The first clinical microbiota test was just released, but is it worth doing? Let’s discuss this test’s pros and cons and help you determine if it’s right for you.
If you need help with your gut health, click here.
Episode Intro … 0:42
Microbiota Test Defined … 1:47
GA Map Test … 3:52
How Can This Test Change Treatment? … 9:11
Crohn’s and Fungal Overgrowth … 19:39
Episode Wrap-up … 21:21
- GA Map Testing
- Deviations in human gut microbiota: a novel diagnostic test for determining dysbiosis in patients with IBS or IBD.
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The First Clinical Microbiota Test Was Just Released. Is It Worth Doing?
Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio, flying solo today with what will be a short podcast but regarding a few things that I think are important for us to check in on.
I guess maybe the most exciting news is that I officially finished the manuscript for my book. And it’s now started in on the editing process, which has a few different phases to it, especially because my grammar is still probably that of a 12-year-old. And we have a pretty firm launch date for March 1. And I am very excited about that.
More specifically to today’s podcast, though, I wanted to check in on a couple things regarding the gut microbiota — big surprise there, I guess, in terms of topic — but in terms of testing. There is one test that has recently become available that is really the first microbiota test that might have clinical utility.
Microbiota Test Defined
And let me just clarify. When I say microbiota test, what do I mean? It’s kind of a broad term that can be used interchangeably. So when I say microbiota test, what do I mean?
When I say microbiota test, I’m not referring to something like a SIBO test or a test that looks for candida or a test that looks for H. pylori or Giardia — more typical, traditional, clinical GI tests. These are what I would term gut tests.
Microbiota tests, at least the way I define them to help avoid confusion, are tests that will assess the world of bacteria in your gut, the microbiota. We have 1,000-some-odd species. Those species can be broken down into maybe four to eight major phyla, or broad groupings. This would be a microbiota test.
American Gut, uBiome — these are both examples of microbiota tests. These are good tests. And I think they’re tests that are important for research purposes. But it’s very important that we draw the distinction that those tests are not clinical.
And even the owner of one of the labs has previously come on the podcast and commented that these tests are not clinical. And therefore, they should not be used clinically. Yet, some people are making that recommendation.
And I just want to politely draw attention to the fact that these tests are not meant to be clinical. They don’t really give us any clinical data. And trying to treat based upon them is just adding in information that does nothing to contribute to the clinical progress of a patient or of yourself.
All it will really do is confuse you because if you’re trying to incorporate what’s happening on those tests into a treatment plan, you’re taking irrelevant data and trying to factor it into a treatment plan. And all that’s going to do is confuse you.
GA Map Test
Now, there is a group in Switzerland that has come up with a test called the GA Map, not to be confused with the GI Map, which is a commercially available test in the United States.
I’m not commenting on the GI Map test one way or the other. I just want to make sure we don’t confuse one for the other. The one I’m referring to is only available, at least right now, via a lab that is associated with a group of researchers in Switzerland, called the GA Map.
And this test has been published. And essentially, what they did was they created their own set of microbiota parameters — some looking at species level, some looking at phylum level or larger, broader groups of bacteria.
And what they did was attempt to see what their test looked like in a group of patients with inflammatory bowel disease (IBD), in a group with irritable bowel syndrome (IBS), and in a group of healthy controls. They had around 300 to 400 subjects. So it was a decent number of subjects evaluated.
And essentially, what they found was their test showed dysbiosis in 70 to 80% of those with IBS or IBD and only in 16% of healthy controls.
Now, this is really the first test that has shown a highly consistent dysbiotic change that correlated with disease. So when we do a test, like an American Gut or a uBiome — again, it’s not to take anything away from those tests. But we don’t have definitive data to be able to say you have dysbiosis or you don’t have dysbiosis.
We can speculate. We can theorize. We can look at diversity scores. We can look at certain phylum types. But there are numerous reasons as to why that’s inaccurate.
