The GA-map test looks for signs of gut dysbiosis (or imbalance of your gut microbiome). This test is closest, clinically, to mapping the gut microbiota. European researchers sequenced the gut bacteria from healthy individuals and bacterial profiles from individuals with IBS and IBD. Then they compared the two, identifying bacterial “targets” that varied between healthy and IBS/IBD populations. If you were to take the test, you could get a dysbiosis index (or rating) from one to five, indicating how healthy or out of balance your gut was. One study used the GA-map to analyze the effects of diet on the microbiota. They noted that the low FODMAP diet markedly impacts the microbiome. In the future, your functional medicine doctor might use your dysbiosis index score to assess what treatments or diets to recommend. In the present, following a gut health algorithm and looking for symptomatic improvement is still a great option.
Dr. Michael Ruscio, DC: Hi everyone. Welcome to Dr. Ruscio Radio, this is Dr. Ruscio. Today I’m here with Dr. Sean Bennet and we’re going to be talking about the GA-map stool test. Shouldn’t be confused with the GI-MAP. Two different tests. This is what I think is one of the tests that is closest to real clinical utility regarding mapping the microbiota. There have been a couple papers published and Dr. Bennet is one of the authors on those papers. He was nice enough to come on the show and talk about some of his research. So Sean, welcome to the show and thanks for being here.
Dr. Sean Bennet: Thank you very much for having me. I’m excited to talk about this and hopefully give as much information as I can.
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Dr. R’s Fast Facts Summary
What is the GA-map stool test?
- Gut microbiota analysis for testing bacterial imbalance in IBS and IBD patients
- The GA-map may be able to predict who would respond to a low FODMAP diet
What is the Microbiome?
- The Microbiota is essentially the world (or ecosystem) of bacteria in your gut
- Made up of bacteria, fungi, viruses, phages (which are viruses for bacteria), etc.
What is Dysbiosis?
- Altered microbiota/uneven levels of bacteria and potentially opportunistic bad bacteria
- Can be caused by many different factors a bout of gastritis, a round of antibiotics or from some other organic cause
What is a Low FODMAP Diet?
- Eliminating foods that are low in FODMAP’s – Fermentable oligosaccharides, disaccharides, monosaccharides and polyols
Effects of Low FODMAP diet
- The low FODMAP diet can result in reduced inflammatory cytokines, reduced leaky gut, reduced histamine, reduced symptoms
- One study showed that Bifidobacteria was reduced in the patients on the low FODMAP diet
- While this finding is interesting, it needs further research and should not be misconstrued as a reason to avoid trying the low FODMAP diet
- As with any protocol, the focus should be on the overall benefits until something more definitive shows otherwise
- Some people might be able to pinpoint which of the FODMAP foods are causing their symptoms and just eliminate those vs going 100% on the diet
Is the GA-map stool test ready for clinical use?
- It is still pre-clinical, some information can certainly be gleaned from the results but further studies and adjustments are needed
Any questions about the GA-map testing?
- Find Dr. Sean Bennet on Twitter
- Get help using this information to become healthier.
- Get your personalized plan for optimizing your gut health with my new book.
- Healthcare providers looking to sharpen their clinical skills, check out the Future of Functional Medicine Review Clinical Newsletter.
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DrMR: Yeah, it’s definitely an area where I think people are looking for a bit of light to be shed. So also very much looking forward to the conversation. Tell people in brief your background and how you got involved in some of the research with the microbiota analyses.
DrSB: Right. I’m originally born and bred in England. That’s where I did my bachelor’s. Then moving over to Sweden, I did a master’s in ecological toxicology. So I’ve been around in different fields here. Then once that one finished, wanting to stay in education, I saw the PhD for researching irritable bowel syndrome advertised. I’d never given a thought about that, but I’d heard about it and had several friends who had that. After looking more into it, I realized that we don’t know too much about irritable bowel syndrome. Research is obviously progressing, but it’s kind of a black box. So I figured it’s a very interesting subject to go into and see if I can help.
