A Scientifically Validated Lab Test for Gut Dysbiosis

Episode Intro:

Welcome to Dr. Ruscio, DC Radio, providing practical and science-based solutions to feeling your best. To stay up to date on the latest topics, as well as all of our prior episodes, make sure to subscribe in your podcast player. For weekly updates, visit 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.

Dr. Michael Ruscio:

Hi everyone. Today I speak with Anita Jusnes and Christina Casén (www.genetic-analysis.com) from the GA-map based out of Norway, which is the only research validated dysbiosis index. We discuss how this test came to be, its methodology, how it has been validated, how it can distinguish healthy controls from other cohorts, and also how we should think about this test’s ability or inability to tell us how to treat a patient. It was a really interesting conversation with some passionate researchers who are thankfully producing a validated measure of dysbiosis. This gives us something that we can be confident has been able to distinguish between healthy individuals and other groups and not make the mistake of over-interpreting from a stool test that hasn’t gone through the requisite validation to be able to say this is/is not dysbiosis. On stool tests, you will get a lot of information. However, it’s not to say that you can just eyeball a test and say, “Well, if there are many things red/high, that means dysbiosis.”

DrMR:

There are important questions of what threshold of finding would tell you that this is an IBS or IBD individual, as compared to a healthy control, because even healthy controls will have a little bit of noise. That is why the validation is so important to go through. So, that is the discussion here to follow. And just a reminder — If you do need some help in terms of how to improve your own gut health, I would refer you to my book: Healthy Gut, Healthy You. It is available on Kindle, in print, and also as an audiobook. Alright – here we go to the conversation.

DrMR:

Hey, everyone, I have a special treat for you today on Dr Ruscio, DC Radio. This is Dr. Ruscio, DC. We have two special guests from Norway – Anita Jusnes and Christina Casén – who are two of the pioneers behind the GA-map test that I’ve mentioned on the podcast before. To my informed knowledge, it’s really the only test that is validating a measure of dysbiosis. This conversation has been a long time coming and it’s a pleasure to have you both here.

Anita Jusnes/Christina Casén:

Thank you very much, Dr. Ruscio, DC.

DrMR:

Great. Your test is not out of reach. Your dysbiosis index has been incorporated into the Doctor’s Data testing here in the United States. Just to clarify for people, you don’t have to go through the labors of international shipping. Shipping a stool sample across country lines is usually not the easiest endeavor, so there is a United States based plug-in. Where to begin here? So many questions running through my mind. Why don’t you start with how it’s been a long road for you to get this test off the ground. Tell us a little bit about the backstory of how you got into the current position you’re in where you have this dysbiosis measure that you’re validating; where you really seem to be the only game in town that’s subjecting yourself to scientific scrutiny and trying to quantify a dysbiosis test.

The Patent Creation of the GA-map

AJ:

I think the best person to answer this and tell this story is Christina. She has been with the company since the beginning.

CC:

I can give it a try, but Anita, you really have to support me because it’s a long story. I can give it a start, at least. We started out in 2008 and that was actually based on the method that was developed at the University of Oslo. We then moved together with these investigators to the University of Science, which is a bit outside of Oslo. They actually patented the method. And we were so lucky to come into contact with these two guys, whom both today are professors. And after a certain time, we actually established a company based on this patent. Later on, we were actually able to take over the patent. To start a company and think about commercialization, the patent is actually very, very crucial. We also were so lucky to collaborate with one of these professors – Professor Knut Rudi – who is still a very active guy at the University of Science. In the very beginning, we were just a few people starting out very slowly. We were actually building these into more and more of a professional type of development. In the beginning it was explorative research, and then we started out doing all this regulatory documentation that is needed to finally make something commercial-able.

