Microbiome Restoration with Dr Jason Hawrelak PhD ND

Welcome to the SIBO Doctor podcast with Dr. Nirala Jacoby, a US trained naturopathic physician and medical director of the SIBO Doctor, an online education resource for practitioners. In this podcast series, medical experts join us to discuss functional digestive disorders and clinical practice and research as relates to small intestinal bacterial overgrowth and associated conditions. This podcast is intended for SIBO treating practitioners and aims to help educate how we may best serve our SIBO patients. If you're a practitioner and want to learn everything about SIBO, from the basics to advanced treatments, head over to thecebodoctor.com you can also join in the conversation on the SIBO Doctor Practitioner Forum Facebook group. If you're a patient, please please note this information is not intended to diagnose or treat medical conditions. Please ask your doctor before initiating any new treatments. And now, over to Dr. Jacoby and the Sibo Doctor podcast.

Welcome, Sibo practitioners to another episode of the Sibo Doctor. And today I have the great pleasure to have with me again Dr. Jason Horlak. And he's no stranger to this podcast or to many of you who have subscribed to the probiotic advisor. And Dr. Horolak is not just an educator and a naturopath and a clinician, but he's also a researcher and has a lot of experience with microbiome research and is on faculty at several prestigious schools. So without further ado, I really want to get right into the topic of today, which is Microbiome restoration, which is a new course that we're offering on the SIBO Doctor. Welcome, Jason, thanks for coming back on the podcast.

Yeah, it's a pleasure to be back and you're very welcome. I'm always happy to chat about anything gout related, but certainly microbiome restoration is one of my passions because it's something that I've been working with patients for a long time, actually, because my PhD was looking at dysbiosis and neurotrial bowel syndrome patients and how we could alter that ecosystem using herbs and prebiotics and probiotics and dietary changes. So that's, oh, gosh, 18 years ago now. So it's just been cool seeing how technology has changed and how we as clinicians, if we're using the right tools, can now see far more of what's going on and how we can best modify that. So it's been exciting to be part of that change and see the growth in tools that went from research settings through to tools that clinicians can now use. And we'll keep Moving in that same direction that I'm looking forward to when we can swallow that smart. That'll do sampling of our small bowel as it traverses through and tells exactly what species are growing overgrowing in the small bowel so we can target our treatments more effectively.

Yeah, that's actually, you know, that. I mean, already I have like a lot of questions off on a tangent about the smart pill and all that. It's very exciting. Some of the research that's coming out, and I was just at the SIBO symposium in. Or the SIBO conference in New Orleans where Dr. Richard McCallum and Dr. Bohm. I forgot his last name, first name. But they both presented on small intestinal aspirates and dysbiosis. So really fascinating stuff coming out in research and sort of also challenges some of our thinking about bacterial overgrowth versus dysbiosis in the small intestine. So anyways. But back to the master of the microbiome himself. You know, one of the things that really helped me a lot was taking your course last year in. I think it was in Melbourne. It really helped me with understanding. I mean, having said all that, you know, we don't really know a lot about all of the different phyla, all the different bacteria that are there, and how to really impact them, how they speak to each other. But generally speaking, it was so helpful to start to understand dietary implication in some of these phyla and how to manage some of these overgrowths by utilizing very simple things that we have available in our practices. And really what I really appreciated was this other perspective of rather than always kill, kill, kill. It was about how do we actually regrow some of these other organisms that have a regulatory effect on the whole microbiome?

Yes. Yeah, I think that's a huge thing. And I think that in some ways we've focused far too much over the last decade on kill, kill, kill. There's been some negative repercussions of that that I'm seeing in my patients on a daily basis, in fact, in clinic. And I think that we really do need to focus on. There's a time and place for killing, Mike, obviously, but there's a time and place for restoration. And I think we really need to focus on that with patients and helping to restore that, because I don't think the gut ever functions optimally or the person can function optimally if their colon ecosystem is not in good condition. And there's a number of tools that we use as clinicians at times from dietary changes that are restricting Certain dietary plant fibers for example to herbs and anti biofilm, things that do have negative impacts on the colonic ecosystem as well. That is essentially collateral in some cases when we're trying to deal with sibo. So I think it's important that we're actually aware of that. And two can assess that in our patients and three can restore because I think our patients health suffers long term if we neglect that aspect of SIBO treatment and just go, let's just deal with microbial overgrowth. Boom, done, put on some prokinetics. No, that's part of the story and we're part of the way there. But we need to, particularly if we're using more stronger interventions in our treatment of sibo, then I think we can't neglect restoration, repair of the clonic ecosystem.

