Why Autoimmunity May Not Cause SIBO and IBS

Episode Intro:

Welcome to Dr. Ruscio 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.

DrMichaelRuscio:

Hey everyone. Welcome back to another episode of Dr. Ruscio Radio. This is Dr. Ruscio with a few updates on whether autoimmunity really underlies IBS. Just a couple quick research updates I wanted to point to – one quick study on low FODMAP diet and one on nutritional status and hypothyroidism. Let’s jump in with the main thrust here, which is prompted by a study that recently flagged and came up in the research briefs of our Future of Functional Medicine Review Plus. As you know, this is our constant commitment to monitoring literature and using that to update and inform our opinions. Now that Gavin and myself are doing this together, we have a broader net. Therefore, there are fewer studies slipping in between the cracks or evading my purview. It is a lot to keep up with and it’s just unsustainable for one person to do it. So, if you’re a healthcare provider or a science nut, I would definitely get plugged in for the FFMR Plus research briefs.

New Study Analysis: Gut Microbiota

DrMR:

The study in question is entitled ‘Gut microbiota profiles and the role of anti-CdtB and anti-vinculin antibodies in patients with functional gastrointestinal disorders.’ The quick primer here, in case you haven’t heard of this, is the great work of someone who I respect and who has been on the podcast before – Mark Pimentel. He is one of the leading researchers in IBS and SIBO research and has postulated to a greater or lesser extent one of the underlying pathways or mechanisms of IBS and SIBO. This is what’s known as post-infectious IBS — traveler’s diarrhea, food poisoning or some type of organism that causes acute gastroenteritis.

DrMR:

This causes the immune system to come in and come to the rescue, but in the process of doing so, it triggers this autoimmune attack. Some of the structures – let’s say it’s an organism of Giardia or Cryptosporidium – look similar to certain tissues of the body. This can lead to the creation of these anti-CdtB – or cytolethal distension toxin antibodies or vinculin antibodies. These structures are part of the motility apparatus in the gut – these interstitial cells of Cajal – or these neuromuscular bundles that help the intestines contract to keep food moving through. When food flows through like running water, it doesn’t stagnate and it doesn’t harbor bacterial overgrowth. However, if there is a breakdown and therefore, a stagnation and a slowing of motility, that’s when SIBO and IBS can occur. This is a wonderful finding.

DrMR:

Anytime you understand more about mechanisms, that is a huge win. However, if you have been paying attention to some of my ongoing criticisms of how to not get too far ahead of ourselves, one of the things I constantly point to is the evidence-based model or the evidence-based pyramid of how we assign value to different types of information. If you’re picturing a pyramid in your mind, the bottom of the pyramid is mechanism or observation. For example, we could observe that people who live in India have less heart disease. This can get us in trouble quickly because people can say, “Ooh, it must be the curcumin and turmeric they’re using because those are anti-inflammatory. And that’s why the people in India have less heart disease. So everyone – take turmeric.”

DrMR:

Well, maybe, but we’re a few steps away from being able to say, “…Because people in India have less heart disease and they eat turmeric … that if you take turmeric, you’ll also have less heart disease.” We would need to take a group of people – 1/2 of them get turmeric, 1/2 of them do not. We can then track heart disease outcomes. If we can then show those taking the turmeric as compared to the placebo have less heart disease and heart attacks, then we’ve now qualified there’s something to that observation. So, at the bottom of the pyramid is observation/mechanism. Mechanism would be what we’re looking at here. This is a mechanism that seems to underlie IBS. Now, as we go to the pinnacle of the pyramid, we have clinical trials and/or summaries of clinical trials (aka meta-analyses.) This trial is a higher level trial because of the setup.

DrMR:

This setup – albeit a smaller trial – was 22 healthy controls (this is key) vs. 65 patients with functional gastrointestinal disorders. This is a broad catchall. It could be reflux, constipation, dyspepsia; it could be some of the symptoms of IBS, but not fully IBS. Up to 40% of the population has a functional gastrointestinal disorder. Whereas, about 10% to 15% have IBS because IBS is a more narrowed constellation of symptoms. So, there are 22 healthy controls and 65 functional gastrointestinal disorder patients. This breaks down to the subsets of IBS-Constipation, IBS-Diarrhea, and dyspepsia. They’re looking at these antibodies – the CdtB and the anti-vinculin antibodies – and what they find is very interesting. In constipation-type IBS, 77% are positive; in the diarrhea-type, 40% are positive; in the dyspepsia or indigestion cohort, 60% are positive; in healthy controls, 63% are positive.

