DR: Yeah, that’s great. It’s on National Geographic.
SM: Yeah, NatGeo. You can search it and DVR it, and it’s probably can it be on YouTube as well I’m assuming.
DR: I love it. I’m always looking for a good way to share the importance of sleep with people that I know without having to beat a dead horse, so to speak. So a cool documentary that has picture and video and stuff like that I think would be helpful in raising awareness. So that’s great. I will have to look that up.
SM: Yeah. So, Doc, today is Part 3 in our series on small intestinal bacterial overgrowth (SIBO).
DR: Yes. There were a couple of things I wanted to expand upon a little bit from our conversation last week on the ICC cells, the interstitial cells of Cajal. Then I wanted to finish off with a listener question on bile acid diarrhea.
SM: OK, Dr. Ruscio. Tell us more.
DR: So, last week we discussed the ileocecal valve. And we had also discussed the the interstitial cells of Cajal.
Ileocecal valve and interstitial cells of Cajal
DR: Just as a quick primer: The ileocecal valve, depending on the circle that you learn from, can be described as a really important, pivotal part of healthy digestion. We talked about that. We talked about where the science is lacking – my personal and clinical opinion on that. We’ve also, of course, been talking about the ICC cells, or the the interstitial cells of Cajal, which, we are learning, have very important impact on gastrointestinal motility and how that proper motility is very important in SIBO. If you deranged motility, you are higher risk for SIBO. If you have healthy motility, you’re going to have better gastrointestinal function overall.
So, the ileocecal valve and the interstitial cells of Cajal actually have quite a intimate connection. Some researchers have looked at the density of these interstitial cells of Cajal through the intestinal tract, and they found that the ilium, the last section of the small intestine where the ileocecal valve is, the ilium has the highest density of these interstitial cells of Cajal compared to anywhere else in the digestive tract (2). So,these pacemaker cells, these interstitial cells of Cajal, are very very dense where the ileocecal valve is. What we maybe able to say is that a more contemporary way of discussing the ileocecal valve may be to discuss the interstitial cell of Cajal function. Does that make sense or am I going way too deep on that?
SM: No, it totally makes sense. It’s like almost anything in the human body – things are so interrelated that you can’t look at one thing without taking into account something else.
DR: Exactly, exactly. I should mention that with this ileocecal valve and the interstitial cells of Cajal are now synonyms for one another. There are a couple important things to remember. Of course we know that in SIBO we can have an autoimmune attack that damages these interstitial cells of Cajal. Now we know that they are highly concentrated at the ileocecal valve. So it may not be, again, that you have an ileocecal valve problem, but that you have this autoimmunity damaging these interstitial cells of Cajal. Since they are so concentrated in the ileocecal region, you see your Ileocecal valve function go down. Now, the good news, and like we discussed in our last conversation, is that these interstitial cells are plastic and able to be regenerated. This is not a terminal diagnosis so to speak. I should also note that there are two key things that may regulate your ileocecal valve and the interstitial cells of Cajal – again, they are synonymous: One is inflammation. Inflammation can derange the function of these valves. That’s definitely very important in, of course, addressing SIBO/addressing your diet can help tremendously with inflammation.
SIBO, ileocecal valve and gut motility
DR: The second is a little more interesting. That is…well, essentially it’s nutrition. But the back story is a little bit more complex. You need nutrition to stimulate motility throughout the gastrointestinal tract. These various receptors throughout the lining of your intestines – as they sense nutrition, it affects motility, right? It makes perfect sense. If there is food coming through, that’s going to be handled differently from a motility perspective than if there is no food. So, nutrition signal sensors that alter motility. Now, we talked last time about the ileocecal break – which is another way of saying the ileocecal valve, which again is affected by these interstitial cells of Cajal. Well, throughout the whole gastrointestinal tract there is a series of mini-breaks that will partially stop and slow down food, and then will also signal motility. So, you have to have nutrition to signal these receptors that alter motility.
Now, what SIBO – small intestinal bacterial overgrowth – can do is actually rob you of the nutrition needed to signal these sensors. Remember, these bacteria eat food, and the nutrition is needed to signal these receptors that alter motility. But if the SIBO is eating food, the nutrition isn’t there to signal these receptors (3). This is probably one of the reasons why that in patients with SIBO, we will see a decrease tone in the ileocecal valve because the SIBO is eating the nutrition that would normally stimulate the valve to close.