And that's certainly part of my program now where we treat sibo but also review the actual causes of sibo because it's not always motility related. It's other factors there as well. But then including microbiome restoration. And that's the title of your new course, Microbiome Restoration and Clinical Practice, which I think a lot of clinicians that are out there are going to find extremely useful, not just in relation to SIBO treatment, but really most conditions that we are seeing nowadays have some aspect of microbiome dysfunction. So it's super helpful for anyone and that, you know, one of the aspects that I found really helpful is how to actually interpret some of these DNA readings, the PCR reports that we get from either Genova or Eubiome and how to actually interpret them because a lot of us don't know what all of the bacteria are doing. So that I think I found that aspect to be really, really helpful. So can you talk a little bit more about that? And I think that's module one. There's three modules to each module has two lessons and just as an overview, the first one is sort of reviews, testing. Right. Then we go into beneficial bacteria and then last module is pathobion. So I'll let you take it there to kind of over do some overview of those modules.

Yeah, certainly the first one is some of the results of an experiment I've wanted to do for years which is sending a single stool sample to six different labs, some using DNA technology, some using the old technology, culturing and seeing the differences and similarities hopefully of what actually showed up and surprising or perhaps not if you know a lot about the area, that there were quite a bit of differences between labs. But I think that the biggest differences Is is really between the labs that still use culturing versus the ones that use DNA, there's a revolution in the microbiome understanding because we've moved to DNA techniques and there's microbiome journals that refuse to publish any research that still uses culturing. I said a microbiome conference in Rome a few years back, and out of all the presentations, all the poster presentations, we're talking about hundreds. There was one that used culturing for rural Czechoslovakia. The rest all used DNA techniques. So I think that if we're wanting to move with the times and, you know, we used to and always have been way ahead of the field as naturopathic practitioners, could be new about dysbiosis. We've been talking about it for 20, 30 or even longer than that. You can go back to, like Lewis Kuhn in the early 1900s, and we were talking about dysbiosis even then. So it's always been part of our tradition. But I think we're at risk of falling behind if we still stick with old tools, using old technology, because there's Reese moving on. So much in our understanding of the ecosystem and what species are doing what has evolved so much, because we're seeing that what culture can pick up maybe 30% of the species that are present in your gut, typically 30%, and it's essentially DNA that's allowed us to see the other 70% that we couldn't see 20, 30 years ago. And that has allowed us to make these associations between Parkinson's and the ecosystem, microbiome and Alzheimer's disease and type 2 diabetes, a whole range of things that we never made the connection before because we're using tools that were too crude to see what was actually there. You know, and when I teach this course 10 years from now, it'll probably go for double the amount of time because we'll know a lot more about the other species that are in there, too. Like, I can get a report, I had several yesterday from using UBiome as a lab that uses DNA. So you can get a lovely picture of the 89,000 species that are actually present there. And there's a whole bunch of. We don't actually know what they do, what role they play. Occasionally you'll find one that makes up 15% of their whole ecosystem, or 20%. And you do a Medline search on it. And it turns out that the only paper that's ever been published looked at the fact that this particular bacteria was found in ocean mud. Okay, Ocean deep sea ocean mud, near volcanic vent and their guts. And now this is at 20% and we really don't know what the significance is. But there's a number of species we do and those certainly ones we focus more on during the course. Things like Akkermansia and Faecalobacterium and the butyrate producing microbes and also hydrogen sulfide gas producers too, that we just couldn't pick up using old technology. So you couldn't see what was there. And once you have a look in ecosystem with new eyes, it's like there's so much more there and it allows you to actually have a much deeper understanding of what's happening with that patient and how we can influence what's happening with that patient too by changing that ecosystem.

So that is module one is where we really learn the differences in assessment and diagnosis and interpretation. And then we move into the beneficial bacteria. And then you mentioned the pathobions. The good, the bad, the ugly I think is how you phrase it. That's pretty good.

Yeah.

And that's hydrogen sulfide producers and Methanobravibacter and although that's not really a pathogen, but in this context of Sibo et cetera, those are the organisms that we really focus on. What about other.

That's right. And we'd probably classify it as a pathobiont would be a good representation that a microbe that in the right amounts actually has health benefits, but when the balance hits too much, it essentially causes.

Harm.

In that category.

E. Coli is also in that category, I suppose.

Yep. And same with Bacteroides too, that they in the right amount, they're actually producing some healthful compounds and enhance our health. But the difference between someone who has a. You look at a triple therapy cocktail for treatment of Helicobacter pylori or some people are being treated that way for Blastocystis these days too. And all of a sudden Bacteroides goes from being at 20% of their ecosystem, which is what we would see typically up to 60, 70% because it just tends to resist antibiotics really well. And there are negative health consequences for that. Microbes being that far out of balance. That's one of our biggest producers of beta glucuronidase, for example, and it's got endotoxin just as part of its structure that is pro inflammatory. And some Bacteroides produce other toxins which cause gut damage and even a bit linked to Alzheimer's disease too. So having at 67% ecosystem is not good. But having a 20% actually it has other health Benefits too. So I think we have a chance to discuss those going where is the optimal range and how can we adjust? Using diet primarily, you can make huge shifts to that ecosystem. And I think sometimes we get very fixated on using herbal agents to modify things and they're certainly effective at doing so. But really, dietary changes can make huge, huge changes to an ecosystem, far more so than what you're ever going to get with probiotic supplements, for example.

