Pre and Probiotic Use in SIBO with Dr Jason Hawrelak

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If you're like me, you're finding that treating small intestinal bacterial overgrowth can be complicated. Patients often present with a myriad of symptoms and associated conditions which require holistic thinking and a methodical approach to treatment. This podcast was born out of a desire to start a conversation with other practitioners, educators, experts and researchers and see if their insights can give us new treatment considerations, especially for our difficult cases. In this podcast series, our guests talk about functional gut disorders, hormonal issues, the enteric nervous system, food and toxins tolerances, the immune system, the microbiome, methylation and genomic issues, and everything else that can make a SIBO case very confusing. I believe that by understanding the often complex interconnection of SIBO with other disease manifestations, we can be more effective in our treatment approaches. I hope you find this podcast useful in your practice and thank you for listening.

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Welcome SIBO practitioners. Today I have with me Dr. Jason Horolak is a friend and an amazing naturopath. He is a researcher, lecturer, naturopath and nutritionist with more than 16 years clinical experience. Jason also practices at Gould's Natural Medicine, a 135-year-old natural medicine apothecary and clinic located in central Hobart, Tasmania here in Australia. He did his PhD examining the capacity of probiotics, prebiotics and herbal medicines to modify the gastrointestinal tract microbiota. Jason is currently the Senior Lecturer in Complementary and Alternative Medicines at the University of Tasmania School of Medicine where he coordinates the evidence based complementary medicine programs. He also teaches the Gastrointestinal Imbalances unit within the Masters of Science in Human Nutrition and Functional Medicine program at the University of Western States in Portland, Oregon. So a highly, highly qualified, all around amazing practitioner and researcher and teacher. So I'm so pleased to have you on the show here with us today, Jason.

Thank you for the invite, Narelle, and it's the pleasure to be connecting with you once again and to have a chance to chat about all things got.

All things got. We're nerd out for sure. So you know Jason, just for those listeners who are sort of a little unfamiliar with him, there's two things that really stand out is he gave an amazing 90 minute presentation at the SIBO Summit here in Australia on pre and probiotics which you can still get on SIBO test.com if you're interested in that topic. We will touch base of course today on the use of pre and probiotics. But to get the full frontal of everything he had to say, I think it's a really good lecture to have and to listen to. And the other thing you're doing, Jason, is this Probiotic Advisor, which is a website that, that lists the research on every probi well on researched probiotic strains which is an incredible resource for practitioners. Do you want to talk a little bit more about that?

That's essentially grown out of teaching that I've been doing for really since I started my honours and PhD. So back in 2000 when I first started delving into the pre and probiotic world, it was, you know, I certainly learned it during my naturopathic training but having it, having an opportunity to spend years delving into it was amazing. And the things that learned that process were quite amazing too. But particularly one of the biggest concepts to take on, certainly prebiotics were because that was very much neglected as part of my naturopathic training. But the strain and specificity of probiotics, it was pretty mind blowing because that wasn't touched upon, upon my naturopathic training and looking at all the research that was around then and has since grown in that area too, really shifted the way that I used probiotics from that time point as a clinician and really using evidence based prescribing of probiotics rather than industry based prescribing of probiotics, which I think that's a trap that many people fall into.

Well, I mean me As a practitioner, I was just so appreciative of a resource that it's pretty affordable at $45 a year. And you can just put in, you know, UTI or some other search terms to look for. What are the actual exact strains and where to find them and what products you can find them in in Australia and in America and I think Canada. Canada too. Yeah. So that's really helpful for anyone who wants to learn a little bit more about it. I think it's a really good place to start playing around with that. And that's prebiotic advice? No. Probiotic advisor.com right?

Yeah, it is. And it certainly grew out of word documents that I used to give to my students. And then it just became, as more evidence grew, which happened every single year, the word documents came bigger and bigger and bigger. And it just became unmanageable to have three separate documents where you're trying to read the condition and the strain and then what country you're in and try to match that with probiotic product. And that obviously changes over time. And sometimes every year new companies add new products in. So the database format made everything far simpler. And we, we've done constantly updating products. We're expanding our range of U.S. and Canadian products as we speak, as well as updating the research base.

That's great.

So it's an amazing area to be in and see how much new research is published every month, which can be quite practice changing when a particular study comes out with a niche. And I think we'll probably have a chance to talk about one of the recent studies that I've come across with probiotics that will be relevant to SIBO practitioners.

Well, let's go right into it because I can't wait. Yeah, I can't wait to hear it. Give me some new stuff. That's great.

Well, this is interesting because, you know, no one, you don't get 100% success rate with anybody with any sort of condition. So you've got your treatment approaches that usually work, and it's great when those approaches usually do work for patients, but when they don't, it obviously gives us a chance to grow as a practitioner and to delve deeper into the research and in traditional literature as well. So I think it's a bit of a, a wonderful opportunity when our initial treatments don't always work with patients because we have a chance to learn and expand our repertoire. I had one of those patients too, who was a methane predominant placebo patient who just wasn't responding to the usual treatment. Approaches. So I had the chance to re dig into the literature and see what new things were there. And I came across a 2017 study using a particular probiotic strain, Lactobacillus Reudry DSM17938.

I'm going to write that down.

Remember name. It's also known as the Biogaise strain or the MM53 strain, which are previous and also current names for that strain. It was looking at people who were, I think they CIBS patients or constipation prominent IBS patients who are high methane producers. They gave them this one probiotic strain, dose of 10 to the 8th CFU twice daily. This particular strain has been researched in a number of different conditions. At that same dose it seems effective at what we'd call lower dose than most probiotics would be 10,8 CFU twice daily. And over a period of four weeks they reassessed methane production. This is interesting because we've known for a number of years that the strain works for functional constipation and constipation patients. It certainly increases number of bowel movements over the week, for example, and softens stool. But the research team was interested to know what's the mechanism by that. Could it be working by reducing methane production? And it turns out it did. And over that four week span, I think it reduced methane output by. And the whole group by 2/3.

Oh my God.

At the end of. But importantly, at 55% of subjects, there was no methane production at the end of the trial. Or very minimal, one or two parts per. And that's all they did.

Oh my God. And what was the, what was the study size? What did you say?

That I can't remember off top of my head. The actual number, the number of subjects involved. Yeah. Okay, but it was recent study. 2017. Yes, but very.

So hopefully they're going to like, is there a probiotic that has that specific strain?