Then looking at the immunological system, the microbiota system, was the focus of my PhD in the University of Gothenburg in Sweden. The group had had some collaboration with a Norwegian group who created the GA-map analysis, and we wanted to see if we could implement that as a follow-up study for a diet intervention study, which had previously been performed at Gothenburg. We wanted to see if we could implement this method. That’s the beginning, basically, of how this publication came about.
DrMR: Is this the second study published with the GA-map, or has there been a third now? I wanted to give this a double-check before our podcast today, and ran out of time on the fact-checking. So I’m hoping that you know what the current status is in terms of published trials. I know there was one showing correlation with skewing of the GA-map results, in a pattern researchers term dysbiosis, and they skewed to associate with IBS and IBD. And then there’s your study. Has there been another one?
DrSB: There has been one which used the same GA-map analysis, that was performed by a Norwegian group. They took the dysbiosis index, which I will describe a little bit later, from the GA-map analysis, but created their own index, if you will. So research since has been performed using this method.
The Gut Microbiome
DrMR: Gotcha. Okay. Just for the audience—and if you want to alter this or add to this in any way, please feel free—I’m sure most people listening have heard of the microbiota. But the microbiota is essentially the world of bacteria. There’s also fungus and other life in your gut. But predominantly bacteria in your gut that may affect your immune system, may affect certain symptoms of digestion, may also affect things like joint pain and metabolism. We’re getting more and more advanced with testing where we can now look at these many, many, many species in the gut and start to say this is healthy, this is not healthy.
The challenge is, it’s not so easy. It’s not as if to say, we have 10 bacteria in the gut and if you have this much of one or that much of the other, it’s good or bad. What’s the current opinion on how many strains of bacteria are in the gut?
DrSB: Off the top of my head, I believe it’s along the lines of being a thousand at least.
DrMR: A thousand, and there are a few hundred fungi, I think.
DrSB: You’ve got a whole ecosystem in there. Just like you say, you’ve got bacteria, you’ve got fungi, you’ve got viruses, you’ve got phages, which are viruses for bacteria.
DrMR: Right, and so one of the challenges is, with having so many strains of bacteria, you’re looking at a thousand some odd species of bacteria and then how they interface with a few hundred species of fungus. And everyone has a bit of a different level of these different species. So it’s challenging to say, all of these hundreds and hundreds and hundreds of bacteria should be at XYZ level in a normal person and at this level in that normal person. I think that’s one of the few reasons why it’s been challenging to get a test that tracks tightly with symptoms or with disease. Would you modify that?
DrSB: No, I agree. I think to try to focus on a select few amount of bacteria or species, for example, isn’t really going to work for other than certain specific infections, like I said, due to the fact that it’s an ecosystem in there. There are a lot of different species, all doing their own roles. And it’s very unlikely going to be just one of these which is going to be causing problems for the individual.
Instead, we need to look at it as a whole and we need to look at it as patents of these species. We call them the gut microbial profiles there, and that’s the way you’ve got to look at it. Because while you can look at one individual species, it’s very unlikely that that’s going to be causing problems.
Developing a Dysbiosis Index
DrMR: So as we’re trying to sort this all out, the researchers who have developed the GA-map test are starting to hone in on what they think a healthy gut should look like and what a dysbiosis-laden gut would look like. They developed this dysbiosis index. Can you tell us a little bit more about that, Sean?
DrSB: Yeah. This group—the paper where they actually presented this GA-map analysis—took about 165 healthy individuals and sequenced their gut bacteria. Then they assessed it for certain bacteria which they’d looked at in the literature, which they’d known to be associated with inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). They used those as a starting point to hone in on what could be differentiating a person with IBD or IBS from a healthy individual.
So you take this 165 healthy cohort and you look at all their individual bacterial profiles. Then you create a sort of meta-profile of what a healthy gut should look like. Of course, you and I are going to have different gut bacterial profiles, but we’re both healthy. That doesn’t mean to say that one bacterial profile is better than the other. It’s just a different variant of a healthy gut biota, if you will.
Then they took the samples from people with IBD and IBS and to a similar fashion, created their IBD meta-gut-biota profile and an IBS meta-gut-biota profile. By doing that, they were able to focus in on which of the bacterial targets (which they’d looked at in the literature) were presenting as significantly differentiated between a healthy gut biota profile and that of an IBD or IBS.