Well, this is always the difficult aspect when we sort of, I wouldn't say over focus of sibo, but very often when we have a SIBO patient that's very much an active overgrowth, it's very difficult to utilize some of these techniques because that might be contraindicated in terms of low FODMAP diet or. And you know, I always tell my patients it's a limited time that I want them on it on these diets. But so this is another really good, I think aspect of the course is that you learn some techniques that after you're done with your SIBO treatment of how to really restore this person's microbiome. I've actually had a really, I had a few interesting cases now of hydrogen sulfide and luckily hydrogen sulfide breath testing is just around the corner. So that will I think really illuminate a lot of our maybe resistant to SIBO treatment cases when we actually know from not just flatlining breath tests, but really from the data that this person is producing hydrogen sulfide. But I've had some really amazing turnaround cases where we completely switched gears even in the middle of SIBO treatment, where we went from a low FODMAP to more of a medium fodmap or even just completely changed the diet. And that was a game changer for a couple of my patients. And then we sort of, that effect was lost after a few weeks and then we sort of returned a little bit more to another diet. So it's just as a reminder that the diet part can also be very dynamic, that you don't have to just stick to one thing, you can experiment. And that's what I find so helpful is knowing what foods are really helpful for some of these overgrowths.

Yeah. And conversely, what foods are feeding those and what we can cut out. Because I think that's the other aspect is not always that well considered out. The long term consequences of certain dietary approaches where they might have a much higher fat content, for example, which in the short term will decrease bloating and distension type symptoms and intestinal gas Production. And there's a whole bunch of flow on effects from that in terms of acute symptomatology. But when we're doing that longer term, we produce more bile and there's sulfur compounds in the bile which feed hydrogen sulfide producing bacteria. So what's interesting to see, and I often see this in clinical practice, is those patients who sometimes you're lucky enough, you've had a baseline test, and the hydrogen sulfide producers weren't a big part of the picture initially, but after treatment, where they've been on very restricted diets with low fiber, much higher protein, much higher fat, is their hydrogen sulfide gas producers have gone up by like tenfold or sometimes even 50 fold from what it was at baseline. And it shows why they still have SIBO might be gone, but they have worsened visceral hypersensitivity than what they ever had before, and they're more reactive to foods now than what they were ever before. And I do think it's very much tied into hydrogen sulfide production and the fact that we've been inadvertently feeding that population by the dietary approaches that we've sometimes been using.

Yeah, I actually gave a whole presentation on hydrogen sulfide. I did a deep dive into hydrogen sulfide because I was so fascinated with it. And it is a really fascinating topic because it can have benefits and it can have detrimental effects on not just the microbiome, but systemically for patients. And one study I came across was that it actually showed that low FODMAP diet was definitely detrimental or not detrimental, but that it increased hydrogen sulfide producers. So not just high fat and high meat, but actually a low FODMAP diet. So, you know, it is important to know that when you're a clinician, because especially when we've been told, and I preach this to my practitioners about using a really phased approach to the treatment and using the diet. But then to really understand that this is just a one step in a dynamic process, I think is helpful. Okay, but we're talking about hydrogen sulfide and also methane as they pertain to sibo. And one thing I was gonna ask you. Cause I did come across this in my research, was that in equal producers, meaning that patients that have certain subsets of bacteria that turn soy isoflavone into the bioactive compound equal, that tended to be in those cases, or the study showed that giving isoflavones to equal producers reduced both methanogens and hydrogen sulfide quite dramatically. So can you just sort of remind us about the equal producers? I think that There was you talk about one of them in this course. But just generally speaking, just so that people can understand that a bit more.

Yeah, I mean, it's always been a fascinating thing that people have noticed for the last 20, 30 years is that some people are able to make equal and some are when they ingest soy isoflavones. And certainly some of the health benefits of isoflavones are tied into equal production. Not all, but some certainly are. So they're looking at, okay, why is that? And eventually, and there's a researcher, Alde Kreutz, who is doing a lot of research on selective estrogen receptor modulators is what we would call them now. And eventually the bacteria that is the main equal producer has since been named after him, Alderkruzia, and that is one of the key players in that. And with new technology, we can actually see whether people are equal producers or not, essentially by looking at their level or whether they have the presence of Alderkrutsia in their gut or not.

And do you see a correlation of like, let's say vegans that eat soy products and that their levels of Adler Crozia is much higher?