AJ:

Maybe I can take over from there, Christina. Today we are actually in the market with a commercialized test. It’s a pre-determined, targeted microbiome test for basically diagnosing dysbiosis in IBS and IBD patients. And we are very proud to say today that it’s not sequencing. It’s based on a PCR pro-based technology, but it’s patented, like Christina said, and has got solid validation. I think the journey, which I’ve not been a part of until last year, is amazing. This small Norwegian company has really focused so much in this field and has come up with a solution to such a complex world of the microbiome. The whole field is booming with different kinds of technology and different kinds of discussions. It’s still just the beginning, but I think we’ve come a long way to put a standardized, validated test on the market.

DrMR:

Absolutely. And to your remark on this massively growing body of research on the microbiota, there’s been this real paucity of data in terms of asking how we translate this myriad of research studies, oftentimes using 16S rRNA methodology? How do we translate that into something that’s able to be used in a clinical setting? That’s really what excites me about your test because we do have this wonderful world of literature documenting that microbiotic profiles will skew in various disease states, but then that’s not something that’s available to a clinician in clinical practice. These are normally tests that are done at research centers, oftentimes with highly advanced computational assistance in determining the skewing of the microbiota and oftentimes done in population samples. So, the ability to translate that into your run-of-the-mill clinical stool test has been largely absent.

DrMR:

This is why I see so much utility in this. It’s attempting to give clinicians an ability to quantify this clinical assumption. One of the clinical assumptions I’ve made with patients is (loosely stated) – “To the degree to which you have symptoms, we can assume some degree of dysbiosis.” Now, that’s more of a heuristic for someone to understand the correlation between what’s going on in their gut and their symptoms. However, now with your test, we’re getting more in the direction of being able to quantify that with your dysbiosis index. For the audience – this index reports dysbiosis on a one to five scale: five being most dysbiotic and one essentially being normal. Perhaps you can define dysbiosis for our audience? Or tell us more about how you think about and define dysbiosis?

The Dysbiosis Index

CC:

I could explain the more technical part of it and Anita could add something. We actually started out with a healthy cohort. Since we were going to make something clinically available and easy to use in a clinical setting, we wanted to make a reference range/reference area for the healthy microbiota. That’s why we started out with a healthy cohort in the beginning. It was a Scandinavian cohort, but later on we added from other countries in Europe – in Germany and Southern Europe. We also have a healthy cohort from the United States, too. We then tried to differentiate the healthy from the diseased cohorts with IBS and IBD. Then, we found the bacteria that were the most changed/different between those cohorts. And based on that, we found what the healthy range was.

CC:

If you think of a plot, you will see those who are grouped together in the middle would be the healthy individuals, while those outside this range, would be dysbiotic and in different degrees. Now, the farther away from the center – of the healthy – the more dysbiotic. In a way, that’s how it works. That is also how the dysbiosis index is working. That’s why one and two is defined as healthy and means the core bacteria and all functionalities are in place. If you are a three, four, or five, you have a distance actually in abundance of the most commensal and important functional bacteria.

The Hybridization Model: PCR &16S rRNA

DrMR:

The fact that you’re using PCR makes me suspect there’s a smaller grouping of keystone species that you’re looking at. And you’re essentially finding that there’s a smaller number of bacteria that I’m assuming are where you see the predominance of skewing as you go from a healthy control to a diseased population. To frame this for our audience (and please correct me if you disagree with any of these statements), if you’re using something like 16S rRNA, you’re going to get a lot of data. With PCR, it’s a more zoomed analysis, but you may be able to get better quantification of that analysis. With the PCR, you’re looking at less, but in further detail, whereas with the 16S rRNA, you’re looking at more, but perhaps in less detail. That’s a rough heuristic, and I’m assuming that you were looking for the specific keystone/pivotal species that skewed in one direction or the other. Is that a somewhat fair representation?