Well, that's even better than yes, because sometimes you find probiotic research. It's like, yeah, that's super exciting. But the strain's only available in Italy. Damn. But this isn't one of them. This strain you can get in Canada, US and Australia now. So you don't have to wait, you can actually utilize it.

Okay, now what is it? What is this product? Tell us.

Well, in the US and Canada, it's sold as the Biogaia probiotic. Yeah. And you can get it as an oil base. So it's actually floating around in some sunflower oil, which reduces the risk. Yeah.

Wow.

I never Heard of oil based probiotics in Australia. That same strain is available in the Blackmores. I think it's called Digestive Biobalance, which is sort of a chewable lozenge. But as of I think a few weeks ago, the Biogaia range has just come into Australia as the oil format too. So my apothecary clinic is just trying to see if we can start selling that strain in that form because there are some people where that cleanness of just floating a bit of sunflower oil is welcome rather than other binders and fillers, etc. You can get with type probiotic, which is the Blackmores one is.

Well, I'm definitely. When we're done here, I'm going to get some more specifics because that's something I'd be really excited about. As you know, for most SIBO practitioners will be probably nodding their head that sometimes with those really high methane levels, it's the toughest thing to treat for us as SIBO practitioners. And what's really interesting is that. Well before I go into the next thing, that's really interesting, but 10 to the 8th, that's that. What's that? 10, 10,100,000,000. 100,000,000. Okay. Oh yeah. So that's basically 200 million a day. Gave those effects. That's great. That's really amazing. That's pretty low.

And they've got that same strain and that same dose has been used for viral, gastro and other conditions. And it works at that condition. But I think it sort of blows. Another one of those other myths that you have to give your hundreds of billions of CFU to get an effect. It's like, no, if you use the right strain with the right action, what is needed is the therapeutic dose. You don't have to go over that. Maybe there's a greater effect with higher dose. We don't know at this point in time because no research has been done at different doses. But that dose works. Okay.

And it was this oil based formula that they used.

Yes.

Okay. Excellent. Wonderful.

From memory. From memory, my. Oh God. It's been a couple of weeks since I read this study and I've just been excited and just started trialing out on patients. So I had a chance to get much feedback from them yet. But the research itself was quite stunning.

Well, it's an invitation to practitioners listening to this, if you can get a hold of this, is to try it out with your methane dominant patients and report back to us so that we can maybe have an update down the road as to what the efficacy is of this particular probiotic. So Biogaia oil based sunflower oil and Lactobacillus reuteri, you said, Right, yeah.

Rheotide DSM17938 is the strain code. So again, the strain specificity is important. I wouldn't use any other rheotor, I would just use that one.

Yeah. I was just at a conference recently where there were several microbiome specialists like Rob Knight. It was amazing to see the research and to start to understand the complexity of microbiome research. And. And it was reiterated several times that strain specificity is really so important and that just because something says Lactobacillus plantarum doesn't mean it's the very thing that was studied for ibs, for example. Can you talk a little bit more about strain specificity?

Yeah, that's a very important point. And I think the more in depth you look at probiotics, you see that this is clearly the case, because there's a whole bunch of research teams all over the world focusing on development of new probiotic strains with therapeutic potential. So they'll sometimes comb through dozens of strains of Lactopilis plantarum to find the one that survives gastric acid, survives bile salts, attach it to the intestine mucosa and produces selective antimicrobial compounds. Sometimes they'll start off with many dozen strains to find the one that essentially goes through the obstacle course and wins and comes out, and then they can start doing animal studies and other studies to make sure it actually has some type of therapeutic effect before bringing through to human trials. So there's a lot of work being done there with all different species. I can take another one of Lactobis fermentum from some traditional food ferments and start off with a couple hundred strains, but in the end there's only a half dozen that actually meet all the criteria. So it's not that all strains within the same species are the same. They're not. They obviously have certain qualities in common, enough genes turned on to make them similar enough to be considered the same species. But the differences in genes, which ones are on and which ones are off, I think is striking and perhaps sort of negative illustration of that is with E. Coli, where you can get the NSSLA 1917 strain, which is used as a probiotic enhancement since the 1920s in Germany, which we used to treat bloody diarrhea and ulcerative colitis, for example, and then you can have the same species, E. Coli. It's the EO157 strain which causes bloody diarrhea, kidney failure and death. All the difference is a few genes turned off and on that can make the difference between a strain that can be helpful and one that's actually harmful. Now, we don't tend to have that extreme condition with bugs within the Lactobacilli or Bifidobacteria genera, but you do have different genes turned off or on, which means that someone would be much more capable of having and producing a therapeutic effect versus others. And it's great to be here. That information was talked about in that conference because as someone who's been espousing hatfirst for 16 years, it's nice to find it gaining traction after that time, because there's been some resistance amongst some in industry to that idea getting out there, which has been hard to overcome, whereas others in industry have embraced it and gone, ah, we can actually have a product that we know works. We can put claims on there based on evidence itself, rather than extrapolate evidence from other people's research on their strains.

Yeah. And that even, like I said, even with strains that have. Like you just talked about in terms of. They have the same name, but if it's V299 versus, what is it, 39, they have totally different actions, these probiotic strains. He. Actually, one of them was.

You can't assume they do the same.

Yeah. So, yeah, I'll talk a little bit more, maybe a little bit later, about that conference. It was really good. Particular aspects were really good of that Microbiome conference. But so moving forward with. As naturopaths especially, and this is always something where I sort of pause and appreciate how far we've come as naturopathic practitioners and just seeing how much the research now substantiates what we've talked about for, you know, many hundreds of years, it seems, and. But now we really have the science to back up some of these things that we've known for a very long time. And one of those old concepts, however, was this idea that you see sort of reseed the gut with probiotics, which now really is an outdated concept. Can you talk a bit more about that?