I think the research tends to suggest that that's the case, that longer term consumption of soy. Yes, and it totally makes sense, would actually nourish that particular species. But in the shorter term it doesn't seem to like, okay, go on, eat some tofu for a few weeks. Doesn't seem to have a huge thing. And I think there's still lots to be teased out around that. It's been a little while since I looked directly at that literature, but my previous understanding was that it was more longer term dietary patterns that determined someone's equal status rather than shorter term. And whether that had to do with if it was passed because if your mom didn't have it or your family didn't have it, you did get it in the first place, then even eating soy from an early childhood isn't going to actually help that situation. But if you were passed on and then you fed it, nourished it over that time period, then yes, it's still going to be there. And I am curious. And again, for me, this is not something that's been teased out adequately. Most microbes will have a bit of variation in their diet and this one presumably does too, but that might be. So it probably just doesn't only eat soy isoflavones, but there might be some other polyphenols that it consumes as well in the intervening time periods. And that I don't think has been teased out all that well yet. So there might be other waves of helping that population survive in the gut in the absence of soy consumption, for example.

All right. One of my areas of interest has always been food intolerances, especially when people have self restricted foods for a long time that not only affected their microbiome, but now every time they then introduce certain foods that become more symptomatic and and so continue to restrict foods further. And I know I've asked you this question before. I'm just wanting to see if there's any updates on whether or not we do know if there's any connection between things like histamine. I know that for example, with histamine intolerance there are certain species that do also produce histamine. But also, for example, when patients have yeast overgrowth, that can actually clog up the aldehyde pathway, with which also histamine can get detoxified. So sometimes it's a roundabout way of association where we see something just be correlated. But do you see any other microbiome disturbances or potential for supplementation of probiotics in cases of histamine intolerance and salicylate intolerance and then moving into more oxalate intolerance?

It's an interesting area. And for those of us who've been in practice for a while will have see this as actually more common now than ever before. I guess there were people who had slyslate issues before, but the number of people that are presenting now with histamine issues and slysllate issues is far more than what it was before. Sometimes I just have some kids that would outgrow their salicylate issues. You just have to put them on a low salicylate diet, which is a horrible diet to follow for any length of time. But it was necessary at this time. But now it's becoming more widespread and I do think it's got to do with damage to the ecosystem. And this is more of a clinical observation rather than based on any research around this topic. But I'm seeing it mostly in patients that I think have actually damaged their ecosystem, often inadvertently through dietary approaches, herbal antimicrobials, sometimes antibiotics mix in that whole sort of mix. And all of a sudden they come and they're like, I used to really eat those foods until I started getting treatment for my sibo. Post treatment of sibo, the sibo might be gone, but now I can't eat these foods anymore. And I'm only eating a Handful of foods is a common story. And then you do a microbiome assessment. It's like, ah, okay, they're generally very high in hydrogen sulfide gas producers, but conversely they're very low in B tree producers, very low in Akkermansia and very low in Bifidobacteria. And this is a common pattern that I observe. And when you realize how important the roles that those three major classes of bacteria play, the butyrate producers, I'm just lumping together, but bifidobacteria and Akkermansia, in terms of ensuring optimal gut integrity, it's sort of like imagine your immune system trying to function without neutrophils, where you're just like, oh, let's just take the neutrophils out and see how it functions. It's going to not function quite right. And I think we have to remind ourselves that we evolved in this, this relationship with bacteria, that they're playing specific roles that we rely on. And things like Akkermansia and bifid bacteria and the B tree producers, we rely on them to have optimal gut integrity and proper gut integrity and proper colonic functioning. We rely so much on it. And you take them out of the picture and you do understandably going to have gut dysfunction, integrity issues. And I think this is the core aspect. And you can keep throwing glutamine and other things at it, but it's sort of putting a band aid over that when the cause is this lack of this microbial communication that we've evolved with. So I think that's the core aspect of. And then it's worsened by the excess production of hydrogen sulfide gas, which we know causes gut leakiness and visceral hypersensitivity, so inflammation in the nerves. So they start being even more reactive to gas forming foods, but lower down in the gut than where it was before. So yeah. So I think the core aspect of treatment is more based around, from my perspective, that restoration of populations of Akkermansia bifid bacteria, butyrate producers, and focusing on healing the gut. And when we're able to do that, my experience has been that patients are able to improve in terms of the diversity of their diet and minimize symptoms and eventually have a diverse diet again without reacting to histamine containing foods or Swiss like containing foods.

Interesting.

It's easier said than done. Some of those people have that eat five. That's the challenge. It's like, I know what will fix up that ecosystem is that you can't tolerate it. And this is the thing where you have to go so slowly, introduce one thing at a time and start to wean up on doses. And I mean most patients we get there, but it can be a slow process. And those people that are only on five different foods.

You know, it's so interesting. I was just thinking about my patients with these high desulfovibrio levels on a Genova panel and that's really a common occurrence. I see this a lot. And also a lot of E. Coli and a lot of Oxalobacter as well. And they're all sort of in that same category, aren't they? They're like in the Proteobacteria, I can't remember.

They are off the graph.

Yeah. So is there a significance to. Because I see actually Oxalobacter be high. Very, very much. And just for those listeners, Oxalobacter famigenes is an organism that helps break down food based oxalates, which are in a lot of healthy foods. So is there any clinical significance to Oxalobacter being elevated?