CC:

In one way, it is because what we have realized is that all human beings actually have a set of core bacteria important for the functionality of the human body. And if those bacteria are intact in the microbiota, everything is fine. However, if there are disturbances within these core, healthy, functional, and important bacteria, then you have a problem. However, when it comes to the technology of the test, we use PCR. However, it’s not sequencing (as Anita already mentioned.) It’s a hybridizing method. We hybridize over target to nucleotide that is added to the test at some step in the lab procedure. What we are doing with the PCR is that we are actually amplifying the complete16S rRNA gene and not only small pieces of it. We take the whole gene, amplify it, and then we add small targets that will fit to its place on this 16S gene. And if it finds its place where it fits, it’s hybridized and a signal molecule is added. So, if you have a positive hybridization, you will get a signal. We don’t sequence nucleotide by nucleotide, so it’s a completely different way of building off the procedure of the test.

AJ:

Christina – Could I just add on for this? Just to simplify it, I think it’s important to say that is a pre-defined approach, right? All these probes that are designed are specifically looking for those species (that Christina mentioned) that we already defined as the most important ones for the dysbiosis index. And then that’s exactly what the test does. It targets only those species that we defined in the test, and you immediately get a report out saying if you are a low level or high level versus a normal population. Right, Christina?

CC:

Absolutely right.

DrMR:

One clarifying question there at the risk of getting really into details here — Is this at the species level that you’re assessing? Or are you going higher up to phylums?

CC:

Yeah. It’s actually different taxonomic levels. Of the 48 bacterial markers (which is in the test today), approximately half of them are at a species level and then another nearly half are at a genus level. In addition, a few targets are also on higher taxonomic levels. It’s phylum and it’s a couple of family and order.

DrMR:

Gotcha. Interesting.

CC:

And that’s the way we actually are able to catch much more than actually the 48 bacteria markers because some of them actually cover a whole phylum and others a whole family. That’s why within those 48 bacteria markers, we say that we detect approximately 300 different species at different taxonomic levels.

DrMR:

Gotcha. Well, that makes sense. It makes sense that you’d want to get (at least in theory) data from different levels of zoom on the colony and you could detect different patterns.

CC:

Absolutely.

Dr. Ruscio’s, DC Resources:

Hey there listeners. This is Erin Ryan with the Dr. Ruscio, DC team back to answer just a few more questions about Elemental Heal. You asked: Will the carbs in Elemental Heal feed fungus or candida? So, there’s no real set research on this yet, but in Dr. Ruscio’s, DC opinion, no. This formula is absorbed in the first few feet of the upper intestines, so it should starve fungus, just like it does bacteria. How to reintroduce foods after the two week Elemental Heal protocol? Okay, so you want to start slow and use a very limited number of foods. Maybe start with steamed veggies or something like that. Stay away from raw veggies or charred meats, but take the time to introduce things very slowly so you can notice how you feel. What about intense workouts while on the two week protocol? Since this is a time to reset the gut and have it rest from digestion, it’s probably a pretty good time to just rest your body altogether. So, if you can do something restorative like yoga or walking, that’s probably even better. There’s a lot more info about Elemental Heal on our website: drruscio.com. There are customer reviews, research, scientific evidence, and ingredients. Anything you want to know about Elemental Heal is there on the shop page.

DrMR:

Does this tie in it all with the concept of enterotyping? Or various enterotypes?

CC:

What do you mean by enterotypes? Maybe I didn’t catch it?

DrMR:

Sure. Well, there’s this theory that gut microbiota assessments may have different signatures. I think, at last, there was roughly three or four different clusterings that you’ll see in the microbiota and they’ve been referred to as enterotypes.

CC:

Yeah, now I understand what you mean. Well, we haven’t gone into that because that was a theory that was presented at many international meetings at the time, but later on it got quite quiet about these types. So, we haven’t really gone into that. What we actually have gone into is looking directly on the functionality of the bacteria.

Functional Profiles

AJ:

Yes. And we also just launched functional profiles. Maybe you can say a little bit about that, Christina?

CC:

Yes. Based on literature, we have put together five different functional profiles. The bacteria represented in these five profiles are represented in the 4k flex test. One example is butyrate producing bacteria. If you somehow have a reduced abundance of two of the three important butyrate producing bacteria, you actually get a low score or a negative score in your butyrate profile or functionality. That’s another way of thinking. We don’t just look at the abundance of a typical bacteria, we also want to look at lacking functionality if some of these bacteria are not present at the level they should be sure.

