SIBO Symposium Wrap Up & Highlights – Episode 18

Dr. Ruscio recently attended the SIBO Symposium at the National College of Natural Medicine in Portland, Oregon. In this podcast-artwork newepisode of Dr. Ruscio Radio, he brings you all the major takeaways from this information packed symposium.

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SIBO primer…..1:48
Episode intro…..2:32
SIBO testing…..3:14
Sulfur producing SIBO…..4:31
Autoimmunity and SIBO…..6:02
Testing markers of inflammation…..8:39
Food poisoning and traveller’s diarrhea…..12:17
3 treatments for SIBO…..14:23
Diets to treat SIBO…..18:52
SIBO relapse…..30:21
Acid and motility…..36:57
Methane and methanogens…..39:26
Small intestinal fungal overgrowth – SIFO…..45:44



  1. (2:28) SIBO podcasts:
  2. (3:42) Meta-analysis validating SIBO breath test
  3. (8:12) New SIBO test podcast
  4. (13:07) Risk of IBS increases 7 fold after acute gastroenteritis, Meta Analysis Trusted SourcePubMedGo to source
  5. (19:21) FODMAP diet increased biodiversity but also decreases Bifido (I could not verify increased diversity) Trusted SourcePubMedGo to source
  6. (28:10) Iberogast more effective than metoclopramide and cisapride for dyspepsia Trusted SourcePubMedGo to source
  7. (28:40) Low IC valve pressure seen in those with SIBO, cites study
  8. (33:51) Wurn Protocol for adhesions
  9. (39:26) Archaea and the human gut: New beginning of an old story
  10. (43:02) Statins interfere with methanogen cell wall formation
    1. Trusted SourcePubMedGo to source
  11. (46:05) SIFO – may be present in up to almost 30% of GI cases Trusted SourcePubMedGo to source


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SIBO Symposium Wrap Up & Highlights – Episode 18

Welcome to Dr. Ruscio Radio, discussing the cutting edge of health, nutrition, and functional medicine. To make sure you’re up today on this and other important topics, visit and sign up to receive weekly updates. That’s

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 to your doctor.

Now, let’s head to the show!

Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. And this is Dr. Ruscio. I am here with the lovely Susan McCauley. And also visiting in town is my sister. We have a little group today to talk about SIBO.

Susan McCauley: Super excited to be here and to meet, virtually meet, your sister.

Gina Ruscio: Yes, nice to meet you as well.

SM: I’m fascinated to hear about the SIBO symposium because I kind of followed along on Facebook. There were a couple of pretty big jaw-dropping, shaking my head, all those different hashtags you can use. To think, ‘Really, I never thought about that way!’ So, why don’t you just get started.

DR: So, real quick, to prevent myself from over-embarrassment, I tried this new coffee shop in Walnut Creek today, which was fantastic. But the caffeine content must have been through the roof because I am literally shaking right now.


DR: So, in case I sound like a cracked-out weirdo, here’s my disclaimer. You may just want to tune out now.



SIBO primer
DR: That being said, a quick primer on SIBO, if you are someone out there listening to this. If you are suffering from gas, bloating, constipation, diarrhea, potentially an osculation between the two, abdominal pain; those are the most common symptoms. But, even people who have mild or almost no abdominal symptoms may have other symptoms – depression, fatigue, skill breakouts, lesions, other neurological involvement. That may be attributial to SIBO, also, the Small Intestinal Bacterial Overgrowth.


Episode intro
DR: Now, we’ve already done a two-part series that is an intro to this. This episode is going to be a recap of the SIBO Symposium, which was at the National College of Naturopathic Medicine in Portland, OR, the first weekend in June (2015). This is going to be a little more advanced concepts, so if you are someone new to the argument, feel free to stick around. But if you want to get an intro-level discussion, we will put links to the intro series Part 1 (1a) and Part 2 (1b) to SIBO, and you may want to start there. That being said, let’s jump in. There are a bunch of things. I tried to orgainize these to flow as best they can. So, hopefully they will.


SIBO testing
DR: Testing: So, I think we’ve all heard about the test for SIBO, called the latherose hydrogen methane breath test. Like almost anything in medicine, there is almost always some kind of controversey that follows any point or position. Dr. Pimentel, maybe the preeminent, but definitely one of the preeminent researchers in this movement, presented data on a meta-analysis validating the breath test (2 Trusted SourcePubMedGo to source). A meta-analysis is, like a systemic review – which I’ve harped on numerous times on the show – with additional statistical analysis. Essentially, researchers will go. They will find all the clinical trials or other high-level studies, looking at this issue. They will summarize them. And then they run additional statistical analysis to show if the overall trend was significant or not. In this test, the latherose hydrogen methane breath test, was supported by a recent meta-analysis. And we will put the link for that in the show notes.