The idea would be that you could then narrow down from these thousands of species and very different types of genre of bacteria to just the key ones… those which are most likely to be different between healthy and symptom, or IBD/IBS profiles.
DrMR: And this is the main set of bacteria they’re looking at, of course, to flag someone that is normal or IBS or IBD? I think we’re referring to the same study, where they showed different profiles for healthy compared to IBS compared to IBD, which is a great first step.
DrSB: Yeah, exactly.
DrMR: I think any clinician needs to caution an eager layperson that this doesn’t tell us if it’s causal or associative. Meaning: it doesn’t tell us, for example, if someone with inflammatory bowel disease has up-regulated inflammation that’s essentially poisoning the milieu in the gut, allowing unfavorable bacteria to grow as a byproduct of the inflammatory bowel disease, not as a cause of the inflammatory bowel disease. I think your study inches us in that direction, but how would you comment on starting to parse between causal and associative?
DrSB: Well, you’re absolutely right. It’s a very chicken-and-egg situation there. Is it something which is caused by dysbiosis (which I will describe a little bit)? Shall I elaborate on this, by the way?
What is Dysbiosis?
DrMR: Sure. I think many people have probably heard that, but for many people who haven’t, it’s always good to redefine these terms so we don’t lose anyone. Absolutely.
DrSB: Right. So you mentioned the gut bacteria living in a healthy individual. It’s a nice ecological rain forest in there, that’s living in symbiosis. They’re breaking down food for the host which perhaps are unattainable, and they’re filling up spaces in the gut wall where they will then stop bad bacteria getting in. There’s a general peace in the valley scenario. But then when something perturbs this milieu—be it perhaps a bout of antibiotics, which might completely wipe out all good and bad bacteria, or a particularly vicious infection, like gastroenteritis—that can shift this peace in the valley state to one of dysbiosis.
So not symbiosis, dysbiosis. In that milieu, you’ll have uneven levels of bacteria and potentially open up for opportunistic bad bacteria. I say bad bacteria in a pathogenic sense. In this dystopian milieu, things might not be going as they should be. Perhaps some species aren’t producing a certain product which keeps the gut healthy, for example. So that’s generally what we might see in some people with IBS or IBD.
Regarding the chicken and egg scenario, unless there’s something which we can definitively point a finger to—like a bout of gastritis or a round of antibiotics which might have caused this dysbiosis—then it’s very difficult to know whether an altered microbiota in an individual has stemmed from an organic cause, or is causing the symptoms of the patient. It’s pretty difficult.
DrMR: Sure, and this is where I think we’re going to learn a lot as we start to look at clinical trials and look at how various patient groups respond to various treatments. When we correlate that to various dysbiosis pre-treatment, I think we’ll be able to kind of reverse-engineer or use response to treatment to figure out, “Okay, this profile of dysbiosis or in this patient’s subgroup seems to be more of a causal dysbiosis. Whereas this other type of dysbiosis, or dysbiosis in this subgroup, is more associative dysbiosis.”
Predicting Response to Low FODMAP Diet
That does lead to your study where—and this is, I think, really exciting—you seem to be able to predict who would respond to a low FODMAP diet. In my mind, that is really exciting, because it could allow someone to have a better ability to navigate the handfuls of diets that are out there for inflammatory bowel disease and irritable bowel syndrome. You can use a low FODMAP diet for either one.
That being said, it doesn’t take a long time for someone to notice symptomatic improvements on a low FODMAP diet. In my experience, usually by one to two weeks, most people will notice an improvement. By the third week, a lot of people will notice improvement. But nonetheless, this may be one tool that could help guide us in the dietary recommendation realm. Again, if you can help someone determine between paleo or low FODMAP or Mediterranean or what have you, that’s definitely a step in the right direction.
DrSB: Definitely. You’ve got to imagine that any diet—we’ve all been there at one time in our life—can be quite arduous and laborious. Even if it is for just two weeks, if you don’t have to go on something for no reason, then it’s obviously easier to take that. You can start with a different type of therapy earlier, which might prove better. If what we need to do is leave a stool sample and then be told, “Yeah, it’s worth going on the low FODMAP diet (or not),” I think a lot of people would appreciate the ease of that. Versus going two weeks cutting out almost everything from their diet.