DrMR:

Sure. So, this is a new component. Is this included inside of the dysbiosis index or is this an add-on that would occur (perhaps in tandem) with the dysbiosis index?

AJ:

I would say more an add-on and in tandem. They’re independent in a way, but at the same time, there are some links. For our European customers, we just added it on the report. It seems like the market and people are really appreciating this angle to the test, as it shows you the profiles on the functionality and clusters of different functions and not only the dysbiosis index and abundance. Basically, you need to be quite educated to understand it in terms of the microbiome. By adding these functional profiles, I feel more people will be able to make actionable calls after looking at the results.

DrMR:

That’s one of the next areas I want to jump into — how these tests guide clinical decision making. However, before we go there, I did want to try to clarify something for our audience (and again, if you disagree with this, let me know.) One of the things we’ve been noticing at the clinic is patients oftentimes have the worst possible interpretation of a lab result. And if there’s something wrong with them, they almost take it too much to heart. They assume it’s more pathogenic than it may be. And I think clinicians struggle to find this balance between using testing results to educate patients (especially if we look at an IBS cohort) knowing that they have a higher likelihood of being anxious. We want to be careful not to fuel the thinking that “I’ve got a bunch wrong with me… I’m sick… I’m ill…” but rather use these markers as something that can be empowering and informative.

DrMR:

All of that is backdrop to say when you do look at some of the studies that have validated your test and documented it can successfully discriminate healthy controls versus IBS cohorts versus IBD cohorts, the amount of distinguishment in between the two isn’t always huge. There was one study that found about 20% to 30% of IBS and IBD patients had dysbiosis, but there was also approximately 16% of healthy controls with dysbiosis. What I’m trying to say there is perhaps some degree of dysbiosis can be normal in some individuals, and it’s not something that we should be overzealous to treat aggressively — especially if there aren’t any symptoms that can be correlated along with it. And to try to state that as clearly as possible — We should be looking for agreement between someone’s symptoms and their dysbiosis index; to be careful not to just treat the labs and to wrap in with that how the person before you was presenting.

AJ:

We totally agree with that. And that’s why we say this test is a snapshot. It’s a profile of the gut. This is not any more than a tool to guide the clinicians with the symptoms and the patients to make the calls. In Norway and in Europe – I don’t know, maybe it’s different than the US – there’s more of a focus on finding the answers rather than the treatment. In Norway, for instance, the use of antibiotics and the use of different therapies for IBS is more cautiously treated. I don’t have any facts to back that, but there is a difference in the way they interpret the results. For IBS patients, for instance, some studies show 30% of them don’t have a dysbiosis. That’s also a finding in an answer for an IBS patient. The purpose of this tool is to give a snapshot and a profiling, and maybe you need to monitor that patient over time, as well.

AJ:

We have FMT studies and we have intervention studies showing that you’re your own control. And this is what I like about it, as well. You can monitor your development, your progression, or your state with this test because it will show you the same answers. It’s clinically validated each time. I think it’s something with the culture, as well. Christina — Do you want to comment on that? On how this test is used?

CC:

Yeah. I think it’s important to understand that. As Dr. Ruscio, DC said, people tend to think it’s much more serious and they get much more afraid to see their results in a way. I’m thinking that what we try to build up with the dysbiosis index system is like a traffic light system. You have the green, you have the yellow, and you have the red. I would say that many of the IBS patients fall in the the yellow area, which is dysbiosis index three and is in the middle. It’s not very serious dysbiotic but, it could be the beginning of something and it could be something that should be followed so it doesn’t get worse. I wouldn’t aggressively treat on number three. However, if it was number five, then I would really study the results. I would look at the bacteria and I would see what is actually going on there. Is it something we should do? Do we have to do something? I really hope that’s the way doctors will think, and it should also be the message they should give to their patients.