DrMR:

This is something I have not yet fact-checked. I want to clarify this podcast is reporting on one or two new studies. It is not a summary based upon my comprehensive review of this issue. My belief – and I could be wrong on this – is the validation studies for the vinculin and the CdtB antibodies, these auto-immune tests that underlie SIBO, have not adequately discriminated between healthy controls. I believe they were discriminating against IBS subtypes, however, I could be wrong there. I will leave that door open for a piece of background that I’m not seeing. Why I feel this would be important is because clinically, I have not found there to be a lot of utility of this testing.

DrMR:

I also feel it’s a bit early – we’re still mapping out how all this works and what kind of meaning we take away from this. As an example, there was a previous study that found there was no significant elevation of these antibodies in constipation. However, this study is finding the opposite. The highest level of antibody is in those with constipation. So, this is why I’m not too quick to rush to a new test. While it sounds attractive and scientific – and when I’m wearing my clinician hat thinking, “Ooh, maybe this will help.” – if we haven’t figured out the exact meaning of this test yet, that actually makes it harder to help an individual. You don’t know if what you’re treating is signal or noise – or as this individual study found, really just inconsequential noise. If this is no different in healthy controls than those with IBS or dyspepsia, then how does this help the clinician treat you any differently?

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DrMR:

Low Level Dysbiosis

DrMR:

A few other notes here that are worthy of mention and where I think there is some clinical takeaway — Dysbiosis, a disruption in the community of bacteria in the gut, was more common in those with elevations of the antibodies. Why this likely matters is also a speculative point, but because it doesn’t change how we treat someone, it’s a safer speculation to make. Another finding – that I believe was a presentation at the last Digestive Disease Week Conference (DDW) and Alison Siebecker made me aware of – is that some researchers were now finding and speculating that part of what may cause those antibodies is chronic low level dysbiosis. That would make complete sense. It would make sense that there is some residual immune activity when there’s a low level of infection the immune system is trying to address. My position has always been work to improve symptoms and reduce inflammation. This will likely get you to the healthiest microbiota or rectify the dysbiosis. This healthier, more balanced, symptom-devoid state is most likely when the body will have the best chance to get over the autoimmune attack and/or repair any of the damage that happened because of the autoimmune attack.

DrMR:

These cells in the gut that are damaged – these interstitial cells of Cajal – can rewire, regenerate or regrow. However, if you have an inflammatory environment, that can’t happen. Zooming way out – we have a crossroads here where we can treat the lab test and say, “This lab showed antibodies that thwart motility and therefore, prokinetics.” That’s one way, but that’s just treating the lab marker and not treating the person. “Cholesterol high – suppress it with this drug.” Another way of looking at this – an alternative hypothesis – would be, “These antibodies are elevated. They’re telling me there is some damage, inflammation and autoimmunity occurring.” Let’s continue to use an evidence-based algorithmic approach with the therapies we know improve symptoms, reduce inflammation and help heal the individual. This should address the most root cause of that inflammation and autoimmunity. The less symptomatic someone is, the less dysbiosis or imbalance they have. Therefore, the less inflammation and the more these things can repair, the more the autoimmunity can be quelled. This is the hypothesis I’ve been trying to champion for a number of years and how I interpret this data.

DrMR:

A few other findings from this study – no other bacterial markers showed significant differences between the symptomatic group and the healthy controls. Now, one of the things I want to weave in here is what they’re doing at Diagnostic Solutions with their GI map test. It kind of hints at this. They are reporting organisms that have a detectable level, but not enough to say that they’re at the “disease level.” This is where Diagnostic Solutions really may be ahead of the curve. For example, you don’t have cryptosporidiosis to the point where it’s a full blown infection, but there is some cryptosporidium on this stool test.

DrMR:

This may be that subclinical or low level pathogen or dysbiosis some researchers are speculating is what underlies the inflammation and autoimmunity that allows these antibodies to occur. What do you do with that? This is another contentious point. I am not convinced that those low level pathogenic or dysbiotic findings mean we have to bull in there with antibiotics – rifaximin, metronidazole, neomycin, Alinia. If it’s a frank infection, maybe. However, the algorithm has so much more merit here. This is partially theoretical, but there’s also some emerging evidence that supports this. If we’re trying to get the dysbiosis quelled and the imbalances in the gut are the ultimate driver of this, then a diet that makes the host feel best, will reduce inflammation. Step one – figure out if you should do paleo, low FODMAP, vegetarian, low-flex, low-histamine… Figure that out, get some improvement and reduce some inflammation that’s already positioning the microbiota in a healthier direction.