Yeah, yeah. I think it's a very worthwhile topic to bring up because I think it's very misleading to stick with that. And I think it's in essence causing patient harm, trying to continue to use an approach which isn't based on what the data tells us is reality. And it does go back a fair while to actually Metchnikov himself is probably the father of probiotic movement who is really focused on why certain people in a certain part of Europe had a good lifespan and a health lifespan. And he attributed to the fermented milk beverage they drank, which we now call yogurt. He isolated some bugs from that two different species, Streptococcus thermophilus, Lactobacillus delbrachii, subspecies bugnavaricus. Essentially the bugs, that's the species that convert milk into what we call yogurt that was in that fermented beverage. And his idea was that if we ingest these bugs, they would permanently call us our guts and they would prevent the putrefaction of proteins. And he thought the putrefaction of proteins in our gut was essentially what caused all disease and sort of aging poorly in essence. So I think a lot of it comes back to that original idea that we could use these exogenous lactobacilli or streptococci in this case to reseed our guts. And sadly, it's not that straightforward. When we actually start looking at clinical trials that have been done using lactobacilli and bifidobacteria based probiotics, or ones based on even Saccharomyces cerevaceae variety Boulardii as well, that we see that they're in essence temporary travelers in our gut, in that when we take them as adults or even as kids, that even if they stick around for a couple weeks, it's considered to be a good outcome. They don't permanently colonize your gut. So it's like you can take a multitude of antibiotics and then to completely wipe out those species from your gut and then just take them off the bottle, off the shelf in a bottle and re inoculate. And I think for me that's the thing is that sort of cheapens the appreciation of your microbiota to think that you can do that and we can't. That's what the reality of the research has shown is that for the last 30, 40 years of giving probiotic strains to people in human clinical trials, that they do not permanently stick. You might get the odd person that sticks around for a few weeks, but in the majority of people, it doesn't stick around for more than a week or two. And that's still considered to be a good outcome. Now that may change when we start making probiotics from Faecalobacterium prosnitzii or Ackermansium buisniphilia or Eubacterium rectil roseberry species, we might find that these strains do have the capacity to permanently stick in your gut. And we know we can do it with a fecal transplant. Yes, we can introduce a whole swag of new species that will stay in a very disrupted gut. But it's not the same as just taking even a so called multi strain probiotic off the shelf. It's not going to introduce the 12 new species into your gut that are permanently going to be there as long as you're taking them, they'll remain there. You can see this pretty clearly even in your own practice. If you use molecular based techniques to assess people's microbiota that you get a rise while taking the probiotic, they stop taking the probiotics up. When it goes back down, you know, it's only a very temporary thing. Whereas you can use other tools like prebiotics to enhance endogenous levels of those particular species quite effectively and a much greater effect than what you're ever going to get with supplemental probiotics for species like Bifidobacteria, for example.

So what did you know? If you take, I mean obviously they have therapeutic benefit depending on what's strain they are, but you know, what kind of metabolic modulation do they do, do they mainly do when we talk about taking a probiotic, are they like known factors that they are that are sort of common to a few probiotic products or is it mainly always going to be strain specific?

It's a good question. And there is some discussion now that there's some qualities in terms of the capacity to produce acids in the gut that are probably are generalized across bifidobacteria and Lactobacilli species and strains. So it's sort of acidification, it probably doesn't matter too much. But I think for the most part, I mean the way I look at probiotic strains is the same way I look at herbal medicines is that I choose the right herb that's got the action that I'm after. It works while they take it, it stops working when they stop taking it. It's the same with probiotics. If you're after one that speeds up gut transit time, you choose that strain, it has that effect, you stop taking it, it's going to slow back down. If you haven't done anything else in the background to sort of fix up more so with dietary lifestyle things that. Or normalize the initial problem or correct the initial problem if you possibly can. But I think that's the best way of viewing them and I think for the most part you should base prescribing based on strains and even for some apparently simple alterations where you think just putting some probiotics in there that can be helpful, like antibiotics. There's a study that used the Coltex strains of probiotics to see if it could treat antibiotic associated diarrhea or prevent it. Very large study. I think it was actually over 1,000 people in this particular study. It was done in the uk, randomized, double blind, placebo controlled, well designed study. They gave, I think it was 60 billion CFU. It's been a little while since I read this study, so some of the details might be a bit off, but maybe 45 or 60 billion CFU per day of four different strains, it did not prevent antibiotic associated diarrhea. Yet you can have other strains like Lactobacillus, rhamnosis, gg, a single strain which consistently shows in the research and we've got meta analysis level data showing it works for preventing that. So it's not as simple as adding anything in. And I think for the most part at the this time point, I would be hesitant to just give it, generally take a probiotic, it's like, no, I want to know what this is doing and give it to actually treat the condition that this person's actually suffering from. And if I'm doing something that just like general give a product that may or may not do anything, I'd rather just have them eat fermented foods in that case, because like a wild ferment in a fermented food, you don't know whether those strains in that supplement or that that food source actually have any medicinal activity or not, besides producing acids and their other sort of basic characteristics. But you're also getting all the other nutritional elements of the fermented food. So I'd rather do that than experiment with high dose probiotic supplements with no evidence of efficacy with my patients.

So speaking about the acids, before I move into the sort of strain specific probiotics that are maybe more indicated in SIBO as it relates to things like abdominal hypersensitivity and things like that. But in terms of the acid, there's a lot of discussion, at least here in Australia, around the whole D lactate and L lactate producing strains. And this is as it pertains to streptococcus and maybe not probiotics so much. But is that what you're talking about with acids? Are you talking about short chain fatty acids and so forth?

When I was referring to acid, it's more the capacity of Lactobacillus and Bifidobacteria have a capacity to produce short chain of fatty acids and or lactic acid as when they eat. That's what they produce. So their capacity to produce that is not strain specific. It's you could argue genera specific. So to go across any strain within those species. But obviously there's differences in whether they're producing acetate or for bilious tribacteria acetate producers, for example. And then lactobacilli will produce lactic acid with some strains being able to produce L lactate and others D lactate.

So this is the same sort of lactic acid that would like. Does it have systemic effects? If you know this whole conversation around D lactate and L lactate some contributing to sort of either metabolic acidosis or being converted. I think it's the L lactate. I always get these confused for some reason, but I think it's the L lactate that can convert easya into pyruvate and be metabolized and actually be a source of energy. And it's the D lactate that seems to increase acidity and cause more problems. Do you have. Is there any evidence for that?

