Is This More Common Than SIBO?

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Dr Ruscio, DC:

Hi everyone. Welcome back to Dr. Ruscio radio. This is Dr. Ruscio. And let’s jump in on something that we may have been overlooking or, dare I say, doing wrong at the clinic. I say that somewhat facetiously, but let’s unpack it. So as you know, we have a clinical model that, in my opinion, has been hard fought for and won. The observations have been a derivative of an exhaustive ongoing review of the medical literature in conjunction with careful examination of how patients respond, what is the best order to apply therapies, [and] what therapies produce enough of an effect to use. And how do we take this massive amount of information and options? [Such as] tests, dietary changes, supplements (when to use, how to use, how long you use, how to know if they’re helping, how to know when to combine, how to know when to shift to a different track of care completely as in, from gut to hormones).

Dr Ruscio, DC:

And as new evidence emerges, we’re always looking for either confirmation that new evidence is supporting what we’re already doing or, conversely, for opportunities to update and/or for holes that may have existed in our model. And let’s look at a recent study that ties into this and poses some challenges. And I have a number of what I’m hoping will be insightful thoughts in light of this.

Dr Ruscio, DC:

This study was entitled “Systematic Review and Meta-analysis on the Prevalence of Nonmalignant Organic Gastrointestinal Disorders Misdiagnosed as Irritable Bowel Syndrome.” Saying that another way, people who are diagnosed as IBS were actually found to have something else that was causing their IBS. And this was a well-performed study. Let me go through it: Bile acid diarrhea [had] seven studies with about 600 participants as one diagnosis that was examined, carbohydrate malabsorption [had] 39 studies [with]10,000 participants (and the carbohydrate malabsorption is namely lactose and fructose intolerance or malabsorption), microscopic colitis [had] 17 studies [with] 5,000 patients, pancreatic exocrine insufficiency [had] two studies [with] 500 patients, and SIBO [had] 48 studies [with] just under 7,000 patients. So this is a very well done study. There’s a number of trials and there are hundreds and tens of thousands total participants. So this is a sample that is really worth looking at.

Dr Ruscio, DC:

Now, consider this. Here is a list from the most common diagnoses, or the most common underlying causes that were missed, that people who had IBS were told, “oh, it’s just IBS.” And which, by the way, I don’t think is necessarily a bad thing because that gives us a constellation of symptoms that we can go to work on. But IBS that was knowingly, upon further investigation, able to be tied to another entity [such as] carbohydrate malabsorption [for] 54% of individuals. This shouldn’t be surprising because of how much we discuss things like elimination diets and the low FODMAP diet. So, check. I think we’ve got that fairly well pegged. But here’s the one really in question: bile acid diarrhea or bile acid malabsorption [for] 41% of individuals. Consider that in juxtaposition to SIBO [for] 19% of individuals via the glucose test and 49% of individuals via the lactose test.

Dr Ruscio, DC:

Now, what I don’t know is [whether they were] using the updated North American consensus criteria for their determination of the prevalence of SIBO. I’m going to assume that since those guidelines only came out within [the last] two years (or roughly so). And given the fact that there were 48 studies, I’m going to assume that most of these studies were probably using the older criteria wherein we should have seen a higher prevalence rate with lactulose, and a subset of those were probably false positives. So the true diagnostic yield, if you will, of SIBO positivity is probably closer to that 19 percent you see with glucose. You could argue that the glucose [received] under-diagnosis. Okay, fine. You can also argue that the lactulose [received] over-diagnosis. So, let’s put the difference between 20 and 50 and say, maybe it’s about 30. And that’s being generous. But we’re still seeing a 10% higher likelihood of bile acid diarrhea than SIBO.

Dr Ruscio, DC:

Okay. So bile acid diarrhea [diagnosis received] 41%, CIBO with glucose [received] 19%, [CIBO] with lactulose [received] 49%, pancreatic insufficiency [received] 4% (technically 4.6, say 4%, 5%). And what’s interesting there is the finding of pancreatic insufficiency—and this is something that Joe Mather and I discussed on the podcast previously—was something very exciting initially (and credit to Lana Gerovich [for] putting this on my radar screen initially, or more prominently so). However, upon further testing and noting this in a patient’s chart—putting it in their hierarchy as something to consider and something to treat, treating this in an isolated fashion (I really want to underscore in an isolated fashion, meaning we weren’t doing other things at the same time, this is a therapeutic trial we would do in isolation, thus giving us a very clean signal), I have not found it to be a very helpful finding. Meaning it’s not as often as I would like that when someone uses pancreatic enzyme supplementation, they see improvements in their non-responsive symptoms. Most namely: loose stools, frequent stools, abdominal gas, bloating, and pain.

