SIBO Testing: Is It Time for a Change in Protocol? ft. Dr. Jason Hawrelak

YouTube discussion (Jan 15, 2026) featuring Dr. Jason Hawrelak, Siobhan Sarna and Dr. Allison Siebecker about SIBO breath-testing protocols. Dr. Hawrelak reports a clinical series (n=130) using triple-sugar breath tests (lactulose, glucose, fructose) and argues fructose substantially increases diagnostic yield for small intestinal bacterial/archaeal overgrowth (SIBO/IMO). Key findings: 15/130 patients were negative on all three tests; 60/130 were positive on all three. If only one sugar were used, detection rates in this cohort would be: lactulose 73%, fructose 85%, glucose 67%. Pairwise combinations: lactulose+glucose 76.5%, glucose+fructose 93%, lactulose+fructose 96.5%. Hawrelak’s clinical interpretation: fructose is slowly absorbed and broadly fermented by bacteria, so it can detect small-bowel fermentation missed by glucose (actively absorbed) and lactulose (not fermented by all bacteria). He reports clinical response when SIBO diagnosed by fructose is treated (patients regain tolerance to certain fruits). Limitations noted: no small-bowel aspirate culture (gold standard) available for correlation; clinician-access and lab-interpretation variability noted (pre-2007 heterogeneity; later cutoffs discussed). The recording includes case vignettes, example breath traces, and discussion of species (e.g., E. coli, Klebsiella, Citrobacter, Haemophilus) that may not ferment lactulose.
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Hi, everyone. I'm Siobhan Sarna. I am the founder of SIBO SOS and the author of Healing SIBO. And I am here with Dr. Jason Harlock and Dr. Allison Siebecker, both world renowned experts in the field of SIBO and the microbiome. And they have a very interesting situation that they wanted to share. And I'm so glad to be part of this conversation. So I'm going to actually hand things over to Dr. Allison Siebecker so she can tell you about why this conversation, why it came to be, and why she in particular is so excited about it. Hi, Dr. See Becker. Hello. Well, many, many years ago, I had asked Jason if he could let me know what he was seeing in the differences between glucose breath testing and lactose breath testing, because he did both on his patients, which is amazing. I didn't, I only did lactal and I knew he liked glucose and I didn't want to be missing anything. And it turns out that recently he prepared for a presentation, some data and actually had triple breath testing and reached out to me, let me know he's got some amazing results. And I was so excited in hearing your results, Jason, that we wanted to just get it to everybody because it was in a presentation in a conference in industry conference and not everyone got to hear it, even including myself. So I didn't get to hear the presentation because I was also presenting at the same time. So that's really how it came to be, is that Jason remembered my question, wanted to provide me with really good data, being a researcher, Jason's researcher, and has that information now. And so, Jason, why don't you give us your background on this?
Thank you. And I apologize. It took some years to actually get the data. I just didn't want to do it until I had like, I was confident with the findings. Yeah. And I think I'll tell more with the presentation, but I think really was trying to work out the best way of diagnosing placebo because we know that there's conflicting information in that. You know, North America is very lactealous biased, for lack of a better word. Europe is often very glucose biased. And for me, I was like, okay, well, I'm going to do both and these things. But then I started seeing some other interesting patterns with fructose. And that's what we'll get into with this presentation and discussion afterwards.
Perfect. So if you want to just start share your screen.
Yep, I will do that. All right. So hopefully you can see the correct screen currently that'd be correct. Yes. Okay, great. So I'll get into it and then we'll have some time for questions afterwards. So for me, it was really asking is the time for a change in protocol around SIBO testing. I want to place this argument within the context of a patient's story because I think this kind of illustrates it quite well why this is important. So the case, this is a 35 year old male presenting complaint, frequent belching, but also diarrhea. And I always think that we always have to dig in deep with that term, diarrhea because it means so many different things to different people. Now, for this person, it was four day bowel movements per day and type six stools in the Bristol stool scale. Definitely diarrhea. But I certainly have had patients who do one type 5 stool a day and classify as diarrhea. So it's like it's not here. We have to dig into it. Definitely. In this case, often greasy and pale, mucus explosive and urgent at times. Episodic bloating, episodic abdominal cramps, what he defined as smelly flatulence. And gut symptoms were worse for white flour products, sweets and many fruits. Not all, but many fruits. And plus there were systemic symptoms like brain fog, fatigue, low mood and anxiety. You know, so patient, you know, presentation pretty familiar to you, I reckon, Alison, Many others were dealing in the world of Sibo, but yes, let's go back a bit further. A 13 year history of gut issues, and it started with increased bowel movement frequency, an abundance of what he defined as foul smelling flatulence and stools. But there was no obvious indicating event. For many people, there's traveler's diarrhea or food poisoning or even, of course, antibiotics that I see as the turning point, moment, but there wasn't with this patient. Now, the first investigation that was done 13 years ago was a test for parasites and that found blastocystis. All right? And then from that point he went to see a naturopath back in 2005. And that natural was me. A less hairy, less gray version of me and a lot less experience. And I'd like to think with less wisdom