I'd say it's overplayed in that if you follow the reference trail back, you'll find that most of the research that people are quoting comes from case studies of small bowel syndrome where people had half their small intestine removed and then had a bit of a blind loop created where lactobacilli go from 0.01% of the population to 60% of what's there. Very unlike anything that could occur in people that don't have half their small bowel removed. In that case, if they do have an ecosystem which is dominated by D lactate producing strains, they can actually have more reaching their bloodstream. And this is particularly an issue in people who've got small bowel syndrome because they're or short bowel syndrome because they actually malabsorb fat as well. And the malabsorption of fat means that they absorb more oxalates and the oxalates turn off the D lactate metabolizing enzymes. It's a whole sequelae that has to happen. And I think it's very unlikely for this to occur in the majority of people. Yes, I keep it on my radar for people that have had half their small bowel removed that this could occur. But I think if you follow that reference to your back that I don't think we should be extrapolating research done on these very unique populations to what's happening to your general healthy person because the levels of bugs do not getting near that 60% of what's there, Mark. And also most people can metabolize, delactate quite fine. And this is obviously going to be a genetic component as to. So some people will be less capable of actually doing so. But I think the absorption bit in terms of the dietary fat and the oxalates is another pathway that has to be considered too. So that there might be some people who are more prone to that scenario because their endogenous lactobacilli are more cake have a greater capacity to produce delactate, but also because they might be on a high fat diet, which means that there's more fat reaching the large bowel, which increases the absorption of oxalates and oxalates turn off your delactate metabolizing enzymes. So I think there is a pathway and there might be some people that might fit that combination of events, but I think it's overplayed. And particularly, I mean, I think the other issue there is blaming Lactobacillus specifically or even streptococci, which are really in most people's guts, relatively small players. Once you start doing using more modern method techniques to assess the microbiota, you find that lactobacilli make up 0.01 to 1% of what's there for most people. And even streptococca, it's often around that same level in healthy folk and itself goes too much above that bar when there's a major sort of disruption and bugs that actually. And I suppose when you look back at what other bugs produce D. Lactate well, bacteroides can produce delactate and Bacteroides can be present in 20% of what's there and some people makes up 60% of what's there. So I think we're maybe actually looking at targeting the wrong sort of bugs. And even E. Coli can produce D. Lactate. So I think sometimes the underlying theory is always blaming those two genera and not going, okay, well, given that D. Lactic acidosis actually occurs as part of appendicitis, has been put forward as a diagnostic approach to help confirm appendicitis diagnosis. But you know what bug is causing appendicitis? It's bacteroides. And how many people do you know that have had appendicitis? I know a hell of a lot more people that have had short bowel syndrome caused by deep phylactic acid bacteria in their gut. It's actually Bacteroides overgrowth is far more likely to occur in populations and Bacteroides does produce diagnostic. So I think sometimes too that we're being too scared to use those particular bugs due to insufficient amount of information around that whole top area.

Interesting. Very interesting. So let's kind of go more into sort of symptom presentation and strain specificity. So if we think about, you know, when I think about the most common presentations or symptoms associated with Sibo that could maybe respond to probiotic use, number one, of course would be motility. And then I'd also think about, like I said, abdominal hypersensitivity, which is more sort of IBS anyways. And then something like food reactions or histamine issues seem to be also quite common, especially in the population that I see. So I'd like to kind of touch on that. But kind of starting with motility. You did talk about it at the summit about Bifidobacterium lactase HN0.19, which I've been using in the Probiomax that you'd recommended. And I kind of get mixed results. So I'm just wanting to hear your take. Maybe I'm dosing it wrong. I give it one or two capsules a day and can you talk more about that?

Yeah, I sure can. I would use a similar dose and I find for some people it works amazingly well. And that could be my methane. Slow gut transfer time, SIBO patients, but also just by functional constipation cases with just slow gut transit time. For some people it makes an amazing difference. Other people less so. And I haven't found any. Some people, none. I haven't found any way of differentiating that besides giving it to them and observing what impact it actually has. And that's why I'm partly excited to have that lactose readry mm5 3 biogiastrain to start using 2 because it gives me another option in those patients that don't necessarily respond to the probiomax or.

Maybe couple them up or something, you know.

Yeah, yeah, yeah. And that's how I'm start. I've just started using it for those people that of actually adding them together and seeing how it goes. And I have had other patients where they've given the probiomax and there's also some research on the BB12 strain of bifiductrium lactis for. For constipation issues. And some kids, for example, I've seen that responded better to a combination of those strains rather than just one on its own.

Okay, so It's Bifidobacterium lactis HN019. And the other one is BB12 for motility, right?

Yeah.

Okay.

That's mostly for. We know it improves constipation, so. Yeah. And the cases I can think of are probably more functional constipation cases with kids that just are pooing once everybody four days or something like that. The combination has been helpful.

And so we don't have any evidence yet of probiotics working on the migrating motor complex, do we?

There's one animal study that used, I think it was a combination of L Rhamnosis GG, the BB12 strain of bifrobacteria and inulin combined, actually improving the migrating motor complex function. Wow. So the importance of inulin in that mix, I'm not so sure what role it actually played because that might make a deal breaker for some, but it would be worthwhile trialling the two strains combined and seeing what impact it has.

Okay. Another good thought of as a prokinetic, potentially just trying it out. So, yes, people listening, just get your hands on some of these strains and try it out. Okay. The next one is abdominal hypersensitivity with SIBO strain specific recommendations.

Yeah. In this case, it's probably more animal model type data that we actually got on those strains. And I think there's some research on the Biforcrum impetus 35624 strain, which is to North American audiences, have been available for a long time, but I think for Australians, it just recently hit the market as meta align.

Oh, yeah, they align, right? Everybody's talking about that. That's right.

Yeah. Now, some of the ingredients of the align are not necessarily on my G I wish to eat lots of it list. I've been pretty hesitant to prescribe it in my entire practicing life because of the other ingredients that are there. But there is research in irritable bowel syndrome, but also research in animals suggesting it works via that mechanism of decreasing visceral hypersensitivity. There's some research in Al Rhamnosis GG on that, working on visceral hypersensitivity in animal models. And we also know it's a useful strain for functional abdominal pain in kids. There's a meta analysis supporting LGG for that population where, again, that fits that sort of picture. So some research on the NSSLA 1917 strain of E. Coli and then Lactus DN 173010, which is only found in yogurt brand Activia that's available in Canada, the U.S. and Australia. And strangely enough, the ingredient list in the US is appalling compared to even the Australian ingredient list. But they used to have a natural yogurt, and I did use it for my constipated predominant patients. Again, this may not be SIBO specifically. It was more people with dysfunctional constipation. And sometimes it would work magically well to both speed up gut transit time because it does have that capacity, but also decreasing pain and bloating, I think with a secondary aspect of working on visceral hypersensitivity. But yet, sadly, it's only available in the yogurt form worldwide, as far as I'm aware.

And then what about leaky gut? There's some, some talk about probiotics like sb, for example, and LGG being very useful in healing leaky gut or helping to repair a leaky gut. Are there any others or are there, like, specific strains of. Is it always going to be rhamnosis? Lgg, is that specific?