DrMR:

Well said. I try to make it a point pretty much every time we discuss testing on the podcast to have a healthy and correct respect for tests. I might be overly sensitive to this, but it’s a byproduct of this drove of patients who come in very worried about their test results. I fear that some tests, especially when they’re not being interpreted by a clinician, end up doing more harm to patients than good because of all the anxiousness and worry that they foster. I fully agree with with what you said.

Anti-CdtB Antibodies, Motility Apparatus, and Dysbiosis

DrMR:

One other thing I wanted to get your take on — there was a very interesting study that you guys published that found dysbiosis was more frequent in subjects with the anti-CdtB antibodies. For our audience, these antibodies may underlie IBS. This is the Mark Pimentel, vinculin, and cytolethal distending toxin antibody test that tells you if someone has autoimmunity against the motility apparatus in the gut that is one underlying factor for SIBO.

DrMR:

I feel it to be a smaller factor, but that’s another conversation. What the GA-map dysbiosis index study found was that dysbiosis was more frequent in those with these motility antibodies, but the antibodies (ironically in this study) did not discriminate healthy controls from unhealthy controls. However, dysbiosis did tend to track with the antibodies. That was really interesting for me. It actually made a lot of sense that the underlying autoimmunity may more tightly associate with dysbiosis. Curious to hear what you think is going on in the gut and this interplay between dysbiosis and this autoimmunity to the motility machinery.

CC:

Yeah. That was really an interesting publication that came out. It’s hard to say something specific about gut mobility antibodies. However, I would say that autoimmune diseases, in general, might be very much linked to leaky gut syndrome. I would guess it’s the same situation here, as in other autoimmune diseases, because we have done studies in other types of autoimmune diseases. We also see that it’s quite a high frequency of dysbiotic patients among these different autoimmune disease scripts.

DrMR:

There was a paper at the last Digestive Disease Week Conference here in the US that my friend and colleague – Allison Siebecker – shared with me. It was where these researchers were hypothesizing that low level dysbiosis might be what’s driving the autoimmunity, turning some of the causal association on its head. And that actually makes a lot more sense to me. If there’s a slow level dysbiosis that’s calling in the immune system to help repair/address it, and the immune system’s has bad aim, it can lead to some bystandard autoimmunity. And that’s why this paper was so interesting to me. Have you come across any of that with your research or any of your colleagues?

CC:

No. We haven’t really gone into that.

DrMR:

It’s one paper, but interesting nonetheless.

AJ:

Can I just comment? The dysbiosis term, I think, is getting more and more accepted and we will see much more research in the future regarding the links between the dysbiosis and different states and conditions. In GA, we’re now also working to see how we can fit this solution and this platform in clinical research, like you’re mentioning. It would be super interesting to see these correlations over time and get these answers. Personally, I think what you just said is very interesting and more and more research is coming in every direction that is linked to this dysbiosis.

DrMR:

This is true. Our email feed, where we get notified about microbiota and gut research, is very hard to keep up with. <laugh> There’s a lot coming through there.

AJ:

The same goes for us. Things are happening every day.

Correlation of Symptoms & Dysbiosis

DrMR:

Absolutely. It’s great for gut geeks like us, I suppose. <laugh> As I mentioned earlier, one of the ways I describe dysbiosis to patients is to some extent we can assume that to whatever degree you have symptoms, there could be this underlying dysbiosis. Let me ask you what your thoughts are about the correlation between symptoms and dysbiosis. I think some of this is fairly obvious. You’ve documented the ability of the test to discriminate between those with IBS and those with IBD. Those are gut symptoms and those correlate with dysbiosis. You’ve also done more documenting that in various autoimmune cohorts that are non-GI in nature (or at least the symptoms are not chiefly manifesting as gut symptoms), those autoimmune conditions also correlate with dysbiosis. Without overstating our case, we could make a moderately confident assumption that an array of symptoms — skin issues… neurological… digestive — correlate to a degree with dysbiosis. That’s a broad statement. It’s probably not going to be defensible in every context, but just trying to get people this rough heuristic through which they can start to make decisions and understand cause and effect. Do you feel like that’s a fair framing or would you modify that at all?

