Back to Blog


What Is Research Telling Us About SIBO?

Guy Daniels
Onegevity

GutbioTM by Onegevity is a test designed for individuals who want to optimize their gut health. It examines your unique gut microbiome and offers personalized interventions for diet, exercise and supplementation. Gutbio is not intended to diagnose, treat, cure or prevent IBS or any disease. Always consult a qualified health-care practitioner


Watch Now: https://youtu.be/GamX7lBE5bU


Slide 1

SIBO – small intestinal bacterial overgrowth, is currently a popular topic, and something we get many questions on. Considering that at Onegevity, we analyze stool samples, you may wonder what role we can play in a microbiome from a different location, that of the proximal small intestine. And that’s a legitimate question. With that in mind, let’s take a look at what the research is telling us about SIBO.


Slide 2

Our first reference lists to the left, two very important considerations in SIBO. First, it highlights HCL output from within the stomach, and how acid blockers can diminish its abundance. Acid blockers may be great for alleviating heartburn when you’ve eaten things you probably shouldn’t have, but they are not good for the long-term health of your microbiome. Keep in mind, you have a microbiome throughout the whole length of your GI tract, not just in the colon. You have an oral microbiota, one in the stomach – believe it or not, in the duodenum, etc all the way to the very end. The microbiota are not the same from one location to another, as factors such as oxygen availability, motility, stomach acid, luminal pH, bile salts, enzymes and substrates are variable in different locations. In chronic use of acid blockers, you’ve not only altered the environment of the stomach, but also the proximal colon, and also what makes its way into the colon, which would be a higher proportion of animal proteins, something that is not good for the colon. So as you can see, the entire microbiome is impacted, but in regards to the stomach, since you’ve changed the environment, bacteria and fungi, who otherwise should not be residing there, can now survive. This is but one aspect of SIBO. Another is what they refer to on the bottom left, that of motility, or how quickly the food contents move through the GI tract. Food is supposed to transit the small intestine significantly faster than the large. When we impact this motility, again we’ve altered the environmental basics, and allow a shift in who can reside where. To the right, is shown 4 trials using an antibiotic, Rifaxamin, along with other agents, in the treatment of these bugs where they don’t belong. As you can see, the success rate is relatively high. This is the go-to pharmacologic approach to SIBO, but doesn’t always work, hence the addition of other agents.


Slide 3

Here we’ll revisit one of our previous concepts, that of transit time. I know this slide is a bit busy with acronyms, but what these researchers are saying, is that those with SIBO have significantly longer GI transit time, specifically for the small intestine. The longer it takes for food to pass through the small intestine, and the more bacteria which accumulate there, the more fermentation you’ll have, and therefore more gas and bloating, in a place where there shouldn’t be gas and bloating. This is a classical symptom of SIBO, and something we aim to resolve as part of an overall approach.


Slide 4

In this paper, once again we see our two concepts, HCL suppression and motility. If you look at table 2, you’ll see highlighted, that those who tested positive for SIBO, and who were on acid-suppressing PPIs, had a much higher rate of their identical comparators, but who were on a “prokinetic”.

A prokinetic, is something that helps you move the food faster, in other words, speed up motility. One point to take away is that even with PPI use, altered motility can improve outcomes on its own. As for the left side, I’m going to read the text verbatim, as it’s quite powerful. The authors from this 2018 paper state, “Chronic acid suppression with long-term PPI leads to hypochlorhydria, which alters the intraluminal environment to facilitate the growth of the bacterial flora in the small intestine and contributes to the proximal migration of colonic microflora”. That last bit, “proximal migration of colonic microflora, means that bugs that are dwelling further down your GI tract, in your colon, are able to migrate or work their way UP, the GI tract, to reside in places they don’t belong, whether it’s in the type of bug or quantity, and this is a result of acid-suppressing agents, namely PPIs.


Slide 5

I’ll try to summarize this dense slide for you. What they are saying, is that when looking at the middle section of the small intestine, in SIBO patients, the types of bacteria that were found, were the ones listed to the left. We’ve identified these bacteria as highly problematic in numerous human fecal analyses. In other words, many of the same bad actors from the colon, are residing in the small intestine, according to these researchers. Are not only are they residing there, but they are also dominant. The microbiome is a two-way street. Bugs from the upper GI tract can make their way to the lower GI, and the reverse is true. Either way, we can be dealing with a situation of what I call, “bugs where they don’t belong”. Ideally, we have a properly functioning GI tract, with more distinct delineations of residents in their proper location.


Slide 6

Once again, we see the now-familiar theme of dysmotility and PPI use. This time, these researchers looked in the duodenum, the first part of the small intestine, just after the stomach. They found several of the same bad acting bacteria identified from our previous slide, as well as another topic we get many questions on, that of candida. Here they use the term SIFO, or small intestinal fungal overgrowth, and candida was the culprit here, all the way up in the duodenum. Again, we have bugs residing where they don’t belong, thanks to environmental shifts, centered around PPI use and dysmotility, both of which were found to be risk factors for overgrowth.


