Nirala Jacobi:

Welcome back to part two of The SIBO Doctor Podcast, and let's jump right back into it. Okay. So that's another good segue to talk about... Before we talk about how would you identify it, let's talk about the different types of stool testing that's available, and I've already given a little teaser on this topic in my previous podcast about different stool tests. So we have your basic culture, we have a PCR test, and we have this metagenomics test called Shotgun Metagenomics. Can you just briefly differentiate between these tests?

Brad Leech:

So you're exactly right, and that's one thing... I'm not sure about yourself, but when I was going through my undergrad degree, there was no training at all or no education when it comes around to sequencing the microbiome. It was basically your patient has dysbiosis, give them a probiotic. That was almost the extent of microbiome training. But when you actually dive deep into the literature, you actually get an understanding that depending on the method used to measure and sequence, the bacteria will actually determine the results and what you can do with the results.

So as you alluded to, we've got a number of different methods. We have culture, we have a 16S PCR, and then we have metagenomics. Now, PCR, a lot of people would be familiar with this term given it's commonly described on the news to identify a virus, especially the COVID virus. The PCR is based on testing and probing for particular bacteria. So you've got 16S sequencing, which uses PCR to amplify a particular region of the DNA.

I like to give the example of a jungle. Okay. So, hypothetically, you're on a safari in Africa, and the tour guide says, "We're on the hunt for an elephant." So all you're looking for is an elephant. You've got your goggles on, you're looking for an elephant, and straight ahead, you have an elephant. Fantastic. That is PCR because we're actually trying to identify that one particular species or genus level. Whereas if you're looking at other realms such as metagenomics, it's almost like you're going on this safari, and it's like, "Well, let's see, and let's count everything that we can actually possibly see." So we've got butterflies, and birds, and lions, and elephants as well. So we're not just focused on the elephant, whereas metagenomics, we can see a much larger variety because we're not governed by the technology, which is basically just a probe where it's like, "Do you have this? Yes or no? How much of that?" and giving out a quantity.

So the other method that's becoming more accessible is metagenomics. Now, to put this into perspective, metagenomics has actually only been accessible to clinicians only in about the last five years. So before that, it was only used in research. It's only very recently been able to be utilized by clinicians and patients themselves. In this method, DNA is extracted through the sample and sequenced. Now, it does this by almost as the name describes, shotgun. It almost breaks it up, and then through a variety of different methods, able to sequence and understand, "Well, who does this line of bacteria belong to? Which bacteria does this belong to? Fantastic. We can group it there."

Now, by sequencing the DNA in the sample, this method not only tells us who is there, but it's able to tell us what they're able to produce. So we know that different proteins are released or formulated from DNA, and that's the same thing with bacteria. So depending on their food and their fuel source, and depending on their genetic makeup, they can produce things such as butyrate or they can produce other functional markers such as LPS purely based on their genetic makeup.

So if you were to compare the two frequently used methods, let's say, here in Australia and abroad, you've got 16S which sequences using PCR, whereas you've got metagenomics, which can actually identify, and I think last count, up to about 6,000 different species of bacteria. So the take-home message here is 16S PCR can identify, let's say, the genus level of bacteria, and it can only identify what it's set out to look for. With metagenomics, you can actually take a step back and look at a larger number of species, almost all the species, and actually understand what they have the capacity of doing.

So what's more important to remember here is its function over gene or function over species. So when I say function, that is what does the microbiome or what does that particular bacteria have the capacity of producing? Is it a good guy, or is it a bad guy, or do we not probably... just unsure whether or not it fits under the good/bad category? The best way to look at that is to go, "Well, what does this bacteria do, and what does it produce?"

