What the New SIBO Test Can Tell You About Your Gut Health

Intro:

Welcome to Dr. Ruscio radio, providing practical and science-based solutions to feeling your best. To stay up to date on the latest topics as well as all of our prior episodes, make sure to subscribe in your podcast player. For weekly updates visit DrRuscio.com. The following discussion is for educational purposes only and is not intended to diagnose or treat any disease. Please do not apply any of this information without first speaking with your doctor. Now let’s head to the show.

DrMichaelRuscio:

Hi everyone. Today I speak again with Dr. Mark Pimentel, who is one of the leading researchers in IBS and SIBO, definitely in the US, perhaps even worldwide. He has certainly pioneered a number of fascinating and helpful findings in the field of IBS and SIBO. We discussed more specifically the new arrival in the gut health toolkit of a SIBO breath test that can now not only test hydrogen and methane, but also now hydrogen sulfide. We discuss the fact that hydrogen sulfide seems to more closely correlate with symptoms than does hydrogen as well as some of what those symptoms are. We discuss how to interpret the test. We also discuss the controversy, and he provided the only argument that I have found to be compelling, making me reevaluate my thinking regarding the use of a glucose test rather than a lactulose test.

DrMR:

So I think you’ll find that quite insightful. We also go into treatment and what I would term a non-reductionistic and inflammatory based hypothesis on motility along with a few other hopefully entertaining musings with Mark. I’m sure you will find them very insightful and enjoyable. I also want to remind you about Healthy Gut, Healthy You, if you are struggling with digestive symptoms and you’re looking for a resource that integrates much of what you’ve read or heard about into an actionable plan, then I would definitely refer you to Healthy Gut, Healthy You as that resource. With that, we will now go to the conversation with Dr. Mark Pimentel.

DrMR:

Hi, everyone. Welcome back to another episode of Dr. Ruscio radio. This is Dr. Ruscio, DC, back again today with Dr. Mark Pimentel and we are going to be expanding on the concept of this new type of SIBO, or at least SIBO gas, hydrogen sulfide. Mark has really been pioneering some pretty interesting and fantastic work in that regard. Mark, welcome back to the show.

DrMarkPimentel:

Thanks so much. It’s great to be back.

DrMR:

It’s always nice connecting with you. Obviously you are pioneering a lot of the charge in SIBO and IBS and for a while, just to get our audience up to speed, we’ve known about, mostly thanks to your work Mark, this third type of gas, hydrogen sulfide, but haven’t really been able to test it. Now we have this test available and it’s something that we’ve been running in the clinic and we’re actually collecting data on. It’s definitely helpful to fill in the gaps for those who have symptoms, but the standard SIBO breath testing comes back normal. But Mark, for people who maybe haven’t heard much anything about this, can you get us up to speed on the evolution of this and how you came to uncover this as well as any other context you’d like to provide.

Breath Testing

DrMP:

Yeah, I mean, I don’t want to go back too far in time and waste a lot of time and conversation about the history of this completely, but breath testing dates back to the seventies and eighties. At that time they were only measuring hydrogen, but we’ve known, at least since the nineties, that the hydrogen that’s produced in the gut is actually used in two different pathways by other organisms in the gut for energy. So hydrogen is like a fuel. I joke with my patients that those are the rabbits and then you’ve got the wolves eating the rabbits, which are the methanogens. So when methane was added to the breath test in the nineties, it was just added. Nobody knew why, nobody knew if it was important. It wasn’t until we started exploring that we found that methane is contributing to constipation.

DrMP:

The gas itself is doing that. You still couldn’t rely on hydrogen for symptoms. In other words, if you had a 100 for hydrogen, it didn’t make you more sick than a person with 40. They’re both abnormal, but you weren’t more sick the higher it was. Because there’s another path for hydrogen eating, or the rabbits as I’m alluding to. Maybe these are coyotes and the coyotes are hydrogen sulfide producing organisms or what we call sulfate reducing organisms. So without knowing the hydrogen, the methane and the hydrogen sulfide, you have an incomplete picture of the fermentation in the gut. We now know currently that hydrogen sulfide is proportional to diarrhea. So the higher that is the more diarrhea you have, the higher the methane is the more constipated you are and the hydrogen and methane organisms are fighting with each other for the rabbits. One is going to win in an individual patient and dominate the symptoms. The benefit to patients or to doctors treating patients with these conditions is you were missing something. Now knowing this extra something could help a number of patients that had a normal breath test but it wasn’t normal. It was hydrogen sulfide.