What could be healthy for one group is not going to be healthy for another group. We don’t know if the changes are cause or effect. There are constantly changes in the testing. When two people perform the same test side by side, they’ll see different results.
In fact, I just received a Facebook message this morning from Richard Nikolai kind of reinforcing some of what I presented in my AHS presentation (which is available on my website, by the way) about how these American Gut and uBiome tests really don’t have a lot of clinical utility, at least from what he has seen, because he was commenting that he would run these side by side and see different results, even doing a side-by-side test on the same day.
So there is definitely a lot that we have to learn with those tests. Again, I still think it’s good to support them so we can learn more that we need to learn. But if you’re a sick patient, someone who’s not feeling well, or if you’re a doctor looking for a test to help get your patients well, those tests are not going to be able to provide you that data.
Now, coming back to this GA Map test, they were able to show dysbiosis. And they factored in for time. They did not find that time fluctuation was an issue because you’ve probably heard me say that the microbiota changes daily, weekly, monthly.
They factored that into their studies with a small subgroup. And they found that even doing repeat samples did not make someone go from dysbiosis to non-dysbiosis. So their dysbiosis score remained valid.
Now, they have a certain parameter for how far away, I guess you could say, from a healthy microbiota one had to be to be considered dysbiotic because we have degrees of change. And to put it simply, you could have what we think is a healthy baseline or a healthy reading. And then if you deviate 10%, 20%, 30%, 50%, 80% — at what percentage change away from healthy does that person become dysbiotic enough to be consistently dysbiotic?
So I hope I’m not confusing you with this. But essentially, they wanted to make sure that they weren’t classifying someone as having dysbiosis if the change was so minimal as to be clinically irrelevant. So they had some pretty good parameters here.
Again, the main finding is that 70% to 80% of those with IBS and/or IBD show dysbiosis, whereas 16% of healthy controls show it.
Now, here’s an important part of how we frame this. What does that mean clinically? Does this mean we should test everyone and tell everyone that they have dysbiosis? Well, we probably know, if someone has IBS or IBD, that they have dysbiosis. They probably have some type of imbalance in the gut.
How Can This Test Change Treatment?
The clinically relevant question is — if you’re a doctor or you’re a patient, the “What do I do?” relevant question is, how can this test help me? How can it help me dictate, “Use this probiotic. Use antimicrobials. Use an elemental diet. Use fiber. Use prebiotics.”
That is what we do not know. Right now, the best data that we have shows that those with gastrointestinal conditions or diseases have dysbiosis. The next step is to then see if certain patterns within those findings may indicate someone will respond better or worse to a particular intervention. Or potentially even better yet still, might that be able to inspire new types of probiotics or other bacterial therapies to help correct the dysbiosis?
But it also still doesn’t answer the question, is that dysbiosis causing the disease? Or is the disease causing the dysbiosis? And we can make an argument for inflammatory bowel disease that there may be a large component of which the disease drives the dysbiosis.
Because, remember: In inflammatory bowel disease, your immune system attacks either your intestinal tissue or your resident microbiota. So if your immune system is attacking your microbiota, might you expect to see a different microbiota that someone who’s healthy? Of course.
It has also recently been shown that those with IBS tend to have increased immune activation against their commensal microbiota, or their good bacteria.
So again, when we look at this type of data — which, by the way, is conveniently left out of a lot of the microbiota enthusiast dialogue. But when we look at this data, it suggests that there is a large component in which the immune system is attacking the microbiota.
Now, how do we then fix that? Well, there may be a degree of this that we can’t change and that we have to try to work with. And here’s what I mean by that. Most of immune system development occurs early in life. And after that, there’s not a high ability of the immune system to change. So someone may have a tendency toward attacking their intestinal bacteria because of how their immune system was hardwired since birth.
So if we go in there and we say, “Well, the people with Crohn’s don’t have enough bacteria. We need to jam more bacteria in there,” and you present more of what the immune system is attacking, you run the risk of making that person worse. And we see this in interventions.