SM: Wow. That is really interesting. It’s kind of like a Catch 22.
DR: Exactly, yeah exactly. We mentioned the ileo break and we mentioned the ileocecal valve. It would be easy to fall into the thinking that, ‘Well, I want to have a super, super, super strong ileocecal valve, and I want to have really strong breaking mechanisms. But remember, if the valve closes too much, that may halt the motility all together. We don’t want to have too much motility; don’t want to have not enough motility. It’s always an issue, like your alluding to, an issue of balance.
I hope what’s emerging here is that the ileocecal valve is secondary to the function of the interstitial cells of Cajal, which really come down, I think, inflammation, and then come down to bacterial overgrowth. To the question that’s been asked, which was what kind of impact does SIBO have on the ileocecal valve – it definitely appears to have a deleterious impact on the ileocecal valve. But does that mean there is some special ileocecal therapy or ileocecal valve supplement that you should take? No, I don’t think so. I just think it comes back to the general principles of motility, like we’re been discussing – again, healthy diet, and then treating any kind of bacterial overgrowth.
SM: Right, clearing the SIBO and any other GI infections; eating a paleo-style diet; stress management; good sleep – all the works.
DR: Exactly, yeah. Absolutely. So, that’s kind of the recap on the ICC cells. And just to kind of bring it home to a brief recap: To have good ICC cell function, you want to make sure you don’t have high levels of inflammation or oxidative stress, both or which are going to be addressed through diet and the flora of the gut. And then, also, if there are obstructions, obstructions can also damage the ICC cells. This would be if someone had, for example, inflammatory bowel disease and the form a stricture, which is a narrowing of the intestinal tube which can cause an obstruction. This is why some patients that have very severe, chronically relapsing SIBO may need to be referred out to a gastroenterologist for a scope examination to see if they do have a stricture.
SM: OK, that was my next question; (it) was, how do you find out if you have that obstruction?
DR: Yep. So that would definitely be a GI referral for that. I should also mention for healthy ICC function, or interstitial cells of Cajal function, methane – of course there is a type of SIBO that secretes methane gas – actually decreases serotonin in the gut. And serotonin stimulates interstitial cells of Cajal function and regeneration. So, again, we’re coming back to…even though the mechinisms are all a little different, we come back to the same core principles for having good gut motility.
SM: SO, we’ve learned everything on all of the ICC and the IC and we’re going to go on to listener questions if that’s what you’d like.
DR: Yeah, we had one gal, Heidi, who asked a four-or five-part question. So maybe we can chop this down into little bits and try to tackle it.
Listener question part 1– bile acid malabsorption (BAM)
SM: Yeah, it’s a five-part question, but three and four are kind of the same. So, I will roll those two together. So Heidi M. says, “Are bile acids deconstructed by SIBO causing bile acid malabsorption (BAM) and chronic diarrhea?”
DR: The answer to the question, Heidi, which is a great one, is yes. I just wantto outline briefly for people if this is kind of a new issue for them. I was interviewed by Sean Croxton in a documentary he did called The Digestion Sessions, released sometime in November, of 2014 of course. I spoke about diarrhea -I was kind of the diarrhea guy.
SM: Oh, that’s a great persona.
DR: Yeah, I got the call, “Can you talk about diarrhea for an hour?”
DR: Sure. There are more fun things to talk about, but why not? Let’s go for it. So, I spoke about diarrhea, and one of the concepts that I discussed was a concept called bile acid diarrhea. The quick primer on bile acid diarrhea is as follows. One or two key points: When people have had their gallbladder removed, it’s oftentimes said that you need to supplement with bile, because now you are deficient in bile. Certainly this may be helpful for some people. However, 10-15 percent of people who’ve had their gallbladders removed will form what’s called bile acid diarrhea. This is because the bile now is…you still have the ability to make bile, right? The bile producing organ, the liver, is still there. It’s just the temporary storage vesicle for the bile, the gallbladder, is removed. So, what ends up happening is you have this constant drip, drip, drip of bile into the intestines. In some people, more drips into the intestines than can be reabsorbed. If you don’t adequately reabsorb bile, by the time it leaves the small intestine – no bile should make its way out of the small intestine into the large intestine; it should all be reabsorbed by the end of the small intestine – if it gets into the large intestine, it can cause a diarrheal response.