DrMR:

You published a few papers on this, but one was entitled A Novel 4-Gas Device for Breath Testing. You essentially found this exact thing. I believe it was diarrhea and abdominal pain, more closely tracked with the hydrogen sulfide than the other two gases.

DrMP:

As I mentioned earlier, it didn’t matter how high hydrogen was. We thought more hydrogen, more bacteria that produce hydrogen, and that may be true, but you couldn’t rely on the gas as a marker because the gas was being eaten. We do see a direct correlation between hydrogen sulfide and abdominal pain and diarrhea. So that means the lower you make the hydrogen sulfide, hopefully the less the diarrhea and the less the pain. We’re working through that now.

DrMR:

A significant finding for patients and for their wellbeing.

DrMP:

Yes, absolutely.

DrMR:

Now we’ve alluded to two of the symptoms, abdominal pain and diarrhea. There’s this kind of budding hypothesis that there are some symptoms that can delineate between regular SIBO and hydrogen sulfide SIBO. I don’t know that there has been nearly enough investigation to really make any strong conclusions, but this sulfur gas odor and intolerance to light are two of the more kind of pervasive or at least proposed symptoms. What are your thoughts on the reliability of looking at those symptoms?

DrMP:

Hydrogen sulfide is a very odorous gas. So if you are producing hydrogen sulfide, it’s likely you’re going to have a more foul smelling bowel movement or expulsions of gas. But I don’t know that anybody’s sophisticated enough to know based on smell alone that it’s H2S versus all the other exciting, odorous material that’s in feces. So it’s not really clear to me that anybody with a good nose can be definitive. Having a test is much more accurate. In regard to light sensitivity. I haven’t heard a lot about that. So that’s a new one on me. I honestly don’t know about that.

DrMR:

What could be happening is people may be over-interpreting just foul smelling gas, which could have a number of kind of underlying components and just kind of falsely connecting it to hydrogen sulfide.

DrMP:

That’s correct. That’s what I think at the moment. Having said that I have to admit that it has happened many, many times that patients say that the smell of their flatus or their bowel movements are much improved when their SIBO is gone. We never put two and two together because we didn’t have H2S measurements, but you would imagine that correcting that could improve those issues. If you seeing on a before and an after sort of scenario, I can imagine that people might say, Hey, that’s different. But at the front end of this, I don’t know that you can diagnose just based on smell.

DrMR:

Right. I’m in agreement with you there. There are also pre-existing conditions. I’m just wondering what role you think some of these suggested conditions, interstitial cystitis, fibromyalgia, peripheral neuropathies, what role do they play? Are they helpful, or are they more kind of this diagnostic red herring noise that we should be careful regarding?

Pre-Existing Conditions

DrMP:

These are all things that are in parallel associated with IBS and SIBO and their relationship to IBS and SIBO are not altogether clear. Let me give you some cross examples of what we’ve seen. The same interstitial cells of Cajal or pacemaker cells of the gut that we think are deranged that cause the poor flow that cause SIBO and IBS are also located in the wall of the bladder. So we often see that if we get disruptions of the motor function of the gut, we’re going to have some disruptions of the motor functions of the bladder or irritable bladder or interstitial cystitis, depends on how you use the terminology. Whether it’s organisms in the bladder or not. I don’t know if that is true. So when we give, for example, serotonin prokinetics one of the things that I commonly see with patients when they take Motegrity, (Prucalopride is the generic name), when we give patients that, they often say they have better urine output.

