How to Use & Interpret the GI-Map Stool Test Part II

Intro:

Welcome to Dr. Ruscio Radio discussing the cutting edge in health, nutrition, and functional medicine. To make sure you’re up to date on this and other important topics, visit drruscio.com and sign up to receive weekly updates. That’s DrRuscio.com. The following discussion is for educational purposes only and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking with your doctor. Now let’s head to the show.

DrMichaelRuscio:

Hi everyone. Today, I spoke again with Dr. Tom Fabian from Diagnostic Solutions about the GI-MAP stool test and how to best use it. One of the reasons why I wanted to have this follow-up conversation was because we got cut short last time. So I wanted to finish off some of the topics that were on the agenda. The other more global reason is that the over interpretation and misuse of testing in functional medicine is an endemic problem that needs to be reformed. This is happening way too much. It is getting out of control and needs to be corrected. So I wanted to have this follow-up conversation to provide as much support for doctors and clinicians as possible to allow them to best be able to use the testing. I think you will find this episode enjoyable for that reason.

DrMR:

One of the things that we cover in the episode is that the resolution of someone’s gastrointestinal issues often requires more of a broad scope of focus. Not just treating one test, but looking at perhaps one or two different tests, plus symptoms, plus history, plus response to treatment, and all this collectively is what informs the approach. This is essentially what you will find in my book, Healthy Gut, Healthy You, which is a personalizable plan to improve your gut health. This plan does not require any testing. Quite ironic considering this conversation, but often the utility of lab testing for gut health is vastly overstated. There are some choice tests that can be used by experienced clinicians but I would argue that most laypeople, probably all laypeople, will grossly misuse these tests. Unfortunately, most clinicians are also probably likely using these tests incorrectly.

DrMR:

I would go as far as to say that a test could likely lead you astray. If you’re using a directional indicator like a test, but you’re interpreting it the wrong way, it could literally move you in the wrong direction. However, a validated clinical algorithm as laid out in Healthy Gut, Healthy You, evidenced by just under 1000 references, which supports the approach is likely to be much more accurate. Now a good clinician can use tests appropriately, but unfortunately, and sorry to be candid here, but good clinicians seem to be much more of a rarity. The field has drifted into a territory of vacuous lab result treatment and not looking at all the other important contextual data. I say that as someone who is trying to help the field. I don’t mean to denigrate, but this needs to be called out because the field, if not course-corrected, is headed for some serious trouble.

DrMR:

In any case today, we will go into part two about the GI-MAP and how to use it. Also remember if you need help before you do a test, go through the program in Healthy Gut, Healthy You. It has been proven, as some of the case studies we’ve published substantiate, to help people who have seen five, six, seven, eight doctors. This is not to discount conventional medicine. Still have your follow-ups, but if you’re looking for a perspective on an integrative approach to your gut, Healthy Gut, Healthy You is where I would direct you. Alright with that, we will go to the conversation with Dr. Tom Fabian.

DrMR:

Hey everyone. This is Dr. Ruscio. Welcome back to another episode of Dr. Ruscio radio. Again, here with me is Dr. Tom Fabian, and we are going to be going into part two on the GI-MAP stool test and some of the facts versus follies of interpretation. I hope it was clear during our last conversation that over interpretation and misinterpretation of the test is a major problem that clinicians are committing fairly regularly.

Treating the Test

DrMR:

Unfortunately, I think it’s pretty darn accurate to say that functional medicine has drifted into a very lazy way of thinking. Often providers are treating the test, treating the test, treating the test and the knowledge of a clinical algorithm, the patient’s symptoms, trying to build a case for an intervention or against intervention all that seems to, unfortunately and in large part, gone by the wayside. It’s more so just treat the test, treat the tests. I can say for a fact, this is one of the differences between the person who is self labeling themselves as a chronic or complex case. For these patients, seeing improvements or not is oftentimes a complicated discussion. Yes, they might have seen seven other doctors. But it’s all been the same paint by numbers medicine, where the tests are being treated and unbeknownst to the provider there may have been a false positive. It may have been not something that could be literally interpreted, but should have been kind interpreted in a greater context. Surprisingly, some of these “more challenging cases” can be fairly straightforward to fix when you just have the right way of using these labs. This is one of the things that I really enjoyed about our prior conversation Tom. We see eye to eye on this and with that long intro here, let’s jump into part two. Welcome back.

DrTomFabian:

Thanks so much, Michael. It’s great to be back again and looking forward to the conversation today.

Exocrine Pancreatic Insufficiency

DrMR:

The last time that we spoke, we discussed the three patterns of dysbiosis. One of the things I thought maybe we could use as a specific launch off point into this conversation is regarding pancreatic insufficiency or EPI, exocrine pancreatic insufficiency. I really appreciate Dr. Ilana Gurevich who made me more aware of the importance of this test, and this has been a fruitful treatment. I say that advisedly, because I think there’s a lot of confirmation bias going on in the field. A clinician sees a positive lab marker, they have the patient take fish oil, probiotics, go gluten-free, go low FODMAP, start meditating and then they think everything that improved was due to the treatment of the one lab marker rather than all the other interventions co-occurring at the same time. In the clinic we’re doing one therapeutic at a time, we get a very good signal to noise ratio.