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So tell people a little bit about the study that you did. I just gave the general take-home. I’m really curious to hear more about the whole inspiration, setup, findings, any clinical pearls that you may have stumbled across that haven’t been published.
DrSB: Sure, yeah. It was done during my PhD. During those times, you’re guided somewhat by your supervisor at the time. In the group, Lena Böhn had produced a study looking at the differences between a traditional IBS diet and a low FODMAP diet, to see how either of them are better than the other at reducing symptoms for IBS. The hypothesis was, when you’re cutting out various foods from your diet to see if they have an effect on the gut biota, you’re cutting out food groups which are definitely going to have an impact on what’s living in your intestines. We don’t know any long-term studies yet on how a low FODMAP diet is going to positively or negatively impact the gut biota.
So we had the collaboration with the GA-map analysis people. And we thought it’d be a great opportunity to see the impact of a low FODMAP or traditional IBS diet (just to reiterate, a traditional IBS diet would be to eat in a calm manner and cut out caffeine in a more patterned eating, if you will, as opposed to the low FODMAP, which cuts out various heavy FODMAP foods).
DrMR: To expand upon that a bit—and I’m not sure how the IBS diet where you are and where I am differ, so there are maybe nuances regionally—you’re essentially, loosely said, cutting out a lot of processed foods, and you’re also cutting out caffeine, alcohol.
DrMR: So it’s a step one, if you’re eating processed and unhealthy food, cut that out and focus on others?
DrSB: Yes. It implies a greater focus on how and when to eat, rather than what foods to ingest. It was based on the dietary recommendations from the National Institute for Health and Care Excellence. So NICE and the British Dietetic Association. So it’s eat three meals a day, three snacks. Never too much or too little. And reduce the intake of fatty or spicy foods, coffee, alcohol. That’s what the traditional IBS diet was, at least regarding the study which came prior to this one.
DrMR: Gotcha. Okay.
DrSB: Moving on from that, stool samples had been taken from the patients, prior to the interventions and then after the traditional and the low FODMAP intervention. We wanted to see what impact these diets had, because in the study by Lena Böhn, it showed that both were certainly effective at reducing the symptoms. But if, for example, the low FODMAP diet was having a grand impact on the gut bacteria positively or negatively, that would definitely be something to try to elucidate.
So we did the analysis where we sent off the samples. Then it came back. The analysis looks at 54 targets. We then wanted to see how those had changed after being on their respective diets.
DrMR: And these 54 bacteria are what’s comprised in the dysbiosis index, I’m assuming?
DrSB: They are. It’s important to state that these are 54 probes, which target over 300 bacteria on different taxonomic levels. So it’s not 54 species. It’s 54 targets. It’s these which then I used. You can analyze them individually as the targets, but also if you have to gauge the dysbiosis index.
DrMR: Gotcha. Okay.
DrSB: We then received the raw data back. When you’re working with such a large data set as this (61 individuals and 54 targets), you have to go into the realms of multivariate statistical analysis. This is looking at Big Data. In a small study you might look at just five different targets. You’d look at them individually and compare them between the two groups. That would work here, but it’s much easier to look at them as a profile. To assess and compare, the profiles of each individual and these bacterial profiles are compared through this multivariate analysis.
We then wanted to see if the bacterial profiles had changed after going on the intervention diets. We went through each target individually and saw that as predicted, Bifidobacteria—which you might have heard is a probiotic species, which helps the gut health and maintains the epithelial membrane health—was reduced in the patients on our low FODMAP diet, irrespective of whether they were a responder or a non-responder.
Gut Bacteria and FODMAPs
That’s something which has concerned people going on this low FODMAP diet, because you’re reducing potentially beneficial bacteria. But it showed that it didn’t matter whether you responded or not, it was always getting reduced. The reasoning behind that is because this bacteria feeds upon certain FODMAP foods. Ironically, a lot of the FODMAP foods are also what’s known as prebiotics. You might have heard of probiotics, which are the good bacteria if you keep taking your Yakult or Activia or whatever, little yogurt drinks. But if you imagine those as the seeds in your garden, prebiotics then are the fertilizer for those seeds. These FODMAP foods work as a source of nourishment for the good bacteria in your gut. It’s just unfortunate that for some people, they work too well, if you will. So that can lead to the bloating as the bacteria in the gut use these and produce gas.
