Gut Parasites with Dr Jason Hawrelak - Part 1

Welcome to the SIBO Dr. Podcast with Dr. Nirala Jacoby, a US trained naturopathic physician and medical director of the SIBO Dr. An online education resource for practitioners. This podcast is intended for SIBO treating practitioners and aims to help educate how we may best serve our SIBO patients. Medical experts join us to discuss functional digestive disorders, clinical practice and research as it relates to SIBO and associated conditions. Head over to thecebodoctor.com where you can learn everything about SIBO from the basics to advanced treatments. You can also join in the conversation on the SIBO Doctor Practitioner Forum Facebook Group. If you're a patient, please note this information is not intended to diagnose or treat medical conditions. Please ask your doctor before initiating any new treatments. We welcome you to head over to the SIBO Lifestyle Facebook group where we post frequent tips and videos to help you on the road to gut health recovery. And now over to Dr. Jacoby and the SIBO Dr. Podcast.

Welcome SIBO practitioners to another episode of the SIBO Doctor Podcast. And with me today I have one of the show's favorites, Dr. Jason Horlak, who is the third time now on the SIBO Dr. Podcast and always such a pleasure to have him on the show for his wealth of knowledge in everything gastrointestinal. Dr. Horlak is a researcher, educator, naturopath and nutritionist with over two decades of clinical experience. He practices at Gould's Natural Medicine, a very very old natural medicine apothecary over 130 years old, and a clinic in Hobart, Tasmania. Dr. Horlack completed his PhD examining the capacity of probiotics, prebiotics and herbal medicines to to modify the gastrointestinal tract microbiota. He's a Senior Lecturer in Complementary and Alternative Medicines at the University of Tasmania School of Medicine where he coordinates the evidence Based Complementary Medicines program. He also teaches the Gastrointestinal Imbalances units at the University of Western States and five years ago he started the Probiotic Advisor, a searchable database for researched probiotic strains which I have certainly found to be an invaluable tool and is a great tool for anyone with a gut focus in their practice. So welcome very very warmly Jason.

Thank you Narella. It's wonderful to be back and to have a chance to chat with you. I always love our chats.

I know we're always just get off on a tangent so I'm hoping I know you're still a little bit under the weather so I'll keep it. Not as long as we tend to usually go but today's topic is so fascinating to many of our practitioners that are in the field of gastroenterology, because we are talking about parasites. And you've just recently released a course about blastocystis and dientamoeba fragilis. And anyone listening, the link to that course will be in the show notes where you can access it really easily. And so I really thought I'd take this opportunity to chat with you about it because a lot of misinformation exists around blastocystis and dientamoeba. So we'll start with that, but we'll sort of have a looser conversation about other parasites, but we really want to kind of hone in on that. But people also can. I really do advise you to take his class because it just will clarify a lot about these two protozoans. So let's get started about. Let's. Which one do you want to start with?

Let's start with blastocystis, which I'll probably just end up calling blasto, because I've been in Australia long enough that we like, you know, shortening everything we do.

We do.

We'll go blasto.

Great. So tell us more about, you know. Well, my understanding is it hasn't even been classified as an actual parasite for that long. And since then, we've had a lot of time to look at it. And a lot of people, when they find it on a stool test, think, oh, eureka, I found the cause of the problems for this patient and proceed to treat it. So can you tell us a bit more as to what you found in your research that sort of demystifies blastocystis a little bit?