It that's an interesting observation and I'm trying to rake through my brain of other tests that I've seen recently to see if I've seen anything like that. And to be honest, I tend to see the lack thereof far more commonly than I do. Higher amounts.

Yeah, I see it high so much. Yeah.

Okay. And you'd know that the lack thereof is very problematic because for a lot of gut function there's a lot of redundancy built in there that there's a number of species that produce butyrate, a number of species that can actually eat that polyphenol, for example, and convert it through something else. But there's only one species that we're aware of at this time point that actually eats dietary oxalate and that's Oxalobacter. So in those people where you've eliminated or wiped out that species, which is a consequence of certainly antibiotic cocktails, majority of people completely wipe out that species, so it goes extinct in that particular person. Then they're always from that point going to absorb a lot more dietary oxalate. And then I think the number of people that now have dietary oxalate issues has increased substantially and I certainly tied in with that. Now the other side of that, I suppose is that the issue with all Proteobacteria, broadly speaking, in that category, and that's something I love about eubiome result, for example, is we get an actual percentage of Proteobacteria that's in their ecosystem it could be 0.1% or it can be 20% of their ecosystem, can't be Proteobacteria. And it's far more useful than a three plus or two plus one in some of the older style stool analysis. Because you work at actually how big of a role are these things actually playing in that ecosystem? Because Proteobacteria are all gram negative, which means they contain endotoxin in their cell wall. But the core thing is that all Proteobacteria have very pro inflammatory endotoxin. And this might be why some microbes that have beneficial roles, like Oxalobacter, if levels are very high, they're still turning over and releasing that endotoxin all the time into the gut. And if you have 0.1% Proteobacteria, hugely different endotoxin pool in your gut compared to if you had 20% Proteobacteria. And you're always going to be absorbing some of that in certain dietary approaches will make you absorb far more of that endotoxin. And then we know endotoxin itself causes gut damage, but then it causes systemic inflammation. Leaky blood, brain barrier totally being linked into anxiety and depression these days and Alzheimer's disease, as well as impacting insulin sensitivity too. So I think endotoxemia is a huge, huge issue. And as a naturopath, it's great coming back to the research on that because it's something that naturopaths have pinged on about for a long time, bacterial endotoxins. So it's nice that the research is catching up to where we've always been.

Yes. And that basically all that coconut oil that's been slathered on everything might not be that great after all in terms of high fat diets being associated with LPS absorption, which is really begs the question. I have patients that definitely they've put themselves on a ketogenic diet and they definitely feel much better. I mean, it's complex, it's not always going to be A to B to C kind of pathways with microbiome. I mean, there's a lot of metabolic issues going on for many people. But it is something that I've seen is where as soon as they get off a ketogenic diet, they start feeling brain foggy and fatigued and all sorts of things. So it's really interesting and time will tell how. And as we gather more information about how these different phyla really respond to different diets, I think this is going to be very fascinating as we find out more.

It certainly will because there is really a policy of research that's looked at that, and there was one mouse study and the author said that the ketogenic diet was like an antimicrobial treatment on the colonic ecosystem. It's like, whoa, I don't think that's what you really want from a dietary approach, broadly speaking, for your gut bacteria. But then there's other research showing that what you'd expect, which would be in humans, increase hydrogen sulfide gas producing bacteria because they eat the bile that they are producing. Lots more of decrease in diversity of the ecosystem and increased numbers of Proteobacteria too, from memory, which might be most due to the hydrogen sulfide gas producers in that instance. But as you know too, that there's people that have their ketogenic diet is eggs and bacon and sausages. There's other people that it's like lots of olive oil on us, huge leafy green salad. And that's obviously extremely different in terms of the impact it's going to have on that ecosystem.

Yeah. Okay. So another overgrowth that I often see and often on a stool test with particularly constipated patients is actually Akkermansia. Is that due to the. Just the mucus that is overproduced due to the constipation? I mean, you know, I just, that time again see that elevated.

Yeah. Okay. I'm just trying to think because I think Genova is, I think less able to give me quite the same detail as what a eubiome does for actual percentage of Akkermansia and Amantha is in the gut. So I see more perhaps variations when I'm using a Eubiome than I am Genova. But I do think, just going back to that observation, that I'm just trying to think, certainly I have seen that raise up in some constipated patients. But the core thing that seems to run through is gut inflammation and increased production of mucus tends to increase Akkermansia, if it's there, you get people where it's extinct from the ecosystem and then it's not going to actually show up, even if you're having lots of mucus there. But I have had patients who are made up 20% of their ecosystem and these are people that were just pooing out mostly mucus and it's like, yeah, okay, because we know that Akkermansia is a mucin eater, so that would make sense. But for me it's usually a sign of inflamed gut when they actually have high levels of Akkermansia when it's like double or triple, what levels are, it's like, yeah, I think your gut's inflamed, that's why. And we treat the inflammation and then the Akkermansia goes down as a consequence because there's less mucus being secreted to try to deal with the inflammation, which.