SM: So I have a question: Since bile is predominately involved with digesting fats, if you’re eating a diet too low in fat could this affect it as well?
DR: Could it affect bile secretion you mean?
SM: No. If you don’t have the gallbladder and you have that steady drip, drip, and you’re not eating a diet not high enough in fat…
DR: Yes, certainly. That’s actually a very insightful question. Yes, if you’ve had your gallbladder removed, and you’re eating too little fat, I would think it would be possible to provocate or worsen bile acid diarrhea. I haven’t seen anything published on that, per say. But, certainly, I think that makes a lot of sense. So, yeah, it may very well be possible.
DR: So, how does this tie in with SIBO? So, SIBO can actually perform deconjugation of bile acids. All deconjugation essentially means is that it changes the structure of bile so that bile becomes more inflammatory, becomes damaging, and it also does not perform as well in aiding fat absorption and digestion. And finally, when bile becomes deconjugated, it’s harder for the intestines to reabsorb it. So, if it’s harder for the intestines to reabsorb it, then you may not reabsorb all of it in the small intestine, and some of it may get into the large intestine. And again, if you picture bile like this: The first section of the small intestine is where the bile squirts into. And then the bile travels down the entire length of the small intestine. And then, at the end of the small intestine, right before you transition into the large intestine, that bile should become reabsorbed. If it doesn’t get reabsorbed, and it gets into the large intestine, it causes diarreal response. So in SIBO, SIBO deconjugates bile – makes it harder to be absorbed – so it doesn’t get absorbed at the end of the small intestine and gets into the large intestine. Yes, small intestinal bacterial overgrowth can cause bile acid malabsorption and cause bile acid diarrhea.
Listener question part 2 – gallbladder, SIBO and BAM
SM: OK. Part 2 – Is a person who has their gallbladder removed more susceptible to SIBO from chronic diarrhea and BAM?
DR: So, this is a confusing one. And it’s a little bit putting the cart before the horse. So, bile acid malabsorption doesn’t cause SIBO, but SIBO causes bile acid malabsorption.
SM: Ah. That makes sense.
DR: When we think of bile acid malabsorption, there are maybe two ways that we can think of it – Either too much is released or not enough is absorbed. If you’ve had your gallbladder removed, it can be too much is released, because you don’t have anywhere to store it, so it’s just constantly being released. If that happens, too much is released, you can’t absorb it, and so you have bile acid diarrhea.
DR: Now, if there is impaired absorbtion, that would be in SIBO or an inflammatory bowel disease. So, in SIBO, like we talked about, when the bile acid becomes deconjugated, it’s much more difficult to reabsorb, you can’t reabsorb it, and therefore it gets into the large intestine and you have a diarrheal response. Similarly, in inflammatory bowel disease, since inflammatory bowel disease can affect the terminal ileum, where most of this reabsorption occurs, if the section that is suppose to do reabsorption is a lesion due to from Crohn’s disease, let’s say, you can’t really reabsorb it effectively. So then you get some of that bile leaking into the large intestines and causing a diarrheal response.So, we have too much released, as when your gallbladder is removed, and then potentially impaired absorbtion, as seen in SIBO or in inflammatory bowel disease.
SM: So, it doesn’t cause SIBO, but if you do have SIBO, it can cause bile acid malabsorption.
DR: Exactly, exactly. And the reason why I say…again, to make it that a little more clear, bile acid malabsorption doesn’t cause SOBO, because SIBO is antibacterial.
DR: That’s why I wanted to flip that around and make sure people understand that bile is antibactial, so it can prevent SIBO. Bile acid malabsorption doesn’t mean bile id absent – bile is there and it is forming it’s antibacterial effect. But, SIBO can deconjugate that bile. And them, if you can’t absorb it, you have diarrhea.
Listener question part 3 & 4 – gallstones, SIBO, gluten and sugar
SM: OK, OK. So, (question 3 and 4) I will put together.: Where the gallstones leading to the removal of the gallbladder result in SIBO? And is it possible to connect gall bladder diseases to SIBO, gluten, and sugar intact? And I am going to add to this: How about low fat and chronic dieting?
DR: So, this is a great question. And it is possible gallstones were the result of SIBO. And to kind of tie together gallbladder disease to SIBO and to gluten.