DrMP:

This sort of coincides with what I’ve just said, that some of the nerves and/or pacemaker cells that are being stimulated by prokinetics are also helping the bladder. Now, whether this is due to the primary mechanism of SIBO, meaning the motility or due to the bacteria itself accumulating causing these other peripherals is not clear. It’s even less clear for fibromyalgia. Although, in the early days, we did publish a number of studies suggesting that SIBO and fibromyalgia were related and can get better with treatment. For reasons that I don’t know, a rheumatologist never followed that train and we got tied up with IBS for many years.

DrMR:

Are you noticing that same improvement in urinary bladder symptoms after the administration of Rifaximin? Or is that unique to prokinetics?

DrMP:

Yeah, that’s a great question. That’s the second part of this. So if it’s the bacteria, if you give Rifaxamin then you should expect the bladder to improve. We just don’t see that. We do see some improvement with the prokinetic, but not so much with the bladder with the antibiotics, even if the breath test becomes normal. So that leads me to believe that it’s the nerve muscle connection that is causing the GI symptoms that is probably also causing the bladder symptoms.

DrMR:

I guess while we’re on the topic of motility, I believe it was at the last DDW meeting, and I may have a few of the details here partially off, but the essence should be essentially accurate, which was dysbiosis. It may have been Campylobacter, like this low level finding, this dysbiotic finding paralleled with dysmotility. I believe this led some of the researchers to posit that underlying dysbiosis, maybe one of the causes for motility impairment. Is this something that you you’ve seen? And if so, do you have any thoughts on that?

DrMP:

Campylobacter contains that cdtB toxin. I think in our previous discussions, we’ve covered that, but just to summarize the cdtB ain Campylobacter causes antibodies in your blood, and you can measure these to diagnose IBS because Campylobacter can trigger IBS. The cdtB also triggers anti-vinculin antibodies because of the similarity in proteins. Vinculin is a human protein in nerves. You can measure both of these as part of the IBS smart test to diagnose IBS. Having these antibodies around will impair your motor function. And that’s what we think is going on. It can also factor into bladder dysfunction as well. We haven’t actually looked at anti-vinculin antibodies as a cause. We are looking for more people with more bladder dysfunction. So I can’t declare that because we haven’t studied that, but I would imagine that the similarity will be there. If Campylobacter continues to reside in the intestine in a few people, and we have some patients where we can detect low grade Campylobacter, I think that’s what your question was sort of trying to get at. Then your antibodies will be much higher because you’re chronically infected and having exposure to cdtB. We do have some patients like that, that we’ve described in the REIMAGINE study.

DrMR:

How is the Campylobacter being detected? One of the things that we’ve discussed in the podcast recently is these kind of newer age functional medicine, PCR, pathogen stool tests, and they’re modifying away from the FDA approved cut-off values to lower values that they’re purporting are better. I haven’t seen, after a fairly extensive look into the literature, any evidence showing that those lower detection values can distinguish between healthy controls and IBS patients, meaning that they don’t suffer this potential false positive. Your comment makes me wonder, perhaps these non-traditional positive levels, a lower level, maybe something that the clinician wants to hone in on and treat. I guess the question is, are these unofficial infections, meaning lower levels that may not be considered a clinical infection that you’re looking at? Or how are you making that delineation?

False-Positive, Unofficial or Clinical Infection

DrMP:

There’s a lot to unpack there. First of all. Because technology requires a lot of discussion and one of the problems with technology is that sometimes the technology goes ahead of the actual clinical relevance. Not that they’re wrong, it’s just that the data hasn’t accumulated enough to prove they’re right. You know what I’m saying? But one of the things that we suspected, but proved in the REIMAGINE study is that measuring stool has hardly any reflection of anything going on in the small intestine. Let’s say Campylobacter is in the stool. It can still be a pathogen, even if it’s not in the small bowel or whatever. But a lot of inferences, for example, of bacterial overgrowth, were made from stool testing.