Is sometimes hard because to convince your patient they're inflamed when calprotectin is normal, Sig A is normal and their eosinophil protein X is normal, or at least not elevated, you know, So I know that there are other ways of being inflamed without those markers being high, but still, it's a good tool.

Yeah, it is. And it is interesting. Just the number of people that poo out mucus, for example, and still have normal calprotectin too. It's like, yeah, I know that there's something. Yeah. And we know that calprotectin is a great marker of gut inflammation, particularly more severe end of things. But I think there is something that's missing in that sort of low grade inflammation type scenario where we're obviously inflamed enough to be secreting heaps of mucin to try to deal with that inflammation, but not actually having markers like calprotectin or lactoferrin go up as a consequence.

So moving into more probiotics, and I know that you have really championed the cause to change our vocabulary, vocabulary to stopping this idea of recent reseeding, which I appreciate. We're not reseeding with probiotics. If you're still using those words, please stop using those words.

Yes, please, please.

What would you suggest we exchange for reseeding or repopulating?

I think restoration is probably the best word that we've got because that's essentially what we're doing in those situations. And probiotics can be part of our toolkit to help us restore that ecosystem. But certainly current generation probiotics are particularly poor at actually colonizing long term. And we've got 40 years of research showing that pretty clearly. You can sometimes find 1 out of 100 studies showing that that particular bifid bacteria strain did stay in 20% of people for six months, but the majority show that they're only there for a couple weeks and each day that the number actually goes down, sometimes they're completely gone for weeks. So they're not receding in that way, but whilst they're traversing through it. And I think their biggest role here is for extremely disrupted ecosystems, like just during antibiotics or during or just post antibiotics or chemotherapy or radiotherapy, where there's a huge ecological vacuum and that, you know, sometimes you have a million fold decreases in certain bacterial populations. So there's a huge amount of empty space for the antibiotic resistant microbes to grow into and or something that you've ingested that normally wouldn't have a chance to take a hold, but does when there's a huge amount of food and space on offer. So I think probiotics come on, and I always explain it like an empty car park versus full car park. Your gut is normally like a very full car park. There's very little space for new microbes to take up a spot and it just sort of pass straight out again out to the car park because there's no place for you. But post those very traumatic gut insults that boom, there's a huge amount of parking spaces. But what the probiotics will do is temporarily take many of those spots and consume some of the food that's available. And also in that process secrete lactic acid. And that's one of the things, or acetic acid too, potentially too, that we can say are pretty broad across Lactobacilli strains and bifidobacteria strains is the capacity to produce acids. And that helps change that ph environment that's more conducive to most of our beneficial microbes in our gut.

And actually, I forgot to mention that you do have a really good segment on short chain fatty acids, I think, in your course. And the importance of not just butyrate but propionate and acetic acid. Yeah, acetate.

Yeah. And we also bust some of the stuff around delactate as well because I think that we got a bit lost in that area and partly due to marketing concerns by certain companies.

Well, actually, you know what, I actually had a very interesting conversation with Dr. Satish Rao, who's this researcher who actually brought SIFO into the limelight because he did a lot of aspirates and found about 25% of SIBO patients. There's a comorbid SIFO, but very interesting conversation. And his research is actually into D lactic acid acidosis. And I'm going to try to get him on the podcast because he actually thinks it is more common than previously thought. So stay tuned listeners. But it is something that has, I think, been over emphasized in certain segments. If you're in North America, you probably don't know what we're talking about, you know, but if you're in Australia, you probably do know what we're talking about. There are segments or sectors that really emphasize the D lactic acidosis.

So.

And which, you know, it's a fascinating topic and certainly we're not trying to discredit anyone. It's just that we, we want the research to show that this is really the case, I think. Okay.

Oh yeah. It's also like who, who gets blamed for the, for the D lactate when there's certain species that seem to. That are producers of D lactate that are currently in that same approach. Are people trying to feed up those species yet they're actually the biggest producers of te lactate. It's just that there's too much inconsistencies there that need to be pointed out and discussed and considered.

Okay. Now you were the one that broke the news on biogaia being used being really effective for methanogens or at least in this study it showed to reduce methane production. Yeah. And did you know that there is a new study using Bio gaia using only five drops that when used concomitantly with PPIs, that it prevented the formation of Sibo or the development of Sibo?

Yes.

Oh, yeah.

I just wrote a book so I.

Could break it to you. Darn it. Okay, fine. You are on the ball with all of these things. No, I just found out about it, so I thought that's really cool. Okay.

It was very cool because it was like a 12 week study where they gave, you know, children PPIs. And what was. There's a few fascinating aspects. One was 56% of kids in 12 weeks developed SIBO in the placebo group. 56% in 12 weeks, which is on PPIs. Yeah, think about that. Three months. And how many people are on PPIs for three months or more and how many people developed SIBO? 56%. Outrageous. But when they gave just five drops of the Biogai strain that was reduced down to 6%, people actually developed SIBO and none of those kids develop new symptoms. Whereas where the number of kids in the placebo PPI group develop new gut symptoms, which is not surprising because they developed SIBO about 56%.