I mentor a lot of newly graduated naturopaths and nutritionists, and I'll give you example here on why metagenomics in the coming years is becoming more frequently utilized. My example I'll give you is if I was to place a list of a hundred different species in front of a newly graduated naturopath, nutritionist, or even functional medicine practitioner, I would guarantee that they would look at this list of species, and there would be limited clinical utility with what they could actually do with that. Whereas if you were to actually provide them with a, "This is what the microbiome has the potential of doing. It has the potential to produce butyrate," they will go, "Ah, uh-huh. This is a beneficial thing. I understand this. Let's support this pathway, which may then, of course, go on to support with the intestinal permeability." But it's interesting whereby the depth and the amount of information that we can gather is significantly more.

So another example I can give you is in most people, you generally have around that 150 different species of bacteria, and that's coming from 6,000 different species that they could have. Now, I had a patient just, well, two or three weeks ago, and I was looking at their metagenomic microbiome, and they actually had 270 species. Now, that's a huge amount, and that is absolutely fantastic. Their diversity was excellent.

I compare this to a patient I had probably about a year ago now who had inflammatory bowel disease, Crohn's disease or ulcerative colitis, and was on long-term antibiotics. Using metagenomics, I could actually see that this particular patient only had 22 species of bacteria in their gut, which when you take a step back and just look at that, it provides a lot more clinically useful information to say, "Well, this patient with 22 species, even if you know minimal about the microbiome, you can generally say, 'Well, hold on. We need to do a lot of work here,' when it comes around to gut health." Where the patient that has 270 species, and the vast majority of those were beneficial, there's less work to be done there. So it's just fascinating the depth of information that you can gather when looking at the whole microbiome.

Nirala Jacobi:

So I have a question about that because first of all, I want to clarify to the listeners that we're talking about stool testing, which means that you will get information about your microbiome that resides in the large intestine. You won't get any information from a stool test about the diversity in your small intestine or if you have SIBO or any of those things because that's just not possible with a stool test.

Brad Leech:

Mm-hmm, mm-hmm.

Nirala Jacobi:

So if there are over 6,000 species or the potential is there, 250 still doesn't sound like a whole lot. I mean, I get what you're saying, but are we getting closer to reporting more than just a few hundred? The lab that you work for, is it possible to... Is it coming soon that we continue to increase our species information and maybe are able to identify it? Because if you're saying that this shotgun is able to basically record everything that's there, then 250 species still doesn't sound like a lot.

Brad Leech:

It doesn't actually sound like a lot, but when you look at that, there's, let's say, a database of 6,000 species that could be in your gut. That's almost a fantastic question. I'd love to know what would happen if you put all 6,000 species into someone's gut. Would that actually be a good thing, or would that actually be a bad thing?

Nirala Jacobi:

No. I think it was like going... You remember that study that was done on... I think it was the Hadza tribe, and they're... Basically, disappearing old species that have always lived with us are disappearing in terms of species of bacteria, and because of our more sterile environments, and our food supply, and antibiotics, we're actually killing out these ancient... or killing off these ancient species, and the study, I think it was... I can't remember exactly when, but it was a pretty famous study that looked at the diversity of people that had very minimal contact with so-called civilization, and they had an incredible abundance of bacteria. So it makes sense that you would also require a lot more diversity when you live a lifestyle like that.

Anyways, I just wondered if what we're seeing is a species loss that's not just macrocosm, but also microcosm, and I think we're seeing that. I certainly see a lot more microbiome issues in my practice than I did 20 years ago, but you're right. Our ability to diagnose that was much more limited because the Human Microbiome Project hadn't really been initiated at that point. We were not even on... The Human Genomic Project was also not completed when I was going through school. So there's all this stuff that we are learning about the genes of bacteria are actually... I mean, this is where we talk about what is your microbiome, what's the ability, what is it producing, and what is it doing for us because that's really where, I think, the mystery still is unfolding of how are these organisms connecting to us, and how are they communicating with us, and what are they doing for us.