DrMR:

Clearly the higher dose pancreatic enzymes has been significant for some patients. So I’m happy to have that kind of finer point on this lab marker, which is fecal elastase and the corresponding treatment, pancreatic enzymes. One of the things that I wanted to get your perspective on is, and I’m not sure if we call it a false positive or a false negative, I guess it depends on what’s happening. But one of the things that we’re doing right now is researching a bit more about EPI. One of the things that seems to skew the labs on this is a history of diarrhea. This got on my radar because we now have patients who have taken the test more than once. Some will have had two stool tests done in tandem, or perhaps there was retesting over a number of months. You don’t always see this marker positive and there’s been a few cases where it was positive, then negative, then negative, then positive. I think for clinicians that’s a bit of a head-scratcher, but apparently it seems like transit time can skew this. So I know that’s a very specific question, but wondering what your thoughts are around exocrine pancreatic insufficiency, the fecal elastase test, how to interpret and how to treat.

DrTF:

Sure. There’s a lot I can say about that. Specifically regarding the effects of transit time. I’m actually not really familiar with the research around that. It certainly makes sense based on all the factors that we know. There’s some variability based on diet and things like that. That said, it’s actually one of our most consistent markers when patients do multiple tests over time. Overall, if they’re improving with treatment, we will tend to see that increase over time if it’s low. It’s certainly overall less variable than some of the microbial markers for example. So we don’t necessarily see a lot of variability.

DrMR:

One quick thing, just for me to clarify for the audience. We’ve yet to corroborate that, that that’s one of the theories behind why there may be false positives or negatives with the test, but we haven’t corroborated that. So I just want to be careful not to put that in people’s heads as fact. It’s a perspective issue, but we’ve yet to verify that one way or the other. Just to clarify.

DrTF:

Okay. Yeah. So definitely that makes sense that it could have an effect. We do know other things that can affect overall output of the pancreas. Diet, of course, is one. Diet content. But mostly what I can speak to is what it tends to correlate with on the test, as well as just recent research on how important that may be as an indicator of just pancreatic insufficiency related to gut function, but even relatively mild decreases in pancreatic enzymes. So I’ll just kind of talk to that a little bit as it relates to GI-MAP. So for most of our markers, we have a cutoff indicated for whether or not that’s going to get flagged as high or low, but of course there’s some gray area in between. It’s not like there’s a sudden cutoff that just above that it’s perfectly fine and normal.

DrTF:

And just below that, it’s going to be a major problem. There’s sort of this obvious gradual decrease in the effects potentially and in the levels based on what we’re seeing on the test. So clinically we tend to see a pretty strong association with symptoms and also based on what clinicians report, when they decide to treat that with supplemental pancreatic enzymes. When elastase is roughly around 300 and below. So we would consider that potentially sort of low normal, or maybe functionally low, but not outright insufficiency, at least based on the numbers. So that can still be significant for many patients, many clients, just the fact that they’re not really at optimal levels, you don’t have to have an outright deficiency to have an impact. Or to have an improvement in symptoms when that’s addressed. Just one other quick thing I was going to mention about elastase. We were kind of curious as to why we tend to see this overall digestive dysfunction pattern on GI-MAP that often includes low elastase, but not always. So we wondered why that seems to be so prominent overall.

DrTF:

When we looked into a lot of the research around that, one of the studies that came up, which was done recently, I think it was published in last year or so, they looked at a bunch of different factors in terms of kind of the whole statistical analysis. Which ones seem to affect the microbiome composition. I think this was a fecal stool test. Which of these factors had the biggest impact. In their studies, they looked at diet, age, gender, a number of other factors, and in that study low elastase was the biggest factor. It’s one indicator that not having optimal levels of pancreatic enzymes in particular, but probably just digestive dysfunction overall, does have a pretty big impact on the ecosystem in the gut and is pretty frequently related to symptoms.

DrMR:

It’s another great example of how fundamentally flawed the perspective is that if you see a abberancies in the microbiota, if you see suboptimal diversity, then you’ve got to feed your gut bacteria with fiber and prebiotics. I think the challenge with that is depending on your reference point, that statement is more or less true. If your reference point is coming from the standard American diet, then yeah, just by improving your diet, no matter what direction you go in, even if you go lower carb, you’re likely going to be increasing your fiber and your prebiotic intake. But if you’re someone who is on a generally healthy diet. You’re within the normal realm of fiber and prebiotic intake, and please know, there’s a fair variance for which people seem to be able to thrive optimally, but if you’re there and you may still be seeing abberancies in the microbiota. The solution in this case of just force feeding more substrate into the gut doesn’t seem to be how we fix things. What’s going on in the gut is more likely a by-product at that point, and not of dietary insufficiency.

DrMR:

So the mistake is trying to force a dietary problem to what might be a non dietary issue. So in this case, if the problem is insufficient hydrochloric acid, an example that Dr. Richard McCollum, gastroenterologist and researcher, discussed on a previous podcast, that can lead to small intestinal bacteria overgrowth from the top down due to a lack of acidification. There could also be a problem with pancreatic release. Arguably that is impacting the food substrate digestion in the GI tract. That opens a door for some type of dysbiosis. There could also be inflammation that is a by-product of certain food reactivities or there could be circadian and sleep disruption. So, yeah, sorry to get on the soap box a little bit here, but one of the reasons why it’s just so damaging to interpret the finding of suboptimal diversity literally is because it misses all these contextual markers that oftentimes are really going to be what leads to the resolution of the symptoms for the individual.