It's just staggering.

Blows your mind. I think In Australia there's 19 million prescriptions for PPIs per year and we only have 24 million people.

Wow. Yeah, yeah, yeah, yeah. It's. I actually had a super fascinating podcast with Dr. Steven Sandberg Lewis and that's going to be released soon. But he's writing actually a book on gourd or GERD if you're in America and he's really an incredible mind and so much knowledge about all the little nuances of esophageal reflux and bile reflux and lots of different aspects of, of what to look for and, and how we've over focused on H. Pylori and all of that. So. And he, you know, it's just a really great podcast for those of you who are fascinated with that topic and, and how to get off of PPIs and all of that and that there's like actually the new guidelines. Yeah, the new guidelines now like even with Barrett's, unless you're symptomatic, you should not be using PPIs, which is huge because most people that are chronically on PPIs are for either Barrett's prevention or they have Barrett and are told to stay on it for life on PPIs. You know, so that's, that's a huge development there. And so that's a great podcast if you haven't listened to it yet. Dear listeners, now my last question as we wrap up is because my research into hydrogen sulfide, the only really probiotic that I came across was L. Plantarum LP8, which is a research strain of Alplantarum. And this is always the frustrating bit when you dive into the research that yes, it looks really promising that you come across a strain that's been used successfully to treat something as difficult to treat as hydrogen sulfide overproduction. Any thoughts on. Well, let me just finish my thought on that. It was LP8.10 billion unit a day or colony forming units a day for four weeks and not only decrease desulf but also increase butyrate and bifidobacterium. So which is interesting with El Plantarum. Now is there any, is there any way that we can use just L. Plantarum? I know what you're going to say, Jason. It's like apples and oranges probably, but. But what can we do if we can't get that strain?

Yeah. In situations like this, and I think this is where it's okay to experiment with other strains of LPlantarm. The problem is you can't guarantee we don't know whether they'll work or not. And I think I gave a lecture on this just last week looking at IBS literature and there's LPlantarm 299V, which most of us will be at least somewhat familiar with, if not very familiar with. Very good research profile on IBS. And there's another strain which I think L. Plantarm MF1298 from memory that clinically trialed in people with IBS and actually made their symptoms worse. People prefer placebo over taking this MF1298 foot plantarum strain. So a few genes turned off or on made the difference between it being an efficacious treatment versus causing harm to these patients.

Interesting.

It's worthwhile just keeping that in the back of your mind that I think again that I'd be happy to experiment with 299V which is a well researched.

Strain that makes sense, that makes a.

Decent body evidence behind it in ibs. So it sort of makes sense and has got some gut anti inflammatory effects, et cetera for sure. But you just don't know whether it will have the same attributes or not because sometimes they might share some genetic capacity to produce certain compounds. Like we can look at. Oh, you know, why does the biogaia strain for example work for preventing sibo and it's most likely due to the production of reuterine, which is an antimicrobial compound that works against E. Coli and bacteroides and streptococci and staphylococci.

Oh, reuterin. Oh, there's a comment.

I thought it was based on motif.

But I guess not.

Well, I think for the methane thing possibly, but I think for this, that's my postulate anyway, is this production of uterine and only some reuterized strains produce it. So obviously a strain that doesn't produce uterine is going to be useless in this instance, whereas other strains that do, even if they don't have that same motility enhancing effect might work because of that, that aspect of production of uterine. So rain seems to be teased out, but I think the reality is that, and I've been stuck in this bubble for 18 years of looking at research going damn, why can't we get that strain? Why can't we get this one? This one? And it's been fascinating to see those things for each the market. Like look at the GR1 strain of rhamnosis and RC14 strain of fermentum that I was reading about for UTIs and vaginal thrush and bacterial vaginosis for a decade, craving them to come into clinical practice and eventually they were available and I was on the moon at that point. So I think the timeline between research and actually reaching the marketplace is less than probably before. But then again also, I mean you and I practice in Australia where the market is slower anywhere else, slightly, slightly slower, bluntly. Yeah. So strains like that will probably become available in Europe and they'll probably be available in North America before they ever reach our shores.

Okay, now I thought it was my last question, but it wasn't. I have one last question because you're also a master herbalist. So I have to ask you, any favorite antimicrobials for disulfovibrio or do you plain. Do you just do it with diet? Do you not even bother? Because, you know, given the fact that it's a proteobacteria, although with desulfavibrio it's one of the most resistant to antibiotics strains, as I've read so. Or bacteria. So is it similar with herbs that you find? Because I just use my tried and proven other antimicrobials. But I just wanted to get your take on, you know, if you use and if it's really sky high, what would you use?