DrMP:

But the bugs in the stool have nothing to do with the bugs in the small intestine. That was a paper we published in the summer. It was really black and white that you can’t make much of a determination from stool about small bowel. Campylobacter really likes the small bowel. So finding minute quantities of Campylobacter is a little unclear to me as to what its relevance is. On the flip side, just being the devil’s advocate, you are really not supposed to have a lot of Campylobacter. Campylobacter is a pathogen, and generally speaking it should rarely ever be detectable. So there may be something there, but I think it just needs to catch up with the science. They’re advancing the specificity or the sensitivity of the test, but they need to prove that it actually correlates with symptoms.

DrMR:

I guess one data point we could look at to kind of inferentially answer that question would be, has there been any data yet, to my knowledge, no, that Rifaximin will help reduce the vinculin and cdtB antibodies. Has there been any data that has demonstrated that?

DrMP:

We should actually publish that study because we did do that analysis and it has absolutely no correlation. It does nothing to the antibodies. We looked at that and I think it was about a hundred patients before and after Rifaximin, whether the Rifaximin made the patient better or did not make the patient better, it didn’t change the antibody levels. That actually makes sense, but we haven’t published that. It’s a negative study. So negative studies are harder to publish. That probably was our thought process, but it’s an important question that should probably be in the official literature.

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Healing the Motility Apparatus

DrMR:

Sorry to kind of pepper you here with questions on motility, but this is something I’ve been thinking a lot about lately. There’s this theory that the interstitial cells of Cajal are plastic and if they’re not in an inflamed environment, if there’s not a lot of oxidation that they may be able to regenerate and/or rewire. It makes me think that perhaps if we can hold an individual in an asymptomatic state with whatever support that they need, we could loosely presume that there’s not as much inflammation. Perhaps that would open the door for the motility apparatus to heal. That might be an overly optimistic perspective, but wondering from your purview, does that hold any weight or is that something that’s fairly disprovable?

DrMP:

Yeah, so you’re absolutely on the right track. This is sort of the type of advanced things that we’re trying to work on because we’ve believed this to be true. Ken Saunders, who’s a very famous interstitial cell of Cajal researcher in Reno, Nevada. He is the world expert in interstitial cells of Cajal. If you cut the bowel during surgery, let’s say you had to take a tumor out of the bowel and you have to cut a piece of bowel. The interstitial cells of Cajal will die off. It’s called a die off. It’s like cutting one root of a tree and part of the tree dies, but then it all grows back again. So the interstitial cells die off about a foot on either side of the cut of the bowel.

DrMP:

Then within three weeks, they are all together back and interconnect again. Even cross the bridge of the scar, or that’s what he tells me anyway from his research. So they’re plastic, they’re able to regrow. Their half-life is similar to red blood cells, about 120 days. So they live that long. Think about the long nerves in your arm. They’re there forever. They’re not plastic. You cut the nerve of your arm you’re never getting function in that arm again. This is not the case here because these are not nerve cells. These are hybrid nerve muscle cells, so they can regrow. He’s shown that. So the pressure of the anti-vinculin antibody on the cells, if taken off, everything should recover. In other words, if you kept the patient, let’s say on Rifaximin for six months, and they were perfectly asymptomatic for six months, the cells would not come back. It’s the antibody that’s doing it. That’s what we think. If we could get the antibody out of the blood, the patient should recover. We have some data on that, but it’s something I don’t suggest anybody do to filter out antibodies. We’ve seen dramatic improvements, but you can’t keep doing that. It’s like dialysis.

DrMR:

This begs the question, of course, are there any of these immunosuppressive cocktails that are used for various autoimmune conditions? I believe you’ve been doing some experimentation with those. We have one shared patient who was on a regimen from you and I was very curious to see the impact. So I’m assuming you’re doing some experimentation there. Are you seeing any viability with that line of therapy?

DrMP:

When we do these kinds of things in the clinic, it’s not under IRB. It’s basically just clinical practice for severe patients and using things off-label and that standard of medicine. We have some patients where they are so sick and their antibodies are so high and nothing’s working and they’re in and out of the hospital or they’re just absolutely miserable. We will try things like Immuran or other agents to block B cells. They are very expensive. It’s not a long-term solution, but just see if we can get some short-term gains and see if they get better. We have some limited success there, but this is really pushing the envelope. It’s only because of the extremeness of the patient’s condition that we try these. For the conventional run of the mill patient with bloating, these are not the therapies you should be using.