Dysbiosis

DrTF:

Exactly. Kind of getting on the topic of dysbiosis. So there’s sort of this general idea that dysbiosis means, at a high level, that there are key measures or general imbalances in the microbiome. You’ll hear that quite a bit. Then there are these specific markers known as diversity measures, alpha diversity, beta diversity, et cetera, and there are different ways to measure that. Those are often given as indicators of the extent of “dysbiosis”. I think that kind of begs the question of what exactly do we mean by dysbiosis? This is kind of getting into your area of diet versus kind of looking at these imbalances. We identify three key patterns of dysbiosis, just based on our experience and then what we know from research and things that kind of connect based on research that also seem to kind of associate together in different clinical scenarios.

DrTF:

So we have insufficiency dysbiosis. This is essentially just a lack of beneficial bacteria and that can occur by itself without any evidence of the other types of dysbiosis or in combination with the other types. We also have inflammatory dysbiosis, which is an overgrowth of known potentially inflammatory species. That can be pathogens on the first page of GI-MAP. That can be a couple of the normal commensals that are known to be potentially inflammatory or associated with inflammation when they’re elevated. The classic example there is E. coli. The normal E. coli is found in the Escherichia group in the normal bacteria section. Enterobacter on that page as well is part of that same general group that can be an indicator of inflammation or inflammatory type dysbiosis when it’s elevated. Then on the opportunist page is where we really really the bulk of them.

DrTF:

So there’s Pseudomonas, Morganella, Citrobacter, Proteus and Klebsiella, and a couple of others. Even candida itself can be inflammatory. Those are the sorts of things you want to look at for evidence of inflammatory dysbiosis. Now, of course we do see cases where patients have elevated levels of those markers, but don’t necessarily have elevated calprotectin. So there are some details to get into there, but that’s one of the key things you want to look at because we know that to get outright inflammation in the gut, sometimes you have to have a combination of factors such as a lack of beneficial bacteria, plus overgrowth of inflammatory opportunists and sometimes another trigger. Antibiotics have been shown to be one of those potential triggers, partially because that can reduce beneficial bacteria. The third pattern is when we touched on last time, which is the digestive dysfunction pattern.

DrTF:

So that’s a pattern generally characterized by overgrowth in the normal bacteria section. Also in the opportunistic section, mostly in that top part of page three, where you’ll see things that are commonly elevated, such as enterococcus, streptococcus, et cetera we’ll see certain opportunists that tend to, potentially, have a causal effect or at least contribute to poor digestions, such as H. pylori. We talked about this last time, H. pylori commonly can contribute to low stomach acid, but then there can be kind of a downstream cascade from these effects. That digestive dysfunction pattern can lead to, and this is based on what we see clinically and interpreting the research, to decreases in beneficial bacteria and also potential increases in the inflammatory bacteria. Those are cases where we often will see all three of them, but we can get really tremendous insights into what’s going on with patients when you start to recognize these patterns and realize it’s not just a simple dysbiosis. Diversity is an important indicator. It has been shown to be linked to a pretty broad range of diseases. So just increasing your diversity is a good thing. But to your point, Michael it is not just all about throwing a bunch of fiber at them. In some cases that may be helpful. Other patients, of course, may have lots of negative effects from excess fiber. So that’s really where it’s helpful to look at these more detailed patterns to get an insight into what’s going on with a particular patient. So you can look at those specific factors versus just kind of this general idea of dysbiosis.

DrMR:

Kind of devil’s advocate question here. How does drawing this discernment change treatment in any measurable way? When I’m looking at this on the one hand, the academic in me really likes having more definitive parameters for how to interpret all of these findings and giving them some context in these dysbiosis types.Then the clinician in me says, well, if it’s low bacteria versus inflammatory, couldn’t you make the argument that the inflammation is going to also cause insufficiency. Inflammation, we also know, has a negative impact on things like the interstitial cells of Cajal and that could impact motility and that could cause overgrowths of the digestive function type dysbiosis. Then at the end of the day, it seems like a real kind of Gordian knot. The only way to untangle it would be going through kind of the SIBO or IBS algorithm and personalizing the therapeutics.

DrMR:

So I want to clarify for the audience that there are two aspects to this question that I’m probing into. We may not be there yet where enough data has amassed to where we know how these things should steer treatment. It may be that there’s only so much clinical information you can derive from this and this is where having a healthy respect for the limitations of the test comes in. I don’t profess necessarily to have the answer. Again, there may not be a good answer, but how do you reconcile or try to parse that Tom?

Insufficiency Dysbiosis

DrTF:

Well, I think I’ll do that by giving a specific example. There are actually quite a few of these. One of the most common scenarios, although clinicians actually do miss this often, has to do with the insufficiency dysbiosis pattern. There are scenarios where we’ll have, for example, consultations with clinicians where their initial take on the test is that there wasn’t really much that they could tell from the test. It didn’t look like it was too bad and not much going on. So we take a look at the normal bacteria section, for example, and we’ll see that some of those keystone species or even the phylum level are deficient. That can have a pretty major effect on the gut. Of course, I think most clinicians are mostly thinking initially of looking at pathogens, opportunists and identifying those versus again, as you mentioned, looking at the whole ecosystem.

