. And I think so far we've put a lot of effort into killing, inadvertently causing damage to our microbe components of ourself over the last 50, 60 years, from intervention, this perspective through to the medical interventions we are using and also the diet that we're choosing to eat. And I think we just need to be more aware that we are part microbe and we need to nurture and look after those components of ourselves if we want to be optimally healthy.

Yeah. Hear, hear. Okay. Your clinic, what you do. I know you're very much in demand and it's taken us a little while to find this time slot for yourself. How can people contact your clinic or even yourself? Do you work with people who are international? I know you're based in Australia and we've got a very wide worldwide audience. People are going to be interested to talk to you and to learn more. What should they do?

A couple of things I do offer some online courses which were around microbiota. Meet your microbiome for the sort of health conscious general public which is designed to introduce you to your microbes and get you to love them and get you to learn this skills are looking after it. So I've got some online courses that you might might find valuable adjuncts to everything else that you're doing. I think that's one thing and I do, and that's@probiotic advisor.com that's my website and we do have a whole database around evidence based prescribing of probiotics. That is a subscription service mostly designed for clinicians, but we have 24 hour free access if you just want to have a look and play around a bit for that that time point. And if you take a lot of probiotics, you may well find the $49.95 annual fee to be quite fine to help guide your decision making in the area. But we do have a range of courses too that could be useful. And then my clinical practice is at Gould's Natural Medicine, which is an old natural medicine apothecary in Hobart that dates back to 1881. So I practice out of there a couple days a week as well.

Okay. All right. Well, well, thank you so much. This has just been fascinating and as you said, we're always limited by time and I wish this were a five hour plane ride, but we're going to have to let you get back to doing the great work that you do. So thank you so much for sharing everything you've done with us today, everything you've talked about. I've learned a lot and I'm really stoked that we've been able to have you on the show and be able to share this knowledge with everyone.

I'm glad to be here. Thanks for the invite, Clint.