Sulfur producing SIBO
DR: Another concept that we discussed is people who thing they have SIB; (but) they test negative. Some of these people may have sulfur-producing bugs. These actually don’t show up on the breath test. However, Dr. Pimentel commented that he is currently working on something in this regard, and is hoping to have an update on that soon. So, hopefully we will have a way of testing for sulfur bugs at some point in the near future.

SM: So, right now it’s still just the hydrogen and the methane?

DR: Hydrogen and the methane, yes.

SM: OK, but it has been validated, which is really good news when we can look to the research to show that these tests that we might be going to ask our practitioners about, they just can’t pooh-pooh them anymore. I know a lot of times I’ve gone…before I got tested for SIBO, I went to a regular GI doctor, and he just looked at me like, ‘Oh, that’s not going to do any good.’

DR: Right.

SM: So, it’s good to have a little more in our arsenal.

DR: Absolutely. And your point about it being important to validate tests is a really crucial point because, as much as love functional medicine, I also believe in thinking critically, in questioning things. And, there is quite a bit of testing in functional medicine that is not really validated at all. And so, not to say those test are wrong; I think some are probably, just to put it bluntly, they are probably BS tests. And some are probably legitimate. When we have high-quality science like this, we can be assured that the test is going to be legitimate.


Autoimmunity and SIBO
DR: So, moving along to autoimmunity. Just recently, we talked about the new test released called IBS check, which is a test that tests for the underlying autoimmunity that causes SIBO – the autoimmunity to some of these stomach cells, or intestinal cells, excuse me, that damage motility and then set the stage for SIBO. Now, Dr. Pimentel had some commentary on this test. He did comment that in his observation, the higher the level of autoimmunity, the more severe the SIBO overgrowth tends to be. He also commented that the higher-level autoimmunity may indicate, or may predict, more treatment difficulty, or a harder case, so to speak. He also commented, and I’m glad he made this comment, that the cells that are subject to this autoimmune attack, regenerate fairly quickly if we get rid of the insult in the gut, which I think is really important to emphasize, so that people go to a total place of fear in this being a terminal diagnosis. And the final point he made in this regard, which I think is very important, was that antibody levels don’t seem to change with treatment. How that relates to relapse is unknown. But Pimentel did comment that the antibody levels seem to remain elevated even after the appropriate treatment. So, again, kind of reinforcing my position as this test being a screening tool; a screening tool, like we talked about in one of our last podcasts, to help differentiate IBS from IBD. And also, it may be a screening to help predict the severity of the case.

SM: So, it’s not like your thyroid antibodies that you actually routinely check to see if they’re going down. If they’re going in the right direction, this test is a tool like that to see if the antibodies are going down. It’s just a screening tool. And we will also put a link (3) to this podcast in the show notes, as well, that talks about the test, the limitations, and what it’s for.

DR: Exactly. And I harp on that point because I am sure that somewhere, someone will say you should track these antibodies. But I wanted to try to give people the most factual and evidence-based information. So yes, these would not be something that you’d want to track as a gauge for your clinical effectiveness.

SM: OK. cool. I like that point.


Testing markers of inflammation
DR: Now, something else regarding testing is markers for inflammation. Now, one of the tests I use is through a lab called Diagnos-Techs. I do a select panel of 15 markers through them. There are really 13 markers that I want, but they bill you for up to 15, so I usually tack on two additional ones because we are paying for 15 anyway.

SM: You gotta get your money’s worth, right?


DR: Right. So, I typically include lysozyme and what is called alpha 1-antichymotrypsin. I really don’t pay much attention to those markers because, when I went into the scientific literature to validate those, there was very little validation for those markers. I remember I had a patient a little while back that was really concerned. And I had to go through the dialogue of, ‘Just because you have a positive on a lab test doesn’t actually mean something,’ which can sometimes be a little bit of a paradigm-shifting experience for a patient, because we tend to think of lab markers as, like, the Bible, right? It’s, like, written in stone; it should be looked at serious, potentially ominous marker…

SM: If you are out of the range, uh-oh, we gotta do something.

DR: Exactly, exactly. But Dr. Stephen Samberg Lewis presented a review of inflammatory markers for gastrointestinal inflammation, and he perfectly supported my position, which was at lysozyme and alpha 1-antichymotrypsin have very little research to validate them.

SM: OK, cool. So now we can put people’s minds to rest.

DR: And, on the other side of the coin, calprotectin and lactoferrin have some very good research to substantiate them. They have been used to track the clinical course of inflammatory bowel disease, to monitor the effectiveness of therapies, and also even to predict relapse. So, those are two inflammatory markers that seem to be ones that may have merit to run and to track. Additionally, leaky gut testing…one of the leaky gut tests is called lactulose mannitol ratio test. Dr. Weinstock who was a conventional gastroenterologist, has been tracking leaky guts testing via lactulose mannitol in his SIBO patients to see if there is a correlation. He saw a very poor correlation, and he speculates the reason why is because SIBO bugs eat lactulose…

SM: I was just going to say that.That’s why we use it to test.