Test Interpretation

DrMR:

No. I’m glad you made that distinction because I think there’s sometimes this desire for patients to reach to the most exotic, esoteric and end of the line therapeutic before kind of going through the algorithm and doing their due diligence. That’s a great reminder. Coming over to test interpretation. My understanding is there’s been two studies that have established what a normal or positive finding would be. That is a rise in the hydrogen sulfide of five. Is that clinically how you’re looking at this also? It’s the rise and not the absolute value, or is there some nuance there?

DrMP:

It’s the absolute value of five. It’s not a rise for hydrogen. We have an abstract that’s submitted to the DW meeting for this spring. It covers that with the new instrumentation and bag collection system combined. The bag collection system for the new breath test, if you don’t know called trio-smart, the bag is very designer in terms of being able to retain all the gases for up to seven days, maybe even longer. We had to validate what the actual number is for diarrhea. The threshold for diarrhea, with the collection system, the transport, the time to transport and the instrument itself at the other end. It came up with five. That could be the first number, or it could be the 90 minute time point. It doesn’t matter. It just has to, at some point, be greater than five parts per million.

DrMR:

Okay. That actually is quite helpful because what I’ve been seeing as we’ve been running the trio smart now for maybe 3-4 months, is that it’s more common for there to be a flat line. I’m oftentimes seeing flat lines somewhere between 13 and maybe 7 seems to be most of where the patients who are positive are clocking in. There’s definitely this trend where there seems to be much more of a flatline presentation.

DrMP:

Yeah. That’s true. I mean, because think about it this way. When you drink the sugar, let’s say lactulose or glucose, depending upon your desire of substrate, that sugar has to get to the bacteria. The bacteria have to produce hydrogen, the hydrogen then have to go to the hydrogen sulfide producers, and then they have to take the hydrogen and make hydrogen sulfide. That takes hours and hours. We don’t see the rise in hydrogen sulfide during a practical time point on the breath test. Whatever hydrogen sulfides is there is either there or not there usually. So the point of giving the sugar then is to make the hydrogen go up to look for hydrogen overgrowth. The hydrogen sulfide overgrowth will be self-evident without the sugar and methane is also self-evident because it’s the same process where you have to have hydrogen first.

DrMR:

So it’s the rabbits that will peak, but it’s the opportunists, so to speak, the wolves and the coyotes that are more of a flat line.

DrMP:

Yeah. Because they’re constantly using the hydrogen right from whatever’s there to make their gasses.

Treatment Options

DrMR:

Gotcha. Okay. That makes sense. Regarding treatment, I know there was one study that found response to Rifaximin, I’m assuming and hoping there will be more studies. The reason why I say I’m assuming is one of the things I’m seeing, at least from my vantage point, a little more in the alternative camp, is whenever there’s something new, there’s a whole bunch of theories that tend to permeate with very little evidence. I try to be pretty principled and evidence-based, and not feed into these things. So that’s why I’m hoping we’ll discover more about how the therapies that already work for the other two types of SIBO also worked for hydrogen sulfide. Just wondering what you’re favoring in terms of therapeutic.

DrMP:

Well, we’ve known for quite a long time that bismuth has some inhibitory properties on sulfate reducing organisms. So we think bismuth, similar to what was being done with H.pylori, can be part of the treatment successfully. I have seen some success with Rifaximin with bismuth during the same 14 days. So Pepto-Bismol essentially. Another cocktail that I’m hearing very good things about is Augmentin and bismuth, combining those two. I haven’t tried it personally, but some of my colleagues and other people in the community have tried it with good success and patients are responding. In a very short period of time, because the community of SIBO having experience with trio-smart are going to start to report their successes and failures. We’ll start to hammer that through. In the meantime, we are doing a clinical trial with a new formulation or new style of giving Rifaxamin specifically looking at its effect on H2S. That’s all I can say about the study right now, but it’s for the diarrhea patient, which is what H2S is. So we’re doing the trio-smart breath test for the study. We’re randomizing people, everybody gets Rifaximin, but some people get the new special cocktail. Then we’ll see what gets better in what group.