DrMR:

Now, maybe you’re not all the way there. So now we layer on top of this probiotics – not just willy-nilly probiotics – but a clinically viable probiotic triple therapy that seems to have more punch than just one probiotic at a time. This further reduces inflammation and – as over 20 clinical trials have found – probiotic monotherapy can eradicate SIBO. Also, a meta-analysis has found that H. pylori can be eradicated in about 1/3 of cases with just probiotics alone. There are even some head-to-head trials looking at drugs, whether they be antibiotics or antifungals directly against probiotics, and they found equivalent results. The probiotics reduce inflammation, reduce leaky gut, help rectify dysbiosis and fight pathogens. Boom – another big step in the direction of reducing inflammation and helping correct the dysbiosis.

DrMR:

If you have a frank parasite, there is more of a justification to go in there guns a-blazing. This comes back to my analogy of cultivating a healthy gut and not just thinking one round of antibiotics or antifungals is going to fix everything. Now, we’ve worked our way up to the point where if we do use an antibiotic, antifungal or an antiparasitic, you’ve done so much groundwork that you should see a very favorable response and reduce the likelihood of a negative response from said agents. There are some studies that have found – as an example – when you’re trying to eradicate H. pylori, it’s much more successful when you use probiotics at the same time. Two studies even more to date show that when rifaximin was given along with probiotics, there was better clearance of SIBO. This study is a good window into this different paradigm of how we look at and treat the gut. Are we thinking antibodies positive and a prokinetic? Or are we thinking the antibodies positive is giving us diagnostic information about an intermediary mechanism, but not the root cause? Contestable, but that’s how I look at this. The data here are not definitive.

DrMR:

So, in close on this study, the commentary here was there was no statistical difference in the antibodies between those with functional gastrointestinal disorders vs. healthy controls. However, there was more dysbiosis in those with the antibodies. Now, we should also mention that the notion of dysbiosis and what exact criteria are used to identify that, are still up in the air. I want to acknowledge that dysbiosis, to date, is still a partially theoretical construct. You can look at a stool test and say there are some of these commensals that are high or low, or some of these dysbiotic organisms that are high and maybe a problem. However, there is still some information I think we have to work out there. I want to be careful in disclosing that, in my opinion, I think dysbiosis is an oftentimes assumptive diagnosis based upon someone’s prominent symptoms and some lab work. As you’re probably accustomed to me saying, we want to look at symptoms in conjunction with lab work to really give us a more complete clinical picture. Especially in GI, a lot of these tests are still being further developed and validated. We don’t want to hang a diagnostic hat too firmly on the hook of a lab finding.

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New Study Analysis: Antibodies as Biomarkers

DrMR:

There is one other study that has a similar finding. It’s entitled ‘Circulating Anti-cytolethal Distending Toxin B and Anti-vinculin Antibodies as Biomarkers in Community and Healthcare Populations With Functional Dyspepsia and Irritable Bowel Syndrome.’ They did find there was a higher mean value of the antibodies in those with functional dyspepsia indigestion vs. healthy controls. If they grouped IBS and dyspepsia together, the antibodies were higher there than healthy control. There is some discrimination there for the anti-CdtB antibodies alone. However, there was no difference between the groups when looking at anti-CdtB in IBS and functional gastrointestinal disorders when compared with patients with organic GI diseases. What that means is – if someone has another inflammatory disease or diagnosable issue in the gut, this didn’t discriminate between IBS and those individuals. This may mean that these antibodies are more reflective of – broadly – inflammation than this very specific finding in IBS that requires this very specific treatment of prokinetics. There’s still stuff here that’s being mapped out, but this is how I’m reading these data.

DrMR:

For the other antibiotic – the vinculin – there was no difference at all between IBS and functional dyspepsia vs. healthy controls. This is important to keep in mind. It’s why sometimes I find myself almost appearing as someone who is lazy. Why aren’t you using this test? Why aren’t you using that test? Well, it’s because I’ve reviewed the evidence and I’ve thought through how this would affect treatment. Unless this is going to give me something I wouldn’t otherwise know or allow me to use a treatment I wouldn’t otherwise use, this is just one in a sea of pieces of noise that don’t really help us improve your health.