DR: This is why we use the lactulose test. So, his speculation was this test is probably not a good test to be using in the SIBO population. My thinking is leaky gut testing has very little clinical utility because we always need to be looking to the cause of the leaky gut. So, if this was an easy test that we could just…say you go to LapCorp and it’s part of the routine blood draw, we could just check it off and have your insurance cover it as a marker to track, sure, I’d be open to it. This is usually a special order urinalysis that you have to pay for out of pocket and do separately. Due to all the rigmarole and expense associated with that test, I just don’t think it’s worth it, because it doesn’t tell you how to treat the cause of the leaky gut.

SM: Yeah, we want to dig into the underlying cause. And then, when we treat that, the leaky gut most frequently resolves itself.

DR: Exactly, exactly.


Food poisoning and traveller’s diarrhea
DR: Segueing into treatment now. I’ve got some really exciting stuff regarding methane treatment. In my notes, it’s organized a little bit toward the end, but we will come back to that; because I really want to drive home a couple of really novel treatments for methane. But a couple things before that.

I know we’ve talked about this before, but I just want to reiterate that when someone has a bout of acute gastroenteritis – so, stomach flu, food poisoning, traveler’s diarrhea – their risk for IBS – and IBS and SIBO very similar – increases sevenfold. So certainly, if someone has a history of stomach flu, traveler’s diarrhea, or food poisoning, that may really put them at risk for SIBO. And the meta-analysis, again, was substantiating that (4). So, that concept has some very good scientific validation. That was a segue into Dr. Pimentel emphasizing the importance of when people have IBS or SIBO, it’s very important that they don’t get food poisoning or traveler’s diarrhea again. He gives his patients rifaximin while traveling as a prophylactic or preventative antibiotic. I do that same thing with my patients who are going to be traveling – we will give them the herbal equivalent, some of the herbal antimicrobials if they are going to be traveling somewhere Third World, outside of the country, or where sanitation is questionable.

SM: That’s really interesting because we do want on vacation. We may want to go to Mexico or Third World countries where it could be if you eat or drink the wrong thing…so, we want to make sure to either bring our herbs are our prescription with us.

DR: Exactly. Yeah, exactly. You know, when people go on vacation, I’d like to let them just go on vacation and forget about health for a while. But, there may be some merit to this you bringing oil of oregano pearls and popping some of those on most days while you are traveling.

3 treatments for SIBO
DR: And then, also regarding treatment, there were numerous case studies presented looking at different treatment methods. The three threatment methods we have for SIBO are herbal antimicrobials, antibiotics (pharmaceutical), and the elemental diet, which is, essentially, liquid nutrition for two-to-three weeks. And they all seem to work better or worse for different people. It was interesting to see other clinicians present – ‘This patient came in, had two rounds of antibiotic, very little success, switched over to the herbs, (and) it worked very well.’ Or conversely,’This patient did two rounds of the herbs, it did not work very well, but we followed up with the elemental diet, and that seemed to work really well for them.’ One of the thoughts that ran through my head while seeing others present cases that were similar to the ones that I’ve seen is, if you are working with a really skilled SIBO practitioner, sometimes you have to give them time to see things through. I’ve made this comment before that, if you start with a doctor and things…and I should really clarify. It it’s a doctor that you have confidence in, right?


DR: Very, very important clarifier. But if it’s a doctor that you have confidence in, and you do a round of treatment and you don’t get better, I’d encourage you not to jump ship right away. Sometimes you have to work through different available treatments or test to find what is going to work for you. That’s one of the first things I say to a patient that comes into the office saying, ‘I’m working with Dr so-and-so. I don’t feel like I am getting anywhere.’ The first thing I will say to them is, ‘Well, do you feel like their competent? Have you given them time?’ The worst thing I could do is take a patient out of a competent clinicians hands and start again from square one in my office.

SM: Right. And you can tell, in my opinion, if someone is competent if you listened to the podcast on SIBO, and you are pretty well versed in the different treatments and what they are for, and what the testing is. If you are going to a practitioner and they are walking you through very similar, you probably have a good practitioner.

DR: Exactly. And that’s what’s nice about some of the resources that we’ve put out is you have away to at least get at an initial sense of ‘Here are some of the major items in the checklist. Is this person aware of those? And, are they working through them?

SM: Right. And if your practitioner or doctor isn’t, give Dr. Ruscio a call.


DR: Yeah. If they call, we are happy to help.


SM: Because, he will walk you through step-by-step everything that we’ve talked about.

DR: Absolutely. A couple of other things that were brought up: I didn’t get the full story on this point, so I want to make sure to preface this comment with that. But rifaximin, one of the antibiotics of choice for SIBO, has a generic alternative called xifaxan. There was discussion about xifaxan having a higher incidence of reactions because, unlike rifaximin, some of the xifaxan becomes absorbed. One of the main benefits of rifaximin is it doesn’t get absorbed, so it doesn’t cause systemic bacterial death…

SM: Right, it’s localized.

