There’s a wealth of information about how prebiotics and probiotics can influence your gut microbiome for the better. And yet, even though SIBO is a type of gut imbalance, there’s less awareness around how these tools work to eradicate unwanted bacteria and encourage the resurgence of beneficial populations.
In this week’s episode, we clear up some of the confusion and talk about how specific probiotics and prebiotics can be used in SIBO treatment, why taking these supplements in pill form differs from getting them through your diet, and what well-established thinking on the low FODMAP diet (which limits many prebiotic fibers) gets wrong when it comes to the health of your microbiome at large.
To break it all down for us, I am joined by Jason Hawrelak, PhD, who is a research scientist, educator and clinician with more than 18 years of clinical experience. Dr Hawrelak did his PhD degrees in the areas of the gastrointestinal microbiota, irritable bowel syndrome, the causes of dysbiosis, and the clinical applications of pre- and probiotics. He has written extensively in the medical literature on these topics – including 16 textbook chapters – and his research has been cited over 800 times. So yeah, he’s a pretty big deal.
A quick taste of what we’ll cover:
- What the microbiome is and the relationship between our bacteria and our immune system
- Why broad spectrum antibiotics might cause a bout of SIBO down the line
- The various functions of probiotics to improve IBS symptoms
- How certain prebiotic fibers can improve motility and reduce the risk of SIBO
- Which types of probiotics and prebiotics to use if you have hydrogen versus methane SIBO
- The best herbs for not disturbing the colonic ecosystem in the large intestine
- Why allicin garlic works to treat SIBO, while garlic in food remains problematic
- How fermented foods and prebiotic fibers in our diet effects our gut health overall, and how they compare to conventional probiotic pills
- Why the low FODMAP diet my NOT be the right approach
- Visceral hypersensitivity and why we might still experience symptoms even after SIBO is gone
Resources, Mentions and Notes:
- Dr. Hawrelak’s website, The Probiotic Advisor
- Study on Proton Pump Inhibitors and SIBO
- Study on PHGG and rifaximin
- General study on probiotics and SIBO reduction
- Dr. Hawrelak’s recommended basic probiotic: Biogaia Gastrus
- Visceral hypersensitivity study
- Partially hydrolyzed guar gum
- Phoebe’s post on probiotics for general health
- Join the SIBO Made Simple Facebook Community Page
- Subscribe to receive a free download of the episode transcript
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USING PREBIOTICS AND PROBIOTICS FOR SIBO WITH JASON HAWRELAK
PHOEBE: Thank you, Dr. Hawrelak, so much for coming on the show.
JASON: It’s a pleasure to be here, Phoebe.
PHOEBE: We haven’t yet covered the question of probiotics and prebiotics. I know it can be a little bit of a misnomer and a little counterintuitive from what a lot of people have heard about SIBO treatments. I want to start from the beginning. I think some people who have been suffering for years, maybe SIBO is kind of their first foray into paying attention and tackling their gut health at large. Since you’re a microbiome specialist and researcher, I was hoping you could just paint people a broad picture of what the microbiome is and why we should care about it.
JASON: The gastrointestinal microbiome is one of the many microbiomes in humans, but it is certainly the one that has gathered the most media hype and research more recently. We have a skin microbiome, a nasal mucosa microbiome, breast milk microbiome, vagina microbiome. We’ve got quite a few for different body sites, but it’s the gut one that has really charged up there from a research perspective in terms of getting noticed and getting attention. When we’re talking about the gastrointestinal tract microbiota, which is the microbes that make up the – microbiome is the term that incorporates the microbes and their genes and byproducts versus the microbiota, which is just the microorganism component itself. When we’re talking about the GIT microbiota and the health consequences or the potential detrimental impacts to health that are associated with a dysbiotic ecosystem, we’re generally referring to the colonic ecosystem.
The colon microbiota is by far the biggest in terms of number of microbes present where you’re looking at 10:11 or 10:12 bacteria per gram of [colotic] contents are far greater than what you find in the small bowel or stomach or oral cavity, for example. Because you essentially have such a large number of microbes and such a diversity of species, we’re talking about 150 to 160 species per Westerner and a slow transit time that food [digestate] might be the best word for it, has got the capacity to stay in that colon anywhere from 12 hours in people with quick transit time to 3 weeks in people with slow transit time. There’s a very large variation there. The bacteria that are in that very slow moving ecosystem have got that capacity in tract with the human cells or gut immune system cells in a different way than where in the stomach they’re only in there for a small time. Typically in the small bowel in healthy people bacteria are only in there for a small period of time.
We know there’s a whole bunch of health consequences and essentially humans have evolved with this special ecosystem in our colon that plays a number of functional roles for us from the production of B vitamins and vitamin K to helping us get energy for our body from otherwise indigestible substrates like dietary fibers and resistant starches and oligosaccharides that actually provide energy for us because of the bacterial fermentation that occurs in the colon. Immune system function is very much tied in with the health of the colonic ecosystem. What research has shown in the last few years is that metabolic health and the capacity to gain or lose weight is tied into the balance of microbes that are present in the colonic ecosystem and even more recently mood is associated. Anxiety and depression are associated with particular dysbiotic patterns in the colonic ecosystem.
PHOEBE: That term, dysbiosis, dysbiotic, I understand it as a layman to just mean some sort of imbalance in the gut. I guess the most basic definition or description of SIBO is an imbalance. We’ve talked a little bit on the podcasts already about some of the risk factors and root causes of SIBO. Are there any other elements of other imbalances in the microbiome that contributes to SIBO?