CC:

I just had to think for a couple of seconds. Actually, I think it’s fair because we have found these correlations. We have done hundreds of studies in different clinical areas. We see those correlations. They’re not 100% though. There are many variations within this field, so it’s not an absolute correlation. I think you have to use the dysbiosis and an additional tool to other clinical symptoms that come with a patient. But I can absolutely agree with you.

DrMR:

I’m glad you said it’s not an absolute. I think that’s just important to maybe quickly echo — this is why at the clinic we use a decision making framework that essentially looks at four components: someone’s history, someone’s symptoms, someone’s response to treatment, and someone’s lab work. And we use all that collectively to make a decision. To your point, there may be some conditions that do not correlate with dysbiosis and there may be some healthy people who have some dysbiosis. We should be careful to use some sort of a decision framework that’s not unifactorial, but rather uses a few different points of evidence to make sure that we’re not putting all of our decisions on one marker or symptom.

CC:

Absolutely. I totally agree with you. That’s important.

The Importance of Validated Tests

DrMR:

Now, as we’re looking at this test and trying to make clinical decisions, we haven’t yet gotten to where a dysbiosis measure can tell you what treatment to use for an individual. That may sound simple in theory, but there’s a lot of scientific groundwork thas to be done for that to happen. Firstly, the test has to be validated, which is not easy. And as we’ve said on the podcast before, there are lots of stool tests that are not valid and it means they have zero utility. Additionally, we’ve also talked about some very popular stool tests that were shut down by the FDA for falsifying their ranges. So, to even have a validated test is a huge step in the right direction.

DrMR:

A lot of work goes into that and it probably takes even more work to use/to develop the nuances of the test to predict who will respond to a given treatment. Now you have not just needing to distinguish between healthy versus IBS versus IBD… now you have three or four different diets you could study… there are probiotics and there are different types of probiotics… there are antibiotics and there are other anti-parasitic or anti-inflammatory agents. There are lots of treatments that then have to be looked at in healthy control versus IBS versus IBD. I don’t know of anything that shows predictive value, as of yet, and hopefully we’ll get there. Any thoughts or observations in terms of the ability to use this testing to predict where to go with a patient?

Predicting Therapeutic Responses & The IBD Project

AJ:

Christina – I think we should share a little bit about our IBD project here. This just shows how we are building on the clinical experience and the evidence we have today on the GA-map and then going into this direction of the future – predicting and monitoring therapeutic responses. Christina – maybe you can share some more about the IBD project?

CC:

Yeah. I just want to divide this into two groups first. You have the one who wants to look at the microbiota composition to see if it’s healthy or if it’s not healthy, and if it’s not healthy, then they would like to know what to do. And then you have to give some advice on how you can change your microbiota. Then you have the other group, which is the diseased group that maybe already has a diagnosis and has a dysbiotic microbiota. And then you may treat the disease and see how the microbiota changes and maybe moves towards a healthy composition. So to me, that’s two different groups in a way – two different ways of thinking – on how to use a dysbiosis test. And when it comes to the IBD project that Anita just mentioned, we are looking at making the test as a predictive tool to say something about the expected disease course.

CC:

This is in IBD patients. Some patients actually go through a very rough and severe disease course, while others actually have an easier and mild type of course. If it was possible to predict which patient would go in which direction at the very beginning at a diagnostic time point, then you could – at a much earlier time point – understand what type of treatment the clinicians should actually give to each of these two different patient groups. That’s another way of using a microbiota test. And that’s what we are aiming for in our next new test. It’s a project so far and it’ll be some time until this is on the market, but we are still working on it. And this is from a clinical perspective – really an unmet clinical need.

CC:

That’s actually to take a dysbiotic test one step further, as I see it. It’s much more concrete. You use it for that particular task, while today’s tests are more general. When it comes to interpreting the profile of a given patient which actually has a dysbiotic outcome, then one should look into the bacteria. Which ones have increased? Which have decreased? If you put your patient on a diet — for example, a low FODMAP diet — you should really follow very closely what is happening to the microbiota during the treatment time because this type of diet actually has a great impact on the microbiota. It changes maybe the composition, but it still might be as dysbiotic as it was in the beginning. We have to be very careful before going into that and follow it tightly. And that’s why I think monitoring during treatment is really an important part of this.