DR: Now, xifaxan was criticized for having a different molecule or binding factor – I didn’t get the full story on this. But, that allowed it to be partially absorbed and cause problems. Now, there was one point I was not able to get clarity on, and I apologize for not having all of the details on this, but it may have more to do with the sourcing of the xifaxan. Part of what I heard – and, again, I am unclear on exactly what the details are – but some patients may have been getting xifaxan that was sourced in India. And it may have been in India, specifically, Indian sourced xifaxan that had this altered molecule that allowed absorption.

SM: So, would that be someone that would be looking at an online pharmacy and trying to skirt the system, and not have a doctor write them a prescription to go fill your local Walgreens and CVS or whatever?

DR: That’s what it sounded like.

SM: Yeah. Stay away from online pharmacies. You never know what you’re going to get.

DR: So, a little bit of caution there, in piece I don’t have all the details on just yet.

Diets to treat SIBO
DR: Something else interesting presented by Dr. Jerry Mullins, who is a gastroenterologist at John Hopkins. He spoke about how the fodmap diet decreases bifidobacteria, while also is very helpful for symptoms. And he also commented that the low fodmap diet actually increased bacterial biodiversity, which would be a really good thing and almost counterintuitive (5). However, I wasn’t able…I pulled the paper that he cited supporting this, and I wasn’t able to verify what he said. So, I guess I am just throwing that out there to waste 30 seconds.

DR: The fodmap diet (is) very helpful for symptoms, and for SIBO, but it does cause a decrease in bifidobacteria, which shows us that we can’t put all of our eggs in a certain bacterial baskets, so to speak.

SM: So, would you still recommend doing the low fodmap diet during the maintenance phase that we talked about?

DR: Absolutely. Yep, absolutely, 100 percent.

SM: A friend of mine just got diagnosed, and she’s like, “I’m starting low fodmap tomorrow.” I said, “Wait! Listen to the two podcasts first! You want to do it after.” She was like, “Thanks. I almost started it today.” I said, “You can eat some fodmaps now.” And she also tried the elemental diet and she was unable to do it. She did the Dr. Siebecker’s…

DR: Uh-huh.

SM: And she just said she wasn’t able to get it down.

DR: Yeah, it can be challenging because of the taste. And on the topic of diet, Dr. Dr. Allison Siebecker actually made a great point, which was, she’s noticed that the better a patient understands the concepts behind the diet, the more compliant they are. I thought that was important and maybe it is worth reiterating that these diets all help get us into the vicinity of a diet that will work for a particular person. We have GAPS, autoimmune paleo, we have low fodmap, we have SCD. And sometimes, people get neurotic about following every rule, or conflicting rules, and it’s really not that complicated, and it really is not that black and white. People tend to find certain things for the AIP work for them, certain things from the low fodmap work for them. So it’s not about saying, ‘Oh, my God. What am I going to do? I like this food, and it’s AIP compliant, but it’s not fodmap compliant. Oh, my God, I’m pulling my hair.” That doesn’t make a huge difference.

SM: The stress over all of that is going to be more detrimental than finding the – and I am using air quotes – ‘perfect diet’ for you.

DR: Right. You just need to…you have some ideas here, and now you play with them. And, maybe you cut out fodmaps and feel better. And then you go through a fodmap reintroduction, like we’ve talked about, and you notice that most of the fodmaps you cut out, you are now OK with. But there are two or three that you can’t do. And so, you avoid those two or three.

And the same thing applies to SCD. There are some principles there, there are some foods you may want to try, there are some foods you may want to avoid and observe and see what works better for your diet. And, don’t be overly obsessed with if you are in one box or out of the other. Really, the way we want to sequence this is, try some of these diets initially. If you don’t respond fully, you have to get a thorough gut evaluation. After that thorough gut evaluation, you go back to some of this dietary tinkering. And you should have a better gauge for what works for you and what doesn’t work for you. The reason why you may not have that gauge initially is because, if you have infections, then your gauge is off. That’s really as complicated as it has to be.

SM: Especially if you are transitioning from a standard American diet. You don’t know what normal is yet until you get further down the healing path, and then you know. Like, for me, if I eat a ton of raw veg, my tummy hurts. But I know where my limitations are; I know when I feel good, and I know when I don’t feel good. You have to get pretty far down the healing path to figure out what’s right for you.

DR: Yeah. It’s a process, like you are saying, and something to be patient with and not be neurotic about. Be patient, observe, experiment, and follow the advice of your clinician, as long as that advice is not ‘You can’t ever deviate from this diet at all, or you are going to cause an up-regulation of the inflammatory pathways for eight months and damage every cell of your…’ That super fear, black and white, 100 percent or you fail sort of mentality creates a lot more damage to people than it does help. Certainly, diet is important. But, when we make it this issue of, ‘If you are not perfect, you fail’, that really hurts people psychologically. So, I really hope people avoid that. And even, like, Chris Kresser came on the podcast recently – talked about how he was getting the same scenario. And then, for awhile, he just said ‘Screw it. I can eat whatever I want.’ And, he did some other lifestyle things to get out of his head. But it was just thinking less about health, and caring more about having a fun, full life. That was really kind of a pivotal moment for him. And I think it’s absolutely true.