I think the research has shifted around a fair bit on this organism. And I can go back to when I first started practicing and how I approached blasto versus now. And I think you hit on a few things there. But certainly what I would see, what's commonplace is that someone presents with gut symptoms and perhaps the first stool test we do in that case, because they might have diarrhea stools, you know, and they may, you know, had had that since they went to Bali or Mexico or something like that. Oh, well, let's check. Boom. It shows up that they've got blastocystis there. Therefore that must be the cause. And I mean, I made this mistake myself in the past too, is you'd stop your diagnostic workup right there. And I do not do that now. Yeah, I've learned better to just to stop actually there and make that. That leap, because there's plenty of research that's really come out of 10 years, 10, maybe 15 years, particularly when we started looking for the prevalence of blasto in healthy populations. And I think that bit of data was missing before studies would be done going, oh, this person's got diarrhea. Oh, look, there's blasto. Therefore this group of people have diarrhea, they seem to have blasto. So we'd sort of make that sort of link that was there. But once they started doing studies looking at how prevalent are these organisms in healthy populations, and I think the first study was that looked at this in healthy populations with maybe 2008 and a small study in Ireland, and they found 82% of the healthy people had blastocyst. It's completely asymptomatic. And I think that sort of blew their minds because, like, oh, we weren't expecting 82% of this sort of healthy control without symptoms to actually carry this organism in there. And I think there's plenty of data that's come out since that time showing exactly how prevalent it is in healthy populations and even that it actually may be playing a role in keeping ecosystems healthy. And I think that's the other fascinating aspect too, of, you know, that since we're dealing with do testing more accurately and see the relationships with ecosystems in greater depth, like we're now associating blastocyst prevalence or presence with more diverse, more healthy ecosystems, lower levels of gut inflammation than people, that they're actually missing that organism from their ecosystem. And it's now possibly that these protozoa organisms like blastocystis play an apex predator role and actually are very important players in keeping your ecosystem, your bacterial components of your ecosystem in balanced and healthy.

I think that's going to blow a lot of people's minds, what you just said, because we're so accustomed to thinking that we would find it in a dysbiotic environment and that there's some problem. But to consider the fact that you find it in really healthy environments is just sort of like a complete sort of paradigm shift. I think for many people when it comes to this particular protozoan.

The research in 2016 was really clear, showing that the presence of blasted cystis was associated with a healthier microbiome status with greater diversity. And when you didn't have it, you're more likely to have sort of typical western ecosystem, which is Bacteroides dominant. And other research in 2018 showed that asymptomatic carriers, so people that had blasto and no symptoms actually had lower fecal cuddle protectant compared to those that did not have blasto as well as a lower BMI as well. The people with blastocyst were shown to have a more healthier body mass index.

And you're going to go deep into that in your class. I know because I had the pleasure of listening to your lecture about this before. So I really do encourage people to, to tune into that now. But there are different subtypes, right? I mean There are about 17 different Blastocystis subtypes and there was a like, I'm sure you're aware of it. But from 2019, that study that showed that subtype 7, the Singaporean strain, did seem to be more virulent than other strains and really affect microbiota around it. So do we think that there it's sort of a strain specific issue around virulence?

Yeah, and I think when you look at the data more broadly and research on different subtypes, it certainly suggests it's not necessarily a subtype thing. And if you look at the conflicting data around subtype and potential virulence, there's tremendous amounts of conflicting data out there. Some research shows subtype 3 is more likely to be problematic, others subtype 4, others subtype 1. Others show complete opposite things. There's really no consensus around that. But there's plenty of research that are indicating that there's probably strains within subtypes that may potentially be involved with that display greater virulence factors that actually might be key here. And this is problematic for clinicians to tease out at this time point because we don't have the diagnostic tools to actually differentiate beyond for the most part the subtype level. But yes, you mentioned that study from 2019 that was looking at subtype 7 and those isolates. I think there's two different isolates, different strains of size subtype 7 that were isolated and used in the study that were originally probably from asymptomatic patients. And they did show that co culture with different bacterial components of the ecosystem sort of stimulated the growth of some microbes, but actually seemed to inhibit the growth of Bifidobacteria. It may be that one in particular was perhaps good at grazing Bifidobacteria, whereas other subtypes seem to be good at grazing on Bacteroides, interestingly enough. And those subtype 7 isolates, when they sort of injected into the cecum of mice, it had sort of induced sort of chronic inflammation as well and decreased their prefecture accounts in that sort of animal model as well. But obviously it's A slightly stretch to inject these things in high doses versus oral, oral sort of usage, for one thing. And two, it is worth flagging too, that subtype Sevin is generally a subtype you find in chickens and birds, and it is actually very rare in humans. So I would suggest that if someone has symptoms, you've done a thorough workup, and subtype 7 is actually there, then that may well be correlative and that may be causative in that particular instance, because it's such a rare thing, versus subtype 3, which is the most common subtype in humans and extremely common in asymptomatic people as well as in people with symptoms. So I don't think you can make any assumptions around subtypes 3 or 4 or 1 because they're so commonplace in. Unlike subtype 7, which is actually very rare. And agree. There's a number, a few other studies that have shown that strains within that subtype may have a greater capacity to cause harm in humans. And even the environmental conditions that subtype 7 likes is a little bit different because they're used to being in birds. So I think they actually like a slightly warmer temperature. So maybe the human gets too cold to be all that happy. So it's like trying to do something to warm the temperature.