DrTF:

When you see a lack of beneficial bacteria, the knee jerk reaction, based on most of the information and training that’s out there, is to resort to probiotics. A lot of clinicians will mention that. They will say I see this one is low, it’s in the normal bacteria section, so maybe a probiotic may help. Now they seem to be very clear on that when things like lactobacillus are low, that’s a fairly more direct connection. However, for things like Faecalibacterium, where there are no current probiotics available for that species, the question is, well, how would you potentially go about increasing that? So they’re normally thinking of what specific supplement maybe helpful. Is there a probiotic that has been shown to increase that, or even prebiotics are another common thing that clinicians will think of. Part of what we do in these educational sessions is help them understand how that can be connected to the overall ecosystem.

DrTF:

Just like you mentioned, it can initially be due to inflammation. One of the first things we help them understand is you want to look for these factors, at least based on the ones that we have evidence for on our tests, which is inflammation. We do see that very frequently. So if you have high calprotectin, for example, you’re much more likely to see low Faecalibacterium. So that’s really the first thing to understand. It may not be just a probiotic or even if you try a probiotic, it may not be very helpful without understanding that first you have to look at inflammation and what may be causing that. The other part of that picture has to do also with the digestive dysbiosis pattern. Again, looking at the whole kind of integrated view of the GI tract. There are a couple key things we need to understand about how poor digestion and especially low stomach acid could contribute to low beneficial bacteria and inflammation.

DrTF:

One is kind of the simple concept of low stomach acid. So of course, if there are pathogens, they are more likely to get through that barrier when stomach acid is low. Even some of the new research that’s coming out about some of the other inflammatory microbes like Klebsiella shows that it usually is coming from higher up. Some studies have indicated that when it’s found in the colon under inflammatory conditions, that potentially can originate from dysbiosis and the oral cavity, for example. So Klebsiella can be an issue there or in the respiratory tract. Again, the stomach barrier is an important barrier that it has to get through, and that can be deficient. More recent evidence indicates that there’s kind of a second acid barrier, not nearly as strong, but it’s the proximal colon that actually has, in a healthy gut, lower pH because of fermentation activity.

DrTF:

That’s been specifically shown to be important to inhibit the colonization of the lower gut with inflammatory microbes. Then those inflammatory microbes go on and inhibit beneficial bacteria. The challenge here is that there are a lot of dots to potentially connect and that can be challenging for busy clinicians to kind of learn all this background information. That is why we always try to direct clinicians to our consultations, as well as the educational information we have on our website. So that can give you a lot of these clinical insights into what may be behind these patterns that then they can use to figure out what kind of treatment approach that they want to take.

SponsoredResources:

Hey, everyone. Let’s talk about one of my favorite tests for digestive health, the GI-MAP from Diagnostic Solutions, who has helped to make this podcast possible. Now if you’ve been reading any of the case studies that I’ve published in the Future of Functional Medicine Review clinical newsletter, you’ve likely seen that this test, the GI-MAP, is a test I frequently use in my practice. Why? Well, one of my favorite things about this test is it has excellent insurance coverage. So this is a few hundred dollars that I save patients. This lab is also CLIA certified, which is essentially the quality assurance bureau for labs. So it’s important that these labs are being monitored, not cutting any corners. That’s where you get your CLIA certification. Now, this test uses quantitative PCR technology. So it’s a DNA test. And you’ll get a good read on dysbiosis with this test because they will assess and report out various types of bacteria, yeast, and parasites including protozoa, worms, and amoeba. They also have some valuable and helpful clinical markers like calprotectin which can help rule in or out inflammatory bowel disease, and zonulin, a marker of leaky gut. So head over to DiagnosticSolutionsLab.com to learn more and to order your test.

Validating the Intervention

DrMR:

How do you know that the recommended interventions for these patterns are actually helping? This is one of the things that I struggle with. I have some major reservations surrounding the idea that if these things are cascade like, how can we be sure that a given therapeutic, dietary change, supplement, medication is treating what is proclaimed to be the causative factor. If it’s a cascade of one thing causing the other, it seems like this gets really messy. On the one hand, I try to be appreciative of the fact that human beings are complicated systems and a single line of intervention may not always be the best therapeutic. On the other hand, we should be able to draw a fairly straight line between a given intervention and that helping an individual. This is where something like EPI seems nice in the sense that there is a marker, and a treatment to address that marker. Then symptomatic response follows anywhere from a couple of days to a week or two later. So I guess the question I’m asking is how do we know this is valid? How do we know this isn’t just some very elaborate placeboing and/or has there been any good interventional data that have shown that these interventions are.

DrTF:

That’s a good question. So we’re starting to see the beginnings of some of these types of small-scale studies published. So an example would be in the case of C. Diff. I know we talked about this a little bit in the last podcast, but there’s really good evidence that low stomach acid, just like is the case for most pathogens that are found in the lower gut, that low stomach acid seems to be a pretty significant predisposing factor. Of course we know that poor digestion, low stomach acid can have a negative impact on protein digestion in particular. Independently, a lot of research found that, and this is true for many pathogens and even opportunists in the gut, that they tend to thrive on excess amino acids. A lot of this is actually really well worked out in the research, especially in the colon, how the whole competition between carbs, fiber, and amino acids takes place and they’re kind of directly antagonistic. We do know that protein in general, higher protein content in the gut promotes the growth of C. diff and various pathogens.