JASON: I would say that clinically you do see SIBO as traveler’s diarrhea and antibiotic use being a key turning point in people’s lives where their gut was doing well. They didn’t have any gut symptoms. Boom, they took a course of antibiotics and that’s where SIBO developed for them and other people with traveler’s diarrhea. Sadly, for those that have traveler’s diarrhea who then took antibiotics, it’s far more problematic than otherwise. It’s a double whammy. You would argue that both of those have a change in the ecosystem as a core driver of the underlying pathophysiology of SIBO and develops from that. I think antibiotics is a clear case of that where you’re getting that imbalance in the ecosystem and it shifts that balance to something that’s different than where it was before.
PHOEBE: What happens? What causes the bacteria to migrate or to not continue on their path to where they should be after killing off the good critters with a broad spectrum antibiotic in the large bowel?
JASON: That’s a good question, and I don’t think research has teased it out nearly as much as what it should have. They probably will keep working on those areas. I think there may be some change in motility that happens as a consequence and certainly low-grade inflammation that occurs. We do have good data on what’s causing long-term low-grade inflammation in the colon as a consequence of their use. By adjusting bacterial populations, we actually adjust motility as well.
It’s bacterial byproducts like short-chain fatty acids like butyrate and acetate, for example, that are key drivers of normal motility. When we start changing the cells that determine our normal motility time in dramatic ways as we can do with antibiotics, then there can be consequences. I do think that inflammation that can persist post antibiotics that are caused by the antibiotics and can also result in dysmotility as well. The nerves that control motility and also sensitivity can get altered by antibiotic exposure.
PHOEBE: This is kind of speaks to your underlying strategy for combating and healing SIBO, which is a little different than what some other doctors and practitioners do. I would love it if you could tell us a little bit about how your approach differs and how actually using prebiotics and probiotics, which many other protocols are generally restricted, how that can actually be contrary to the other approach.
JASON: I think I’d have to go back in time a bit to explain how I came to my approach to using probiotics and prebiotics in SIBO. That really goes back to the fact that I did my PhD looking at the role of dysbiosis in irritable bowel syndrome and looking at ways that we can manipulate the microbiota to beneficially shift that ecosystem and change the underlying environment and symptoms in patients with irritable bowel syndrome. Part of that was looking at clinical trials using probiotics in the treatment of IBS. I started studying that area in 2000. That was my full-time work for the next number of years.
PHOEBE: Did people know about SIBO? Was that subset of IBS sufferers known?
JASON: No. This would predate the popularity and rise of SIBO. This is the other interesting aspect too that SIBO was discussed in the medical literature in very isolated instances where people thought it would only occur after small bowel surgery where you had a decent chunk of your small intestine removed. Then a portion of them would develop severe enough SIBO that they would be hospitalized with a degree of symptoms and malabsorption that they would get. That was the SIBO that was discussed up into the early 2000s when Dr. Pimental published stuff that suggested that SIBO was far more common and a key driver in irritable bowel syndrome pathophysiology.
When I was getting into that area of probiotics and IBS, that was pre SIBO being a popular diagnosis or pre SIBO being connected to IBS. What we could say at that point is there’s research that goes back to the 1950s showing clearly that probiotics in general were very efficacious in the treatment of irritable bowel syndrome. That’s pretty consistent from 1950s up until now if you look at the clinical trials. When this idea came out that SIBO was the underlying driver of IBS and some of the original research suggested that 84% of people with irritable bowel syndrome had SIBO as the cause, if that was the case, then we already know that probiotics are efficacious in the treatment of IBS. That’s clear from the data up to that time point.
If that assumption is correct that SIBO as the key driver, then obviously probiotics are going to be helpful in SIBO. That just made sense these two things were correct that probiotics would be helpful. That’s the point that I came at because I already knew that they were helpful in IBS. It’s a matter of going I didn’t have that inherent block there that probiotics shouldn’t be used in IBS because it’s going to be too much bacteria there, which is I think is the underlying assumption, at least the way I take it in the arguments that go against the use of probiotics in SIBO.
PHOEBE: Where did you go from there? How did your research on probiotics and IBS dovetail with the SIBO movement?
JASON: I suppose for the first little while I was a little bit hesitant to take on board that SIBO diagnosis because it was so new and it was being put out by what I would consider vested interest at the time, people that had strong ties to antibiotic pharmaceutical companies. Their idea that probiotics were unhelpful for that condition didn’t fit the preexisting data, and there was debate in the IBS field. To be honest, there still is. The role of SIBO in IBS was much more with traditional gastroenterologists. If you’re looking at the whole data set, it certainly doesn’t suggest that 84% of people with IBS have SIBO.
Because there’s so many different ways, and I’m sure you’ve touched on this of how do you diagnose SIBO, how do you define it in the first place, this is where there’s so much confusion and why there’s hesitancy amongst more conservative aspects of the gastroenterology community to take on board the existence of the diagnosis, let alone how to treat it and move forward from there. I was a little bit hesitant to take it on board, but I’ve always been a clinician as well. I’ve treated IBS as the core aspect of my practice as a clinician for nearly 18 years. I’ve done clinical trials in patients with IBS where we’re using probiotics and prebiotics, so I saw them work from a clinician perspective. It’s also a clinical trial perspective, so it didn’t make sense that these things wouldn’t be useful if SIBO was an underlying driver. Then we really had that chance to start experimenting with patients when breath testing became more commonplace in testing my IBS patients for SIBO, and I was still giving them probiotics and prebiotics, etc., and getting very good results, that didn’t fit in that they shouldn’t be used. Then if you look at the scientific literature about the use of probiotics in SIBO, the clinical trial data is extremely positive for the use of these agents for that condition.
PHOEBE: What does your tool kit look like today? Can you take us through some of the various pre and probiotics that you use in your practice and how you decide who gets what?
