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Abbreviations:

CFU/mL: colony forming units per milliliter.

ESS: euthyroid sick syndrome

GI: gastrointestinal

PPIs: proton-pump inhibitors

SIBO: small intestinal bacterial overgrowth

SIFBO: small intestinal fungal and bacterial overgrowth

SIFO: small intestinal fungal overgrowth

 

Today I want to revisit two verified risk factors for small intestinal fungal and bacterial overgrowth (SIFBO). A study published in June of 2013 found that dysmotility (or what many of us call impaired intestinal peristalsis) and proton-pump inhibitor use were significant independent risk factors for developing either small intestinal bacterial overgrowth (SIBO), small intestinal fungal overgrowth (SIFO) or SIFBO. (1)

Now this should surprise none of my faithful readers. Anything that impairs gastric barrier function, and that includes any medication that raises stomach pH or actively inhibits hydrochloric acid production, lays out a veritable welcome mat for any swallowed bacteria to take up residence in the small intestine. I explained all this in my GERD series so there’s no reason to rehash it here.

Nor is it surprising that compromised peristalsis is a risk factor for SIFBO. It is, after all, those muscular wave-like movements of the small intestine that prevent bacteria normally confined to the colon from migrating their way into the distal small bowel and beyond.

But what I found most interesting about this study is that these researchers were not content with administering breath tests to arrive at a diagnosis of SIBO. All patients who presented to this gastroenterology medical center underwent an upper endoscopy to collect small intestinal fluid (aspirate) to assess what was really causing their unexplained gastrointestinal symptoms.

I say unexplained because all patients had tested negative for gastric or intestinal abnormalities after being screened with the following diagnostic procedures: gastroscopy, colonoscopy, CT scan, blood work, anti-tissue transglutanimase testing for celiac disease, thyroid dysfunction, ultrasound and Barrium X-ray.

And what makes this study even more fascinating was that while performing the endoscopy, they also placed sensors in the stomach and small intestine to record motility. A wireless recorder of this data was placed in a shoulder bag allowing patients the ability to walk around and spend the night at home giving these researchers invaluable real-world information.

Monitoring continued until 11 AM of the following day. Participants were encouraged to mark any events like eating, walking, sleeping or any gastrointestinal symptoms they experienced on an event marker that was attached to their recording device.

Now here’s what these researchers found. Of the 150 patients evaluated, ninety-four or 62.7% were positive for an overgrowth. Thirty-eight of the ninety-four had SIBO. Twenty-four others had SIFO. And thirty-two others had an overgrowth of both yeast and bacteria.

As for those that tested negative for an overgrowth, I suspect these people were reacting to FODMAPs. No indication is given as to whether any of these patients were advised to eliminate these foods from their diet.

The criterion for determining who had small bowel overgrowth was having an aspirate culture that contained organisms at or greater than >103 colony forming units per milliliter (CFU/mL). When using the less rigorous, yet conventional standard of >105 CFU/ml, the rate of diagnosed SIBO and SIFO was dramatically lower, suggesting that too many patients with either are being missed in clinical settings.

According to these researchers:

“The predominant aerobic bacterial organisms that were cultured included: alpha hemolytic Streptococcus species (n= 32); non-hemolytic Streptococcus including Enterococcus and Stomatococcus species (n= 10); Klebsiella species (n= 8); E. coli (n= 6); Neisseria sp (n= 5); Staphlococcus sp (n= 4); and Enterobacter sp (n= 3). Eight patients had positive anaerobic cultures including Veillonella sp (n= 5); Clostridium species (n= 1); Bacteroides (n= 1); and Peptostreptococcus (n= 1). Fungal growth was predominately due to Candida species (albicans or torulopsis).”

Courtesy: Dysmotility and proton pump inhibitor use are independent risk factors for small intestinal bacterial and/or fungal overgrowth

Now let me just say that I really appreciate a study that also screened for an overgrowth of fungal organisms.  As I’ve said in the past, yeast is a woefully unrecognized cause of gastrointestinal symptoms. All current breath tests are incapable of detecting these organisms, and it’s no doubt a major reason why for some conventional antibiotic treatment for SIBO fails. Given what I wrote here, I also believe it’s an overlooked contributor to more serious gastrointestinal diseases, not to mention increased intestinal permeability in general.

As per these researchers:

“Although candida infections are usually seen in the neonatal, elderly, or immunocompromised, individuals or those on steroids, or repeated antibiotic use, our findings suggest that fungal organisms are not uncommonly present in patients with chronic GI complaints. In one study, candida was the most common organism identified in nasogastric aspirates from the proximal GI tract of preoperative patients with GI disorders (malignancy, inflammatory bowel disease, and benign conditions). Another study identified fungal growth in stool cultures of six patients with diarrhea and abdominal pain. Apart from these anecdotal case reports, there has been no systematic study of the prevalence and clinical presentation of small intestinal fungal organisms in patients with chronic, unexplained GI symptoms.