Dr Ruscio, DC:

I think we’re probably seeing the fact that [pancreatic insufficiency] is tacked on to stool testing probably gives you a lab finding that’s a bit out of context and we might be seeing some false positives, so to speak, there. But the pancreatic insufficiency A) is not very prevalent (4.6% of the population) and B) we haven’t found it to be very effective. Every once in a while, yes, it is. But on the whole, I’d say it was more of a disappointment rather than something that really was a hard-fought addition to our clinical model.

Dr Ruscio, DC:

So zooming way out, the main thing to take away here is: if you’re using a glucose breath test—which isn’t going to have the false positivity rate—bile acid diarrhea is twice as common as SIBO. So how do we interpret that? What do we do about this? Well, I also want to flag that this is something that, since this paper has been published, we have been discussing. Mainly Joe, Gavin, and I have been talking through: what does this tell us, how do we interpret this, [and] what do we change in light of this?

Dr Ruscio, DC:

So, a number of thoughts here. I am not seeing very much non-responsive diarrhea. And I’m sorry, let me take a step back and just explain what bile acid malabsorption is. Bile acid malabsorption, as the name implies, is when your body isn’t able to absorb bile. So your gallbladder squirts out bile into the small intestine early on (duodenum). And from there it makes its way through the small intestine, helping you to absorb fat. And then at the end of the small intestine it’s reabsorbed in what’s called the terminal (or end of the ileum). If it’s not absorbed or reabsorbed, it causes diarrhea and discomfort when it gets into the colon.

Dr Ruscio, DC:

So this is bile acid diarrhea (also sometimes known as bile acid malabsorption). So this presents as chiefly a symptom of loose stools, frequent stools, potentially greasy stools, abdominal pain, and discomfort. And I am not seeing very much of this. Why? That’s the next question my mind asks. Well, very likely because of improvements in gut health by addressing SIBO. Which credit to Allison Siebecker, I think the 2016 SIBO symposium initially brought to my attention that SIBO can deconjugate bile and make it harder to reabsorb in that terminal ileum. So by addressing SIBO, you’re addressing part of the cause of the bile acid malabsorption.

Dr Ruscio, DC:

Also, I’m assuming that there’s something happening when addressing dysbiosis that does the same. And maybe this is the terminal ileum can be irritated, damaged, or dysfunctional when there’s dysbiosis present. So similar, but different to what happens with SIBO—addressing microbial imbalances may help address the root cause of the bile acid malabsorption. And also, with everything else that we’re doing with low FODMAP dieting, elimination diet facets, repairing of leaky gut—that also has an ability to restore the absorptive capacity of that terminal ileum, thus allowing people to reabsorb their bile—[we’re] preventing and essentially addressing the root cause of this bile acid malabsorption.

Dr Ruscio, DC:

So I suspect that we are treating the root cause of the bile acid malabsorption and—whether it’s SIBO, dysbiosis, leaky gut, or just the person’s IBS symptom-picture improving—we’re achieving the endpoint of hitting that terminal ileum repair. And this is likely why I am not seeing very much non-responsive loose stools and diarrhea. Now, this is also in our model, in the back end, when myself or anyone on our clinical team is looking through, what I feel now is such a wonderful dashboard of reporting and biostats that are laid out in juxtaposition to the person’s data (so you can very easily make decisions and problem solve), this is in the model—bile acid diarrhea (we use the abbreviation BAD).

Dr Ruscio, DC:

But in light of this, we’re making a few changes. We’ve made this flag a touch more prominent in our list, or at least we’ve all made a mental note to be a little bit more on the lookout and to consider this mid-to-end phase with patients. We’re also going to make a couple minor modifications to our paperwork, to flag some of the historical findings that may associate with this. One of which is cholecystectomy, or previous removal of one’s gallbladder, and also greasy stools. And we’ve also been looking into: what are some of the best natural bile binders? There’s also welchol and cholestyramine, although our preference is to start with natural agents.