DrMR:

Do you have any thoughts on diet? One of the things that has been posited is a low sulfur diet. When you get to a certain level of patient presentation, the resolution gets really hazy because there are lots of symptoms, lots of ups and downs, and they oftentimes tend to self treat with different things. So I want to just preface my statement by saying it’s a hazy read, but there does seem to be a subset of patients who have done better on a lower sulfur diet. I haven’t had any chance to correlate that to the breath test because it’s newer in terms of my use of it. Wondering if you feel a low sulfur diet or any other diet besides perhaps low FODMAP or low residue has merit here.

DrMP:

Imagine now that we’ve got the complete picture of gases. That we might have actually three different styles of diet for these three different types of intestinal dysbiosis, whether it’s intestinal methanogen overgrowth. Methanogens have certain needs, and maybe there’s a diet for that. Sulfate is a little less complicated, a little easier actually, because there is data from the nineties talking about low sulfur diets and how they could reduce sulfate, but in this new world of this new breath test, there’s not a lot of data yet. I am telling patients who are high H2S to consider less eggs, less red wine and things that might contain higher amounts of sulfur. But I don’t have a lot of experience, meaning not a lot of patients coming back after two months of doing that because the test is only been out for a couple of months. So I think we will gain that experience with time.

DrMR:

Gotcha. One of the things that we’re going to be embarking on soon, or midstream, depending on when this podcast goes out is just collecting data and monitoring our patients to see what sort of impact probiotics and probiotic triple therapy has on the hydrogen sulfide gas levels. I don’t know of any research being done there, but just wondering if you have any suspicions, yay or nay regarding probiotics and hydrogen sulfide?

DrMP:

I’ve always been of the mind, and this goes back to conversations I had 10 years ago with a company that was making probiotics, I won’t name the name, but maybe the key is to find the coyotes and the wolves. Or the patients who have coyotes and wolves. That’s where the probiotic may be beneficial. Maybe it is a methanogen colonized individual, or maybe it is the sulfate reducing organized colonized individual, and maybe boutique use of probiotics there is what will make probiotics more successful. We just never measured these things before. So I’m curious to see what you find. There’s no data as yet, and I’m not familiar with any studies yet. So it’s a good niche to get into because it’s so new.

DrMR:

Sure. Well, fingers crossed.

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Managing Expectations

DrMR:

Something else I wanted to ask you. This is more theoretical. One of the things that I’m increasingly becoming concerned about with the patients coming into the clinic is, I guess for lack of a better term, they get so fixated on their health that they’re thinking past the solution. Meaning something’s helping them and they’re unable to really take any joy in the improvement and they go on to “what else could be causing my problems”? I’m just wondering if you have any thoughts for the audience and for clinicians on how to grapple with that.

DrMP:

No disrespect to patients whatsoever. I do try to educate the patients ahead of treatments as to what the expectations would be. Back in the early days of Rifaxamin, I remember one distinct patient. She’d been around the block, she’d seen 10 different gastroenterologists. She comes to me, we give her Rifaximin and she comes back and I say, so are you better? She says, yeah. I said, how much better, what percent? She says, 80%. I said, that’s fantastic. She says, how do I get the other 20? I was totally taken aback because as the doctor, knowing the history of IBS and SIBO and knowing that sometimes we only get 10% better so 80 sounds terrific.