Well, we know that that strain. Yeah, we know that strain does it. And we also know that the biocodex preparation of Saccharomyces cervaceae, Varadi boulardii, people often call SB for obvious reasons, works for healing up damage guts, irrespective of the cause. And I've certainly been using the biocortex preparation in my celiac patients for many years to speed up the process, but also use it in Mycebo patients if we believe or we've got evidence of they're having a damaged small bowel alongside that. And you have before and after evidence with patients showing you're not doing a placebo run there to see what happens in that time point. But it certainly does seem to be helpful for speeding the process of healing.

Great. Now, you know, histamine intolerance is one of my sort of pet subjects, and I'm sort of fascinated by it because. And I seem to see a lot of people that do have reactions to either histamine containing foods or they, you know, I mean, one of the hallmarks of SIBO is the infiltration of mast cells into the small intestinal wall. So there is reason why histamine intolerance exists. And there are studies and research out there that people with functional bowel disorders often have high historic histamine intolerance, regardless of whether they have SIBO or not. So it's a large percentage of people that seem to have this with functional bowel disorders. So I'm not sure if you're seeing that as well, but my understanding is that there's kind of sparse research on probiotics and histamine degradation and there's some thought that some species like LKCI and Bulgaricus, Lactobacillus bulgaricus actually would increase histamine or do produce histamine and that L. Rhamnosis alprantarum and B. Infantis might be helpful with reducing histamine. So I just kind of want you to myth bust that if that's incorrect or.

Go ahead.

This is based on a couple of studies that I looked at. Granted, one of them was an. I think one of them was a rat study. This is always the problem, you know, how do we get good studies that actually demonstrate this in a human population? But you know, barring that, there isn't. Yeah. Since we don't have any, we just gotta experiment, you know. So that's what I've been doing. I've been experimenting with single species and you know, it's sort of early days. I've only had. I've only been doing that probably for the last three, four months. And I mean it's looking good so far, but maybe you can shed a bit more light on that.

Yeah, no, I hadn't had anybody who would probably be. I'd call histamine sensitive for a number of years of my practice. But I do see them more commonly now. I think partly because I'm seeing some of the harder to treat patients now. Whereas before I'd often see first diagnosis when you're the first practitioner who's diagnosed them versus people that have actually been diagnosed five or 10 years ago and have tried lots of things along the way. I'd be curious to hear your view on this one. But I've seen that histamine type reaction more commonly in people that have been on very restricted high fat diets for periods of time. And I've certainly had patients that there was never an issue before the diagnosis of sibo, for example. Then they get treated and they go on these restrictive diets and now they can't. Now they react to histamines where they didn't before. And I'd be curious if you see that in your patient population or there's some people that I see.

Well, first of all, I do sort of see also much more difficult to treat cases than I did before I specialized in sibo. And so people have already. They're sort of self restrict. I talk a lot about this where yes, they're down to the chicken breast and five brussels sprouts and they've sort of painted themselves into a corner when it comes to species diversity because they've just selectively feeding a few species. And so anytime they increase their foods, they will react to it. Now, I'm not sure that's a histamine reaction. I'm talking more sort of classic symptoms of hives and stuff. And I would say, yes, I see that mostly in people that have very restricted diets, but it's, it's that they had to restrict it because they were reacting to the food. And typically people that restrict their food more and more and more will be more reactive. Right. So it just seems to kind of go hand in hand with food restriction. But I don't know what came first. I mean, are you suggesting that because of the food restriction they have more histamine intolerance and then that just builds.

Too and they get more and more restricted? I've certainly seen that in patients. Yeah. And I'm just curious if other people have observed similar things. And when you. And again, from a pathophysiology mechanism, you can look at, you know, higher fat diets essentially increase bile salt output and bile salts feed up hydrogen sulfide producing bacteria like bilophyllin to sulfavibrio. And hydrogen sulfide gas causes leaky gut, for example, and it allows greater sort of contact. And there's also, it's been a little while, a few months since I read this particular study, but there's some animal research looking at higher fat intake actually causing the DAO enzymes in the small intestine to be essentially overused, which means that there's none left over for other sort of food detoxification. I thought, ah, that's an interesting link. And again, it's only animal research at this point, but it would sort of explain that observation that I've actually seen with some patients. Now, that doesn't necessarily help you with you've got a patient who's like that. But I think it should be perhaps on our radar in that early of trying to prevent patients from going down that particular pathway at an early stage. Because I certainly have had patients where if they would have been treated differently initially, they wouldn't have gone down to that point of being on chicken and a couple of foods.

Well, I mean, that kind of leads me down the thought like the new thing is the ketogenic diet, you know, and ketogenic diet has been around for a while, but it sort of seems to have made a bit of a resurgence. And it's like I've had patients where overnight their symptoms were 60% better because of ketogenic diet. Which begs the question, you know, like what's going on there with their microbiome? Are they just sort of, you know, they were on like on a low fodmap diet, then they changed to a ketogenic diet. And I'm not suggesting that's a good idea. I'm just wondering if you see those people as well and, and what do we make of that and is that sustainable? Is that.

Well, that's a very good question and I think that's the answer that similar to even doing a low fodmap diet will reduce symptoms in the short term. No doubt. And if you remove fermentable substrates from someone's diet, essentially the gas weighted symptoms are going to go away pretty dramatically. So it doesn't surprise me that someone with bloating and distension from fermentation, when they go onto a diet that's mostly meat and fat or insoluble fiber that doesn't really ferment very much if they're lucky, will essentially have a production in gas related symptoms because gas production will go down dramatically in that scenario. The downside is that you actually end up starving out decreasing diversity as part of that process, starving out your butyrate producers, starving out your Akkermansi and fecalobacterium which are important for gut integrity as well as bifidobacteria, and also upregulating the levels of disulfavibrio and bilophylla. And you can see this pretty clearly again when they're using molecular based techniques where these bugs can from normally 0.01 or 0.05% of a population, but in a sort of higher fat type diet can be 5% of what's there, which is actually a massive change, which means the actual production of hydrogen sulfide gas is absolutely huge comparatively. So I think that a, unless planned very very well with prebiotics and fiber supplements, et cetera, that there's a lot of risk with following that dietary approach long term. Certainly. I have no doubt that you cut out those fermentable foods and symptoms related to excess fermentation that gut are going to go. That's clear. But I just think there's a high price to be paid for that over the long term.

Yeah. And then how do you actually like when you see someone like that, how do you reintroduce foods in your case now, like how do you do it that you reintroduce foods to people that seem to have reactions to Everything. Do you have a certain sort of pathway that you follow or you just introduce one Brussels sprout at a time?