Dr Ruscio, DC:

So we’re making some tune-ups in the model to do two things: 1) make sure we have the structure as sharp and as clear to see this, and then move on this when appropriate and then 2) reappraising the best therapeutics. And to lead to the endpoint of 3) getting a signal for (in a subset of individuals who, let’s say, haven’t responded well regarding their diarrhea, looser stools, or abdominal discomfort) do bile binders seem to make a big difference? And again, my experience here and my intuition is going to be that this will not be a high yield intervention, but only because of the context that we have in our clinic.

Dr Ruscio, DC:

I’m thinking that if you are a primary GI care center, which is I’m assuming is where most of this study was pulling its data from, then I’m assuming these people have not gone through this methodical, “Are you sleeping enough? Are you eating inflammatory foods? Let’s do lower FODMAP for a bit and then reintroduce. Let’s use probiotic triple therapy. Let’s use gut reparative nutrients. Let’s reassess, then potentially do an elemental reset”. [These steps would heal] the gut and presumably, ostensibly address the underlying cause of the bile acid malabsorption. So if that’s not present, would someone respond—potentially very notably so—to a bile acid sequestrant (something that will bind that bile and prevent it from causing irritation in the large intestine)? Yes. Will we see that same effect in our clinic? My thinking is no. But we’re going to evaluate this and we will see. And, you know, at worst case, we’ll keep doing things the way we’re doing them. Best case scenario, we’ll make a modification to how much of a root cause, from the individual’s problems list that we create, bile acid malabsorption occupies and the therapeutics we use therein.

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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, and, also, we offer health coaching independent of the clinic for those perhaps reading the book and/or looking for guidance with diet, supplementation, etc. 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.

Dr Ruscio, DC:

Coming back to: how does this fit in with my remarks about new evidence influencing our model? And how do I reconcile that, but also my suspicion that this evidence may not be very helpful for us? Because you may recall me criticizing that we have to be careful when people say “my clinical experience,” right? They can’t just play that card because clearly there are people who are saying that (in my opinion) who are biased. And I think many of the people proclaiming that treating the adrenal test is helping their patients, they’re getting those results because of the therapies that they’re using—like adrenal adaptogens—not because of the treatment of the tests.

Dr Ruscio, DC:

And what I’m arguing for here—and this is, I think, a really important philosophical clarification to distinguish— what I’m advocating for is moving into a direction that is more patient-centered and more about treating the person in light of this evidence, rather than moving more in the direction of treating a lab marker. So we’re making the patient outcome the primary thing that helps us dictate that balance between being evidence-based but not evidence-limited. That’s the opposite of the people who will argue for treatment of a test or treatment of a mechanism. So if new data emerges that pushes you more in the direction of treating numbers and not people, I would argue that would be a time and a place where the other philosophical construct that we have—which is be evidence-based, but not evidence-limited—would apply. Or treating people, not numbers would apply.

Dr Ruscio, DC:

So hopefully, that all makes sense because all these things are running through my head: making sure that we are consistent with our clinical model and, more importantly, the philosophical characteristic or the epistemology through which we examine this information is consistent. And I think in this case, it is. Said perhaps as plainly as I can, we are going to look at this evidence and we are going to test in our clinic. And we’re going to use it to move, hopefully, progressively in the direction of even better-treating people. And not perhaps [stopping] these treatments that address symptoms upstream (or root cause) and just chase this number of a baseline bile malabsorption test and then treat it with binders. And this is where evidence has to be put into a model. Because some evidence will give you information about treating a cause and some will give you information on treating more of a mechanism.

Dr Ruscio, DC:

And in this case, I would argue while this is fantastic data—I want to really give a lot of credit to the group that put this meta-analysis together and all the hard work that went in behind it—however, how do we integrate research into clinical practice? In this case, we don’t want to necessarily say, “well, the data shows that bile acid diarrhea is more common than SIBO, therefore, we treat bile acid diarrhea first.” Because that would be devoid of the context of—at least from a reasonably speculative perspective (and there’s some preliminary data that supports this)—if you treat things like SIBO, dysbiosis, leaky gut, and repair that terminal ileum, you are addressing the cause of the bile acid diarrhea. Therefore we have to integrate these data points into a sequence or into a model.