SM: Yeah, perfection in this arena does not help.

DR: Exactly.


DR: Ah, biofilms. So, there seems to be a split opinion on the need to treat biofilms in SIBO. I have been randomly assigning patients to either receive biofilm treatment or not receive biofilm treatment – I probably shouldn’t be saying this because some of my patients will be listening.


SM: They’re going to call you up and say, ‘Which one did I have?’

DR: Screwed now.


DR: I haven’t analyzed the data yet, but I have all the data on an Excel sheet. Actually, Dr. Siebecker asked me to get up and speak about this during the symposium, and a couple other things, and from my cursory examination of the data that I have, I can’t say that it looks like using antibiofilm agents in SIBO makes a big difference. Now, that may be different after we run the statistical analysis on it. But, just from my initial examination, it doesn’t seem to be making a huge difference. And that’s what Dr. Siebecker agrees with; that’s here own opinion on this also.

However, Siebecker does feel that it is important for fungus. I’ve talked about a particular fungal case that responded really well to antibiofilms. I’m open to it. I’m still not sure they are fully needed for fungus, at least not initially – maybe if someone has a really recalcitrant, reoccurring case, then I’m much more open to biofilms, but there are a lot of patients that will initially respond very favorably just to a course of antifungul herbs. So, the biofilms may be best used as a second-round follow up if someone doesn’t respond fully the first time.

SM: OK, so in the second round, maybe, depending on the person. But not needed…it’s not a standard protocol.

DR: The reason for this is because, if we took the treatment that worked for the most severe cases, and we applied that to everyone, we would be overtreating everyone.

SM: Uh-huh.

DR: That’s a really important thing for people to keep in mind. People hear about these chronic cases, and what does the methylation expert do? What does the GI expert do for the chronic cases? They want to come in and do all of that. I had a patient yesterday that was on 23 supplements…

SM: Oh my goodness.

DR: …from her integrative MD. I was just like, “What the…” And I get irritated by this, because I really don’t think that’s necessary. I said to this patient, “How do you feel about scaling this back a bit?” She said, “That would be amazing.” I said, “Good, because I think you are about to turn into a powder mound with all of the pills that you’re taking.” So, we don’t always need to do the most (incomprehensible) treatment, yeah.

SM: More isn’t always better. I had a client one time that came in. He had a functional medicine doctor. And he had, I think, 30 supplements. I would ask him, “What did he give you this for?” And there were some esoteric ones, like, ‘That one’s to lengthen my telomeres.’ And, ‘This one’s to do this.’ I was like, “How do you feel when you take it?” “Oh, the same.” So we started taking things out.

DR: In my opinion, these things should be used, for the most part – I mean, there’s always going to be some exception – these things should be used as part of a short-term intervention plan to rebalance, get rid of things that shouldn’t be there, fix the issue. And, in the long term, healthy diet and healthy lifestyle is going to be pretty much all you need.

SM: Yep.


DR: Quickly, a couple of things on prokinetics. Resolor, which is available through Canada – You can have a script written in the states and fill it through a Canadian pharmacy, is probably the prokinetic of choice, it appears. From Pimintel and Siebecker on their use of it. Second to that would be low-dose erythromycin – difference than low-dose naltrexone. In fact, the commentary there was that’s not really a great prokinetic. It may have some other nice utility, but it doesn’t appear to be a great prokintic. Iberogast (6), which is the herbal prokinetic, was used in a study for dyspepsia, which isn’t SIBO but another gastrointestinal disorder. It was actially found to be more effective than two pharmaceutical prokinetics – which is cisapride and metoclopramide; I hope I’m pronouncing that right. I’ll link the study also (6). As you will see, Iberogast was well-studied in that regard. There was also a study (7) mentioning ileocecal valve pressure was lower in those with SIBO. We’ve talked about the leocecal valve…actually, I think that episode will be going out in the near future; we’ve already recorded it, though. Essentially, we spoke about the density of the interstitial cells of cajal – these motility cells is highest around the leocecal valve. My speculation is that we may not need to do treatments for the leocecal valve itself. But, if we can restore motility, we should see leocecal valve pressure regained, or restore itself, because these cells that regulate motility are very dense in the vicinity of the leocecal valve.

SM: So, here’s a question for you: Why is Resolor only available in Canada?