to that matter. And I didn't do any further diagnostic testing with this patient. I was like, okay, you've got symptoms that sound like that could be caused by this thing blastocystis. Let's just focus on killing that. So, you know, we did a blastocystis herbal protocol, probiotics for six weeks. Was there some improvement? Yeah, there was certainly some temporary improvement. All right. And Then right, right after that I moved interstate, you know, hadn't been in touch. And then seriously, 13 years later get contacted by the same patient again with the same presentation, the same symptoms and it's like wow, here's an opportunity to do redo. And you don't often get that in life of a chance to redo something to see if you can do it much better. And I'd like to think that I could 13 years later and I think we did. But it certainly a lot to do with diagnostic workup which I think we were, me and a lot of other practitioners over the years as we'll soon see, were quite lazy in terms of diagnostic workups. So relevant family history. Brother and daughter recently diagnosed as celiac disease and father had a long history of gerd. And the reason I kind of flagged the GERD is that some people with celiac when the main presented complaints is gerd, it's not super common but it still is and it's often non responsive to typical treatments. So kind of should be a red flag for us there. Previous investigations, just a lot of stool tests showing blast. And that was all that was done for about 10 years. Astronomers just stool test after blasted. Let's try to kill it test again, kill test, kill test with you know, not much change. But after his family members were diagnosed he had oh let's get sub done, normal antibody levels but he hadn't actually been eating gluten leading up to the test. And this is again another one of those things that drive clinicians crazy. It's like there's no point doing the test if you haven't gorged on gluten for six weeks leading up to because it's not going to be accurate. Gene test positive for the genes, not surprisingly for celiac again. And that was all More recently after the family member was diagnosed, some clinicians, a new clinician decided to do a bit of a deeper workup which was great because it gave us some additional data that we didn't see before now. Previous treatments were all really based on trying to kill the blastocystis. So lots of flagyl, sometimes with short term release and essentially a decade on herbal antimicrobials and probiotics off and on, mostly on over that decade. 2012 there's a place in Sydney here in Australia called the center for Digestive Diseases that really focuses on antibiotic cocktails to try to eradicate things like blastocystis. He did that, which is a pretty full on triple N. Bought a cocktail, felt horrible during and some short term change, improvement in signs and symptoms afterwards. But again short term tends to be the thing that runs through this case. Currently following anti candida diet. And yes, signs and symptoms were significantly better when he followed. So if he avoided the white flour products, avoided most fruits, avoided sugary things, symptoms were generally much reduced, not gone, but much reduced. But nobody did much in the way of investigations except for follow up parasite tests. That's it until very recently. So here's my chance of going, okay, seeing this person again. I didn't do a very good diagnostic workup at all when I first saw him back in 2005. Here's my chance to do a better one. So what we do, sibo is obviously a top of the list. Now I can forgive myself a bit my 2005 self because Sibo wasn't really talked about much in 2005. It's just barely out there in the literature. So breath testing wasn't really talked about. So I can give myself a bit of forgiveness for not looking at sibo back then. You know, C. Lack disease is obviously going to be on there along with gluten sensitivity, fructose intolerance because he seems to be reacting to fruit, specifically inflammatory bowel disease because of the diarrhea. We should always check and I put two at the bottom. Blastocystis infection, you know, over the last 15 years I look at blastocystis quite differently than I did in 2005. And I think the literature has come out showing that for many people it's normal and commensal and potential. We treat that, we treat the sibo and they no longer have fructose intolerance. And this differentiate from the classic fructose intolerance were the rise of gases in the colon and there kind of is lifelong low fructose diet. You can't just treat it with some herbs and it goes away, but it can when it's actually sibo induced fructose intolerance. And yes, I think he's probably got celiac as well. But we need to do, you know, gluten binge gluten challenge and full of biopsy and such like that. So we'll leave that to the side for the moment. And by treating the sibo and I think you had symptomatic improvement each previous time he took certain antimicrobials because it was inadvertently targeting the sibo. It just because the herbs weren't necessarily put together quite right for targeting sibo and there's no maintenance strategies put in place to prevent it from coming back. It would always just come back in this patient. But now we know what it is, we can get much better treatment outcomes from it. Now I'm going to whip through these stuff on breast test interpretation because I think most people are going to be up on this. But I just wanted to flag it for those people because we're going to look at a few different test results for some people that are don't look at breath test results all day every day like Alison and myself. And I think part of this is flagging too that pre 2007 this is kind of cowboy country where different labs had completely different interpretive guidance and some Labs are using 3 parts per million methane as being positive and some labs are using any rise of 12 or 15 parts per million hydrogen, even 3 hour mark as being positive. So I love this stuff in 2017 where they