Brad Leech:

Mm, and it's interesting. We look at 150 species, and we're like, "Oh, that's not a lot." But if we actually take a step back to 10 years ago, the level of microbiome sequencing that you could get in clinical practice, it would basically be... You've got lactobacillus species. You've got bifidobacterium species, one or two pathogens. It'd be less than 20 genus level organisms that testing facilities had the capacity to do. So this is actually a huge jump forward to be able to say, "Well, hold on. We can actually identify down to a relative abundance of about 0.001%," which is a very, very, very small amount, and maybe what you just said there in relation to these smaller quantities of bacteria, they could be dying out whether it is through the exposure of glyphosates or whether it's through our diet, reducing the type of diversity in our diet, and then thereby, the fuel sources for many of these bacteria.

Nirala Jacobi:

Mm, and antibiotics that are in our food supply even. So, I mean, think we're both agreeing. It's just always so fascinating to me that we're discovering so much about the microbiome, and we're seeing its decline. It's almost like we're exploring the rainforest while we're seeing it being chopped down, so it's interesting.

Brad Leech:

It's fantastic. When I measured my microbiome probably about 6 or 12 months ago, and this is someone... I've never taken antibiotics. I've been vegetarian my whole life. I grew up on a farm. I've got everything going. I was breastfed. I was born vaginally. Probably too much information for the listeners, but to look at the species and to look at the number, I had around that 200 mark. So that's somebody who's almost ticked all these boxes, no diseases, exposed to nature, and from that perspective of, "Oh, wow. Okay. That's actually a substantial amount of bacteria."

Nirala Jacobi:

Okay. So the benchmark is... I think I did when I did that workshop with... I did a workshop a while ago, many years ago with Dr. Hawrelak, and I won the prize for species diversity. So we should have a species diversity.

Brad Leech:

Oh, congratulations.

Nirala Jacobi:

Like a microbiome show-off. That'd be cool.

Brad Leech:

Sounds wonderful.

Nirala Jacobi:

I know. I was like, "Okay. I should just probably package and sell my poo for FMT." But anyways, it made me feel good because I also have a very pristine diet, some would say, and that goes a long way. Okay. Let's move on to... We talked about that microbiome imbalances can induce intestinal permeability. So what are some of these markers that we're looking out for if we're considering that the microbiome has induced somebody's intestinal permeability?

Brad Leech:

Mm-hmm, mm-hmm. So, generally speaking, when I look at a report in my clinical practice, there's five... Five? Yeah, five major markers that I'm looking out for. The first of which is the capacity of the microbiome to produce Hexa-LPS, whether or not there's any beef, B-fragilis-toxin-producing bacteria, hydrogen-sulfide-producing bacteria, and then you've got your good guys, which are your butyrate-producing bacteria and your IPA-producing bacteria. So IPA stands for 3-Indolepropionic acid. Maybe, if you'd like, I can dive into each of these in a bit more detail.

Nirala Jacobi:

Yeah. Sure.

Brad Leech:

So starting off with... Let's not be bias here, but my favorite marker when it comes around to looking at intestinal permeability, especially when it's induced by the microbiome, and that is Hexa-LPS. So in vitro and animal studies actually have indicated that Hexa-LPS increases intestinal permeability through the activation of the immune receptor, TLR4. Okay? So most clinicians would actually be aware of LPS, but many would be, for the very first time, going, "Well, hold on. What's this Hexa that you're putting in front of LPS?" LPS in itself can be broken down into many different subgroups. You've got Penta, tetra, hexa. It all depends on the makeup of the Hexa... sorry, of the LPS. Now, what the research is actually indicating is that it's actually the Hexa-LPS, which is the most pro-inflammatory of all the other LPSs. So many different bacteria have the capacity of producing or releasing LPS, and it's really interesting to quantify and really look at, "Well, what does somebody's microbiome... What is their capacity to produce LPS?"