And I cited this study in my AHS presentation. For example, they took a group with Crohn’s disease who are quiescent Crohn’s, meaning they were in remission. They were doing fine. And they put half on a low-FODMAP diet, the other half on a high-FODMAP diet. There was a near doubling of symptoms and disease severity in the high-FODMAP group.
So in interventions that feed the microbiota, like in this case with a high-FODMAP diet, a high-prebiotic diet, we see people become worse, potentially, because we’re feeding the thing that the immune system is attacking.
So it’s important sometimes to turn that argument around and look at it that way because it’s not always that we can put more bacteria or better bacteria or the right bacteria in the gut and have a favorable impact on the immune system. There may be a degree here where the immune system is already programmed. And now we have to just try to create the best intestinal environment for that person’s immune system.
And for someone with inflammatory bowel disease like Crohn’s or ulcerative colitis or someone with IBS, that may be an environment that doesn’t harbor a ton of bacteria. This is another reason why I’m very cautious about how we interpret the research from Africans who eat a high-carb, high-fiber diet and are super healthy because their immune systems are wired very differently than ours.
So these are all important things to keep in mind when coming back to the initial comments I made about this test. This test is showing us dysbiosis — the GA Map test. But is that dysbiosis a cause or a consequence of the disease?
So those are a few big picture things that I think are important to keep in mind regarding how we look at the gut, and not to have, I guess, a misguided view on looking at observational data — which, much of this is going to be observational data — and saying, “Because we observe X in a healthy person, we need to force that change into a sick person to cure the disease.”
What we’re missing there and what — I’m sorry — the functional medicine community at large does a terrible job with is making sure to be reserved and cautious and thoughtful before making a recommendation and making sure that a given idea at least has some preliminary clinical data to support it.
Now, I also understand that sometimes there is no data. But in the area of gut research, we have a lot of this data already. So we can’t use the excuse, “Well, I’m in the clinical trenches. I’m trying to get sick people well.”
In my opinion, that is often used as a cop-out because there are many areas where we have ample data to guide our decision-making. So we can’t just use that excuse because we didn’t want to do the hard work to fact-check, think, dig, and think critically.
So all of this is important because we just don’t want people to do things that are going to make them worse, A. And we don’t want people doing lots of testing. There are some gut tests that are now tacking onto the gut test a microbiota component of the test. And this takes the traditional gut test from maybe $250 to $300, and now in some cases jacks this up to maybe $500 to $600 or maybe even a little bit more.
And now this is something where if the practitioner wants this person to test this ($600), do some treatment, test it again (another $600), and then do some more treatment and test again. You may have just under $2000 of lab testing there. And a lot of that lab testing may be useless.
So, yes, you can do an American Gut or a uBiome for around $100, which is great. But I’m speaking to many of the tests that are available to doctors that combine the microbiota testing with the more traditional clinical gut testing. They tend to get kind of expensive. And again, if that’s not helpful for you, then this becomes a very problematic issue.
So the immune system is something very important to keep in mind. And it’s not always as simple as saying, “We don’t have enough ‘bacterial exposure’ in Western societies. And that’s why we have autoimmune conditions. So if we just had more bacterial exposure, we would undo these autoimmune conditions we see in Western societies.”
The problem with that argument — I agree with it conceptually. And it does need to change. But when you’re an adult, a lot of your immune system has already been formed. And yes, there are things that we can do like diet, sleep, certain probiotics, all the gut therapies that we talk about, like treating SIBO, trying to have an anti-inflammatory environment in the gut — all those things are sound.
But what we can’t expect to do is take an adult and just cram a bunch of bacteria into their system and expect that to rewire an immune system which is predominantly wired in the first few years of life.
So we want to create that environment for our children as their immune system is forming because that’s going to make their immune systems better wired, if you will. But it doesn’t mean that’s going to be a good approach for people who are ill and have autoimmune conditions in a Western society.