Interesting. So what do you mean actually about apex predator? Does it really go after, like, what does it go after if it's a.

Predator, it eats bacteria, is the current thinking around it. And with that idea, what the research tells us that people with Blastocystis generally have healthier, more diverse ecosystems. And the thinking there is that they essentially graze off bacterial populations and prevent one particular genus from dominating. And certainly the research today suggests it's generally prevents Bacteroides from dominating. Yeah. Which I think is fascinating because I think again, you talk about misinformation in the blogosphere or in the World Wide Web. And it totally is because people will make the assumption that blastocyst eats wheat or eats sugar. All these things are such widespread ideas. But we know it actually eats bacteria. That's what it's eating. And you've got trillions of them to have sat in your gut independently of whether you eat those things or not. Yeah. And I think if you get symptoms because you're eating wheat, it's not because it's blastocystis or something else going on the gut that we should try to suss what it is.

Right. Well, and you mentioned. I think this is really one of the reasons I wanted to talk to you about this. Because I know that there are a lot of. There's a lot of misinformation about parasites in general and a lot of very generalized recommendations about parasites. And I think our thinking of, you know, I'm not negating, obviously there, there are some pretty bad parasites out there. But in my practice, I think the most common two are Blastocystis hominis and Dientamoeba fragilis, both of which you address in your course as really not very problematic for the most part. So that really leaves me with very occasionally I find a worm, you know, or I find there's. There's sometimes even beneficial helminths or what we think of as beneficial helminths in certain circumstances or worms. So it's really. There's just not really a great authority I find on parasites out there because also the testing arena is, I think, lacks real accuracy in many, many circumstances. So it's really difficult because we want to be sure as practitioners as that we're treating something that is obviously a pathogen, like for example, Giardia, that is in the same class of group of parasite, so a protozoan that is very different from these other two, that causes a lot more damage and diarrhea and so forth. So, yeah, I think it's interesting. Now, getting back to Blasto for just a moment, talk to us about. Oh, actually, no, I'm on the wrong protozoan because it's Dientamoeba fragilis that uses pinworm as a vector. Right. Like in terms of potentially.

Potentially. There's been so much debate and discussion around how defragilis gets, or defrag, I'm going to call it for short as well, gets passed around. And I think there was this hypothesis a few years back suggesting that pinworms were vector and that hasn't necessarily been disproven. But one of the main supportive arguments for that was the fact that no one had ever seen a cyst form of defragilis. And it's like, well, if we don't see cysts, it's got to be passing some of the way. Maybe it's through that, through pinworm eggs. And yeah, if we do testing, we can see some defrag DNA and pinworm eggs. So maybe that's it and there's certainly data around that. But within the last few years, people have actually seen the CIS form of defrag for the first time too. So that has led some of the newer defrag researchers to think that pinworbs are not really all that important with the sort of passing on or the spread of defrag. And you know, defrag is just so common. And you start looking at research in Western Europe and I talk to my patients about this all the time, but it's, you know, 55% of asymptomatic kids have got defrag in their guts. So I mean, what do we do here? Do we just give them all antibiotics? Which some people would argue with suggest because defrag is present. I mean it brings up a bunch of questions around appropriate, inappropriate treatment to the presence of microbes that are extremely widespread. And this is the thing, once we start testing healthy populations, we start seeing how common these organisms are and we're starting to tease out what role these protozoals play in a healthy gut ecosystem because we're not absent of these bugs. They play important roles just like the fungi do, just like bacteria do. And these protists all have these entwined ecosystems. Never mind the consideration of what happens if some of those organisms out and change that balance that you actually get in that scenario too. But it's such a frequently found microbe and there's some research that found that kids with defrag actually had less incidence of soft watery stool, less instance of diarrhea and less instance of fatigue compared to those who actually didn't have it.

So why do you think it ever was classified as, as a parasite dientamoeba now?