DR: As I understand it, it’s because there were some cardiovascular side effects with the tegaserod, another prokinetic. As soon as that happened, the marketplace for prokinetics in the United States became very hostile – meaning, it became very hard…

SM: Get some through…

DR: …yeah, in keep a prokinetic on the market. Now, Dr. Pimentel had some commentary on tegaserod, which was there was some initial evidence showing that it may have negative cardiovascular side effects. But apparently, when further-up studies were done in Europe, that was disproven, and (that) it’s actually safe. But, he said because of those findings, he said, a lot of prokinetics got pushed out of the market.

SM: Bummer.

DR: Yeah, yeah.


SIBO relapse
DR: If the migratory motor complex or your motility is damaged, it will not cause a fast relapse – like a relapse that occurs within days to weeks. A fast relapse may be caused by abdominal anatomy abnormalities or adhesions.

SM: So, what do you mean by a abdominal…

DR: Abdominal anatomy abnormalities?

SM: Yeah.

DR: Anatomical abnormalities?

SM: Yes.

DR: This may be someone who has a highly torturous colon, a redundant colon. They may have pockets of inflammation, like strictures that impede the lumen or the opening, causing a narrowed junction in the intestines. This was something very interesting to hear more from Dr. Pimentel about…sometimes patients we will refer or come in already having had a barium study done, or another kind of anatomical examination. I was not aware of this, but Pimentel commented that you need to have a very thorough study done to really get a full assessment of normal intestinal anatomy. This may be very important for a really chronic relapse in case SIBO. There may be anatomical abnormalities that may be the reason for that.

He commented that they, for example with their barium study, 27 photos to ensure a full assessment. And he said, some radiologists will only do four photos.

SM: Whoa, that’s a big difference.

DR: He said it’s very easy to miss something if that’s the case. So, that was something that may be very helpful for a few of the very, very challenging GI cases that they had – which was the proper study, including berium swallow, and what’s also known as antroduodenal manometry, which studies the motility of the intestines, which only a few centers in the United States do, but Dr. Pimentel also does.

The take-home there is, if you are someone who has really chronic, relapsing SIBO – and, again, when I say that, you have tests that have cleared and replased cleared, not the theroretical SIBO where I’ve never done a test. When you have lititament, diagnosised, chronic, relapsing SIBO, then a proper referral for a good GI study may be very important. And along the same lines, these adhesions – one of the things cause structural problems. There was a physical therapist who presented there. He’s developed something known as the Wurn Protocol – W-U-R-N. He is at – we will put the link in the show notes. They have published a remarkable amount of peer-reviewed literature on their method. They have cleared up abdominal adhesions that have been causing blockages and causing chronic SIBO. They mentioned that endometriosis is one of these conditions that can cause occlusion. And they also mentioned that people who have had any kind of abdominal trauma or abdominal surgery, it is very likely – if they have chronic GI conditions – that there may be some kind of abdominal scarring or adhesions that can be manually broken up to restore the appropriate open-tube clear passage, so to speak – that’s probably why his website is Clear…


DR: …and that can have very nice effect on restoring motility and allowing someone’s GI function to return to normal (8). I have reached out to him, and I’m going to try to get him on the podcast. I have to admit that sometimes I hear about these visceral manipulations…

SM: Uh-huh.

DR: While I’m open to it – again, I say this with all due respect; this is just my scientific thought process that goes on my mind – it just seems so pseudoscience-y to me. I’ve never seen, in some of these circles I have investigated, any kind of science to accompany it. It was always just super ‘This is what we do; this is why it works.’ I said, “Has anyone ever seen if this actually works?” They have really done that. They have published the studies with valid measures showing symptomatic relief or structural relief with different studies. They have done an excellent job of documenting this scientifically. And I was really pleased to see that. I am looking forward to having them on to discuss this more.

SM: That’s so fascinating. I am the same way. You hear muscle testing, applied kinesiology, rubbing something on your stomach or wherever. And I’m always like, ‘Yeah, I don’t know about that.’ Like, where is the science behind it? Tell me more. And usually, when you’re talking to people like that, you don’t get a lot of the scientific backup. So, I’m going to check out this website.

DR: Yeah, and a lot of times, at least from my experience – again, said with all due respect – I’ve found that some of those people in those circles don’t ever seem like the people that would question ‘Is this actually working?’

SM: Uh-huh.

DR: They are so jazzed about what they are doing. It could not work at all, but they are just so jazzed about it, that they just totally placebo effect themselves into thinking it is working.

SM: Uh-huh.

DR: That’s why I’ve struggled with adopting a lot of those therapies – because of a lack of what I consider objective proof. These guys have nailed that, so a hat tip to them.

SM: And I think why a lot of those things don’t work on me is because I always have that skeptical mind that…’That can’t really be working.’ You can’t be pushing on one arm and telling you where my back hurts. All that stuff. So, I think, like, if I saw science behind it, I’d be more likely to…it would be more likely to work.


DR: Me too. And that’s all I would really need, just some clinician to say, ‘OK, I’m going to track this scientifically for three months with my patients. I will draw up a number of case studies and publish them.’ It’s funny because I’ve never seen that. Maybe the people who have a different sort of mindset gravitate toward that type of work. But I don’t think it’s unreasonable to say, if you have something that you think really works, jot down some notes and try to document its effectiveness.