THE BEST PROBIOTICS FOR SIBO
JASON: I think the choice of probiotic agent is important. I don’t think that all probiotics are helpful for the treatment of SIBO. I think this is where clinicians and people in the general public who are self-treating run into trouble because they’re not always well-versed in how to define a good probiotic supplement or when that might be useful for the treatment of SIBO. That would be if we’re talking about eradication or reduction of numbers of excessively grown microbes, we’re after probiotic agents that have demonstrated antimicrobial activity or they produce a compound that has antimicrobial activity against the microbes that are most commonly present in the small bowel in people with SIBO, which would be things like E. coli and streptococci, etc., and occasionally some anaerobic microbes like Bacteroides.
For me it’s a matter of looking at what bacterial strains in terms of probiotics have got actions against those species that are present and overgrown in patients with SIBO or produce compounds that are active against those same species. That narrows the list down to a few more. Then you start looking at the data around them, and they may be useful for decontamination component of SIBO and those other strains that can improve gut transit time and help work as a prokinetics. I use probiotics as prokinetics in my patients as well as to help with the decontamination phase. I use them as preventative agents for SIBO too. I think this is an interesting area.
You can look at proton pump inhibitors, which we know are a huge risk factor for the development of SIBO. I think the most recent analysis I’ve seen showed that people on proton pump inhibitors, which is the main class of meds used to treat reflux disease, have a 7-1/2 fold increase, so 750% increased risk of developing SIBO, which is absolutely huge. There’s a window of opportunity here to assess to see if certain probiotics can help prevent that development.
There’s a very recent study using the Lactobacillus reuteri DSM17938 strain of Lactobacillus reuteri, which was tested to see whether it would prevent SIBO development in patients taking proton pump inhibitors for their reflux disease. There were a few aspects of the study I found fascinating. First one was that after 12 weeks on a proton pump inhibitor, which in the big scheme of things is a relatively short period of time in that most patients on these class of medications are on them for months to years, not just 12 weeks; even just in that 12-week period, 56% of those who are in the placebo group developed SIBO within 12 weeks of being on a proton pump inhibitor.
PHOEBE: It’s really scary. They give them out like candy over in this country.
JASON: They do it here too, and they do it in most Western nations. These days, at least in Australia, you can just go into a chemist or pharmacy and just buy it without any doctor oversight, which is even more problematic. Going back to that study, we get that scary result of 56% of people developing SIBO. In the probiotic group of people that took the probiotic and the PPI, it was actually only 6% of those who developed SIBO. You get this very clear example of the right probiotic preparation that prevented SIBO development in the vast majority of people. It was a major difference between those two groups.
PHOEBE: What is it about them that’s making the change? I know you just described two different prongs, a probiotic that can act as an antimicrobial and one that can act as prokinetic and improving motility. In that study, what were they doing?
JASON: It’s a good question, and it wasn’t necessarily teased out with the study design. What we do know about that particular strain of Lactobacillus reuteri is it has a capacity to produce an antimicrobial compound called reuterin. Reuterin is active against the main bugs we see overgrowing in SIBO like E. coli and Klebsiella and streptococci.
PHOEBE: It’s doing the stomach acid’s job for it.
JASON: In essence you could argue that. Normally it’s a stomach acid that breaks down and kills those microbes that you’re swallowing on a daily basis, either in your saliva or in food items and drinks, etc. When you’re taking a proton pump inhibitor, you don’t get that anymore. It’s a weak stomach acid that doesn’t kill anything. Then we have this strain that comes in who does have that capacity to produce that compound. They use relatively low dose of one times ten to the eighth CFU, which is colon forming units. From a probiotic perspective in terms of what’s in the marketplace, that’s a low dose.
PHOEBE: That’s one billion?
JASON: A hundred million; even less.
PHOEBE: Not even a billion.
JASON: We know this strain works at that dose. Most strains that would be below what would generally be considered a therapeutic dose, but with this strain it works at that dose. Maybe it works better at a higher dose, but we know that at that dose it works. Through its production, in my opinion, of the reuterin it was able to prevent the overgrowth of most microbes that otherwise would have that opportunity to grow in that environment.
PHOEBE: That’s so interesting. When you’re tackling your cocktail of probiotics as part of a treatment plan, are you combining different strains? Is there one product that has both the strains that you just described?
PHOEBE: It’s complicated.
JASON: If someone comes to my practice with irritable bowel syndrome symptoms and I suspect SIBO, we do some breath testing. I do a different suite of breath tests than what typical clinicians would do. I do glucose, fructose, and lactulose, so I get a much clearer picture of what’s going on and what microbes are present by what is actually consumed at different time points. Let’s say they show up positive on breath testing. Then my treatment approach, depending on whether it was methane dominant or hydrogen dominant, would actually change what probiotic I would use or whether it’s mixed. I would always use something like partially hydrolyzed guar gum, which is a probiotic fiber that we know can be helpful in both different main types of SIBO where you’ve got the hydrogen dominant SIBO.
There’s a study where they gave partially hydrolyzed guar gum alongside rifaximin, and the eradication rate of SIBO was 62% in the group that just had rifaximin versus 87% in those that took the partially hydrolyzed guar gum and rifaximin. This is hydrogen dominant SIBO. I’ve always seen PHGG as a useful adjunct of treatment alongside antimicrobials for hydrogen-type dominant SIBO, but it also decreases methane output in those people that have methane-type SIBO. It’s something I use in both sorts, but I do change my probiotics, depending on whether I’m treating hydrogen dominant or methane dominant.
Then obviously I use different herbal antimicrobials, depending on what those two main presentations are. I also tweak it bit depending on what the breath test results show. If they have negative or a flat lined lactulose but have a spike in glucose and fructose, it gives me a bit of a feel about what species might be present. At the moment it’s mostly guess work because we don’t have an easy way of telling which bacterial species are present when someone presents with a raised breath test value.
PHOEBE: Not to get off track, but back to what you just said about the guar gum and rifaximin study, would that be an argument for why you shouldn’t be on a low-FODMAP diet while taking rifaximin?