So, remember that inflammation negatively affects the interstitial cells of Cajal that regulate motility. So, anything that causes inflammation can damage or decrease motility. Now we know that SIBO can cause inflammation. We know that gluten, of course, can cause inflammation. So, definitely, SIBO and gluten can cause inflammation that can damage motility. How does that connect to gallstones? It’s been found that these interstitial cells of Cajal are actually contained in the gallbladder (4). And those with gallstones had a lower density of the interstitial cells of Cajal in the gallbladder. So again, anything that causes inflammation can damage these cells – so, of course, SIBO and gluten can cause inflammation and, therefore, damage these cells.
DR: These cells are contained in the gallbladder. You can throw off gallbladder motility if you will. And if gallbladder motility is thrown off, you can have sluggish bile. If the bile doesn’t flow properly, then you can form gallstones. So, definitely, that’s one mechanism. If you are eating too low-fat of a diet, it’s also possible that you are just not requiring the gallbladder to contract and squirt out its bile. So, you can also potentially have stagnant bile.
She didn’t ask about this specifically, but there has also been some discussion that estrogen dominance can cause biliary stasis or sluggishness of the bile. These interstitial cells of Cajal are really interesting because they answer a lot of these questions where we see associations between celiac and gallstones. Now we are starting to figure out why. That’s a great question.
SM: I do know a lot of people with a diagnosis of celiac that also have had their gallbladder removed previous to being diagnosed with celiac.
DR: Yeah absolute, and that’s fairly well-established I think because of the…in fact, I remember Robb Wolf discussing this, boy, had to be eight years ago, that people with inflammation, it throws off peristaltic function and that peristalsis may go all the way up to the gallbladder. We are learning now that, ye,s that does occur. And what mediates that are the interstitial cells of Cajal.
SM: And then the one part about her question, she asked about sugar intake as well.
DR: So, sugar intact is more speculative – I haven’t really read much about sugar intact specifically affecting these things. But we do know, of course, anything that causes inflammation could potentially cause a problem here. So, inflammation – be it eating lots of sugary foods – is one mechanism. If it’s the type of sugars that feed bacterial overgrowth, that’s potentially another mechanism. It’s a little more speculative, but I certainly think it would be possible. But I haven’t read a study that definitively ties those two things together.
SM: Yeah, and I think you can make a connection as well if your trying to do the standard American diet and you’re trying to cut fat and cut calories – your carbohydrate intake is going to be very high as well. And your diet is going to be inflammatory, so they kind of all meld together.
DR: Exactly, yeah. Yeah.
Listener question part 5 – guidelines on treatment for BAM
SM: The last part of this question is, (Dr. Ruscio is) asked to recommend dosages and treatments for supplements and/or prescription medication.
DR: I’ll give some general guidelines but I don’t want to get into – for any potential liability reasons, I don’t want to get into specific protocols. Sorry that I can’t do that, but I don’t want to get myself into any kind of trouble. For natural agents we have boswellia propolis. These are often agents used to lower cholesterol, because if these agents can bind to and excrete bile, then the body has to use more cholesterol to regenerate the bile. So, oftentimes these, what are called bile bile acid sequestrants or bile acid absorbers, are also used to lower cholesterol levels. So, boswellia propolis. There is also a pharmaceutical known as cholestyramine. Usually these agents, either natural or pharmaceutical, are taken either between meals, either an hour before or two hours after. And, in terms of a dose, really there is a guiding principle with dose – again, I am not making dose recommendation. But, if your dose is 20-percent right, you will see a 20-percent improvement. If your dose is 100-percent right , you may see 100-percent improvement. If you’ve experimented with a range of doses and seen no change at all, then it’s likely the wrong mechanism, right? If you do have bile acid malabsorption, and you take a bile acid sequestrant, you should respond to that. If you don’t, it’s not a magical dose, meaning if you are off by 5 mg it’s going to work incredibly well or not at all. So, an easy way to figure this out is just to slowly titrate your dose upward. Again, you should always check with some kind of physician to oversee with this, because there are other parts to this story that depend on each person’s individual medical history. So, always run this by your doctor or your practitioner. But, a really easy way to wade into these things is to slowly increase your dose and see if you notice a slow, incremental improvement that matches with your dose. If you do, you can experiment to find the ideal dose. If you notice no chance at all, then the mechanism of your diarrhea probably isn’t bile acid malabsorption.
SM: OK. And then, as you are tritrating up, is there a point where your dose is too high. Are there any symptoms of that?
DR: And then you may see the other end – you may see constipation, yeah.