SM: Uh-huh.

DR: Now that we’ve thoroughly pissed off everyone in the muscle-testing crowd…

SM: Yeah, sorry everybody.


DR: I respect muscle tests; I don’t have the issue with that. It’s just love to see more objective proof. The reason that I’m tenuous there is because I would hate to recommend someone spend money on treatment, and undergo treatment, that doesn’t have any affect for them. That’s the main reason. It’s not about the clinician; it’s about saving the patient from something that may not help them.

SM: Uh-huh.


Acid and motility
DR: So, we talked about…I did a Dr. Evil picture, a Facebook post, how hydrochloric acid may inhibit motility. Dr. Pimentel discussed how, when you have a lot of acid in your stomach, the body things you are in digest mode. The initial phases of digest mode, there are a lot of acidity (that) impedes the migratory motor complex. This is why one of the recommendations we make to stimulate the migratory motor complex is intermittent or periodic fasting – because fasting does stimulate that.

So, he made that commentary that seems to be validated. But, on the other hand, acid seems to help kill bacteria. So, Pimentel’s commentary on the this was it is a little bit unclear. He things, and I agree, that HCL probably helps. His comment was, ‘You may want to avoid HCL at night so as not to inhibit the migratory motor complex at night, because that’s when you’re going to have your longest fast and your highest chance of having a good, healthy migratory motor complex.

SM: Uh-huh.

DR: My thoughts are that, with acid, a balance is likely going to be key. If you are taking eight pills, probably not a good idea, because you very well may be inhibiting motility. But if you notice you do better with a couple, then great. That comes back to my over-arching philosophy: Let’s always try to find the minimum amount of therapy needed to achieve the result. So, what I do with my patients routinely is, once they’ve been stable for awhile, we try to ween them off any digestive enzymes or acids to evaluate their need. And if they maintain improvement on nothing, beautiful. If they notice when they come off that some of their symptoms regress, we have them go back on the lowest-needed dose to maintain those improvements.

SM: And that makes sense, especially if a lot of people coming into this – like I said, standard American diet, or they may have taken proton pump inhibitors, so they may have low stomach acid. So, maybe the HCL in the beginning is just getting you up to normal amounts. And then, as your body starts working properly, then it’s too much. And then it would inhibit the migratory motor complex.

DR: Right. Exactly. I like that thinking, which is you need a little more therapy initially. And then, as you heal you need less.


Methane and methanogens
So, the final couple points about methane and methanogens (9). So, one of the hardest types of SIBO to clear is methane. I’ve clearly seen that in my patient population. It’s something I’ve been frustrated with and thinking about: How can I get better results with methane?

Pimentel has a term/syndrome that he’s coined, which is, and I quote, “Pissed Off Methanogen Syndrome.” I thought that was…because he said, “What we will see is we will do one round of treatment and someone’s methanogens or methane levels will actually increase.” I’ve seen that same thing. It’s irritated me, and sometimes I’ve said, ‘Man, do I suck? Is that why this is happening?’ To see that other, highly respected clinicians are seeing the same thing makes me think it’s not an issue of the treatment. It’s maybe how the methanogens in the hydrogen-producing bacteria interact with each other, or the resistance to treatment, or what have you. But, it’s definitely been observed that methanogens or methane can be the hardest to clear, and can sometimes initially get worse. So along that backdrop, there are some things about methamogens that I’d like to discuss.

One of the things Pimentel cited, and it totally goes in alignment with what I feel on the microbiota, is that methanobrevibacter smithii, or the one of the main methanogens, seems to have some beneficial characteristics. Now, let me come full circle with this point so it all makes sense. But, they seem to help with energy harvest, and they also seem to slow motility, which we talked about, which also helps increase choleric absorption. This explains probably why we see the highest colonization in Sub-Saharan Africa, because they have a diet of what we call low-quality food, meaning highly fibrous, dense vegetation that can be hard to breakdown and also less calories. So if you can slow down digestion with these hard to break-down foodstuffs – like a cow eating grass – you can digest them better and harvest more calories. If you are not eating a ton of calories, or there aren’t a lot of calories in your environment, then the methanogens may actually garner…

SM: They may save your life.

DR: Yeah, they may garner a benefit. And, this is another reason – and I’m working on this, I’m trying this out as hard as I can – we have to be very careful in how we interpret studies from the Hadza and trying to interpret those and try to apply those into Western populations. What works for them is likely an adaptation that is specific to their environment.

SM: Um-hum.

DR: I’ve seen so many citations of, ‘Oh man, the people in Burkina Faso ate more grain, higher carbs, and they were healthy weight; we need to mimic that. And they have this high amount of bacteroidetes, and we need to do the same thing.’ They ate half the calories that we ate – half the calories. And they literally had to grind their grains by hand. So, they had a totally different environment, so we can’t just say, ‘Their microbiota works well for them. Us as Westerns are typically much more overweight and unhealthy. We need to do what they do. If we do, we’ll be healthy.’ It doesn’t work that way. This is a great example of that.