DrMR:

Regarding low FODMAP intervention and its impact on dysbiosis scores, I know your group published one study that found dysbiosis index increased in some patients, even though symptomatically they were improving. And there was just a study published only a month or two ago that essentially found the opposite of that. Or partially the opposite in that patients who went on a low FODMAP diet actually saw an improvement in their dysbiosis index. I’m not sure if you saw that other study and I’m just wondering if you have any thoughts? I think we still have a lot to learn in this next evolution of usage of the test, which is how it guides treatment decisions.

CC:

I remember this study. Yes, we see differences. I think that’s due to the baseline microbiota of the patients because it very much depends on the type of profile you have from baseline; how much you actually are able to restore your microbiota based on a really special diet. Low FODMAP is a very special diet because you remove all the fibers, which are the best food for many of your commensal bacteria. It’s kind of dangerous to really remove all that from your diet, especially long term. Maybe you can live with it for a week or two, but then you should slowly reintroduce the fibers to see which one of the fibers you are okay with and which ones you should not take in. That’s possible, but it’s a long run and you have to really go through it very slowly and very detailed to find in the end your special low FODMAP diet which is good for you. Maybe then most of the patients will slowly restore their microbiota.

DrMR:

And this does beg another question — What impact are we having on the small intestine? There does seem (at least from the few studies I’ve picked up) to be some correlation between what’s going on in the large intestine and the small intestine. But I don’t know that that’s really been studied enough to be able to establish what degree of connectivity you see in between the two. And part of what I’ve seen is many of the clinical interventions that seem to help with IBS/help with IBD maybe having a positive impact on the small intestine, but perhaps not necessarily the large intestine. And one of my posits has been that we may be making a lot of our healthcare decisions too large intestine-centered. And this may be why we see (as one example) low FODMAP dieting being so helpful. It has been shown to reduce inflammation and leaky gut. I think its impact on dysbiosis is still being figured out. Thoughts on that comment and/or the connectivity between the dysbiosis index and what’s happening in the small intestine?

Saliva Testing & Fecal Testing

CC:

Well, we really haven’t been studying this. It’s very interesting because there are still many correlations there we don’t know about. We haven’t really studied the small intestine. We have actually been focusing on the colon.

DrMR:

Right. And it’s presumably much harder to do. I think this is one of the reasons why there’s less research on the small intestine. How do you <laugh> get a sample without having a patient have something shoved down their nose or their mouth or up the other end? Either way is not really something that patients will volunteer for, in most cases,

CC:

That’s difficult. What we have been thinking about though is if it’s possible to somehow compare saliva tests with fecal testing. Are there any connections there? That could be really interesting. We are currently doing some saliva studies to see if it’s possible to find any connection. Is it possible that a saliva test could give some answers about the condition in the colon? These are really interesting questions.

AJ:

This will also lower the threshold for sample collection and the wide use of this test, as well. We want to simplify this and find new correlations.

DrMR:

That would be fantastic if we can start getting assessments from both ends – saliva and stool – to give us a more global understanding. Perhaps those two could give a better inferential read on what’s going on in the small intestine. That’s fascinating and that’d be fantastic if we’re able to get there. Maybe you can pair that with a breath test and get a decent, non-invasive measure of the small intestine through that.

Dr. Ruscio’s, DC Resources:

Hi, everyone. If you are in need of help, we have a number of resources for you. Healthy Gut, Healthy You – my book and your complete self-help guide to healing your gut. If you’re not a do-it-yourselfer, there is the clinic – The Ruscio Institute for Functional Health – and our growing clinical and supporting research team will be happy to help you. We do offer monthly support calls for our patients where I answer questions and help them along their path. Health coaching support calls every other week. We also offer health coaching independent of the clinic, for those perhaps reading the book and/or looking for guidance with diet, supplementation, et cetera. There’s also the store that has our elemental diet line, our probiotics, and other gut health and health supportive supplements. And for clinicians, there is our FFHR – The Future of Functional Health Review database – which contains case studies from our clinic, research reviews, and practice guidelines. Visit drruscio.com/resources to learn more.