I'm contemplating on that because I think most of the people where I see it sky high, I see that their ecosystem is completely disrupted. So often the last thing I want to do in that instance is put more antimicrobials in, to be honest. And I'm really focusing more on improving, changing the environment so it's less conducive to its growth and depriving it of food sources. Those are probably my core, core approaches. And we know that some, I mean, there's some research on galactoligosaccharides by amino gauss for decreasing disulfavibrio, so I would try to use that in patients. And there's also research on inulin phos for decreasing bilophylla, which is the other one other main hydrogen sulfide gas producer that doesn't show up in Genova but does on a Eubiome. So those things might be part of my toolkit. Depending on people's degree of gut visceral hypersensitivity, certainly gauss would be probably more likely to be the case. And you do see it go down and you can deprive it. And this is where I said it's challenging to work with people's diets because they have to reduce their fat intake, which is essentially creating all the bile that's they're eating the bile acids and often produce their protein intake and have more fiber. And this is where it's working with that patient to see what's actually possible in that scenario. Having more polyphenols, I think are helpful too, anything that changes the ph, because I do see clinically that the growth of those microbes is PH dependent, as it is for most Proteobacteria, there's the odd exception, but most respond to anything that ups short chain fatty acid production in the gut substantially or in the colon will create a more inhospitable environment for proteobacteria, including those two. But you're also trying to focus specifically on depriving them of bile to eat and also sulfur compounds too. And I think, you know, you do similar things too. I know Neurala, where we're cutting out obviously the sulfur based preservatives. Sometimes you've got to go beyond that with some dietary things too. And overall protein intake too. Because the sulfur containing amino acids seem to be involved with increased production of hydrogen sulfide gas too.

Yeah, there is some slightly conflicting research on that, although the research I came across was quite compelling. But Alison Seebaker just sent me another research study regarding that, but it's too soon. So I think that, you know, I think that whole hydrogen sulfide issue will become so interesting when we have the capacity to measure breath hydrogen sulfide. Because if you have a motility impaired person with hydrogen sulfide production in the small intestine, that's gonna be really interesting. As far as not just dietary approaches, but I find like it's, it's tough for them to really utilize some of the prebiotics. So I do think finding herbal solutions that are short term just to reduce that number would be really helpful. I just, you know, I use same approaches for like E. Coli or so I use berberine containing plants and stuff and you know, tend to have some pretty good success with that. But I have a feeling that there's other, maybe more potent herbs out there.

Yeah. And I think you're right that once we have tools with quicker turnaround times, which means we can probably experiment and see acute changes. So we can give. And I think it's approaching it systematically, which, and perhaps if you really want to find out what herbs are doing, just give that herbal mix and then you can do some pre and post testing with hydrogen sulfide gas test if that becomes something that becomes easily available. I think that will certainly help us guide our decision making in a far more quick manner. Because certainly for stool testing it's often weeks before you get results back. So it's hard to gauge things and you certainly just don't want to just try one thing. It's like you often just throw a few things at it and yes, there's a change, great. But you couldn't put your finger on exactly which of those aspects is brought down. But I think that's exciting actually, because, because I think you're right and undoubtedly there will be herbs that are effective. But because these microbes are only things we've only recently been able to see properly because we're using DNA that there's been obviously very little if no research on them showing what herbs kill what which we often have for a lot of other pathogens or fungal pathogens, but.

Not well, we've done we know certain, like berberines are pretty good for, for proteobacteria in general, but because they're so they have different mechanisms. But you know, I know that it's in it's DDW week, I think right now weekend where it's like the Digestive disease week where Dr. Pimento is going to make some big announcements regarding hydrogen sulfide. So we'll hear about that at the SIBO Symposium next week in Portland. So anyway, stay tuned, listeners. But back back to the wrap up in terms of this amazing course that Dr. Jason Horlock, who's obviously the master of the microbiome, is presenting. And if you'd like to find out more, you can look at the show notes to this podcast or go to thecebodoctor.com where this course is featured that will run a promotional if this is the introduction to the promotion, we'll run it for three weeks. And so hopefully you can join us for this course. And also I'm always reminded by my staff to include in the end two things. Number one is join the conversation in the Facebook practitioner group called the SIBO Dr. Practitioner Forum. And also if you've liked this podcast or other podcasts, please leave a review in itunes. We would really appreciate that. Okay, Jason, thanks so much for your time. Once again, I know you're going on vacation before we're launching this course, so I wish you all the best on your vacation. I hope you get a lot of R and R and warmth where you're going.

I am looking forward to some warmth, yes, I can assure you, and warm ocean water very much.

Nice. Very good. Okay, great. Well, we'll touch base again. For those of us joining in the course, there'll be a live Q and a with Dr. Horlak upcoming. So we stay tuned for that. But for those of you who are joining us for the course. So thanks again and all the best.

Thank you for listening to the SIBO Dr. Podcast. We hope you found the information this episode useful in the treatment of your SIBO patients. Thanks to our sponsors, Sibo Test.com, a breath testing service with easy online ordering and Quintron, maker of outstanding breath testing equipment. Tune in again for another episode of the SIBO Dr. Podcast. Thanks again for listening.