DrMR:

I would even go so far as to argue that it could actually make it more difficult. Part of the reason why I think I’ve become fairly well attuned at helping patients improve their gut health is because I have filtered out as much noise as I can. I focus on signal. Think about it this way – If you were in a room and the person next to you had a very important message they were trying to whisper to you, but I came in there with a huge stereo system, cranked it all the way up and blasted it while the person was trying to tell you the signal, would you be able to establish the signal versus the noise? Probably not.

DrMR:

If you’re a clinician seeing 10 or so patients every day for years and you’re not reducing the noise, you can’t see the signal. If you can’t see the signal, you can’t learn. If you can’t learn, you can’t improve your model. That’s why I am quite fastidious about reducing variables, filtering out data that’s not relevant and listening to patient response/outcomes; using that to inform how I practice in addition to using tests and research that impacts how we treat someone. There’s so much speculation, conjecture and lower pyramid observation or mechanistic noise that you have to have a pretty tight filter.

New Study Analysis: Low FODMAP and the Intestinal Barrier

DrMR:

A couple other things I want to touch on is a study entitled ‘Psychological and Gastrointestinal Symptoms of Patients with Irritable Bowel Syndrome Undergoing a Low FODMAP Diet: The Role of the Intestinal Barrier.’ It’s a small trial. 20 patients with IBS were given a low FODMAP diet. After 12 weeks, an improved quality of life was noted. There was improvement in anxiety, psychological stress and intestinal permeability (as measured by zonulin and a sugar absorption test – this was the lactulose:mannitol test). There was also a decrease in dysbiosis and inflammatory markers.

DrMR:

Albeit, it’s a small study and there is no control, but it is still pretty amazing to see. I think it’s pretty validating for many that when you withhold prebiotics, which feed bacteria as you do on a low FODMAP diet, you see improvements in gut health. This is something I’ve been trying to champion and get more to the forefront of the conversation in gut care for a long time. Thankfully, it seems this message is gaining momentum. It’s antithetical on the surface when you think of mechanism. If we were like robots, it would be… prebiotics feed bacteria –> we want more good bacteria –> therefore, take prebiotics and all your problems go away.

DrMR:

However, when you look at the clinical trials, you see some evidence showing that prebiotics and the higher fiber can help. By all means, there’s a time and a place. However, when you go into the cohorts I think we’re most concerned about – people with more acute or more symptomatic gut symptoms – this is when you see a higher probability that higher fiber and/or higher prebiotics have an increased likelihood of flaring an individual. And interventions that reduce fiber and prebiotics – like a low FODMAP diet – actually improve symptoms.

DrMR:

Shockingly (wink, wink – as I say this facetiously), as the individuals feel better, there is less dysbiosis and less inflammation as I just went through with the other studies. Without even trying to make all this connect down to a root system philosophically, I hope you can see how even though I just plucked these studies from the research thread, they are all perfectly congruent with the philosophy that we’re using at the clinic. I think that’s really important. If you see contradictions in someone’s philosophy, that gives you a huge red flag that there’s probably bias.

DrMR:

This is a quick aside. There’s someone out there and I appreciate their work. They do some blogging and some consulting. What I’ve noticed is that they are hypercritical of probiotics. They go into uber detail about the strain, specificity and dependency. Yet, they seem to be very keen on supplemental butyrate, even though there is far less clinical trial evidence on it. Perhaps in the past 1.5-2 years since I’ve reviewed this literature robustly, there’s been about 300 clinical trials published to be more on par with that of probiotics. This is something that just came up as a credit to this individual online – something for me to have another look at.

DrMR:

I did have a patient the other day who really felt that butyrate was very helpful for him. However, it wasn’t the only change made at a time so it decreases the probability, but it was enough for me to jump back in. This is something that we are currently doing – a review on what clinical trial data or interventional data with butyrate tells us. Maybe this is something we can start bringing into the clinical model, at least experimentally, to see if there’s a viable signal. The point I’m making is about being hypercritical regarding probiotics. There is an ample amount of clinical literature showing that we don’t have to be that fastidious with our application. Yet, making a hallmark of their treatment something that’s more speculative and has much less evidence, is a philosophical contradiction.