Well, it's an interesting one and I think a lot of the excitement around treatment came from case studies like published case reports where subject A presents with symptoms and diarrhea. We give them antibiotics, their symptoms go away, defrag is gone. Therefore defrag must be the cause of those symptoms. That's I think, where most of the difference comes from. And you look at some of the earlier, sorry, published research on defrag and they're all these case reports, the results look pretty positive. Some of the early ones were like 85% kids got better from taking course of flagyl. But then some of the more recent studies suggest that really and probably most importantly that the one double blind placebo controlled study showed that there was no improvement with antibiotic treatment versus placebo and that placebo, the effect of improvement was about 30% which is you would expect from placebo in an IBS like population. And it was exactly what they saw with placebo. In fact, there's no improvement. And I think that really starts to put some questions around that. But there are people who are still really attached to that approach and are still can easily quote those earlier case reports that have, I think Unrealistically high sort of improvement levels. And really we should be looking at placebo controlled studies if we're going to look at efficacy. And the other aspect is when you give a course on antibiotics, it's not like we're just impacting that one organism's population. We are impacting dozens of, if not more species of microbes. And so it's not necessarily surprising that sometimes we give antibiotics and people's bloating and distension goes down because we probably kill off a whole bunch of their hydrogen gas producing bacteria and their colon too. That probably is only temporary until their populations come up. But it makes you just think of, there's a study published in Gut last year, they're looking at one individual. This slight tangent here. We like going on tangents. They gave him a course of eye, IV antibiotics, ceftriaxone, I think it was, IV antibiotics went off shot and nine species went extinct. Wow, nine from that one course of antibiotics. And you're like, well, who knows what impact we're having on that gut by giving that course of antibiotics. It's not just the defrag, it's not like you're specifically targeting that. You're changing a whole bunch of different things in that ecosystem.

Well, you know, that really brings up this whole idea of sort of ancient species that we co evolved with and Blastocystis potentially is one of those. And we're making our environment more and more sterile in a way. But you know, actually where I was going with that is that some of the research that came out of or the research that I looked at in terms of parasitic studies that have looked at migrants and people coming from developing countries into the western countries and not just adopting the lifestyle, but when they had stool testing, they had lots of parasites and they were asymptomatic. And then when they received antibiotics for those parasites, that's when their problems started digestively.

Yeah, I'm sure you see this all the time. I certainly do. Where sometimes they had a certain level of symptoms and after antibiotics symptoms flared up dramatically or they've never been the same since. Their sort of antibiotic cocktail they took to deal with the blasto, that's pretty common. And I think there's a bunch of reasons that for species lost, for example, and loss of ancestral bacterial organisms that play pivotal roles in their gut that are now extinct to long lasting inflammation that occurs post those antibiotic usage. Plus the potential impact on those protozoa organisms themselves and the role that they're playing in the gut. But there was some fascinating research published recently showing that antibiotics actually could enhance the virulence factors, the virulence of blastocyst isolates as well, which I thought was fascinating. So we're actually encouraging them to behave poorly by exposing antibiotics. Another potential reason why that's problematic.

Yeah. And really one of the reasons I wanted to bring up this topic is because so many, like I said at the beginning, there's so many patients that I see that have been through this very journey where they have been first diagnosed with blastocystis. I think you shared a case very similar to this, but I see many people like that where they're like, oh, yeah, finally I've got my blasto under control, it's finally gone. But my symptoms aren't gone or my symptoms are worse. So it's that really common scenario that we see because we both have basically functional gut clinics where we. Where we deal with a lot of the fallout of this type of approach and really clarifying this for practitioners, because you need to keep. If you find blastocystis and dientamoeba and. Or dientamoeba fragilis, I think basically the message here is keep looking as to a cause of that patient's symptomatology. Right. Would you agree with that?

I totally agree with that. And as I said, I was guilty of not doing that in the past. And I had one of those scenarios of seeing a patient, I think it was 12 or 13 years after I saw him the first time and had a chance to see how I change as a practitioner, both in terms of treatment, but particularly from a diagnostic workout perspective. And it makes me realize that whilst I did the best I could at that time, with the knowledge that I had and my skill set, we essentially miss pivotal diet. And I've seen this before. Other patients have come to see me recently where diagnosis like celiac disease was missed because a number of practitioners were so enamored by the blastoise, the cause of the symptom, that they stopped the workup right there. And then what are the consequences of that person having celiac disease for another three or four years until it gets potentially diagnosed? It's absolutely huge. So I think it's vital that we as clinicians don't stop at that time point that we go, okay, that's interesting, but let's actually keep digging. Given that how common these two organisms are in healthy populations, we can't make the assumption that these are the causes of symptoms in this person.