Now, there’s something else that’s important to mention, which is that something like feeding gut bacteria tends not to have much, if any, of a chance to cause problems the healthier you are. The healthier someone is, the higher the probability that you’ll do fine with fiber, prebiotics, and resistant starch. So that’s important to mention.
So depending on who you are, how you’re feeling as you weigh your way into this argument, you may or may not be able just to jump right into some fiber, prebiotics, and resistant starch. And there are definitely some patients who find that that really helps them. So it’s important to mention that.
But it’s usually the people who are a little bit more ill, a little bit more progressed in having lost their health, who are going to get into the deeper aspects of this conversation. And it’s these people, I think, who are done the greatest disservice, unfortunately, by functional medicine in a lot of regards.
These people are motivated to do lots of testing and lots of treatment. But a lot of the testing and treatment that we recommend in functional medicine is simply not needed. And I think we’ve talked through one specific example of this regarding the microbiota in the gut.
So one other thing that ties in, kind of, with this rambling that I’m doing… Without Susan to keep me grounded, I feel like I just ramble.
Crohn’s and Fungal Overgrowth
But Robb Wolf just posted or recirculated a post something along the lines of, “People with Crohn’s Have a Higher Risk of Having Fungal Overgrowths.”
And if you remember back, if you caught — I think it was my last appearance on Robb Wolf’s show, I discussed the Dectin-1 and CARD9 — just two of a few different polymorphisms that are more common — or at least some research shows they are more common — in those with Crohn’s disease.
And these polymorphisms decrease these people’s ability to regulate fungal growth in the gut. And it’s believed that this leads to fungal overgrowth. And then the immune system comes in to attack this fungal overgrowth. And this initiates the autoimmune attack of Crohn’s disease.
So again, this theme of the immune system being important. And we may see fungal dysbiosis in a Crohn’s person. But that fungal dysbiosis may not necessarily be the cause of the disease. It may be secondary to the disease.
So what this really all comes down to is that the results a patient gets are really, in my mind, the most important thing. And guess what clinical trial data gives you. It gives you results. Half the patients were treated; half the patients were given a placebo. Or half the patients were treated, and half the patients were given the experimental treatment as a comparator. What results do we see?
This is why clinical trial data is so important. Because it tells you what happens when you intervene, when you have an intervention.
So I think that’s everything that I wanted to go through. I have reached out to the research group that has put together this test, and I’m going to try to orchestrate a few things. One, have them on the podcast to discuss.
Two, try to start using this test in our clinic and see if we can tease out any correlations. And a large part of if I do that depends on the cost. If it’s not cost-effective, then I’m not going to bring that into the clinic because it just wouldn’t be worth it, in my opinion, unless maybe this research group wanted to fund the testing. Then maybe we would do it.
But in any case, A, have them on the podcast. B, potentially start running this test in the clinic and looking for certain trends, seeing if this might be able to be used to help steer the recommendations that we make — this type of probiotic or an antimicrobial intervention or maybe even using fiber or a prebiotic in a subset. Or an elemental diet might be better for this person.
That might be nice because it may help you get to the best treatment a little bit more quickly. And if we can do that, then it has clinical utility.
Okay. I guess just one other note as I’m rambling here. I’m excited now that the book is done because I have so much information that I’ve been wanting to share. It’s just, the book has taken up really the majority of my bandwidth. Yes, I’m still doing podcasts and videos, of course.
But there’s another level of information I’d like to bring to the conversation. And I’m excited to bring that to the podcast. It’s been great having these guests on.
But I kind of miss feeling like I’m throwing a lot of heat, so to speak, to use a pitcher analogy. I miss getting into some of these details and trying to debunk myths, set the record straight, give you the best information to get healthier.
So that is coming just around the corner. And I’m looking forward to getting back to more of Susan and me on the mic and digging a little bit deeper into a lot of these issues.
So in any case, I again thank you for your continued support of the podcast. And I will keep you posted on everything regarding the book and testing and the microbiota and everything else in subsequent episodes.
All right. Thanks, guys. I will see you next time. Bye-bye.
If you need help with your gut health, click here.