The final point – sorry I’m rushing; I’m trying to keep this from going too far over time here. The final point, and this is something I am extremely excited about, is a few papers have been published (10a Trusted SourcePubMedGo to source, 10b Trusted SourcePubMedGo to source, 10c) showing that statins actually inhibit cell wall formations of methanogens. It’s been theorized, and this was in a live cow stock model, that stantins should be given to all livestock to help prevent methane-induced diseases. What I am thinking about, and something I will start evaluating in the clinic, is the use of a non-drug stantin, like red rice yeast, which contains active statins in conjunction with our core methane SIBO treatment, to see if has an appreciable effect on a clearing methanogens. We don’t know, we have no data in that regard. What I may start doing is probably treating some patients with this (and) not treating others, tracking the results, and then maybe as the research scene that I am putting together gets little more developed, we can do to try a retrospective chart analysis and publish the results. Because, I am dying to know if this is going to be a useful clinical tool.

SM: Sounds really fascinating, because we are so,in the natural health community, so apt to, when you hear the word statin, just be like, ‘Arrrrggghhh no, no. No statins ever. They are the most evil thing – stints, whatever.’ They’ve always thought that maybe it’s not the cholesterol-lowering effect of the statin but maybe it was the inflammation-lowering effect. Or maybe it’s the methanogen-lowering effect. We don’t know what it is, but there might be something there.

DR: Yeah, just theorizing here: Maybe the mechanism through which statins lower cholesterol is through killing methanogens, which have been correlated with…treating SIBO has been shown the ability to lower cholesterol. Maybe that’s part of the mechanism. But, I want to be careful in telling people, because I know this is going to be one of the, ‘Dr. Ruscio, bruh bruh bruh bruh.’ I’m not recommending that you use this like a cholesterol-lowering agent for years on end.

SM: Right.

DR: This would be part of a one month, two-month, maybe, protocol to treat SIBO.

SM: Our bodies, we need cholesterol people.

DR: Yeah, so just to head-off those things at the pass, this is not to be used in that application. It would be using that in a short-term application therapeutically. And, for someone that has recalcitrant non-responsive methane, this could be godsend, if it works. We don’t know if it works. But, we will be tracking that in the clinic. And I will put in the three references that statin inhibiting methanogen-inhibiting cell wall formation in the notes (10a Trusted SourcePubMedGo to source, 10b Trusted SourcePubMedGo to source, 10c).


Small intestinal fungal overgrowth – SIFO
DR: And the final point – really quick I will sneak this in. For people that test SIBO, have all the SIBO symptoms, but come back negative, it may be small intestinal fungal overgrowth – what’s called SIFO.

SM: Oh, I’ve never heard that.

DR: Yeah, yeah. I mean, it’s being discussed. I’ve heard of it before. You don’t hear a lot of it, but I have seen a couple papers – I will but a link in here to one paper (11) that showed that, in perhaps 30 percent of cases that have gastrointestinal manifestation but are negative for SIBO, they may actually have SIFO. How can we then test this? Well, there’s no official test. But one of the things that I theorize, and I actually mentioned this when I had a chance to speak briefly at the symposium, was I always want a fecal yeast culture in conjunction with a serum or blood fungus antibody profile. If it’s in the colon, you’ll probably find it on the culture. But, if it’s not in the colon, you won’t find it in the culture. And there is a fair likelihood that you may find it on the blood test. So, my speculations, not proven but it’s doing the best with the data we have, are that the blood test may be a way to rule in or rule out if there is SIFO.

SM: OK, so I think we’re probably going to be hearing a lot more about SIFO in the months and years to come.

DR: And it just goes back to the importance of having a thorough gut evaluation – and maybe this is perfect point you made Susan to remind me of SIBO is an entitiy that is receiveing a lot of attention right now.

SM: Uh-huh.

DR: But I don’t put all of my eggs in the SIBO basket. When people come in, they almost always get a full gastrointestinal workup that would screen for things like SIFO, and also other pathogens and parasites. We don’t want to lose focus or sight of things that are also important just because they are dwarfed by the immense attention one item is receiveing at the moment.

SM: That is a really good point – don’t put all your eggs in the SIBO basket.

DR: Exactly.

SM: OK. We are really out of time. Are there any thoughts you want to leave us with before we say goodbye to our good listeners?

DR: No, that’s it. Just thanks, guys, for hanging in for the extra 15. I know this is kind of a deep one, but I am sure the people who have hung in the whole time are probably people that are looking to get deep into this issue. So, hopefully you are still awake.


DR: We will see you all next week, and thanks for listening.

SM: Thanks everyone. Have a great rest of your day.

DR: Bye-bye.

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