DrMP:

Patients really want to want to feel better and once they feel better, I think they think we know the answer to what’s going on for them. So the 100% is in sight. So they chase perfection, but unfortunately it’s hard to get perfection. This is a chronic disease. Whether it’s the antibodies that we still can’t get out of the bloodstream or other factors that are yet to be discovered, it isn’t always perfect. There is some lifestyle stuff that remains. On the flip side, let me do the other way around. I have patients who come in my office and they say, doc, I feel 40% better, this is great. I look at them and say I’m looking for 80. So let’s keep going because my goal is 80% better. So when patients are satisfied with 40, sometimes I push them a little further. So I have both sides of the coin in my clinic. I don’t know if that answers your question, but these are the anecdotes of medicine.

DrMR:

I think maybe one of the things that connects to is you may be better served by having an optimistic perspective. The glass being half full and also locking arms with your clinician and trying to get you to that point where I tell my patients, you probably won’t ever be able to go out and eat a pizza and have six beers and feel nothing. But we will be able to get you to a point where you can have a pretty darn normal quality of life. Yes, you may be affected by some foods, most people are. Even the healthiest people have some fluctuation in how their gut is feeling. I try to just reassure them that, you know, very few people can eat whatever they want, any quantity and not feel anything. If we’re not aiming for perfection, but instead a livable human goal, then we can definitely get you pretty close to that goal, if not fully at that.

DrMP:

Yeah, I agree. That’s the approach I take as well. Trying to set those expectations before treatment is help goes a long way because then the patient’s not looking for a cure. Look, I mean, the other part about the whole antibiotic side of this with Rifaximin is that patients are used to the idea that if you have a urine infection, you take an antibiotic, it completely goes away. So the expectation is that you take an antibiotic for your IBS and it’s going to cure SIBO and it’s going to completely go away forever. It’s not quite as simple as that in this context.

DrMR:

One other thing, sorry to shift gears here, but I was just remembering that there is an ongoing debate between lactulose and glucose. With hydrogen sulfide specifically, did the same rules apply or are you thinking about that any differently regarding glucose versus lactulose?

Glucose vs. Lactulose

DrMP:

What sort of bothers me and sort of makes me reassured that there’s interest in breath testing, I have a stack of papers on my desk with a lot of new research that has come up over the last couple of months. What’s disappointed me is that there are a couple of papers on glucose there, which is not what’s disappointed me. What’s disappointing me is that these investigators are not using or following any of the guidance from either the SIBO guideline or the North American consensus on how to interpret breath tests. Some of them are saying 12 parts per million of methane. I don’t even know any publication of 12 parts per million of methane being a cutoff of any sort. With the North American consensus, what we were trying to do is to level the playing field and say, you can do whatever criteria you want, but use these as well, because these are the standard based on the experts currently.

DrMP:

And yet, rogue characters are just picking random cutoffs still and succeeding in publishing them. I suppose it depends on who reviews them. Those things bother me and it muddies the literature. I just saw a paper on glucose breath testing for that same reason. I prefer lactulose, and here’s the argument. In the IBS trials, if your lactulose breath test was positive, you were way more likely to respond. Literally by 30% more likely to respond to the antibiotic if your IBS. Of the target three trial, 44% of people responded to Rifaximin 44%. If we had done breath tests and only treated those, in IBS only about 25 to 30% of IBS are positive on breath test using glucose. So if we used glucose, only 25% of a hundred people would have gotten antibiotic. But 44% responded. So 20% of that population would have missed the opportunity to get a drug that could have helped them dramatically. That’s almost double the baseline. So yes, glucose is more specific, but you’re missing a whole bunch of people who benefit from therapy by simply doing glucose. That’s my argument. If I was giving chemotherapy to a patient, I would say, okay, maybe it’s risky, but I’m not. I think it’s better to have more people get better than to have less people get better.

DrMR:

That that’s actually the best rationale I’ve heard. It actually sways my thinking, in the direction to be more empathetic to glucose. I remain open on both, and I think the main way I’m able to do so successfully, is because I look at patient presentation and symptoms in conjunction with lab testing, and I never make a decision based upon treatment just based upon their lab testing. In that case, we could still reserve the use of anti-microbial therapy, even for someone with a negative test. Your point is very well taken in the sense that if someone is going to be fully by the book and only administer anti-microbial therapy to a positive test. Even if the lactose let’s say does suffer from false positives, would it be harmful to treat someone with a “false positive” test, if that therapy had a likelihood of helping them, and it did not carry severe potential side effects. That makes a lot of sense to me.