DrTF:

This has been narrowed down to a few amino acids, especially proline. So they’ve looked at small scale studies, both animal, and I believe just very small human studies at this point. They’ve intervened with low protein diets and also low proline diets and shown that can help reduce the burden of C. diff. So there are definitely some interventional type studies out there. They are few and far between, unfortunately, because those are not the type of studies that get well-funded. So unfortunately, we are not likely to see studies supporting every possible interpretation. So that’s really where the combination of knowing the research well and what sorts of things are well worked out and highly likely versus things that are just a couple of studies and it would be much more in the realm of speculating. That said, feedback from clinicians is also key. When they see these types of cases, and then we discuss possible scenarios that may be contributing to that and the research behind it. Then they decide to come up with the plan, especially with addressing digestion that seems to help tremendously with symptoms, as well as how the test appears on a retest. That kind of real world clinical validation from retesting as well as how the symptoms change with those types of interventions then becomes a resource.

DrMR:

Right. I appreciate that there are certainly, in any clinical model, spots in that model where the clinical science, if you will, is ahead of the published science. That’s all fine, fair and good. For our providers, I just want to underscore that so that you understand that we’re still early in our understanding here, which is why you can’t shut off your brain and not think about the results of the test in juxtaposition to the response, to treatment, to symptoms, to history. This is one of the most common problems, as I said at the open, that I see when patients walk in after having had seen 5, 7, 10 doctors, many of them functional or naturopathic, is that there’s been too literal of a treatment of the tests and not all of the other considerations related to the patient. So again, I just want to underscore, we want to use this data, but I look at it as maybe one fourth of the data needed to make a good clinical decision.

DrTF:

Right. One thing I would add to that is that we do have these clinical anecdotes. Again, they’re not formal studies, so take them with a grain of salt. However, the C. diff scenario is something we see pretty frequently, and in almost every case, at least that I’ve seen, what we know from research really syncs up with what we’re seeing on the test. Including several recent cases I’ve reviewed with C. diff where I’m talking to the clinician about these studies that suggest that low stomach acid or high protein, whether it’s from consuming higher protein or from not digesting well, could be contributing to the growth of C. diff. In several recent cases when I mentioned high proline foods have been shown to promote growth, they’ll respond that this patient takes a collagen shake every morning or something similar.

DrTF:

That’s just an example where it’s not really hard proof. We do get some clinical feedback frequently that supports what we’re seeing. But it’s also giving them additional suggestions to look at. A lot of these are not necessarily high risk type interventions, for example, if a clinician decides to tell them to hold off on that collagen supplement and we’ll see what happens. That sort of information can be helpful, but again, clinicians need to know what’s has really solid research behind it. Especially if there are great clinical studies that have shown a result versus just animal research for example. And then what’s just anecdote. So you have to always qualify that if you’re relaying any information.

DrMR:

Right. Then there are also a number of C. diff cases that will be asymptomatic, essentially asymptomatic carriers, where a treatment isn’t necessarily required. I’m assuming that if someone is at a doctor’s office and doing a stool test, there are symptoms correspondent to C. diff. It is something else to be cautious with. For example, and let me use some loose labels here. Stool testing is often done in the context of someone with gastrointestinal symptomatology. When we start running tests outside of the population where the test may have been validated in, we run the risk of seeing what could be called a “false positive”. This is something that you’ll see with SIBO. You’ll see patients who have literally no health complaints, but they have a positive SIBO breath test.

“False” Positive

DrMR:

So that’s just something else to kind of factor in. One of my suspicions and Tom, if you disagree with any of this, please let me know. One of the things that I have seen is people will come into the clinic who are very healthy. They are essentially health enthusiasts who have gotten to the end of the road and they’re feeling great. They decide, as part of their ongoing health pursuits, to check in with a functional medicine doctor. They run a stool test on this perfectly healthy asymptomatic individual. Then the provider says, well, you’ve got this, that, and the other thing, and we need to do all these treatments and all these therapeutics. Then the patient will come to me and say hey, Dr. Ruscio, I kinda wanted to get your take on this. One of the things that I think is happening is we’re running tests on healthy populations that are meant to be run on someone who has symptoms, someone who is part of a sick population. We have to factor that into how we interpret the tests. So a couple of different topics there. First about C. diff, some people are asymptomatic carriers, at least that’s my understanding and then how to look at some of these findings in otherwise asymptomatic individuals. What do you think, Tom?

DrTF:

So I would say the vast majority of cases that we review that we come across that have C. diff are what would be considered sort of classically asymptomatic. I mean, these patients are symptomatic in some ways because typically that’s why they go to see the clinician, but in terms of the classic recognizable symptoms for an outright C. diff infection, particularly diarrhea, a lot of the patients just don’t have any evidence of that. So that, of course, leads to initial confusion sometimes by the clinicians. The patient has a high level of C. diff, clearly the pathogenic strain or strains because we’re detecting the toxin gene presence. So clearly they have a high level, but the patient is not symptomatic. Clinicians really want to understand how is that possible? There’s potentially a lot of complicated information here, but mostly what we’ve found or what researchers have found in regard to a wide variety of pathogens is that for them to express their virulence factors, that has to happen under pretty specific conditions.