JASON: It depends on how you envision the PHGG is working. If you think it’s only working because it’s feeding microbes and making them more susceptible to antibiotic usage, then that argument would be correct. I don’t think that’s how it’s working. The study didn’t think that’s how it was working. There’s some people involved with antibiotic companies that suggested that’s how it works.
There’s a study where they were using it as a probiotic compound, probiotic fiber. That’s the rationale for actually giving it alongside so the antibiotic would kill off the microbes that were there and the prebiotics would help encourage the growth of more beneficial bacteria, which then can suppress the growth of more pathogenic or gut inflammatory species. Perhaps that was their main way of rationale for its use. What my research did is we did a systematic review of all the studies that looked at the use of partially hydrolyzed guar gum in patients with IBS. I’m just going to say PHGG in the future because it’s so much easier. If the argument was right that essentially PHGG worked because it fed bacteria, you would expect that it worsen people’s symptoms with irritable bowel syndrome. That would make sense from their perspective.
You’re feeding bugs and they produce more gas. You get more symptoms. More bacteria creates more symptoms. That would be their argument. If you look at the research on partially hydrolyzed guar gum in IBS, and we did a systematic review grabbing every single study that had been published back in 2016, we found that every study published to date showed a reduction in symptoms of irritable bowel syndrome, including reduction in bloating, reduction in diarrhea, improvements in constipation, improvements in quality of life. It was clear that the probiotic fiber itself dramatically improved IBS symptoms, which is not what you would expect if it was working via the mechanism that you mentioned before.
PHOEBE: What does that tell us? Does that mean that just PHGG and certain other specific probiotic fibers are beneficial versus when you’re a regular diet and taking in all sorts of prebiotics at the same time? Why does one exacerbate the symptoms and one improve it?
THE BEST PREBIOTICS FOR SIBO
JASON: That’s an interesting question. Prebiotics are selectively fermented fibers. The selectivity is the key component there. Even the different microbes that are fed by the different probiotic fibers that you’ve got, the main four probiotic compounds are lactulose – even though it’s not widely used in the US because it’s classified as a pharmaceutical for some strange reason over there – galacto-oligosaccharides, fructooligosaccharides, and then partially hydrolyzed guar gum. Other people would add in acacia fiber or xylooligosaccharides to that list, and I think they’re arguably prebiotic compounds too, but there’s less research on them than the other compounds that I’ve mentioned.
PHOEBE: What about psyllium husk?
JASON: That would be a dietary fiber that I do use in practice, but it’s not a prebiotic fiber.
PHOEBE: That’s the list. That’s the full list.
JASON: That’s a pretty broad list. There are probably some other compounds. People argue about resistant starches, for example, whether it’s a prebiotic or not. It’s an ongoing debate around that, but the other four compounds totally meet that. You’d say things like xylooligosaccharides, acacia fiber probably meet that [21:50], but those ones have a far smaller data set in support of them as prebiotic agents in terms of their types of microbes that are fed, which ones go up, which ones go down. That’s the thing to remember with prebiotics is that when you take them, certain bacterial populations actually decrease as a consequence and others go up because of the selectivity of fermentation that occurs.
If you look at partially hydrolyzed guar gum, it is a food source primarily for butyrate-producing bacteria. Research shows that we don’t get much in the way of gas. In fact, we probably get a reduction in gas-related symptoms when people ingest partially hydrolyzed guar gum. The butyrate-producing bacteria produce butyrate. Butyrate can, for example, inhibit the growth of the main microbe that’s responsible for methane overproduction, which is [22:35]. That’s a mechanism by which we’re actually changing the gas dynamics.
Other research has shown that the supplementation of galacto-oligosaccharides decreases hydrogen gas ouput, for example. Conversely I’d say that we know that fructooligosaccharides/inulin tend to increase breath hydrogen counts in most people, so I think that group of prebiotic compounds tends to be problematic in patients with SIBO and patients with IBS more broadly, hence the popularity of the low-FODMAP diet. Dietary sources of galacto-oligosaccharides that we find in legumes, stachyose and raffinose specifically, tend to be poorly tolerated in those two patient population groups as well. Supplemental galacto-oligosaccharides, which have some small tweaks to their chemical structure, tend to be better tolerated. It’s not 100% better tolerated, but tend to be better tolerated in that patient group and be therapeutic in those 2 patients groups.
PHOEBE: This might be a silly question, but are the butyrate bacteria also present in the small bowel with SIBO but it’s just not the type that’s causing the symptoms and the problems? It’s the key to the solution.
JASON: That’s a good question. Sadly, many of those butyrate-producing microbes are not ones that we can culture, which means if we go in there and scoop out some bacteria and try to grow them out, we won’t find many of those butyrate-producing species that are present. I think there’s a lack of data surrounding the level of butyrate-producing bacteria in the small bowel.
PHOEBE: If it’s helping, it must be there. It couldn’t be helping from the large bowel, could it?
JASON: No, it would seem unlikely. Whether it’s helping by currently unknown mechanism is possible too because we’re always hypothesizing about how things are working. Our hypotheses come from animal data or from in vitro data, but it’s not always the case of how it works. We just know that it does. We know that if we give it to people with methane dominant SIBO, it will decrease methane output. Not in everybody, but I can say as a clinician in a lot of people it works very well.
PHOEBE: PHGG specifically for methane. What are some of the prebiotics that are better for hydrogen?