It's a tricky thing and this is different per person. And I've had some patients that were down to that low level. I can think of one patient and we did a eubiome analysis on microbiota 2 when we first started and she had been diagnosed with SIBO a couple years previously, had done heaps of antibiotics and herbal antimicrobials and very restricted diets. And we looked at her, her microbiota diversity was the third percentile, which meant that 97% of all the stool samples in the eubiome library were more diverse than hers. So her ecosystem was in really, really bad state, including levels of beneficial bacteria, all basically non existent or below detectable level was the term that I use with my patients because they can sometimes be brought back to life with a bit of love and care. Yeah. But she, through a lot of persistence of starting with low doses of prebiotics like partially hydrolyzed guar gum and bimino galactyligosaccharides, slowly worked her way up, slowly introduced a greater diversity of vegetable foods. And I think she had to put up with a bit of, you know, some discomfort and symptoms as part of that process. But what was, I think the most interesting in her case is we did a eubiome 10 months later she was eating a. And I don't necessarily think this is a typical case, but in terms of someone who's willing to put up with a bit of symptoms and maybe the time was just right for the shift in her gut too. Her diversity score was 78th percentile and I'd given up hope at that point. It's like, I'm not sure if there's much here to work with. You might actually have to do an FM fecal microbial transplant to actually reintroduce those species. But it was amazing what could be done over that 10 month span. So I think sometimes it's just slow and steady and other times it's trying to do stuff to heal the gut as you can first and decrease inflammation and maybe work on that allergy access first. You can allow people to increase their dietary diversity. It's certainly not an easy, straightforward thing. I concur and.

Well, you know, my comment to that is, or my question is, would you say in those cases maybe that are super, super reactive to foods that you start with prebiotics? Did I hear that correctly?

I often would with partially hydrolyzed gorgon yeah.

Okay, we're going to talk about that in just a second because that is a huge topic that very specifically. And I've been using a lot more prebiotics and it's sort of still a foreign concept to a lot of practitioners that have not listened to your lecture as to why would you use prebiotics. But I'm going to actually think about that because I use a lot of eubiome and unfortunately they're such heel draggers with their test results. But that really would be great if they could give us a little bit more of a clinically relevant time frame to work with it. But I also use the GI effect.

Express posting back and forth can, can make it a six week span, not always compared to a, you know, 14 week journey.

Yeah, like it's, it's kind of crazy, but so definitely. And I use also the GI effects, you know, because they do the, like sometimes it's a bit like overwhelming when you look at the review biome results and like, you know, most of them, I don't, I don't know these, these strains or species or, you know, I have no idea what they do. So. And, and that was actually one thing that Professor I think it was, what was it Greg Reed who talked about like there, we don't really know yet what to do with the information that we get from the ubiome. But I'm always just like, well, we're practitioners, we always push the envelope, we try things, we, you know, we learn things, we just kind of get anecdotally some experience under our belt. So that doesn't really faze me because that's how you, that's how you learn.

But anyway, so I do and some of the species, we know what they do in the gut. But you're right that there's a whole list of ones. In new biome tests you might come up with 80 different genera or more if you're lucky, and there'll be 65 of those that we have. We don't, as microbiome researchers don't even know what they do yet we know that they're there. So I don't necessarily work with those ones. I work with the ones that we do know what they do, both the pros and cons. And you can still make some dramatic shifts with dietary changes and prebiotics specifically to those species to move things in a much more beneficial way. The species that we do know and decreasing levels of bugs like Bilophylla and the sulfur vibrio in patients where we know, they're probably contributing to what's going on with their ill health.

Gosh, I just lost my train of thought. I had a really good question for you, but. Oh, yeah, that's what it was. So I am very happy to report that I'm in the 97th percentile in terms of species diversity. But others who are in that really super low smell of an oily rag, a kind of percentile where they're really very low in terms of species diversity. Also, my understanding about probiotic use is that they don't seed, but they do have this somehow miraculous effect of bringing some species back and aid in sort of the recovery, if you will, of the microbiome. Is that accurate or, you know, they.

Definitely do that after an insult, and I think that's one of their strong points. And again, there's some strange specificity stuff here too, that some we know, when used, will increase Faecalobacterium populations, for example. So I think there's some strange specificity there too. But yes, so certainly after chemotherapy, after radiotherapy, after antibiotics, where the ecosystem is really mucked up and really different than it was before, that supplementation with probiotics, even just a simple Saccharomyces cerevices biocodex or lgg, will actually help restore the ecosystem more quickly than otherwise. And part of that's to do with perhaps the alterations to the environment. And that goes back to producing acids, as I said before, that making it a more acidic environment, which the probiotics are going to do, actually will encourage the growth of more acidic type flora, which, generally speaking, are the bugs we want more of. And the bugs are growing in alkaline ph. We are, generally speaking, more pathogenic.

That makes sense.

Yeah. So I think, yes, there's that, but we also know from research on, I think there's a systematic review published a couple years ago that got lots of newspaper press going. Don't take probiotics, they don't do anything.

Oh, yeah.

The systematic review is looking at do probiotics alter the ecosystem in healthy people? And I think across the board, it doesn't make much difference to healthy people. And that for me, it wasn't surprising. It's like, yeah, for sure. If you really want to make difference to a healthy person's ecosystem, change their diet or give them prebiotics, it's unlikely that adding a few billion CFU is actually going to change anything much. But when the ecosystem is very much altered, then, yes, adding those few billion can actually make a difference for how quickly things Actually shift. But certainly if you really want to shift things, prebiotics and changes to diet will have a far greater impact.

Okay, so let's kind of dive a little bit into the topic of prebiotics because that's something that you certainly love to talk about. Right. So we have about.

Yeah. And you know, as I said back in 2000 when I started that, this was a new concept to me. It was very barely touched on, if any, in my naturopathic training. So it was like, what the hell is laculose? I'd never heard of it before. And then you start reading going, wow, that does some pretty, pretty cool things. And that was my first introduction to lactulose, for example. And I started playing around with prebiotics, including lactulose, in clinical trials I did on IBS patients as part of my honours and PhD program. So I got to familiarize myself with them with that patient populations, but then also in clinical practice since that time point. So really I've been using a lot of prebiotics for a lot of different conditions for 17 years.

Wow, you have a lot of experience. So. So if I can just sort of summarize just briefly as to what you were using and you can correct me. Right. But just for the sake of time. So you use mainly three prebiotics. Right. Which is the partially hydrolyzed guar gum and that's. Do you mainly use it for methane producers or I think also bacteria?