Dr Ruscio, DC:

And that’s what I think the real value of a good clinical team, clinician, or clinical model is. It’s, how do you apply and modify your approach based upon incoming evidence and incoming data? Because one thing a study like this can’t do, and it’s not designed to do, is give you a larger construct through which to interpret and address these findings.

Dr Ruscio, DC:

So hopefully, that all makes sense. This is a great paper. It’s a great finding. And, at very least, we will tune-up and add a couple questions to our paperwork that will give us an even more accurate notation in our problems list next to bile acid diarrhea. And then maybe something as simple as history of gall bladder removal and notation of greasy stools, right? So, that’s a win. And then if someone’s getting mid-to-end phase in our model and they’re still having frequent stools, then that makes the trial much more likely, or much more warranted, and slightly tuning up the therapeutics that we use for that.

Dr Ruscio, DC:

So, anyway, in recap, this study found that bile acid diarrhea is, depending on exactly how you look at it, perhaps twice as likely as SIBO. However, that finding may be an artifact, if you will, of intestinal dysfunction. And the way of addressing that finding may not be treating that finding or treating that lab, but rather treating the person by personalizing their diet and using the available tools we have to address things like SIBO, dysbiosis, leaky gut, and inflammation, thus repairing the root cause of that bile acid malabsorption (which is a damaged terminal ileum).

Dr Ruscio, DC:

So hopefully, that all makes sense. One other thing I just want to flag, because you may be saying, “well, what about the people who’ve had their gallbladders removed?” I think the same rules apply. Not everyone who has their gallbladder removed has this problem. In my suspicion—and this is admittedly speculation—but my suspicion is that if we look at intestinal health on a gradient, it’s the people who have the poorest intestinal health who will have the most bile acid diarrhea post cholecystectomy or after having their gallbladder removed. And it’s the people with the healthiest intestinal tissue, or gut health, who will have no bile acid diarrhea after their gall bladder is removed. But this would be a historical finding that would make us a bit more suspicious that in a person who has non-responsive symptoms mid-to-end phase, that we’d want to consider using bile acid sequestrants or binders (things like charcoal, welchol, what have you).

Dr Ruscio, DC:

Okay. So hopefully, that all makes sense. And, rest assured, these findings are already on their way into integration into our clinical model and something that we will be thinking about to make sure that we are always bringing you the best care. And I hope it’s also evident that our clinical model (again, hard-fought and won) really helps to bring clarity to the gazillion things that you could do. And that’s why I really advocate for treating people in this kind of process-driven fashion and not treating labs. And this would be a great example of where treating a lab might lead you to treat a symptom or a mechanism and not the cause. Okay. Hopefully, that helps. And we will talk to you guys next time. Take care.

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• A systematic review and meta-analysis on the prevalence of non-malignant, organic gastrointestinal disorders misdiagnosed as irritable bowel syndrome
  • Looking at the rate of the following conditions in those originally diagnosed with IBS:
    • bile acid diarrhea (BAD), 7 studies, 597 participants
    • carbohydrate malabsorption (CM), 39 studies, 10,115 participants
      • E.g. lactose or fructose intolerance
    • microscopic colitis (MC), 17 studies, 5,068 participants
    • pancreatic exocrine insufficiency (PEI), 2 studies, 478 participants
    • and small intestinal bacterial overgrowth (SIBO), 48 studies, 6,779 participants
  • The following diagnoses were correctly identified in those w/ an original diagnosis of IBS:
    • CM – 54%
    • BAD – 41%
    • SIBO – 19% (glucose BT), 49% (lactulose BT)
    • PEI – 4.6%
    • MC – 3%
  • Commentary: This study showed a notable prevalence of organic disorders in those w/ a past diagnosis of IBS. BAD, SIBO and food intolerances (e.g. lactose intolerance) are the most common types of missed diagnosis. Keep these differential diagnosis in mind next time you see a patient that looks to have IBS.

• Dr. Ruscio’s, DC Resources