The clinical manifestations of SIBO are non-specific and include symptoms such as gas, bloating, abdominal pain, and diarrhea. More serious manifestations of bacterial overgrowth of the small bowel include malabsorption syndromes, weight loss, malnutrition, vitamin deficiency, and anemia. Symptoms of SIFO are however not known but based on our study we believe that SIFO shares the same set of symptoms as SIBO. Our study was unable to identify a single symptom or cluster of symptoms that can clinically recognize patients with either SIBO or SIFO. Thus, symptoms were generally poor predictors of bacterial and/or fungal overgrowth. However, SIBO and/or SIFO were prevalent in over 50% of this patient population with dysmotility and chronic use of PPI and should be considered in the differential diagnosis of patients with non-specific chronic GI complaints.”

All I can add is Amen to that!

Examining the association between proton-pump inhibitor use and overgrowth, and utilizing the same 103 cutoff level, these researchers found that sixty-five of the 150 patients evaluated were using these drugs. Forty-nine of the sixty-five were on prolonged PPI therapy. There was a significant relationship between the use of these drugs and both SIBO and SIFO irrespective of motility disorders.

These findings were echoed in a double-blind, placebo-controlled trial assessing the efficacy of using probiotics in children treated with proton-pump inhibitors as a way to prevent SIBO. (2) What these scientists found was that after a month of taking PPIs, 30% of these children developed SIBO as assessed by a hydrogen breath test.

As breath tests are far less sensitive than endoscopy and incapable of detecting fungal overgrowth, you can be certain that the rates of both SIBO and SIFO were actually much higher in these kids. Unfortunately, taking probiotics was discovered to be ineffective for preventing SIBO while on these acid-suppressing medications. Probiotics are wonderful things, but they are incapable of counteracting the harm caused by compromised gastric-barrier function.

Now returning to the original study, these researchers also found that dysmotility was significantly associated with SIBO, SIFO and SIFBO. Fully eighty patients out of 150 had some form of dysmotility. These results confirm what has been seen in numerous animal and human studies.

Dysmotility is a common symptom of gut dysbiosis. A gut populated by diverse and healthy gut flora is one that propels chyme and feces in a timely manner while simultaneously preventing colonization of the gut wall by bacterial and fungal pathogens. But dysmotility is also a function of diet which leads me to discount some of the conclusions derived from this study for the following reason.

After their endoscopy and insertion of gastrointestinal sensors, a meal was fed to all participants before they were sent home. This meal consisted of the following: a chicken sandwich, 6 oz. glass of milk, a cookie and a banana.

Anyone see a problem with this hospital feast?

The sandwich bread, cookie and likely milk would all have produced opioid peptides upon their digestion. Recall that humans lack the digestive enzymes to break proline bonds. While there is some speculation that certain species of beneficial gut flora may be able to do just that, the last thing in the world most of these patients could claim to have are healthy colonies of gut flora.

Eating both the sandwich bread and cookie would lead to the formation of various gluten opioid peptides. The milk served was likely from an A1 beta casein dairy source as that is the typical dairy type consumed in the United States. Ingesting it would have formed beta-casomorphin 7. What these peptides do to antioxidant status via inhibition of cysteine uptake would also negatively affect motility via up-regulation of inflammatory cellular processes that would maintain an environment hospitable to pathogens.

No indication was given regarding what else was eaten by these participants once they left the medical center. However, given that the study was conducted at the University of Iowa in Iowa City, IA, I’ll leave it to your fervid imaginations for what other gluten and dairy opioid forming delicacies were ingested during the off-site monitoring period.

As ALL opioids slow gastrointestinal function, the conclusions drawn from this motility study are inherently confounded. We have no idea how much of this dysmotility can be blamed on gut dysbiosis as opposed to diet.

Conclusion

Again I reiterate that flinging open the gastric-barrier door by taking PPIs or impairing intestinal peristalsis predisposes to small bowel overgrowth whether by bacterial or fungal organisms or both.

Powerful drugs always have powerful side effects, and PPIs are no exception. For more on what those side effects are, I again refer you to this post.

As for delayed transit time, evidence is robust that the more often peristalsis is inhibited, the more likely a person is to suffer from recurring small bowel infections. Diet is surely a factor with both opioid peptides and binge drinking high on the list, but it’s not the only one.

Opioid drug use and thyroid disorders like Hashimoto’s thyroiditis or euthyroid sick syndrome (ESS) are also contributors. But even here, ESS is related to diet as it’s often caused by either prolonged fasting or very low carb dieting.

At some point in the future, I would love to see a study done in healthy subjects outfitted with gastrointestinal sensors and followed in an in-patient metabolic ward where food composition and caloric density are strictly controlled. One group would be fed foods that form opioid peptides and the other given similar foods devoid of the same. Each would be monitored for detectable changes in motility over an identical period.

To make the results even more robust, I would design the trial in a crossover manner so that each participant was in both arms of the study. Maybe then we could finally determine just how gut stopping these foods truly are.

And that, Dear Santa, is what I want for Christmas!

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