JASON: I would still use PHGG in hydrogen dominant too. In that case I’d be seeing it however it’s working as improving the eradication rate alongside my herbal antimicrobial approach. Lactulose can be useful as a prokinetic agent in those people that don’t test positive for lactulose breath test. This is going to sound strange to people who think that the only way you test SIBO is using a lactulose breath test. If you’re positive on a lactulose breath test and have a rise of hydrogen gas or methane within the 60 to 90-minute mark or less, lactulose breath testing would not be a tool I would use in your case. Because I’m using glucose and fructose and lactulose, you get a lot of patients that the bacteria in the small bowel don’t eat lactulose, but they do eat glucose and fructose. In that case I use lactulose as a prokinetic agent and as an agent that is metabolized and utilized by the beneficial bacteria in the small bowel, which actually changes that environment and helps lower levels of the microbes that are overgrown in that situation, which are often anaerobes like bacteroides and some [26:02] bacteria like E. coli and Klebsiella based on the data that we’ve got.
PHOEBE: That’s another complicated thing about SIBO. The lactulose can cause extreme symptoms for certain types of bacteria. It can improve conditions if those specific bacteria aren’t present. Did I sum that up?
JASON: Right, in that some people who don’t have lactulose-eating bacteria in large amounts in the small bowel and lactulose works as a prokinetic in that population group versus people who get bloating distention, heaps of gas production from lactulose because it’s been consumed by microbes in the small bowel. Then I wouldn’t use lactulose as a tool for them.
PHOEBE: You mentioned the herbal microbials. How do all three of these things kind of interact? How do you use these combinations of prebiotics, probiotics, and herbal antimicrobials?
JASON: I do this all the time. I do give probiotics, prebiotics, and herbal antimicrobials concurrently during treatment, but not in the same mouthful. I space out the herbal antimicrobials by a couple hours from the probiotics. We might do probiotics at lunch time and before bed. Then we will do the herbal antimicrobials at breakfast and dinner time. There’s at least a couple hours they’re not floating around in the stomach at the same time.
I think this is where you would negate the activity of the probiotic if it’s bathed in the herbal antimicrobial. It’s unlikely to be therapeutically useful. If you separate it out by a couple of hours, you’re still going to get the actions of those probiotic strains. I think that’s the key point to reiterate too is we’re after specific actions of these strains. I’m not expecting them to permanently stay in the gut, but I am expecting them to have specific actions which are working as a prokinetic, for example, so speeding small intestinal transit time along or speeding colonic transit time along.
They do that whether or not they’re permanent residents. If you stop taking it, you stop getting that effect. It can help people with chronic constipation without SIBO. Whilst they take it, their constipation gets better, their transit time improves. When they stop taking it about a week later, things slow right down because the microbe population is decreased on a daily basis. I’m expecting them to do their action.
When I’m using something like the DSM17938 strain of Lactobacillus reuteri, I’m using it because it has antimicrobial actions. I’m expecting when they take that at lunch time, for example, that when it traverses through the small bowel it is secreting its reuterin, which then inhibits the growth of the microbes in the small bowel. It’s an adjunctive antimicrobial in that case that tends to be much more selective in what it’s doing and not causing collateral damage to the colonic ecosystem, which is a big bonus in my opinion.
PHOEBE: Why use the herbals at all if various probiotic strains can achieve that kill action?
JASON: You get better results. From a clinician standpoint, I’ve got some patients that come to me who have a history of intolerance and can’t any herbs and they have rampaging SIBO. How do you move forward in that case? I have had patients where we’ve just used the right probiotics and the right prebiotics and actually made a dramatic shift in their SIBO and quality of life and their gut symptoms.
PHOEBE: Do you usually start there? Do you prefer to start with the prebiotics and probiotics and see if they work on their own and then add herbals to the cocktail, to the arsenal if not? Is that just for patients who are very sensitive?
JASON: That’s for patients that are very sensitive. What I tend to do is try to choose herbal agents that are less likely to cause collateral damage to the colonic ecosystem.
PHOEBE: What are those?
JASON: I think that would be things like pomegranate husk, for example, would be a very clear selective acting antimicrobial agent. Garlic would fit in that same category too, where it works against a range of the pathogens – or not pathogens, probably too strong a word. Pathobionts might be the right word, essentially bugs that, in the right amount, are fine but in too large of an amount are problematic. The pathobionts we find commonly in SIBO patients, we find something like garlic and pomegranate are active against the pathobionts but tend to leave the beneficial bacteria in the colon untouched, which to me is absolutely perfect.
I would use other herbs. I often use some things similar to what other people would, like oregano and thyme and things like that, but I would tend to use them as a tincture rather than as enteric-coated essential oils. My experience doing a lot of follow-up microbiome analyses in patients who have taken relatively long-term or high doses of enteric-coated essential oils tells me that yeah, undoubtedly they work to kill SIBO bugs, but they’re also killing bugs pretty indiscriminately in the colon as well. I tend to reserve those for treatments of last resort and use my herbal tinctures first off because they essentially pull out some of the volatile components that you find in the essential oil but at a lower concentration. Plus, you get a whole balanced plant extract that also has things like polyphenols.
Polyphenols, broadly speaking, tend to work against the pathobionts we find over-growing in SIBO but not against beneficial bacteria in the colon. We end up having a much more selectively acting, yet effective, agent when given in tincture form, because it’s perhaps broader in some ways in terms of its number of compounds that are involved with the antimicrobial activity but less concentrated on the ones that are less selective in what they’re doing.
PHOEBE: You mentioned garlic allicin. I think that’s one I would love more of an explanation on, because it’s another contradiction for people who have maybe experimented or been told immediately to go on a low-FODMAP diet. Public enemy of the low-FODMAP diet number one is garlic. How does allicin, again, help to eradicate SIBO while garlic, when eaten in your diet, can ramp up symptoms?
JASON: Garlic is a complex herb. We see it as a food, but essentially it’s a medicinal herb that very complex in terms of the numbers of different types of compounds it contains. Garlic does contain inulin, which is fructans, which is why it’s public enemy number one on the FODMAP list.