So I recall one patient, and I alluded to this patient just before, the one with the 22 different species. So lots of antibiotic use, but when looking at his overall microbiome, 80% of his microbiome had the capacity to produce Hexa-LPS. So just think about that for a moment that 80% of the bacteria in his gut were the E. Colis, had that capacity to produce LPS. No wonder he has constant flares and his ulcerative... and Crohn's disease. It'd almost be impossible. This is where your magic poop might come in handy is to do an FMT to actually almost introduce some of these beneficial bacteria. So Hexa-LPS is definitely one to keep your eye out for when it comes around to identifying if a patient or if you have microbiome-induced intestinal permeability.

Nirala Jacobi:

Okay. So let me ask you something about that because I don't know any other lab other than your lab, Microba Lab in Brisbane who checks for Hexa-LPS. So what are the bacteria that... We know that LPS is produced by gram-negative bacteria, so Klebsiella, Acinetobacter, E. Coli, and E. Coli and Klebsiella are the primary or the dominant bacterial overgrowth in hydrogen-dominant SIBO. So is both of them species that produces Hexa-LPS? Do we know the exact species that produce this?

Brad Leech:

That's a very good question, and the ones that you've just mentioned, they are Hexa-LPS-producing bacteria. So if a lab can actually identify them down to the species, then you can quite confidently say, "Oh, yes, they are producing Hexa-LPS," but there's around... My best guess is that there's probably around a thousand different species in the gut that have the capacity to produce Hexa-LPS.

Nirala Jacobi:

Okay, and with Klebsiella, we have several different species of Klebsiella. Are they all producing Hexa-LPS?

Brad Leech:

No, not all Klebsiella species are producing Hexa-LPS. It's a very good question. Something I don't know the answer to off the top of my head, but there are a select few of species that can actually produce Hexa-LPS.

Nirala Jacobi:

Okay. Okay. So LPS, right? So lipopolysaccharides is one thing you look out for.

Brad Leech:

Mm-hmm.

Nirala Jacobi:

So if somebody doesn't have access to your lab, and they just do a stool test, and they have a preponderance or a real big overgrowth of these, what we call pathobionts, right?

Brad Leech:

That's correct.

Nirala Jacobi:

So these are organisms that are normal in low amounts. But when they overgrow, they pose a threat, and they become pathogenic. So you can if you are listening and you're just a bit lost in the woods from all this techno talk, but basically, if you've had a stool test and you have a huge amount of gram-negative bacteria present, it's not unreasonable to assume that you also have high levels of LPS as part of your microbiome. So moving...

Brad Leech:

A lot of labs will do that E. Coli, and so E. Coli being a Hexa-LPS-producing bacteria. So that can be a good indicator, but something to consider is because there are so many different species that produce it, you want to collectively go, "Well, hold on. Is it just one species that's producing Hexa-LPS, or are there multiple species?" So that's really what it comes down to looking at species level microbiome. That is quite interesting.

Nirala Jacobi:

Okay.

Brad Leech:

Okay. So others I alluded to was B-fragilis, so B-fragilis toxin. There's been studies to show that this actually impairs intestinal barrier integrity, and it does this by binding on to colonic cells and stimulating the disassembling of tight-junction proteins, so resulting in intestinal permeability. So, basically, there are some strains of B-fragilis that have the capacity to produce this toxin, so B-fragilis toxin, and that's the toxin that results in intestinal barrier function, and then diarrhea. This is a common species that is measured, and it has got a lot of research out there for linking up with diarrhea.

Nirala Jacobi:

It's bacteroides, right? So, bacteroides fragilis?

Brad Leech:

Bacteroides.

Nirala Jacobi:

Mm-hmm.

Brad Leech:

That's correct. So if a patient presents in my clinical practice with diarrhea, I would actually want to go, "Well, hold on. Yes, there's multiple different causes for diarrhea, but is B-fragilis toxin a contributing factor here?" Exactly what you've alluded to earlier on in the podcast, is that... Loose stools is a clinical symptom of intestinal permeability, and it could be that through the B-fragilis toxin.