It always helps when I tell my patients, look, I've got blasto. I'm fine. You know, I'm fine. Even if I wanted to treat it, it would just come back, you know, no problem because we live in an endemic area.

So, like, I did a stool test for, you know, for an experiment, you know, one my lab at my stool left a whole bunch of different labs, and it turns out, oh, I've got blasto and defrag and I've got symptoms. I'm not fatigue. You know, I don't have any of the symptoms people associate with that. So I think I agree. I tend to share that with patients too. And now I shared it with the whole world.

Great, Fantastic.

And I'm proud.

It's like, you know, it's like getting back to that kind of rewilding of our gut in a way. But I can also imagine a scenario where you would have, like, where it could cause problems if it eats bacteria and you start off as somebody that has a really, really low diversity and really just low in everything, that it could potentially cause problems if it's something. If it's an organism that likes to feed off of other bacteria. You know, I mean, I could imagine a scenario like that.

Yeah. And I think it comes back to those naturopathic ideals we have of that the train is most important, not the organism that would. If we change the train and improve the microbiome health, improve their health, host health, improve gut functioning in general, that we change the environment. So it's not so conducive to sort of more pathogenic side of a range of organisms in the gut that we would classify as pathobion. So those that in long balance, the wrong conditions can cause harm, but in the right amounts actually have a healthful role to play in that ecosystem. And I think we, as you know, natural medicine practitioners have got that important aspect of our philosophy that I think sometimes we've forgotten that the train is important. And if we actually optimize them, optimize our overall health, then it's maybe at first surprising, but later off not how your patients are improved. And they still have blasto or defrag. And it's completely irrelevant because they're doing great and their gut's going great and they've got a lovely, healthy ecosystem now.

Yeah. And it's definitely been, you know, I can understand that that journey is sometimes difficult for practitioners because it's easy to kill something. You know, it just seems. It seems easy to use antimicrobials and things like that and use much more of a judicious approach for the terrain is sometimes or a more measured, I should say, approach. And I have to say that in my years of doing this, I'm much more hesitant to just go in there and start killing. So definitely that's been my experience. And I hope that people listening will also kind of pause and think about using caution when you're dealing also with parasites now. Okay, so the mesh. The message here with those two blasto and defrag is just keep looking. If you find them, they may not be the cause of your symptoms and patients listening. Obviously, this is not meant as medical advice. You still need to talk to your doctor and your medical provider because we don't know your certain. Your circumstance. Would you say that there is a concern in those that are perhaps immunocompromised or is that that totally irrelevant?

I don't think that's backed up with the data to date. In fact, plastic seems really uncommon in colorectal cancer, extremely uncommon in inflammatory bowel disease. Patients like Crohn's and UC patients are far less likely to have blasto present than healthy controls and things colorectal cancer. So I think the data today doesn't suggest that that's necessarily the case. I mean, there's still lots more research to be done. So we'll see as we start, as long as we can start doing studies, case control studies a bit more appropriately, where we're actually matching to healthy controls. And I think this has been one of the biggest issues with blasto studies to date, is that they're looking at a disease population and then going, oh, look, there's an association rather than going, okay, well let's age 6, match healthy controls and see whether they've got blasto or not. And we start doing that, we start getting different test results. It reminds me, there's a study that was done in Senegal, I think in Africa, and looked at kids with chronic diarrhea. And 100% of these kids had blastocystis. And if they would have stopped there, they would have gone, hey, 100% of these kids who are blasted, that's obviously problematic. But they tested healthy controls as well, and 100% of them present too. Okay, we can't make the same leap that we would have made before that. So I think for some of the things that we're talking about here, I think probably remains to be teased out better. You would guess, based on the data that we have, that in people whose ecosyste systems are far more, you know, less healthy, less. Less diverse, more levels of, you know, pro inflammatory species, pathobiome crappier, sort of west, you know, sorry, more standard American, Australian diet. Lots of, you know, food chemicals that cause gut damage, lots of antibiotic usage that might increase the virulence of some of these protozoal organisms. Then yeah, there's probably an increased chance of them actually being problematic in certain populations versus not if you put that same microbe in a healthy person's gut. Wouldn't be a problem.

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. Thanks to our sponsors, Sibotest.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.

Sam.