DrTF:

They are sort of waiting for the right conditions to express them which turns on the whole program for infection. Conditions are not quite right for infection, in terms of what the species is detecting and so it won’t express those pathogens or toxins, at least not at a high level. That’s likely the scenario for patients that do have the pathogenic strains, but do not have symptoms. There can be that sort of gray area in between where they may have subclinical issues. On our test, the main thing to look for would be an elevated calprotectin. Potentially, if they’re being expressed at a low level, that could contribute to some inflammation. This may be an additional sign that clinicians want to take into account when determining whether or not it’s something they want to treat.

DrTF:

Whether or not to treat, of course, is the big question that faces clinicians. Again, we can’t answer that them, but we can give them information to help them understand that better. Mostly with C. diff, as I mentioned, what we know from the emerging research is overgrowth, just like a lot of these other opportunists, can be a sign of other imbalances. Then we’re starting to see some of these interventional studies that suggest correcting those imbalances can be helpful. So once again, if you do see, for example, elevated C. diff, but the patient is not classically symptomatic, we would suggest looking at calprotectin. Is there any evidence of inflammation and then consider the answer with the rest of the picture. I would say the vast majority of time, we do see that evidence of digestive dysfunction type pattern, suggesting that there are some things that could be done potentially to lower the burden of C. diff. Some clinicians may still elect to do an antimicrobial because they may feel that having the pathogenic strain present does pose a future risk. For example, if the patient needs to be on antibiotics, that can be a risk factor for C. diff infection. It’s really clinical judgment once again, but also understanding how that, at least based on what we know from research so far, how that scenario may be related to a given patient.

DrMR:

Great points there. Obviously a very important point to look at. If the toxins are being released by the C. diff, because that will obviously give you a much stronger rationale to intervene. I love the perspective of kind of building a case. Looking at the one marker, looking at their symptoms like you alluded to, looking at are their inflammatory markers elevated. I’d also say, we should all keep in mind that there could be non-classical symptoms that are manifesting. If someone potentially has brain fog or joint pain. I learned that myself. I had amoeba histolytica, which is known to cause dysentery diarrhea, and I had none, but I did have insomnia, brain fog and fatigue. So it’s definitely a balance where we don’t want to be these charlatans proclaiming that the gut is causing every symptom, but we should also remain sensitive. Someone can have an inflammation or just an issue in the gut, pathogen, dysbiosis, infection that may not be manifesting with classic GI symptoms. But may be manifesting as gut/brain, gut/joint, gut/skin. We do see some of this being substantiated in the literature. Most notably is celiac and/or non-celiac gluten sensitivity that may only manifest as neurological or rheumatological symptoms. There is evidence showing that someone can have an active issue in the gut that is only manifesting outside of the gut.

DrTF:

That actually brings me to a couple of things. First I want to answer the other part of the question that you asked about about the asymptomatic scenarios. I’d like to tie into that. Everything really comes back to clinical judgment and the focus of the clinicians. So we do see occasional GI-MAP tests where there’s really nothing wrong with the patient as far as symptoms or health issues. They’re just doing it as kind of a general checkup on gut health and to see how they’re doing. Still, in a number of those cases, we’ll see significant imbalances. That, of course, begs the question is it worth intervening in some way to correct those imbalances, to prevent some sort of future issue. That is a bit speculative and runs a risk of sort of disturbing the ecosystem. If it’s not broken, why fix it sort of a scenario.

Prevention

DrTF:

There’s the flip side of that is prevention. It really gets into a gray area and also the focus of the clinician. Now, I think one particularly interesting example is something I’ve come across a couple of times recently. It’s not enough to really say this is a hard and fast pattern, but I’ve seen results for a couple of patients that were on a carnivore diet, like a strict carnivore diet. No plant intake at all in both cases, from what I recall. This was mostly due to the clinicians conclusion that a big part of the issue was some sort of carbohydrate intolerance. For whatever reason the preference was to try out the carnivore diet. In both cases, the symptoms actually improved dramatically. And yet when we looked at the GI-MAP tests in most of the standard ways that you would interpret results, the dysbiosis, in both cases, looked pretty significant. Lots of overgrowth, lots of inflammatory species. Along with the inflammatory species, a somewhat elevated calprotectin.

DrTF:

So evidence of inflammation. Because we know that too much protein or not digesting protein well has been shown to promote the growth of opportunists and pathogens in many cases, that does beg the question of is that setting the stage for a long-term problem? Again, I think it’s certainly extremely important to take symptoms into account. But that’s kind of where that conundrum of treat to the test or treat to the patient comes into play. Every clinician has to make their own judgment as far as what they think is best.

DrMR:

That’s definitely a case by case call. I definitely lean in the direction of symptoms, knowing how early some of these tests are and that, in my opinion, the appropriate validation to weight a test finding as a primary evidence point has not yet been established. So personally I lean towards symptoms first. We also want to bear in mind that something like the carnivore diet long-term, I have some serious reservations about it. It just seems too restrictive. To me, more of an indicator that there’s something else wrong in the gut that needs to be repaired. So it wouldn’t surprise me that people have inflammatory issues or inflammatory markers positive on a GI-MAP test because the fact they’re having to go on a carnivore diet in the first place likely indicates that there’s some active issue in the gut. Was there a pre-post? Meaning was there a pre-carnivor baseline, and then a post during carnivore where you showed almost a causal change from the carnivore diet. I’m not advocating for the carnivore diet. I’m just trying to make sure I understand the, the observation here as best as I can.

