Irritable Bowel: SIBO, Dysbiosis and Diet

In 2010, I read a paper in the journal, Nutrition, that really rocked my world:  “The concept of small intestinal bacterial overgrowth (SIBO) in relation to functional gastrointestinal disorders.” [i]  To summarize one of its many key points:  we don’t know how to test for it and, “Controversy will continue until concepts are broadened, consensus in definition is reached, and evaluation of efficacy of candidate therapies is more rigorous.”

I’ve been watching this research for over a decade now, and guess what – SIBO is just as controversial as ever.

For many years, SIBO was thought to be the cause of IBS-type symptoms, like constipation, diarrhea, gas, bloating and pain, and testing was mainly done by sampling breath to look for products of bacterial fermentation.  The “gold standard” was more invasive, probably done during endoscopies, I’d imagine: aspiration (collection through suction) and culture of bacterial content from the small intestinal contents (specifically from the duodenum, the upper part of the small intestine, next to the stomach). However, tremendous controversy surrounded this testing as its accuracy has always been in doubt, and for years the search has been “… on for alternative diagnostic strategies with much expectation surrounding the application of modern high-throughput molecular approaches to the study of the gut microbiome.”[ii]

A new paper has taken a step forward in sorting all this out.[iii]  I found the findings really surprising.

In the first part of this research, the scientists compared the results of the above-mentioned “gold standard” aspiration and culture of small intestinal contents to those of a much newer, RNA-based microbiome analysis, on 126 people with GI symptoms.  They also had 38 healthy controls in this study.

1. The usual duodenal aspirate culture showed that only 52% of those with GI symptoms had SIBO (while none of the controls did). So there was not any kind of accurate correlation between this test and GI symptoms.
2. There was a correlation, however, between SIBO and recent antibiotic exposure.
3. Dysbiosis (defined as the biome being compositionally different from the controls) WITHOUT SIBO, as measured by the RNA testing, was much more accurate at diagnostically differentiating people with symptoms and without. Those with GI symptoms had reduced microbial diversity.
4. SIBO does not correlated with microbial dysbiosis.
5. In patients with symptoms, “…pathways associated with simple sugar metabolism were enriched…whereas complex carbohydrate degradation pathways were more prevalent in healthy individuals.” This suggests that healthy individuals eat more fiber than  those with dysbiosis.
6. Believe it or not, some of the healthy individuals with no GI symptoms actually had SIBO,  which…”suggests that healthy individuals can have SIBO without any symptoms or alterations in microbial composition.”

The 2^nd part of this paper talks about what happens in healthy individuals if they switch to a diet low in fiber, high in simple sugars.  They had 16  healthy people (who ate at least 11 grams of fiber per 1000 calories of food)  go onto a low fiber diet (less than 10 grams per day) for a week and then reanalyzed their microbiota using the RNA technology.  They also recorded any GI symptoms experienced and looked too at epithelial barrier function (i.e. the presence or lack of leaky gut).   “All patients developed new symptoms with 80% developing GI symptoms during the dietary intervention and the symptoms resolved within a week of discontinuing the diet.”  That is, in only a week of eating a low fiber diet, almost all developed GI symptoms which resolved as soon as they went back to eating their healthier, high-fiber diets.  They also found that,  “…diet-related changes in the small intestinal microbiome were predictive of symptoms (such as bloating and abdominal discomfort) and linked to an alteration in duodenal permeability”[iv] – so to the development of leaky gut.

To sum up their findings:  while SIBO exists, it does NOT necessarily correlate with patient symptoms.  Some people have it and are asymptomatic. Some people have IBS-type issues and don’t have SIBO.  But what does correlate is dysbiosis:  abnormal gut bacteria.  And once again, diet is a key factor in determining the composition of the gut bacteria and the avoidance of leaky gut:

“Diet has a significant influence on microbial composition and the enrichment of pathways linked to mono- and disaccharide metabolism in symptomatic patients supports this notion. Our pilot dietary intervention study showed that switching to a low fiber, high simple-sugar diet for a short period can trigger GI and systemic symptoms that improve upon resuming baseline diet. The correlation of decreased microbial diversity with increased duodenal permeability and appearance of symptoms suggests that this effect may be driven at least in part via gut microbiota…”

I wish these scientists had given more information on what exactly they mean by simple sugars.  For example, fructose – found in fruit and veggies – is a simple sugar.  I’ve double checked the methods section of the paper, but can’t find any information on exactly what diet they were fed.  I’m assuming they mean processed sugars, like table sugar, but they don’t specify and it’s never safe to assume anything, really.  And is it the sugars that are really the issue – or is it the lack of fiber?

As I mentioned earlier, I’ve been watching this research for many years now and will continue to do so.  Considering the number of people with GI issues these days, this is super important work.

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[i] Gibson, PR and Barrett, JS. The concept of small intestinal bacterial overgrowth in relation to functional gastrointestinal disorders. Nutrition. 2010. 1-6

[ii] Quigley, EMM.  Symptoms and the small intestinal microbiome – the unknown explored.  Gastroenterology & Hepatology. 2019:16;457-458.

[iii] Saffouri, GB, et. al. Small intestinal microbial dysbiosis underlies symptoms associated with functional gastrointestinal disorders.  Nature Communications. 2019. https://doi.org/10.1038/s41467-019-09964-7