That’s one thing that came from the study. And it’s something that needs further research. Perhaps as a way to get the benefits of a low FODMAP diet while keeping the levels of these beneficial bacteria up, you have to realize the low FODMAP diet in full is a very restrictive diet, but some people might be able to pinpoint which of these FODMAP foods are causing their symptoms and just eliminate those. FODMAPs, just to retread, are fermentable oligosaccharides, disaccharides, monosaccharides and polyols. It might be that just one of those is causing your symptoms, but you’re fine to eat all the others.
That’s one thing which would definitely need to be researched further and something which you might want to try, just to remove one of these foods and see if your symptoms clear up and then reintroduce it.
Regarding the traditional diet, we didn’t see any dramatic impact on the gut bacteria, actually. It stands to reason, because it’s not as hardcore, if you will, as the low FODMAP diet. All you’re doing is reducing portion size and changing the method, as opposed to the type of food. The gut bacteria is somewhat resilient to change there. When you’re not doing massive change in diet, then you’re not gonna see massive changes in the gut bacteria composition.
DrMR: Sure. And the thing here I think is most noteworthy is the fact that you were able to find a certain pattern that predicted the outcome. To reiterate this for our audience, my position on this is—and I don’t claim to have a crystal ball that gives me the “right opinion”—I’m not very concerned about changes that we see in bacterial populations with the low FODMAP diet.
It seems that when we look at the totality of the data, we see reduced inflammatory cytokines, reduced leaky gut, reduced histamine, reduced symptoms. So it seems many positive things are happening at the same time we’re seeing the reduction of a bacterial population. To put it quite plainly, if a sick person is feeling healthier on the diet, then for me the outcome trumps what’s happening with the bacterial population underneath the surface, as long as it’s applied (as you very aptly put it) in the context of later reintroducing foods, and trying to find the broadest version of the diet that still keeps their symptoms at bay.
Metabolite Profiles: Gut Health of the Future?
DrSB: I agree, definitely. One thing you have to consider is that with this particular GA-map analysis, it’s a targeted analysis. There are broad analyses which take a massive look at everything which is in the gut there. It might well be that right now, we see a reduction in bacteria species X, but we haven’t even measured bacteria species Y which has come in and is producing the same metabolites (metabolites being the products which are formant when the bacteria breaks down through to your gut).
One thing which I’m going forward with now in my own research is to look at the metabolites of the metabolomic profile, if you will. Not to segue too much, but we’ve been looking at a lot of the bacteria species living there. At the end of the day, you and I and a healthy person have different bacterial profiles and yet we’re still functioning fine and healthy. It must be instead that the thing we share, perhaps, is the metabolite profile. So it doesn’t matter if you have species XYZ, and I have species 123, they’re still producing the same things to keep us functioning.
DrSB: I think that in the future it might not be so unusual to see, “Okay, this bacterial profile is completely different from this one,” but when you look at it, the metabolite profile is similar. Of course, research is ever-progressing. It might just be that we haven’t found the definitive bacterial profile if there is one, and the metabolite profiles that are up-and-coming research-wise.
DrMR: Agreed, and that’s why I caution people about not being too worried about some of these findings regarding the low FODMAP diet. There’s still a lot there that we have to learn. And if it’s really helping someone with their symptoms—as long as they’re not doing it in a highly restrictive way for a long period of time that’s unneeded, and they’re trying to eventually move to the broadest possible diet—then, at least for the time being, I have little reservation about a low FODMAP diet, for the very reasons that you’re outlining.