DrTF:

That’s a good question. So I don’t recall that there was a pre-test in either case. There may have been, but I don’t recall that we looked at a previous test or that it was mentioned. So again, to your point, it may not have been due to the carnivore diet if there wasn’t a pre-test. That can’t be said definitively. I’d have to go back and look at those cases just to make sure that there wasn’t a pre-test. It would be certainly great to have that data.

DrMR:

Nonetheless, these individuals are likely people that are going to need to do more than the carnivore. I have no problem with the carnivore diet used like an elimination diet. The autoimmune paleo protocol can be great. I don’t think it’s where people should be forever. An extreme vegan diet I think can be very helpful for some people, but omnivary, even if you’re more like an 80/20, where you’re primarily plant based and in a smaller amount enjoying omnivorous foods, that is fine. Either extreme, I think could be problematic. The same thing with the carnivore. I look at that as an elimination diet, almost like a low FODMAP diet, it’s a helpful clinical tool. Should someone be strictly low FODMAP forever? Perhaps there are some cases who can only do that. Maybe some cases of very marked as an example, inflammatory bowel disease.

DrMR:

And they’re going to see a flaring of disease activity if they deviate. Is that better than being on Humira? It’s a tough call. I lean in the direction of the low FODMAP diet in the long-term being better than Humira. That’s just my gut sense. I don’t think anyone’s really adequately studied that question. These are the things that we start having to grapple with as clinicians when advising patients. For the carnivore crowd, keep in mind that if that’s the only thing that you can thrive on, there’s likely something else going on in your gut that is leading you to have to be on such a strict diet.

GI-Map and SIBO

DrTF:

Yeah. I couldn’t agree more. It does seem pretty extreme, but maybe for some people can be on that diet longer term and maybe not have significant consequences from that. When you talked about the low FODMAP diet that also brought to mind another set of scenarios where we do find GI-MAP can provide some pretty significant, helpful insights to help clinicians get through certain barriers. A common one has to do with SIBO. SIBO gets a lot of attention these days. There are a lot of seminars and training programs, et cetera on SIBO. There is really a lot of focus on that. When patients have common gut symptoms like gas and bloating or abdominal discomfort, there is often almost a jumping to conclusion that it is SIBO. I’ve even heard some clinicians say they don’t even test for SIBO, they just assume it and treat accordingly.

DrTF:

One thing to keep in mind, and this has definitely been our experience, SIBO, especially SIBO treatment, is just not as efficacious as I think the clinicians had hoped in many cases. Low FODMAP diet is one key example. Do you want to stand up forever in order to kind of keep symptoms managed. When clinicians run a GI-MAP in those types of cases, where either SIBO was suspected, but the breath test was negative or the breath test was positive and the patient didn’t necessarily respond well to treatment or only responded partially. They’ll often run a gut test like GI-MAP and they can get a lot of great additional insights into specific factors that may not have been addressed as part of that SIBO approach.

DrTF:

Just kind of a set of clinical pearls. Under those circumstances by far the most common scenario we see is that general digestive dysfunction type pattern, particularly with high H. pylori and/or Candida. On our test Candida seems to be clinically significant even when it’s not flagged as high. So just something to keep in mind that even if it’s at the E2 level, for example, which is just below that high level, it does seem to be consistent with being clinically significant for some patients. So that reminds us not to take the cutoff levels too literally. Also Pseudomonas, that’s one I mentioned before as well. We often will see that, sometimes just present, but usually elevated, in these patients that are not responding well to SIBO treatment or were suspected of having SIBO, but were negative. So I think stool testing can be quite a useful tool in some of these cases where SIBO treatment is turning out to be a bit challenging. So I’m just kind of curious also as to what your experience has been with that combination.

DrMR:

I agree that we want to be careful not to be SIBO tunnel vision, and that seriously seems to be a problem at current. SIBO is the thing that’s getting a lot of attention. So now what you’re seeing is people testing SIBO, treating SIBO exclusively, and there are just too many factors in the gut to hang your hat on any one diagnosis. There could be SIBO co-occurring with hydrogen sulfide SIBO, with SIFO with EPI, with low HCL, with problems with motility, with slow transit constipation. That slow transit constipation could be skewing and causing a false positive on the SIBO breath test. So there’s a lot here to parse, but I agree that we certainly don’t want to look at one evidence point in isolation. Even at best, our testing is probably only telling us a fraction of what’s actually going on in the gut. Hydrogen sulfide has only recently become available to test. SIFO, we still can’t test. Something like hydrochloric acid, as you aluded to earlier, there are only kind of inferential markers. So yeah, we have to take in a lot of data and then parse it, overlay that with the patient’s symptoms and their history and use all of that collectively to make an informed decision. But I would agree that any one evidence point for the gut is not going to likely be enough to really accurately steer the ship.