When consumed, inulin is fermented and increases gas. That fermentation process can cause [32:39] effect too, but it’s typically the gas that is most problematic as part of that process. When we’re taking garlic as an antimicrobial, most people end up using an extract of garlic which has essentially taken out the fibers and the inulin content and just left the antimicrobial components of garlic, so it’s working as an antimicrobial rather than – then you don’t get that inulin gas-inducing substance. I think that’s probably the clearest explanation of the apparent dichotomy.
PHOEBE: Got it. Obviously, this is all above my pay grade, probably above most sufferers’, laymen on their own’s pay grade, and yet I feel like there are many people in my audience who are trying to figure this out all own their own. I definitely don’t advocate that people don’t seek out medical treatment and the guidance of a practitioner. I’m just curious for people who are diving to the depths of the Earth, so the the internet, and trying to figure out solutions. A question I often get asked is do I take a probiotic while I try some of these compound herbal antimicrobials or rifaxmin? What does someone kind of shooting in the dark – what can their approach be to probiotics? How do they find these specific strains?
JASON: Yeah, you can’t trust label claims. That makes it a bit more tricky because companies can add a whole bunch of different things onto label claims that may or may not be relevant to their particular product, sadly. Navigating the field of probiotics is tricky. I’ve got a whole website, called The Probiotic Advisor that’s designed to help clinicians navigate through the minefield of probiotics. We just summarize the research done on specific strains found in certain supplements, and it gets around. I’m relying on industry information or label claims as to what a probiotic strain actually does do based on the human data from research settings. I think it’s challenging for clinicians to navigate, let alone members of the general public, sadly. The reality is that different probiotic strains within the same species have potentially very different therapeutic effects few clinicians know, let alone the general public.
PHOEBE: Right. Is it – I wouldn’t say dangerous – but should the general public just not even try to use probiotics, any probiotics they find on the shelf or any probiotic that’s recommended generally by trusted physicians but may not necessarily be for SIBO? Should they just steer clear and stick with the herbals if they’re not sure?
JASON: That’s a hard question to answer. I know it’s challenging to seek out the care of those people that are better qualified and better skilled in treatment of SIBO, but I would suggest you’re going to get the best results if you do do that. That, sadly, means it’s often not someone who lives locally to you. It might be that you’ve got to actually do some sort of phone or internet consult or travel to actually get to a practitioner with experience and specialist knowledge to deal with it because it’s not a simple condition to treat. If it was, it would be great.
I can say – and speak to anybody who treats a lot of SIBO – everyone’s different. We look at the breath test results. We do the best with treatment. We don’t have a lot of clinical trial data to steer our direction with treatment yet, particularly in terms of the herbal medicine world. There’s only perhaps one study that has used herbs for the eradication of SIBO, but we’ve got lots of clinicians, including myself, that actively use herbs and get very good results. We just don’t have as much good clinical trial data as we would like to dictate treatment. It makes it much harder for people that don’t have time and inclination and experience of treating mostly IBS or SIBO patients to guide or navigate patients through this problematic era. As I said, even the diagnosis area is tricky in terms of what breath test do you use, what’s normal, and what time point.
There’s been so many differing opinions on this. Up until recently, there’s been some trial or attempt to making some consensus agreement about what a cut-off is for where it reaches the small bowel, the colon, for example. There is still debate around that despite the consensus decision. You see people that don’t have SIBO, but in my opinion should be diagnosed with SIBO. You have other people that the SIBO was missed because people didn’t interpret the tests the way that I would interpret it, which is hard for people to navigate, as I said.
PHOEBE: That’s a whole other podcast episode right there, “How to Read Your Breath Test Properly.” Back to the layman’s approach to probiotics, how do fermented foods fit in? Is there anything we can do to kind of hedge our bets through diet?
JASON: I don’t use fermented foods as tools in SIBO patients because of the – essentially, they’re wild ferments. In wild ferments, you don’t necessarily know what you get in the end and in what amount. I think, in general, you’d get probably a therapeutic amount of microbes. Research tends to show that things like sauerkraut and kimchi have 10 to the 8th CFU per gram which is 100 billion bacteria per gram per mil of contents which is pretty easy to get a therapeutic dose, in theory, assuming the strains contained in that product are actually therapeutic beyond just the fact that they ferment cabbage very well.
This is why the strictest definitions of probiotics don’t even include fermented foods as a component of probiotics. They’re considered to be foods that contain live and active cultures rather than probiotics. Because of that wild nature that we don’t necessarily know what we’re getting when we ingest them, I would be hesitant to use them or expect any sort of definitive therapeutic effect when it comes to – the main reasons I’ve been using probiotics in SIBO would be, as I said before, as prokinetic agents, as antimicrobial agents or things to improve healing of a damaged, leaky gut or things to decrease visceral hypersensitivity which is a common condition in IBS patients and in my experience, many patients with SIBO. I might be using probiotics to work on all of those areas, but I wouldn’t expect my sauerkraut that’s in my fridge to necessarily have any organisms that are going to help with any of those four.
PHOEBE: Why do various microbiome researchers who purport a “good gut diet” suggest that fermented foods are so good?
JASON: As someone that’s been researching the microbiome for 18 years, the vast majority of research around improving the health of the ecosystem is around using dietary fibers and prebiotics. There’s far more evidence using those tools to improve the health of the ecosystem. Improving diversity dramatically increases in levels of anti-inflammatory gut healing species and decreases of pathobionts through the use of those tools. For me, those are, from a research perspective, by far the most effective interventions and from a clinician perspective too of actually seeing changes in microbiota. Nothing comes close from a probiotic realm. If you want to change the ecosystem, you change diet, you use prebiotics, and you’ll see a dramatic shift in that ecosystem, far more so than taking a few hundred million, or billion, CFU of a probiotic will ever do.