DrMP:

Yeah. To be my own devil’s advocate, because I never want to be black and white, with hydrogen sulfide being added with this new breath test, maybe we’re catching all the diarrhea because you don’t even need glucose or lactulose to detect the hydrogen sulfide similar to methane. So maybe you’re picking up the extra characters anyways. I’d have to reevaluate that whole thinking or notion once we have hydrogen sulfide and we’ve finished the trial we’re currently doing. So it could change again. I’m not fixed, I’m just fixed on facts.

DrMR:

Sure. Why I’ve been a bit more circumspect with the testing is because I see so many patients who have been clearly incorrectly labeled as a SIBO positive. Or they tested positive one time, three years ago, they’ve had two or three subsequent tests that have been negative since then, but they’re still labeling themselves as SIBO. Or someone who had SIBO four years ago and still proclaims that their SIBO is flaring every time they feel a little bit tired or feel a little bit bloated. I think there’s this runaway neuroticism that many in the field haven’t done a good job of explaining this the right way to patients and also being judicious and discerning before doling out the diagnosis. There may be some of my bias there, but that’s where it comes from.

DrMP:

Yeah. We don’t want a SIBO cult, we want a SIBO diagnosis. I tell patients when they come to my clinic, I literally do, that I’m not giving you a diagnosis of SIBO until I’ve ruled out everything else and feel comfortable that there isn’t anything more worrisome. You’d be surprised how many times people, like you said, are labeling themselves as SIBO or even their doctors have labeled them as SIBO and they actually have something else. Cancer or otherwise. SIBO was a distraction. It may have been there, but it was a distraction to other symptoms. Medicine is not a game and patients can have other things that can account for that.

Episode Wrap-Up

DrMR:

Yep. I think that’s a good reminder for our audience and why I’ve always said, I think it’s helpful for someone to have a provider on each side of the fence. I know some patients come in and they gripe that their conventional doctor isn’t privy enough about diet. Then they go to their alternative doctor and their alternative Dr. may say, well, you don’t need to worry about your colon cancer follow-up screening based upon your family history. I think it’s really good, firstly, for people to know their lane, but then also to have a perspective on each side of the fence. Mark, your words are a really poignant reminder of in some cases of why that can be so important.

DrMP:

Definitely

DrMR:

I Know you have to go here in a minute. Do you want to tell people a little bit about the trio- smart test or anywhere else you’d want to point them to learn more about this?

DrMP:

I think we’re moving to the next level. The trio-smart test is an at-home kit test, you don’t have to worry about going to a center. It’s COVID time now. So a lot of people are doing the trio- smart because it’s a home kit, very easy to do. You get all three gases for practically the same price as two gases. More is better in my view. I think the H2S is very valuable. It’s diagnosing patients who would otherwise have been missed. Where we’re lacking is not exactly clear on what treatment works best yet. Although we now are narrowing in that bismuth may be part of the treatment or necessary part of the treatment, but stay tuned because we are doing a randomized trial on other therapies. So I’m super excited. It’s the next level. There’s always another level. That’s why I’m so grateful that you take the time to talk to me. It’s good to educate some of the folks out there because there are always changes. Keeping up with the changes is really hard. I have a pile of papers on my desk, just with SIBO that I’m trying to catch up on, let alone the microbiome, which is almost impossible. There are so many papers these days. So education is important.

DrMR:

Right? Absolutely. It’s a team effort. I really appreciate the role you’re taking on that team. Clearly you’re really the charge in a lot of pioneering ideas and research and tests and therapeutics. I probably speak on behalf of many a clinician when I thank you for all the work that you’re doing. So thank you for that. And also thank you for taking some time to elaborate on some of this new stuff with us today.

DrMP:

Thank you so much. I’m just grateful to help some patients out there. Appreciate it.

Outro:

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