Gut Health Biases, Dysbiosis Ratings
I also wonder about other things where perhaps there’s a bias. At least, there seems to be a bias in the literature where I think many researchers are expecting feeding bacteria to be a good thing for you. It seems to permeate deep into the field. For example, there don’t seem to be many that think, “Maybe not everyone needs to feed their gut bacteria.” Although we have it in Tarek Mazzawi, who I believe is in Norway. He’s published some studies showing that the low FODMAP diet can reduce inflammation and leaky gut and histamine and actually may even lead to improvements in some of the serotonin and PYY cell densities in the intestines.
So I think we’re starting to see some of this flower, where people are looking at this from other angles and not setting up a study to say, “Well, if there’s any bacteria decrease, that automatically means bad.” But they’re zooming their lens out and saying, “Well, these bacteria decrease, but we’re also seeing less inflammation, less leaky gut.” So I wonder—as our lens broadens from just the bacteria profile to some of these systems or mechanisms—if we’ll start reevaluating some of these opinions.
DrSB: Yeah, definitely. We’re coming in leaps and bounds research-wise. I think to focus on the overall benefits is definitely the way to go, because you can’t give the stigma too much to the low FODMAP diet. It’s the same with antibiotics to a degree. You don’t hold back giving someone life-saving antibiotics because, oh, it’s going to wipe out their gut bacteria. You take the bigger benefit over the other risk there. So I think it’s the same here. Yeah, there are no really long-term studies on the impact of the low FODMAP diet. But in the short-term at least, if the patient’s feeling better and you’re seeing all these other benefits, then if it ain’t broke, don’t fix it!
DrMR: So you found a certain profile predicting response to a low FODMAP diet. But if someone mail-ordered a GA-map test from Norway, I’m assuming they’re not going to get this on the printout, because there are some meta-analyses or meta-data crunching you had to go through to be able to pinpoint this? I don’t know if this is being incorporated into the analysis. And if there’s a clinician- or user-friendly way to look at the results and say yes or no, I should do well on a low FODMAP diet.
DrSB: Yeah. Actually in the services which GA-map provide to clinicians, I believe they do give a printout and a dysbiosis index. This ranges from one to five, and being between one and two is a healthy gut profile dysbiosis index there. But anything three and on the verge, and anything above a three is considered dysbiotic. In their study, for example, they showed that people with IBD had higher dysbiosis than those with IBS, even compared to healthy. But what we saw in our study was that those who were non-responders to the low FODMAP diet actually had a higher baseline (so, before the intervention study dysbiosis compared to the respondents).
What’s interesting there is, it could be that if you have a high dysbiosis index before you go onto a diet, you might be, if you will, too far gone to have any benefit from going on a low FODMAP diet. So they do the GA-map, do provide a printout which gives you a brief overview of certain species or targets where they’re increased or decreased, as well as a dysbiosis index. If it holds true, after further validation, that if you have a dysbiosis index of five, for example, that a low FODMAP diet is not going to help, then that’s pretty simple. In our study, yes, I did a lot of later analysis with the multivariate analysis and that. But in this simple aspect, to maybe just use the dysbiosis index if that’s efficient, that could be a potential tool.
DrMR: Yeah, and that’s such a great point. Those with a more severe dysbiosis index may still benefit from a low FODMAP diet. But we may—I’m putting my own spin on this—have to use some additional therapies like probiotics, antibiotics, or antimicrobial herbs to get that dysbiosis a little bit loosened up, so to speak, so then at least the impact of a low FODMAP diet can start to impact the ecosystem. That’s kind of how I look at that. That may be proven, but that’s a really brilliant insight.
Follow a Gut Health Algorithm
DrSB: Yeah, I think that from my understanding of IBS and the therapies which are available, it’s very seldom just one method which helps. A combination regarding the gut, and trying to rectify that to become more of a “healthy profile,” I think is a definite bad way to go. Like I said, just one method like the low FODMAP might not be enough. But I like the idea of combining it with prebiotics and, yeah, keeping a broad version of the low FODMAP diet, if you will. So you’re just eliminating those which cause symptoms.
DrMR: Absolutely, and this is exactly why in Healthy Gut, Healthy You, I introduce an algorithm. I spent years and years in the clinic working with different patients to figure out that some patients respond to anything. They just need one line of IBS therapy and they do great. At the other end of the spectrum, you’ve got to work for every 20, 30% improvement that you get. For some people, they get a little bump from low FODMAP, a little bump from probiotics, a little bump from antimicrobials, a little bump from the elemental liquid diet. You add all those little bumps together and they finally get to that near complete resolution or complete resolution that we’re trying to get to.