Nirala Jacobi:

Not many labs test specifically for that, so let's move on, but it's great. It's good to know. I think I've only ever had one person have this, so I'm not sure how common it is, but it is a good marker to keep an eye out. What about the hydrogen sulfide? We know that high levels of hydrogen sulfide certainly causes a lot of gut inflammation.

Brad Leech:

Yes, yes.

Nirala Jacobi:

One of the interesting evolution of us having... in terms of experts I've talked to also is the evolution of our understanding of hydrogen sulfide producers. We used to just think desulfovibrio and bilophila species. Now, we understand that other species can upregulate their hydrogen sulfite production, which is a curiosity to me. Under what circumstances are other species driven to produce hydrogen sulfite?

Brad Leech:

It comes around to the fuel source. Now, this is a fascinating one when it comes around to hydrogen-sulfide-producing bacteria is that the fuel source or what amino acids they're exposed to in the large intestine and possibly even the small intestine will result in the capacity to produce hydrogen sulfide, and the biggest one here, now this is going to be a huge aha moment, is cysteine. So what the research has shown.

Now, a lot of this is mechanistic research, is cysteine or the supplemental form NAC, N-Acetyl Cysteine. Those who have bacteria that produce hydrogen sulfide, if they're exposed to cysteine or if they take a cysteine-based supplement, so NAC, which is a very common supplement in the functional world, that can actually make their production of hydrogen sulfide more severe, thereby resulting in more intestinal inflammation and greater permeability. So it's one thing that I like to... Before I prescribe NAC, I'd like to assess someone's microbiome and go, "Oh, hold on. Is me giving NAC going to actually cause more harm than good?" Now, the vast majority of the time, there's no problems at all, but there are some individuals and I've had a client who had a adverse reaction to NAC, N-Acetyl Cysteine. I actually put it down too that they had too many hydrogen-sulfide-producing bacteria, and that was actually exacerbating intestinal inflammation and permeability.

The other thing to consider here is that in low levels, hydrogen sulfide is protective, but in high levels, it can actually inhibit the uptake of butyrate in the intestines. Now, that almost leads us onto the next marker of microbiome-induced permeability, and that's butyrate. It's almost one of these things where you want to take those hydrogen-sulfide-producing bacteria in combination with someone's butyrate. So we know, and butyrate is probably one of these metabolites, these markers that is probably the most researched out of all of them, and so we know that there's a lot of research. It's protective for colon cancers. It's protective for intestinal permeability, and it's one of these metabolites that we could talk all day about, but some of those research that I actually came across earlier this week, and it was a study published in diabetes, and it was... The title was along the lines of "Butyrate-Producing Bacteria and Insulin Homeostasis." It was this amazing longitudinal study that used metagenomics studies and actually looked at participants' ability to produce butyrate.

Now, the study assessed different butyrate pathways and insulin markers, so fasting glucose, insulin resistance, and so on. What they actually showed was there was about 10 butyrate-producing bacteria that were associated with a beneficial outcome for insulin resistance and insulin, fasting insulin. So the reason I thought that this research is quite fascinating is because in 2019, my own research, we actually came out and shocked the intestinal permeability world a little bit. We said that intestinal permeability is very closely linked with metabolic conditions. So I'm just speculating here. Okay? This is my educated opinion is that I wonder whether or not the link between intestinal permeability and metabolic conditions is actually governed by the microbiome and in particular, their capacity to produce butyrate.

Nirala Jacobi:

Yeah. Pretty cool.

Brad Leech:

Interesting.

Nirala Jacobi:

Yes, very interesting. I mean, for the listener, butyrate or butyric acid is one of the three main short-chain fatty acids that are often measured on a stool test, and butyrate has a lot of benefits, including energy production, anti-inflammation, even motility in the digestive tract.

Brad Leech:

Mm-hmm, that's correct.