DR: And then you can also, in the long term….you have to be careful with monitoring fat-soluble vitamins, because remember you are now taking an agent that blunts bile, and bile aids in fat absorption. So, if you take too much for too long, you may run the risk of certain fat soluble nutrient deficiencies and other fatty acid deficiencies.
SM: OK, that’s a really good point. So, with these herbs, do you have to take them forever, for the rest of your life? Or, as you address other issues, should the bile acid malabsorption go away?
DR: Well, generally the way I like to approach these things…well, let me give you a direct answer to your question – maybe.
SM: That’s a common answer, right?
DR: Right, yeah. And it’s like many other things. If you can really decrease your levels of inflammation in the gut, if you can take steps to treat…let’s say you also have SIBO along with this bile acid malaborption, and you treat the SIBO, and the SIBO stops causing inflammation, and the SIBO stops releasing gases that throw off your motility… So, if you can change your diet, deinflame, fix the micro ecology in the gut – all these things will start to allow motility to come back. If motility comes back, along with intestinal healing, then there is a very good chance you’re going to need significantly less, if not any of this at all. But, you may have had very bad damage to the terminal section of your ileum. That may hinder your ability to reabsorb, so you may need some from an ongoing perspective. Or you may not be very compliant with your diet, and so you still at a low level of inflammation that’s going to affect bile acid reabsorption and motility.
So, it depends really on a number of factors. What I like to do is be very strict with their therapies in the short term. And them, once someone has been stable for a number of months, we try to slowly curtail back the therapies and try to find the minimum dose that allows him to maintain improvement.
SM: OK. This brings up the point I am always making, because I’ve tried to do this stuff on my own, but finding a qualified practitioner to walk you through all of this…because then you get from beginning to end, you get help, and support, and scientific knowledge to get you through the process.
DR: Yeah, you can certainly get there much, much, much more quickly. Maybe a way to think about that is: I see a number of different types of patients. But, there is always that certain patient that they just read about X. So, now everything is going to be X. And for awhile, every patient came in thinking that resistant starch was going to be the Holy Grail.
DR: I think what’s important to appreciate is that a tenured clinician has been through that ‘Oh my God, this is the best thing ever.’ And then, six months later, understanding it wasn’t as great as you thought it was going to be. They’ve been through that for five years. And then they finally chilled out and saw the big picture emerge.
And so, that’s one point. And the other point is, the nice thing about working with and experienced clinician is that, they’ve tried these things on a number of different patient; and you start to figure out what works for who, how to troubleshoot problems, how to know if it’s going to work, how to know if nothing else is going to work. So you really learn how to troubleshoot. You know, instead of treating this from a perspective of an N of 1, now you’ve got someone who’s been through an N of 700. And so, they have all that to draw upon. So, I am all for tinkering. But, if at some point the tinkering is getting you anywhere, and the tinkering is becoming non-cost effective, or even a little damaging to your health, then yeah, call in somebody who can hopefully help you through this, because you’ll potentially get there a lot quicker. And I’ve made that exact mistake myself, where I had a parasite, tested for it once, treated, I was dumb and arrogant and thought that I had cleared the parasite, so I didn’t retest because I didn’t want to spend the $300. Little did I know, the parasite was still there. I got worse for six months, while I continued to pop all sorts of herbs for libido, performance, energy, mental clarity. I wasted $100s treating symptoms only to end up back with Dr. Calish, who was the doctor I was working with. And he asked, “Have you retested?” I said, “No.” And he said, “Why don’t you retest?” I retested; the parasite was still there. And I was really, really mad at myself. So, I’ve been there.
SM: Yeah, Chris Kresser gave me some really good advice a couple years ago. I was a patient of his. I said, “I feel better. Do we really need to retest?” He said, “Susan, you’re going to be a practitioner soon, too. And I need to tell you – Always retest.”
DR: Yeah, absolutely. I can really save you from a lot of heartache. Even though you don’t want to spend the money sometimes…
SM: I know. Some of those labs, they can get pricy. But so do the supplements, too. If you keep going off on tangents, like you said, you know? It’s a $100 here, $100 there. And pretty soon you’re at $700 where you could have spent $300 and had the test done.
DR: Yeah, exactly. Yep.
SM: So, that looks like about all the time we have for today. Do you have anything coming up in the future? Any future topics? Anything you’d like to talk about before we end?
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