DrMR:

I don’t mean to be critical of the person. I’m just critical of the thought process. Also, I am not perfect. I am still trying to work a lot of this out, but I try to share my thought process because that’s the most valuable thing that we have. If we think more effectively, we will eventually find our way to being a stellar clinician. If we’re not thinking correctly, we’re going to spin our wheels. Also, I’ve been doing this for awhile. I have the fortune of having some time and reflection on my side. Certainly when I was early on in my career, I had a lot less of this figured out.

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DrMR:

There’s this emerging theme in my opinion. When you see improved symptoms, you’re likely going to see accompanying that less dysbiosis and less inflammation. That’s what all these studies so far have reinforced.

New Study Analysis: Antioxidant Status & Hashimoto’s

DrMR:

Pivoting for a moment over to thyroid, this study was entitled ‘The Level of Zinc, Copper and Antioxidant Status in the Blood Serum of Women with Hashimoto’s Thyroiditis.’ This was a sample of 42 women with Hashimoto’s and 30 healthy women. There was no difference in zinc, copper or antioxidant capacity. This begs the question – How important are these nutritional status assays? I have not found them to be very clinically useful. Part of the reason why is because I don’t think they’re treating the deepest root cause. If you have someone with Hashimoto’s who has symptoms, the likelihood that a deficiency in zinc alone as a primary driver of that, is fairly unlikely. That’s more of a cherry-on-top, end phase refinement. It’s not usually the deepest root cause that we can address. Diet quality could be and that should eventually rectify imbalances nutritionally. If you really wanted to go more specific, track your food for a few weeks in something like Cronometer. Then, do a report, see what deficiencies you’re eating your way into and make those changes. The other thing that may be occurring here is that people may be avoiding foods due to intolerances. This is where improving gut health comes in.

DrMR:

On one of our last clinician round table training calls, Dr. Rob from the clinic shared a recent snippet with me that I thought was pretty insightful. He accidentally ordered zinc two times – once at either LabCorp or Quest and then once at another functional medicine lab. It was the same marker and it was the same sample, but the values were very different. Something like 80 vs.150. This is also a project to have on our list to go through the evidence on nutritional testing – what’s accurate, what doesn’t distinguish healthy vs. non-healthy, what’s littered by false positives? There’s a lot here to unpack. There are different methodologies and different sampling. Do you do whole blood? Do you do serum? Do you do white blood cell? Suffice it to say – outside of a few that we’ll look at like ferritin and vitamin D amongst a small handful of others – generally speaking, the “let’s test all of our nutrients” I haven’t found to really be something that addresses the root cause of one’s health issues.

DrMR:

I just wanted to share this one study. On the one hand, I am absolutely open to and hoping that wherever there is a nutritional or natural solution, we will deploy that. I also want to be careful not to let that bias me. I don’t want to become the natural health advocate that doesn’t have a healthy respect for limitations; an ability to be self-critical. I want to be able to delineate between when a nutrient helping someone is a meritful claim compared to when it’s a dogmatic claim.

Episode Wrap-Up

DrMR:

In any case, those are just a few thoughts I wanted to share. The most important thing is understanding this deeper philosophy that informs a lot of the actions we take at the clinic – having a filter, being discerning in how you interpret data, using that data to inform a clinical model and looking for all of the new information to be either informing and updating your clinical model. Or if new quality data is antithetical to your model, then you have to reconcile your model. This is why I feel so confident about the model. Even these three different studies really reinforce the same root philosophical points from the model. I want to really call attention to that. It’s not something that I was able to spackle together in a couple of years. It took many years, lots of thinking, lots of research and lots of frustration.

DrMR:

For example, I went to this conference and this person said X, Y, Z. However, it’s really dissonance to what I think I’ve been seeing in the clinic. How do I reconcile this? Or many situations of being told how great these tests are and I’m using them, but I’m just not seeing it. Am I the idiot? There was a lot that had to be waded through and determined to figure some of this stuff out. I feel like there’s really something prized there that helps people not get sucked into dogma or speculation and really helps give us a unifying framework to work through so that we can be more efficient with how quickly we help people improve their health. Hopefully this has been insightful. I definitely welcome any comments anyone has.

DrMR:

If you’re in need of help, please feel free to reach out to the clinic anytime. The more time I spend in the clinic, the more I really do feel honored to be doing the work we’re doing. As I shared recently with my foray into sleep medicine, it’s scary what you can be told. It’s really given me a renewed perspective on how important progressive yet, conservative and cost-effective clinical care is. So if you need help, the clinic is always there as a resource. All right, guys. Hope this helps. We will talk to you next time.

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