tried to standardize this a bit more of looking at that 20 parts per million on lactulose and glucose methane, 10 parts from any time point. And I'll probably move through this relatively quickly. I just wanted to more flag that one what the cutoffs were and even one of the flag just in the UK they see things a little bit differently in that they're using a 10 part per million hydrogen rise at the 60 minute mark rather than 90. And they see any rise between 60 and 90. You've got to have some clinical judgment in that is like could that be in the colon or is it going to be in this. It's still in the small bowel at that point. And then obviously the change of just, you know, our old SIBO methane into intestinal within an overgrowth because they obviously occur in the colon as well and they aren't bacteria, which is all very true. So essentially my approach to SIBO breath testing is this lactulose and glucose all makes sense from the literature as we talked about at the very beginning. In Europe they're often using glucose and recommending glucose and North America often using recommending lactose, sometimes exclusively on both. And here is Australia is trying to grab the best of both worlds and go let's do both. But what I started seeing is this. So the top graph here is what fructose intolerance is supposed to look like. So you just the fructose, you have no rise until that fructose reaches the colon. And there you see this expansion in hydrogen at that point. Or it could be methane, but in this case we see it in hydrogen. That's what it's supposed to look like. That's what all the papers on fructose intolerance talk about. How often do I see this in my patients? Almost never. I had to search and search my files to find this first graph. What I see my patients is this, the bottom diagram and almost all my patients where we see this massive spike in breath gases at an early time point, at that 30, 60 minute mark, we see that giant spike. And this just blew my mind at the time because I'm like, that's not what's supposed to be going on. We're supposed to be this fructose intolerance, according to all literature, is this colonic fermentation that's going on. What we're seeing is small bowel fermentation. And also it's exaggerated breath results in terms of often the 100, 200 sort of mark of parts per million of breath gases. And sometimes I noticed that fructose would pick things up that glucose and later did not. So that sort of made that, oh, gosh, that's interesting. I want to start doing this in everybody. All my patients will now get lacticliff, glucose and fructose, so have the best chance of seeing it and then hopefully eventually get enough data that I can do something slightly more formally with it, which is what occurred recently. So let's look through some example breast test results that kind of formulated my approach. Here we have a patient or the lactulose, again, you see a kind of centrally flat line. So it's not much rise up at the 2, 3 hour mark a little bit, but that's really not much glucose. Nothing to see there. You know, maybe a slight blip there. But again, no, not, not close, quite close enough to the positive cutoff criteria. But here, look at that with the fructose, you know, you see this massive spike in gas at that early time window. Once again, another test result where again it kind of flatlines glucose. Again, nothing to see here. And here again we see it on fructose, less exaggerated response this time, that it just creeps over that mixed sibo kind of 15 part per million cutoff, but dramatically more symptoms from the fructose as well. But again, it was at that early time window, not later on in the colon from the fermentation perspective. So essentially for a presentation I was doing recently and to help answer Allison's question, or both, at last I decided to go, I want to take the last 130 patients that we've done this triple breath test, sugaring on to work out, you know, what the results Were the sugars equally good or was one particularly better than the others, et cetera. So, and here are the results in graphical form and I'll walk you through it. I think the next slide, between this and next slide probably all come together, but all three were negative in 15 patients. So there was no rise in any, any of the three sugars. So I define them as being negative. So, so 15 out of 130, no SIBO was not there. But what's interesting is 60 out of 130 were all, all three were positive. So if I looked at any of the sugars, they would have showed up and you know, that's a pretty decent amount. But what I think is here is more telling. Lactulose picked up SIBO eight occasions that the other sugars missed, only eight occasions. Fructose picked it up 19 occasions that the other two sugars missed, glucose only four, four times. You know, because I think all that's what I was observing with the fructose. I think really kind of I started thinking more about what happens with fructose in the gut. You know, glucose, we know its main limitation is that it's actively absorbed in the upper small intestine. So if you have SIBO in the upper small bowel, yeah, it's usually pretty accurate at sugar picking it up. But because your body so avidly grabs it, there's no glucose left in the middle to last bit of the small bowel, which is the main concern with, with using glucose alone. Now lactulose we know is not absorbed. So it small first bit, the small bowel, middle bit, last bit, it's still there. But the issue with lactulose is that it's only selectively fermented, that not all bacteria have got the machinery to eat it. So they can be there in large amounts in small bowel, but you won't see it on a lateralist test result. But they need glucose. But I think that what happens with fructose is they do. Fructose is almost universally consumed by bacteria and it is slowly absorbed. So unlike glucose, where it's added, we know glucose or fructose is, I think it's carrier mediated. Facilitated diffusion is a technical term, but it means it's slow, slow absorption