Nirala Jacobi:

There are a number of key species who produce this, including faecalibacterium prausnitzii and a host of other bacteria, but this is a fascinating connection to blood sugar, really, regulation. Would you also think that it has some role in hypoglycemia not just through... well, through insulin because we do see a lot of people with hypoglycemia that also have microbiome disorders? Hypo. So these are reactive hypoglycemia and anything that... if you came across that in your research as well.

Brad Leech:

Yes. So that same study actually identified two other species, which were butyrate producers that were actually associated with hypoglycemia, and I thought, "Oh, that's interesting." They just alluded to it. They didn't discuss it in too much detail because it's a very new area of research, but oh, I wonder there as well if it could go the other way when it comes around to regulating blood glucose.

Nirala Jacobi:

Now, and did you...

Brad Leech:

Yes.

Nirala Jacobi:

Did you have another marker that you... or a marker?

Brad Leech:

The last marker is IPA. Now, this is...

Nirala Jacobi:

Oh, yes, IPA. This is not India Pale Ale microbrew, but...

Brad Leech:

I wish, I wish. It would make a life a little wonderful, but no.

Nirala Jacobi:

Yes.

Brad Leech:

It isn't IPA, the drink. It is 3-Indolepropionic acid. I like to shorten it to IPA because that's a bit of a mouthful. Now, the beauty of this one is it's beneficial. So a lot of what we've touched on have been detrimental, excluding butyrate, of course, but when it comes around to IPA, the research is actually suggesting that it's a beneficial antioxidant, and it actually has a role in glucose regulation, inflammation, and maintaining intestinal barrier function. Now, this is where it gets really interesting is that low levels of IPA. So there's only a few bacteria. So the last time I counted, there's probably about 15 species of bacteria that actually have the capacity to produce IPA, and some of these, their name is like CG83. Very bizarre species, but how this actually works is these species that have the capacity to produce IPA, they do that through the breakdown of tryptophan. So when they break down tryptophan, the IPA enters into the bloodstream.

Now, there were some fascinating research that came out in 2020 from Yang. Now, this was an RCT trial out of the USA. Basically, they did an intervention of a particular pomegranate juice called POM Wonderful. Now, this pomegranate juice, it had a polyphenol in it called ellagic acid. Okay? What they actually found was participants that consumed this for a year, it actually maintained their plasma IPA levels compared to a decreased theme in control. So when it comes around to microbiome-induced permeability, IPA is something... It's a protective factor and something we actually want to increase. It almost appears that the number one factor to increase it would be ellagic acid.

Nirala Jacobi:

Hmm, and no other polyphenols or like nothing else works quite like that? I mean, surely, there are other foods that are microbiome-supportive, and usually, plant-based foods, one of the reasons we love them so much is not just because of the fiber content, but also because of the polyphenols and other phytochemicals that really seem to communicate. I mean, plants or bacteria... Our microbiome loves plants, right? So I'm sure that if we come across something else, we'll find something else other than just... because pomegranate juice is fairly... It's not that easy to find. So surely, there's got to be other foods.

Brad Leech:

So it's not just the pomegranates. So the research actually put it down to consuming 120 milligrams of ellagic acid. Now, if we actually put on our research up, we can find other foods that have around 120 milligrams of ellagic acid, and the number one would be chestnuts. So you can get these amazing Chestnuts from Costco. Absolutely to die for. If you do some maths, it's about 15 grams of chestnuts that someone would need to eat.

Nirala Jacobi:

That's like one Chestnut or something, right?

Brad Leech:

It's not. It's two or three chestnuts. It's a very small amount. The other big one is blackberries. So a pan of blackberries actually have enough ellagic acid to actually have that prebiotic action to support IPA production and then thereby, intestinal permeability.

Nirala Jacobi:

Great, and also, I think all those foods also support Akkermansia or at least a few of those foods. That's great. I mean, look, I could talk to you for hours because this kind of microbiome nerding out is... I love that kind of stuff, but we are nearing the end or we're at the end of the podcast. So, before we wrap it up, I wanted to see... The wonderful thing is that you're a practitioner and a researcher. So what are some of the clinical pearls that you can share with us of how you treat intestinal permeability?