Slide 7

Here we have a slightly different take on a now-familiar theme, Once again, the researchers looked at the duodenum, and found that there was significantly more bacterial overgrowth in the duodenum of the SIBO subjects, vs the non-SIBO ones. In addition, we’ll now introduce the connection of SIBO to IBS. Here they showed that those with IBS had significantly higher levels of duodenal overgrowth, as compared to non-IBS. So just a refresher. IBS is something we associated the dysbiosis in the ileum and colon, but here we’re looking way up next to the stomach, in the opposite direction. If we put this together, with the bad bugs from previous slides, and the knowledge that those same bad bugs drive dysbiosis in the lower gut, we see the smoking guns of the same bad actors which can cause problems in one location, can migrate under environmental changes to cause problems in another location.


Slide 8

This slide is a continuation of this 2012 paper. Here we join the two concepts of IBS and PPI use, in regards to SIBO. Although they sound like separate concepts, they are highly correlated. Remember, PPIs changes the entire microbiome, and the bad actors in IBS cam migrate up the GI tract and potentially cause a condition we identify as SIBO. But we can’t think about the GI tract as different segments or even different diagnoses. Bad actors, or more accurately, opportunistic pathogens, are bad

for any condition. It just depends on a variety of factors. But it’s this same large group of opportunistic pathogens which have been strongly associated in many human trials with a wide variety of conditions ranging from Crohn’s, Ulcerative Colitis and IBS, to depression, anxiety, metabolic syndrome, dementia and more. Here we see that SIBO was found in 60%! Of IBS-D sufferers, and that, once again PPIs were linked to SIBO. In addition, those with IBS had more than a 6 fold risk for also having SIBO. Something that makes sense as we now understand the bidirectional effects of the GI tract.


Slide 9

In this Duodenal aspirate study from 2019, I want to hit on some new points. One – it’s the symptoms that are the main driver. In other words, SIBO testing is not failsafe. Just because you are told you haven’t tested positive for SIBO, that doesn’t mean you don’t have it. Although this is aspirate, and in office testing is via breath, the concept remains the same. As you can see in the middle of figure A, many symptomatic patients came back as SIBO negative. Point two – in those with symptoms, prevotella was low. We’ve identified the genus Prevotella as a key player is gut health, particularly in diarrhea, which is you recall, was highly correlated to SIBO in a previous slide. The last point here is that of simple sugars. As expected, they triggered symptoms for these patients, and this is not a surprise. As we now know, there is an excess of bacteria fermentation away in the upper small intestine is SIBO, and if you give them a favorite fuel, that of simple sugars, then they’ll do what they do best. Of course, a part of any SIBO protocol should be to limit simple sugar consumption.


Slide 10

To take the last point, a quick step further, if you recall, when a high fiber diet was shifter to low fiber, but high simple sugars, symptoms got worse for SIBO. Well here, the opposite was the case. Again, we see the use of rifaximin, an antibiotic designed to stay within the GI tract, to reduce those extra fermenters who’ve worked their way up, along with a prebiotic we often recommend, PHGG. Here fiber was added, and with success, as eradication of SIBO was more effective in the Rifaxamin plus PHGG group, than Rifaxamin alone. Prebiotics are at the cornerstone of what we do.


Slide 11

Lastly, I want to touch on a couple of new points. If you're familiar with my webinar series, you may recall that the microbiota produce thousands of enzymes. Well, some of those enzymes change the structure of bile salts. Now we’re not going to dive deep into bile for now, but know that it’s released to primarily digest fats. In a properly functioning gut, the correct microbiota resides in the small intestine, and all goes according to plan. But in SIBO, these extra bugs reside too far up the GI tract, and some of them are now able to perform their enzymatic action on bile salts, changing the structure and function such that it reduces fat absorption. This has multiple effects. One of which is similar to PPI use, in that we now have extra fat making its way into the colon. Although bad bugs tend to like animal protein, fat is also a substrate that can make them happy. Another point from this paper is that of ileal braking. When these macronutrients make their way down to the distal small intestine, the body reads this as too much food escaping digestion, and slows down motility. If you recall, from our first slides, motility plays a huge role in SIBO. So as you can see, it’s all connected. The overall proper functioning of your entire GI tract, is tied into SIBO, something we consider isolated to the proximal small intestine, from a limited point of view.


Slide 12

And since we can identify dysbiosis from your stool analysis, and we have the clinical expertise in gut conditions, to include SIBO, which includes some simple things, like food choices, what we do is

relevant for the SIBO sufferer. In review, we touched on a small component of dietary consideration, gut transit time, proper digestions, and large quantities of bad bugs migrating to places where they don’t belong. Therefore, if you or a loved-one suffer from SIBO, or any gut condition, as well as conditions outside the gut, visit our website at Onegevity.com. There you can find more educational material for what concerns you, and you’ll be able to order up one of our kits and begin the process of feeling better finally.


GutbioTM by Onegevity is a test designed for individuals who want to optimize their gut health. It examines your unique gut microbiome and offers personalized interventions for diet, exercise and supplementation. Gutbio is not intended to diagnose, treat, cure or prevent IBS or any disease. Always consult a qualified health-care practitioner