rather than quick. And it means it's there in the middle small bowel. And I assume it's probably there at least to some degree in the last bit of a small bowel too. But it feeds a broader range of microbes and I think that's why it is Actually so good at picking up placebo cases because it's kind of got some of the best of both worlds of the glucose and the lactulose. That's my theory anyway, to explain the results. And I think this next table hopefully makes it pretty clear too in that with these patients they have said 115 and 130, I would seem as positive because one of the sugars were positive. If I'd done lactulose only, I would have picked up the SIBO or emo 73% of the time. 73%. And that kind of correlates with some of the data we have in terms of comparing it to some of the so called gold standard of aspirin culture, which we know has got some issues with it for sure. Fructose only would have picked it up 85% of the time if I'd only done that one thing. Glucose only 67% of the time, you know, so, and what I used to do, just combining the lactulus and glucose doesn't actually increase diagnostic yield much. You know, 76.5% versus lactose alone was 73, you know, so it's not really, probably worth, worth doing it just, just doing the glucose only. But if we just did glucose and fructose, we'd pick up 93% of time or even better, lactulose and fructose 96.5% of the time. And certainly since I've correlated the data together, that's what I've been doing with my patients, is I've actually dropped glucose from the mix because there's, there's a small drop in diagnostic accuracy arguably from that, you know, 100% down to 96.5. But it's an extra cost, extra hassle of doing it and a few more days, potentially a week before you get your results in as well. So for that decrease in, slight decrease in diagnostic yield, I don't necessarily think it's worth the expense. And I've really shifted since I put this data together to working on just using lactulose and fructose based on that. And that's probably the bulk of the data that I want to share. Now obviously there's some, some caveats here that I wish that I had like access to a, you know, the gold standard small bile aspirate culture so we could do some, you know, correlative sort of data around that. I don't, you know, I'm a clinician, I'm a researcher, but I don't have access to that type of equipment, you know, so that. That is a limitation. But what I found with these people that have that essentially sibo picked up on fructose is you treat the sibo and they can eat apples and pears and mangoes and watermelon, cherries again, you know, which is. Which is not the case when it's a classic fructose, where you get that rise in the colon. All right, so I'm open to questions or any discussion.
Oh, that was it. Okay. That was a very.
That's essentially it.
Wow. We were like, on the edge of our seats waiting for more brilliance. You just keep topping yourself. That was fantastic. Thank you so much. How's your patient? So how is the patient?
Now, listen, there's. There's still ongoing stuff that we're still trying to tease out, but much better after that for the first little bit after that, that treatment, because I still think we're trying to work out the celiac component of that. It's. There's some interesting aspects of this case in terms of low fecal last days and a few other things that fit the CBAC picture.
Very cool. Very cool. Allison. Doctor. See, Becker, what questions do you have? Okay, I have a bunch. This is just absolutely amazing. I was just, like, smiling the whole way through. Okay, first question would be for. For people who might feel unsure to start using fructose just based on this data, you know, just because they haven't done it. Can you put our minds at ease that are you seeing good clinical correlation? So the people you're picking up on fructose who you didn't pick up on the other tests, you're treating them for sibo and you're seeing improvement?
Yes, definitely. That was the case earlier on in that it's funny because I remember this one patient who had had a 10 year diagnosis of fructose intolerance. She comes to me and she had a breath test she did 10 years prior. And I said, can I see your breath test result? And she'd been suffering with ongoing symptoms despite going on a low fructose, low FODMAP diet about that time 10 years ago, some ongoing symptoms, it was better but not improved. We look at the breast test result, and it's like, that's sibo. It's like this huge spike, early window here. Let's treat the sibo. She can eat all those foods again. And that case, to me, just illustrates it beautifully because she was kind of not misdiagnosed. Perhaps an over. Over description of what occurred, being labeled as fructose. Intox because she was. It just wasn't treating the cause. The cause was sibo. You treat that and all of a sudden people's diets open up again and all the whole bunch of other symptoms improve in a way. So, so I. Yes, definitely I'm seeing that clinical correlation and I'm suspecting SIBO in these patients as well. It's just that I wasn't finding that last year was always interesting enough picks it up, whereas fructose did in a lot of patients.
Actually on that note, I know you have said in the past it's mainly proteobacteria that don't ferment lactulose. What are some of the names of those Proteobacteria? Are we familiar with them?
Yeah, so that would be things like E. Coli, Klebsiella, for example. Citrobacter haemophilus are common gram negative bacteria that don't really have the capacity to ferment lactulose. And this is the interesting thing because for me, I started doing research in irritable bowel syndrome back in 2000 and I was treating my IBS patients with lactulose as a prebiotic, as a substance to feed up good bacteria. And then someone came up with this idea using this breath test and I'm like, aren't you just testing for good bacteria in the gut? Like what's the. Just kind of blew my mind because all.
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