So certainly my clinical experience has borne that out, and I think that’s something important to reiterate for the audience. If you are struggling with IBS, don’t look for the one miracle treatment. Again, I talk about this in the book, because that will elude everyone that’s not a simple case. Simple cases will likely respond to any good treatment, whether it’s fiber or probiotics or antimicrobials or antimicrobials or dietary changes or peppermint or what have you. But it’s the people that need a bit more of a robust plan, if they jump from miracle treatment to miracle treatment and they keep doing that, they can spend a lot of time and money to get nowhere. And so be a little patient and try to find a good system to work through or an algorithm to work through. Oftentimes that is the difference between success and failure, in my clinical observation.
DrSB: No, definitely. I’m no clinician myself, but from what I’ve heard doing my PhD, for some people it’s just being listened to. Saying, “Yeah, you have IBS,” that can be enough to help. Yeah, I couldn’t agree more.
DrMR: So how would you recommend using the GA-map test? I know you’re not using this in a clinical setting yourself, but from what you’ve garnered in your study and maybe anything else you’ve seen in your research here, would you say there’s a way? I get that there’s a lot that we have to learn here… so maybe I should ask you this way just to make sure we have every caution out there. Feel free to amend this, I’m assuming you think this test is probably pre-clinical. But maybe you have a word on: “If you’re trying to be as progressive as possible, you could consider X use…”? Is that fair, and if so would you add in a certain recommendation there?
DrSB: Yeah. I think that’s a fair assessment to say it’s very much pre-clinical. They’re always tuning up and improving the GA-map analysis. I think that if you are treating a patient and you want to see if there’s dysbiosis, then it’s a great method to do that. Then if you really want to try to see if they have a high level of dysbiosis, perhaps changing the diet might not be the route to go. The easiest thing to do, from what I’ve heard, when you have a patient with IBS, is to change the diet. But to go to an extreme like removing certain foods, perhaps if you’ve done this test and it’s a high dysbiosis index, it’s not your first line.
DrMR: True. So maybe you go to—if it’s someone with diarrheal-type IBS and you’re more of a conventional provider—the FDA-approved for diarrheal-type IBS, rifaximin. Or if you’re a natural provider, perhaps you use some of the herbs that have been shown to be equivalently effective (if we’re assuming that the herbs are treating an underlying bacterial overgrowth). And then maybe consider the diet as a follow-up or maybe even not at all. Maybe just treat and reassess. Do you know anyone who’s doing anything like this, or is anyone looking at additional treatments relative to the GA-map test, and trying to suss out how to use the test to guide clinical interventions?
DrSB: Not that I can think of at the moment. I know there’s research going on to validate if, in a completely blinded method, the GA-map analysis can be used to predict response to various diets. But as to whether or not it’s to guide therapeutic aspects, I’m not aware.
DrMR: Gotcha. Okay. Well, I think we’re still early here in our understanding, despite what some circles on the internet would have you believe. I think we have to still exercise some caution. Sean, are there any closing thoughts that you have for the audience?
DrSB: I’d say: listen to your gut. It’s considered the forgotten organ for a reason. It’s a massive part of you. And be mindful of what you eat. I think someone once said, food is nature’s medicine.
DrMR: It’s definitely a good place to start. And is there a website or a book or anywhere that people can connect with you on the internet?
DrSB: Yeah. I just have my current email address at the moment, so that’s email@example.com. That’s my most active e-mail address. If you have any further questions, I’d be happy to hear from you.
DrMR: Awesome. Well, Sean, thank you so much for taking the time. It was a really interesting study. I’m really glad that you published it. Hopefully we’ll continue to refine this test to help clinicians and patients navigate the sea of IBS treatments in the most efficient way possible.
DrSB: Excellent. Thank you very much for having me and I’d like to thank everyone who was a part of that project. Thank you very much.
What do you think? I would like to hear your thoughts or experience with this.
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