In terms of quick ways to increase diversity by adding another two, three, four, five, ten different species in there from a fermented food perspective, then yes, that could certainly do so, but it’s only a temporary effect. I still eat fermented foods pretty much daily, like sauerkraut and kimchi, despite the fact I don’t think they’re colonizing my – I know they don’t colonize my gut permanently, but there are compounds in those foods, in the foods themselves, that are more nutritious.
For example, we have better absorption of vitamins and minerals, creation of new vitamins and minerals from that fermentation process. We get lactic acid and other short-chain fatty acids being produced which lower the glycemic index of any meal I consume with those foods. There’s a range of benefits as to why we’d be consuming those things, but their impact on the microbiota pales in comparison to changing one’s diet and using prebiotics. Those will have the biggest impact on that ecosystem.
PHOEBE: That’s so interesting. would you say – I’m drawing a conclusion from what you just said. For those at home who want to experiment on their own with pre and probiotics, skip the probiotics. Maybe look into the PHGG.
JASON: Yeah, I think that that one is generally well-tolerated, not always. I must say I was lucky that the first 30 or 40 people I treated with IBS and SIBO patients with PHGG tolerated it beautifully well. I was at the point of, this stuff is like heaven, everyone tolerates it well, before I had my first person who didn’t. I had confirmed efficacy data from a clinical perspective before I had someone that didn’t. There are some patients with SIBO or IBS who don’t tolerate it well. I’d say thankfully, it’s in the minority of people. I think that’s something you could safely play around with. You could certainly play around, I think, with the BioGaia probiotic because I think it’s got potential usefulness in both hydrogen-dominant and methane-dominant SIBO.
When you start experimenting much beyond that – interesting question because if you look at the data set of probiotics as a whole in SIBO, you combine the data together from just any probiotic, there’s a mass analysis published just a few months back where they did that. They said, okay, let’s grab every single study looking at probiotics in SIBO, combine the data together, which I think is a bit problematic, but nonetheless, that’s what they did. They found that there’s a 63 percent decontamination rate by just using general probiotics for the treatment of SIBO. 63 percent of people cleared it from just taking probiotics. There was a 37 part per million decrease in hydrogen gas from taking just a random probiotic, and its reduction of abdominal pain.
You could argue that even just taking a random probiotic would probably, from a research perspective, be helpful. I can say from my clinician experience, and speaking to other clinicians, that certain other clinicians see people who randomly experiment with probiotics who have issues. For me, I only use very select ones that I know about the action that I want. I can’t necessarily comment on people randomly taking probiotics and their end results.
PHOEBE: Okay, that makes sense. Finally, to round things out on the question of diet, do you have a specific approach when you’re using these other treatments? How do you feel about the low-FODMAP diet? Tell us what you recommend.
JASON: Yeah, and I think I might differ a wee bit from many of my colleagues in terms of not recommending a super-strict diet when I’m treating my SIBO patients. Because I often will do fructose breath testing with my potential SIBO patients, I will actually ascertain whether the bacteria in their small bowel can eat fructose or not. You can get a bit of that from symptoms, but you get a very clear picture from looking at breath test values. I do often use a low-FODMAP diet in patients when I’m in that treatment phase. Most of that’s around reducing symptoms, rather than worried about feeding the bacteria in the gut. The reality is, if you started eating just meat and fat, you’re still feeding bacteria in the small bowel. You’re just feeding different ones, the ones that don’t produce gas.
This is the thing. Just because it’s not producing gas doesn’t mean it’s not feeding something. You’re eating lots of fat, you’re producing lots of bile, and you’re not feeding the hydrogen sulfide gas producers, which I can tell you, long-term, is not a good thing. Eating big chunks of steak with no other sort of fibers – you’re feeding protein petrifiers who just don’t produce gas, but you’re still feeding microbes as part of that process. I don’t go by this idea of, you can starve them off by cutting out carbohydrates because I don’t think that’s the reality of what’s occurring. You’re just feeding different species that actually can cause more gut damage and more tissue inflammation, just lesser key symptoms.
Sadly, you see this clinically, that people that have been on those very restricted diets for long periods of time, and their gut health’s deteriorated dramatically. Their ability to deal with any sort of fiber often deteriorates dramatically over that time point, too. Yes, I do often temporarily use a low-FODMAP diet whilst we deal with the SIBO aspect. Let’s say I’ve got a patient that is lactose intolerant and fructose intolerant because of the SIBO. Essentially, it’s bugs in the small bowel. They’re eating the lactose. They’re eating the fructose. People are getting symptoms when they’re doing it. I’ll cut those things out in that short-term. Once the SIBO is gone, then that’s, in my experience with most patients, is under the 12-week mark, we’ll often introduce fructose or lactose back in.
It’s generally well tolerated, but we might be more cautious with the introduction of the oligosaccharide component of the FODMAP, the O because many of these patients have got low-grade gut inflammation and visceral hypersensitivity that makes their colon still reactive to the gas it’s produced. We’re supposed to produce gas when we eat oligosaccharides. Everyone does. You’re not supposed to get pain, bloating, and distention. You’re supposed to just fart. That’s how it’s supposed to happen. All of us produce more gas. It tells you there’s something wrong if you’re getting pain, distention, and bloating from it, not that there’s something wrong with that food, but there’s something wrong your gut. We work on treating that, that thing that’s wrong with their gut. Then often, after another three to six months period of time, we get them to the point where they can consume oligosaccharides once again as well.
PHOEBE: What’s that process? If it’s not the SIBO, which I think many people think if they reintroduce, even though they’ve come back with a negative SIBO breath test and they feel those symptoms, that it means the SIBO’s coming back. What are these other issues?