I use both, but I do probably more. It's an always one in my methane crew and my functional constipation crew.

Yes. And do you use it for any other situations?

SIBO specific. SIBO specific. I'd also use it in people who didn't have methane type SIBO too. I mean, certainly look back at that research using rifaximin plus or minus partially hydrolyzed bar gum, the efficacy was significantly better by a wide margin with, with all the phgg in that cohort, even though they weren't methane type SIBO patients. So I'm quite happy to use it in that situation too. And I use it for, I mean, I use it broadly for other diarrhea type stool conditions too, because it tends to help normalize stool and I think that's one of its strong points.

And then bimuno or galactooligosaccharides. That's more to bring bifido back. Right, that's kind of what I've been reading. Is there any other. What do you use that one for?

Yeah, so certainly it's a Food. It does work well for bringing Bifidobacteria populations back up. And also Faecalobacterium prostnate populations too.

And what's that one good for again? Like you, you, you like talking about that one too. And Achromansii. Those are like the, the two superstars or the, the sleeper hits right. Of them.

They are a bit because. Because we didn't know about them until recently, so they had really got out to the practitioner world yet. And probably because many of us are using tests, don't even pick those species up. So we stay ignorant of the populations in our patients because they're not using tools that can see them. Yeah, but Fecalobacterium is generally in healthy people is the single species with the highest prevalence or highest amount in people's guts. Now sometimes they might have eight different species of Bacteroides and that add up together a little bit more than the Faecalobacterina, which is a single species that's there, but it's a single species that, that's most common in healthy people. And it's interesting because I do workshops for people in terms of healing or working with the microbiomes and to get a chance to see healthy peoples test results as well as unhealthy peoples that I see more in clinical practice. It's interesting seeing the variation of what can occur with fecalobacterium, but generally you want it to be 10 to 15 to 20% of what's actually there and it often is, and that's of time points. So it's actually quite a significant player in most people's guts. And it is in essence a predominant butyrate producer as well because it's there in such high amounts. And butyrate is one of the short chain fatty acids that it actually outputs. And it's also seen to be helpful for inflammatory bowel diseases that people with Crohn's and ulcerative colitis tend to have low levels of Faecalobacterium and those that respond to treatment, treatment responders tend to have higher levels of Faecalobacterium. So it produces another sort of anti inflammatory gut healing compound besides butyrate. So it sort of heals the gut by two different mechanisms. And higher levels tend to be protective against metabolic syndrome and type 2 diabetes.

I just had a patient data. Yeah, that's interesting because I had it like for the first time I've seen a patient come back and it was flagged as too high. Is there such a thing as too High faecalibacterium?

No, I don't think so. And that may be something that shows up on the GI effects more so than it would on a you biome. And no, and I haven't seen any research to suggest that's the case. Now I do think that can be the case with Akkermansia that I've seen a couple patients with. I had one patient where it's made up 22% of what was there and usually healthy focus in 1 to 3%. It was massive. And because it eats Akkermansia actually eats mucin that when some people, when their guts are really inflamed, they're producing lots of mucus that Akkermansia can actually produce. She overgrow in too high a quantity in that situation.

That makes sense. I've seen that too. So that correlates with what I've seen clinically. Okay. And then lactulose, that was a bit of a shocker when you talked to us about lactulose at the SIBO summit. Can you talk about that in terms of its use as a prebiotic? Yeah.

So lactulose, it's used as a prebiotic, goes back, I think to 1960s, and it was at one point added to infant formula. It's a way of trying to make it more like breast milk to increase bifidobacteria counts in infants. And it certainly worked for that. And yes, so it's been long used as a prebiotic. And yes, it tends to increase bifidobacteria to a great degree in higher doses. It increases lactobacilli and it also increases faecala bacteria and prosnitzii and also Akkermanzi levels too. So it does feed a range of beneficial bugs. And it's very good at changing the ph to make it in an environment that's much more acidic. And I suppose that's mostly probably with the bifidobacteria and the acetate, for example, which is the main byproduct of bifidobacteria, that can actually change things because there's a number of pathogens. Salmonella, for example, there's research using lactulose to treat Salmonella carrier states where essentially by just changing the environment to one that's not conducive to its growth. And I use it, in other words, bugs that are more ph specific in what sort of environment they like growing in that. You can use lactulus as a ph changer in that respect, but it is a pretty fantastic prebiotic. And it's even got some both animal research and even a pretty interesting human case study for a patient with Quite severe type SIBO2, where giving lactulose, not only did it decrease symptoms in three days, but it decreased bacterial counts from 10 to the 12 down to 10 to the 7, which is a pretty massive of decrease by the ingestion of lactulose. And that, I suppose, is the other aspect of lactulose, it does have an amazing capacity to decrease Bacteroides numbers. So when I have a patient whose bacteroides is way out of whack, and this may have often happens after multiple courses of antibiotics, when people do those antibiotic cocktails to try to kill off supposed pathogens like dientamoeba, the ecosystem is disrupted for years afterwards. But interesting enough, bacteroides often bounces back. And rather than being at 15, 20% of what's there, it can be 50, 60, 70% of what's there, which is way too high. So lacticulose can work more effectively than other prebiotics to decrease levels of bacteroides.

But then, of course, a word of caution is for those that do show SIBO positive on a lactulose breath test, probably a good idea to eradicate SIBO first or get that under control before using lactulose.

Yeah, yeah. So certainly when I'm. I mean, I've used lactolase as a prebiotic for lots of different conditions, even like recurrent urinary tract infections, there's research on it for that. And it generally works well in clinical practice too, because it decreases levels of E. Coli in the gut by about 100 fold. So essentially you're decreasing the reservoir of urinary tract pathogens in the gut so less of them can make that perilous journey from anus to vagina to urethra, 100 fold less, in fact, can make that journey if we're using lactulose as a prebiotic. And clinically, I've not been using that for probably 15 years for that indication, it works well. But you're right, certainly in my SIBO patients, that and something I probably did speak about at the summit, but I generally will do three different sugar tests for my diagnostic, figure out my diagnosis. So I'll do a lactulose, a glucose and a fructose. And if I have a patient that that is a positive on the glucose breath test or has a very early rise on fructose breath test, so at the 20 or 40 minute mark, but no rise in the Lactulose, then I can use lactulose in that patient population both as a small intestine motility enhancer, it's a prokinetic, but also in terms of just changing the population dynamics so we have less bugs that are endotoxin rich that essentially will be worsening inflammation and potentially worsening systemic inflammation as well.