Question Everything

DrTF:

Yeah. That’s definitely something we encounter quite a bit with GI-MAP and I’m sure that’s true for gut testing in general. You started off mentioning that there’s just so much focus on taking these markers too literally, and you really have to take that into context. To me that is kind of one of the key take home points. From my experience with interpreting gut testing and also being very familiar with the research and seeing how it plays out clinically, you really do have to look at the bigger picture. Take into account the patient’s symptoms, et cetera, and really connect those dots. The more you know, especially about the microbiome and understand how a given lab intends to have their tests interpreted. We kind of mentioned that as well, that misinterpretation is pretty common and we do see that pretty frequently with GI-MAP as well. Again, I just encourage everyone to focus on continuing to educate yourself about the markers and patterns, and then you can better connect those dots.

DrMR:

Yep. Fully agreed. And also remember to think and to try to poke holes in your own hypotheses. That, for me, has been one of the most helpful things. Every differential I put on my list, I’m half expecting to be accurate and half trying to disprove. I really think the field is stretching into a territory where everyone’s drinking the Kool-Aid and that does not make a good clinician. Interrogating all of your thoughts, your principles, your philosophies, your differentials, and trying to pare those down so only the absolute best remain, that is, in my opinion, the hallmark of a good clinician. Something for us all to keep in mind is that we would be far better clinicians, I would argue the same principle holds for politics, for spirituality, for anything, if you’re constantly trying to criticize and disprove anything that you believe. That is a self-correcting mechanism. If you have any poorly supported beliefs, you’ll eventually catch those and you’ll update. So something there I would just leave people with is try to be your own worst critic, in a non destructive way. That is a good auto-correct mechanism for if you end up having a differential or a principle that really isn’t adequately supported.

DrTF:

Couldn’t agree more. My background is in science. I was trained as a scientist and what you are speaking of basically the scientific method. I think that has benefited me in the clinical area as well. Just to your point, I think the more that clinicians can learn to adopt a more scientific, skeptical approach, not overly skeptical, because at some point you’ve gotta hang your hat somewhere, but questioning things. Especially now that we see a lot of information on social media. There are a lot of clinician groups on social media where a lot of misinformation gets propagated. I would definitely encourage everyone to question. If X person says something and it seems to not fit with other things, maybe take some time to research that a bit more, or wait until you see further confirmation before going too deep down that rabbit hole.

DrMR:

Yep. I fully agree.

DrRuscioResources:

Hi everyone. This is Dr. Ruscio. In case you need help, I wanted to quickly make you aware of what resources are available to you. If you go to drruscio.com/Resources, you will see a few links you can click through for more. Firstly, there is the clinic, which I’m immensely proud of. The fact that we deliver, cost-effective, simple, but highly efficacious, functional medicine. There’s also my book, Healthy Gut, Healthy You, which has been proven to allow those who’ve been unable to improve their health, even after seeing numerous doctors, be able to help them finally feel better. There’s also our store where there’s a number of products like our Elemental Heal line, our probiotic line, and other gut and health supportive supplements. We now offer health coaching. So if you’ve read the book or listened to a podcast like this one, or are reading about a product and you need some help with how or when to use, or how to integrate with diet, we now offer health coaching to help you along your way. And then finally, if you are a clinician, there is our clinicians newsletter, the Future of Functional Medicine Review. I’m very proud to say, we’ve now had doctors who’ve read that newsletter, find challenging cases in their practices, apply what we teach in the newsletter and be able to help these patients who were otherwise considered challenging cases. Everything for these resources can be accessed through drruscio.com/Resources. Alrighty, back to the show.

Episode Wrap-Up

DrMR:

Yeah. I think that’s why these conversations are so important to have. So we help people have the most reasonable way of using a tool. In this case, the stool test. Tom, is there anything that you want to leave people with as we transition to a close and then please tell us about the test and where to plug in for that?

DrTF:

Absolutely. So I think we’ve hit on the main things that I’d want to emphasize. Certainly there’s the idea of taking into account the full picture, the more integrative view of the GI tract. Realizing that some of the research is pointing at other things beyond what we’ve been typically trained to think or think of as being key factors. One of them with the gut is the oral cavity. We’re really emphasizing that a lot more in our consultations, for example. Have they asked the patient about oral health? Is there any evidence of gum disease? That can be a potential source for some of these opportunists that may reoccur, for example, after treatment. It’s that sort of perspective, you just want to keep an open mind. If it’s brand new information you want to make sure that it is vetted carefully before it’s applied. A lot of this new information can really be helpful in helping to get a more integrated view of the GI tract. That’s really where I think we’re going to get the most powerful results as far as connecting the dots and treating patients. Then of course, as I mentioned, there is additional educational information on our website. So I’d encourage everyone to check our learning section out. If you’re a clinician that uses GI-MAP, certainly encourage you to take advantage of the 30-minute consults for clinicians. Then lastly, we do have a page dedicated to GI-MAP and all the ordering information is on our website as well under the clinicians tab.

DrMR:

Great. Well, Tom, it was a great follow-up chat. Thank you for taking the time. Hopefully, for our audience, this helps you navigate this tool and use it as accurately and effectively as possible.

DrTF:

Thanks so much, Michael. It was a pleasure.

Outro:

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• Diagnostic Solutions
• GI Map white paper
• GI-MAP Interpretative Guide
• Dr. Ruscio Resources