JASON: What you’ll typically see is change of timing of when that gas is produced or when those symptoms occur. Typically, with a SIBO patient, they’d be getting those symptoms occur in 20 minutes, half an hour. Around that time, would be pretty typical for SIBO patients. Let’s say they ate Mexican black beans with onions and garlic, which I love. They’d be in horrible pain. It’s a very bad meal for some of these people at the 40 to 60-minute mark when they’ve got SIBO. When you treat that and the far end of it, they may get bloating, distention, and discomfort, but it will often happen at the two, three, four-hour mark from that point. That’s telling me that it’s no longer happening in the small bowel, but in the colon.
At this point, it’s an issue with their motility and the gasses being stuck because the colon transit time is very slow. That’s often part of the story, but also, they’ve got visceral hypersensitivity where the nerves in their colon just don’t – they fire off with a small amount of gas that’s produced. This is clearly shown is IBS patients, where they put a special balloon in their bums, and they pump up that balloon. People with IBS will get pain and experience bloating when the balloon is only a quarter full, versus other healthy people would be like, the balloon is full before they get the same degree of pain or bloating sensation.
PHOEBE: How do you heal the hypersensitivity?
JASON: Yeah because that’s not dealt with. People’s typical SIBO treatment – they just focus on killing the bugs and go, okay, they’re gone. See you later. I think I’m oversimplifying things. Hopefully it’s not usually like that. I think you need to focus on healing up and decreasing inflammation in the colon tissue. One of the key strategies for me is ensuring that they’ve got the right microbial populations around whose job it is to decrease visceral sensitivity. That’s the butyrate producers and species like bifidobacteria and Akkermansia, whose jobs are to maintain good gut integrity and decrease inflammation’s that’s present. The production of butyrate a core aspect of that. This is another reason why I worry about those restricted diets longer term and some herbal antimicrobials longer term. They actually diminish populations of butyrate-producing bacteria, and makes it harder to actually fix up what’s going wrong in the colon.
PHOEBE: Are you just, as part of that healing period for hypersensitivity, using, again, another cocktail of pre and probiotics? Is there anything that can be done through diet, either removing or adding?
JASON: I think you’ve got to be watchful there because there’s certain dietary components like – I know high fat’s very popular at the moment, but high fat diets increase bile output, which then tends to feed hydron sulfide gas-producing bugs like bilophila [48:11] specifically, which then worsens visceral hypersensitivity. There’s certain things you’ve got to take out of the diet that are worsening that visceral hypersensitivity or contributing to it, at the same time, encouraging the consumption of foods that are going to nourish and feed those butyrate-producing bacteria, Akkermansia and bifidobacterial, within what’s allowable with that person’s symptom picture.
PHOEBE: What are those foods?
JASON: Butyrate-producing bacteria will often grow well on partially hydrolyzed guar gum as a supplemental fiber. Psyllium, that you mentioned before, does tend to increase butyrate production, so it’s something that I would use in some of those patients. Foods that contain resistant starches and other types of soluble fibers also increase amounts of butyrate that’s being produced. You just have to tailor that per person, in terms of their individual tolerability to different foods. In general, that’s the approach.
PHOEBE: Closing the loop on the low-FODMAP diet question, how long is too long? What’s your sweet spot there?
JASON: We know from looking at the research on it and impact on the microbiota that there are detrimental negative shifts to one’s colonic ecosystem when consumed for – I can’t remember the duration of the study, whether it was 8 or 12 weeks onwards. You start getting negative shifts in terms of decreases in gut protector species like Akkermansia, bifidobacteria, and [49:35] bacteria. That makes sense because you’re not giving up this much food. Therefore, their populations are going to decrease unless you’re very proactive and do something to try to attenuate that. What I would often do is try to limit around – with a SIBO patient, it’s really around that three-month mark is where most people are – the SIBO is gone, and we move into a maintenance phase aspect of things, in which case it’s reducing some of the limitations of that low-FODMAP diet at that timepoint.
Some of them are more slow than others, but I’m also supplementing with fibers that are going to nourish the same species that are otherwise being starved out on low-FODMAP diet. I think that’s perhaps a good thing to keep a mind, that if they need to be on a low-FODMPA diet for any long length of period of time, that if you can supplement and ensure you feed those species that would otherwise be negatively impacted by the low-FODMAP diet. Since we’re trying to attenuate the negative consequences of that, they still get the benefit in terms of reduction of symptoms with that diet. Then they can follow it for a long period of time while we try to sort out the causes of that.
PHOEBE: That’s with some of the prebiotics you mentioned before.
JASON: Yeah, like partially hydrolyzed guar gum can be a very useful pool in that population. Galacto-oligosaccharide is another one that’s often but not always well-tolerated in those patient groups that benefitted from a low-FODMAP diet.
PHOEBE: That’s a great recommendation. To leave the layman like myself with some advice, is there anything else you would tell people to keep in mind to advocate for themselves in asking practitioners about pre and probiotics or experimenting themselves? Is there anything that we missed in terms of what people should keep in mind?
JASON: I think we’ve covered things pretty well – I think to have cautions about being on very restricted diets for longer periods of times. I’d caution to anyone who says that we can’t take anything, probiotics or prebiotics. I don’t think they’re familiar with the nuances of the literature. Those perhaps would be red flags for me, rather than looking at things on a neutral basis and looking at the data, but individual prebiotic-like fibers and individual probiotic strains.
PHOEBE: Wonderful, thank you so much for coming on the show today and sharing a tremendous amount of knowledge. I have a lot to think about, I think, going forward. It also just rings home how important it is to find a practitioner who’s well-versed in all the intricacies and all the strategies for fighting SIBO.
JASON: Yeah because I think you will shorten your SIBO battle dramatically if you find the right practitioner.
PHOEBE: Wonderful, well, thank you so much.
JASON: You’re welcome.
Disclaimer: The information shared in this podcast is not meant to provide medical advice, professional diagnosis, or treatment. The information discussed is for educational purposes only and is not a substitute for medical or professional care.