Brad Leech:

When it comes around to intestinal permeability, my biggest advice to the listeners is identify the subgroup. Determine whether or not it's alcohol-induced, or microbiome-induced, or exercise-induced. Once you have that information, then create targeted therapies to address that subgroup. So given that we're on the topic of microbiome-induced intestinal permeability, there's three major things that you could consider when it comes around to supporting microbiome-induced permeability, and that would be considering the whole microbiome, the use of targeted treatment interventions, and then what I just mentioned previously of the ellagic acid.

So when I refer to the whole microbiome, I'm referring to fiber, fiber, fiber. I'm really emphasizing the importance of fiber supporting that whole gastrointestinal health coming down to inflammation, digestive secretions, peristalsis, and so on. When I refer to the targeted treatment interventions, especially for microbiome-induced permeability, it's really understanding what the microbiome is doing. So, for example, if somebody has high Hexa-LPS and that's driving somebody's intestinal permeability, there's research to suggest that GOS at for about 4 grams per day is beneficial when it comes around to reducing LPS-producing bacteria.

Nirala Jacobi:

So GOS stands for Galacto-oligosaccharides for those of you who are listening, and that's a prebiotic powder. If you're in the UK, that's usually... We usually recommend Bimuno. If you're in Australia, there are distributors that sell GOS. Just for those of you listening in America, I think... I don't actually know who makes it over there, but Bimuno is a very well-known brand of GOS. So GOS is a good one for LPS.

Brad Leech:

Mm-hmm, and it's one of the only things that has been shown to actually not just reduce serum LPS, but reduce the bacteria that have the capacity to produce LPS. So the patient I was alluding to earlier with 22 species and high amounts of LPS, giving GOS can go on to help with that patient's presentation because it potentially has that capacity to bring down those pathogenic LPS-producing species.

Nirala Jacobi:

Great. That's a really good tip. Fantastic. Anything else? What about the old glutamine, and zinc, and the typical stuff that we do? Do you use a lot of that?

Brad Leech:

When it's not microbiome-induced permeability, then yes. So exercise-induced or stress-induced. Then, that's when I'll bring out glutamine at 5 grams three times a day. That's when I would utilize glutamine. The other big one is [inaudible 00:39:44] blotting. In my own PhD, that had a high level of evidence to support with intestinal permeability. Other big ones would be zinc. We can't go past zinc, and it's clinical utility not just to support with intestinal permeability, but to support with digestive secretions and wound healing, and it's such an important mineral.

Nirala Jacobi:

Fantastic. Gosh. I'm sorry, but we have to wrap it up, but it's been really amazing to talk to you. Where can people find you? I know you're probably too busy to take on more patients, but I've always want to promote people that are in practice or also your lab. I don't normally mention or promote labs or companies on this podcast, but I like Microba. I like what you're doing up there. So do you want to just give us a bit more information about where people can find you?

Brad Leech:

Yeah, definitely. Well, if there's patients, I see patients, and I do a lot of mentoring with practitioners. You can find more information on my website, bradleech.com. If you want to know more about Microba and Microba Testing, then you can visit Microba's website and gather a bit more information on measuring whole microbiome.

Nirala Jacobi:

Right. Okay. We have all that information in the show notes, and Dr. Leech, I'm so glad I get to say that. You finally completed your PhD. A huge congratulations to you on all this work that you're doing. It's been an absolute pleasure to have you on the podcast. I'm sure that I'll invite you again for further diving into our favorite topic, the microbiome.

Brad Leech:

Nirala, it's been a pleasure and absolutely love chatting with you.

Speaker 3:

Thank you for listening to The SIBO Doctor Podcast. We hope you find 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. Thanks again for listening.