DrMR:

There is one other thing I wanted to ask about. Let’s say there’s certain bacteria that are high or low in the constituent report for the dysbiosis index. I have not been able to find that treating those bacteria in terms of giving or withholding certain probiotics or giving or withholding certain prebiotics tends to be any better than treating someone symptomatically based upon the randomized control trial evidence we have for probiotics or prebiotics or low FODMAP.

DrMR:

I think this it’s quite important to flag this because one of the growing concerns I see in functional health is that practitioners treat the tests, even when we don’t have evidence showing that treatment of the test numbers improves results. If one finds themself in a paradigm where they’re treating tests where we haven’t validated if treatment of those numbers is a good idea or not, and they’re doing so while ignoring other clinical trials – for example, ones that show you a probiotic cocktail that works really well for IBD or a probiotic cocktail that works really well for IBS – then they’re likely going to get far worse results because they’re throwing out what works at the expense of more speculative treatments. That’s where I have concern that a test like this could really be misused.

DrMR:

It’s done with good intentions. I’m assuming all clinicians are doing whatever they’re doing to help someone. For example, if we haven’t shown that withholding Lactobacillus acidophilus probiotic supplementation in someone with high Lactobacillus acidophilus scores on their test is a good idea and you do that, you’re just wildly speculating and that may be the wrong way to go. I’m hoping we get there. Do you guys agree with that? Or is there maybe some information that I’m not aware of that leads you more in that direction?

AJ:

I think you’re totally right. And that’s why more and more probiotic companies that we are speaking to are interested in doing this and showing more evidence-based results. And we are happy to support that. We are doing a lot of collaboration now with finding new monitoring projects or restoring the microbiome projects, and I think it goes in that direction. I also know that more and more probiotics are now starting to look at clinical research and research trials, which is a good trend. It should be going in that direction. We hope future markets will be more evidence-based, and this is the whole beauty of GA-map. It has always been science- and evidence-based from the beginning. We hope that the probiotic market will also go in that direction. Diagnostic is also needed in probiotics.

DrMR:

Fully agreed. Well, I think we’ve gone through at least most of the high priority questions with your test – how we interpret it and how we use it. Was there anything else that you wanted to make people aware of?

Episode Wrap-Up

AJ:

Like we said when we introduced ourselves, we are really proud and happy to be working in this field. We are from the smallest country of Norway, but we are really seeing a global reach now. For the functional medicine research to accelerate, I think it’s important that we start paying attention to what the gut is telling us in a very simple way. And it’s very complex – that’s why GA is focused on making it simple and also clinically validated so it can be useful. Hopefully, we will get more results and show you more tests so that you can be even better when you treat your patients in making the right judgment calls. Christina – Do you have anything to add?

CC:

No, I think you said it very nicely, Anita. I just want to say I’m so interested in the microbiota and I wish that people really understood the importance of a healthy microbiota. Think of your bacteria as your best friends and treat them like your best friends. <laugh> That’s my motto.

DrMR:

You’re certainly preaching to the choir here. <laugh>

DrMR:

Well, thank you guys. Thank you so much for taking the time for not only this conversation, but the years and countless hours that have gone into pioneering this test so that we can start to rally behind a somewhat unified definition of dysbiosis that can be obtained via a test available to clinicians in routine clinical practice. Again, I really appreciate the work that you’re doing and I wish you well with your future endeavors. Hopefully you have more and more insights that you can pull from your test to provide to us clinicians with your future research agenda.

AJ/DrCC:

Thank you. Thank you so much for having us.

DrMR:

Absolutely. It’s been a pleasure.

Outro:

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