Yeah, interesting. Yeah. I have sort of gingerly treaded around the use of lactulose in my SIBO patients, you know, so I have used it in those that show more positivity on a glucose, as you've just mentioned, and it seems to be tolerated definitely a lot better. But I think you did give a word of caution also at the summit where it will produce gas. Right. So you don't be, don't be alarmed if you're expelling gas a bit more, but it shouldn't be like that. You're terribly bloated and I mean, that's obviously not a desirable effect.

Yeah, that's right. So if you're farting more, all good, that's fine. But if you're bloating into this and you didn't know alcohol, I won't use or cease use of lactose if someone reacts that way. Now, luckily with the breath, tests tend to get an idea of whether they get symptoms to it as well as actually gas production. So you get people that will take that 10 gram dose of lactulose and get no symptoms and have no rise in breath gases. So I'm pretty confident using in that population and generally it's well tolerated. But I still will start with a lower dose and work up in that population because things adapt to lactulose quite effectively in time, over time.

Excellent. Okay, so also, just wrapping things up, I want to talk a little bit about other issues like, you know, what do you think about spore forming probiotics? There's a, like a, you know, that there's a lot of talk around that. And also soil based organisms as it relates to clinically relevant use of, you know, basically controlling symptoms. There's a lot of talk about that. So can you, can you address that as it relates to not just sibo, but in terms of functional digestive disorders?

Yeah, interesting question. And I suppose for me it comes down to evidence that I'm quite happy to use a probiotic whether it's found in the soil or a cow's gut or a human gut or the skin of a lychee, as it may actually be with terms of saccharomyces, if there's evidence to show it does something. And I suppose that's my caveat. Whereas if all I've got is is information from a company saying yeah, use it, it works, but no data to show that it actually does. I'm not willing to experiment on my patients in that way. And I think sometimes that generalization of okay, it came from soil, therefore that all bugs taken from soil have the same effect. It's like you can't make that generalization. Not all bugs found on the skin of lychee do the same thing as the saccharomyces biocodex does. You can't make that sort of connection that's there. So yeah, when there's more research on spore based probiotics or importantly soil based ones, I'm totally happy to use them in practice. Once we have that data and there is some research on the gbi. I can't remember the code of this one because it's only recently hit the Australian market. GBI6630 or something like that in diarrhea, IBS and other conditions. I'm happy to use that strain because we've got data showing it, it works. And when research comes out on the other side strains, I'm quite happy to do so too. But I think we just have to be cautious with prescribing things because the company tells us that they're good. But I suppose once you start using it and you see effects, fair enough. Then we are clinicians. I'm a clinician too and if I see something works consistently, patients, I'll use it even if the data isn't there yet. Fair enough. But yeah, my caution is around if it's an initial use when we don't have that, particularly if we're using it to treat a condition that we do have good research on other strains perhaps. That's my biggest.

Yes, I wholeheartedly agree with that. I don't, you know, and I used the soil based organisms a little bit but it's the ones that I either got no effect or had more reactions, you know, in my patients. So I just was not really game to go down that road anymore.

Yeah, and you could, you could argue that certainly for some of them it's a new agent that, you know. Yes, we used to eat dirt on vegetables, but that's our food and I'm all for that. But it's still very different from concentration, fitting up dirt organisms and giving species in a dose that we haven't encountered before in terms of what impact they may have. On our gut, because the species in our gut are not the same as what's in the soil for the most part. There might be odd species out of the 150 that are in you, that's also found in dirt, but most are not. And the environment is obviously quite different between a gut and soil.

I'm always so fascinated, like, how did they actually figure out this whole estate, the thing on the lychee, you know, like how what?

That was an observation by Henry Ballard, who actually saw people in Southeast Asia treating cholera with. With lychee skin tea. And he was a microbiologist, so he said, I wonder if there's a microbe in that lychee skin. And he isolated out Saccharomyces, which he then named after himself, Saccharomyces boulardii. And then they started doing research with it. So. So that was essentially observation of traditional use of a nutritional herbal.

Fascinating. Wow. I know that every question that you answer spawns so many more questions, but just for the sake of timing, I think we need to get off of this podcast so that people can get on with their lives and start prescribing some of these single strains that you've mentioned and try to source them. Any last words of wisdom from you, Jason?

I don't think so. I think we've covered lots of extra interesting topics.

Yeah, well, I got one thing that I learned at this other conference, which is I was optimistic or at least heartened by that they did research on this colony collapse situation with the bees and the pesticides that was responsible for that. And they used this Lactobacillus plantarum. And when they used it, it restored the bees pathway to detoxify the pesticides. So something like that is just so encouraging and optimistic in this. Otherwise, you know, every day we get bad news about other destructions and decimations of not just our outer sort of microbiome or macrobiome, but also of our microbiome. So I thought that was a really encouraging story. I don't know how they're going to use it if they're going to just spray the bees with this Lactobacillus. But it's doable. It's doable.

Yeah. That's a very exciting story, actually. I like such positive news stories. I was at a conference last year, the Australian Society of Lifestyle. You were there too, actually, the Australian Lifestyle Medicine Conference. And it was. I found it fascinating hearing one of the lecturers whose name totally slipped my mind. Dr. Voelquist.

Yes.

Dr. Volquist was talking about, like, lack of food diversity in terms of, you know, we used to use 60 or 80 different species of lettuce or types of lettuce. Now we're down to like four, what people are commonly consuming. Just in my brain I was going, wow, we're just losing all that diversity in that outer world in the same way we're losing all that diversity, the inner microbiota, because of antibiotic use and changes in diet and probably chlorinated water and all those other aspects of modern life that have had a massive impact and hit to our diversity in a similar way. So what's happening outside is also what's happening on the inside.

So, Jason, thank you so much for your time and your insights. It's always incredible how much knowledge you have and how, how freely you share it with all of us. So I really appreciate that. And again, practitioners get on probiotic advisor.com check it out, put in your search terms for different conditions and be amazed at the amount of information that you can get from there about species specific strains for different conditions. So thanks again and I hope we have you on the show again very soon.

Jason, you are very welcome. It's a pleasure as always to connect.

Well, thank you.

Thank you for listening to the SIBO Dr. Podcast. We hope you found the information in this episode useful in the treatment of your SIBO patients. Head over to our sponsor, SIBO Test.com an online testing service for your patients and home of the Practitioner education portal. Tune in again for another episode of the Sibo Doctor podcast. Thanks again for listening.

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