Is SIBO caused by dysautonomic gastrointestinal motility?

[Pyrrhus]

Small Intestinal Bacterial Overgrowth (SIBO) is a common diagnosis these days in ME/CFS patients.

• The most common reported symptoms are gas, bloating, and constipation, although there may be others. Diagnosis is often based on a breath test such as the lactulose breath test.
• Some people report that they cured their SIBO with diet, probiotics, antibiotics, colonoscopy prep, or other means.
• Other people report that they put their SIBO into remission with antibiotics or other means, but it keeps coming back.

Partly due to the fact that SIBO commonly returns after each treatment, some people are saying that there must be an underlying condition that needs to be addressed. Some of these people feel that the cause of SIBO is slow gastrointestinal movement (motility). Basically, the autonomic nerves that are supposed to stimulate the intestinal muscles to move food along the digestive tract are not providing enough stimulation to move food along fast enough. (a type of dysautonomia) As food sits around in the small intestine, there can be growth of bacteria, archaea, and fungi, just as food that sits out of the refrigerator for too long can become rotten.

One paper looked into the possibility of slow gastrointestinal movement (motility) and reported:

Small Intestinal Transit Time Is Delayed in Small Intestinal Bacterial Overgrowth

Background: Altered small intestinal motility is thought to contribute to the development of small intestinal bacterial overgrowth (SIBO). The clinical manifestations of SIBO and consequent malabsorption are wide ranging and include abdominal pain, bloating, diarrhea, weight loss, and nutritional deficiencies. However, due to the nonspecific nature of symptoms, the diagnosis may often be overlooked. To date, few studies have illustrated a direct relationship between impaired small intestinal motility and SIBO. In addition, further study has been limited by the technical challenges and lack of widespread availability of antroduodenal manometry. The development of a wireless motility capsule (WMC) (SmartPill) that evaluates pressure, pH, and temperature throughout the GI tract offers the potential to identify patients with small bowel transit delays who may be at risk for bacterial overgrowth.

Aims: The primary aims of this study were to: (1) characterize the relationship of prolonged small bowel transit time (SBTT) in patients undergoing [Wireless Motility Capsule] with SIBO as based on a positive lactulose breath testing (LBT); and (2) to assess the relationship of prolonged gastric, colonic, and whole gut transit times (WGTT) and additional motility parameters with SIBO (positive LBT).
[...]
Results: Of the 37 patients who underwent both [Wireless Motility Capsule] and LBT, 24 (65%) were LBT positive. The mean SBTT among those who were LBT positive was 6.6 hours as compared with 4.2 hours in those who were LBT negative (P=0.04). Among patients who were LBT positive, 47.6% had prolonged SBTT (≥6 h), whereas only 7.7% of those who were LBT negative had a delay in their SBTT (P=0.01). In addition, patients who were LBT positive were more likely to have prolongation of both colonic and WGTT versus those who were LBT negative (CTT: positive LBT=64.4 h vs. negative LBT=35.5 h, P=0.02; WGTT: positive LBT=70.5 h vs. negative LBT=44.1 h, P=0.02). However, there were no statistical differences observed between the groups for gastric emptying times or other small intestinal motility parameters (SB motility index, contractions per minute, and peak amplitudes) between the 2 groups.

Conclusions: Patients with underlying SIBO have significant delays in SBTT as compared with those without. The association between prolonged SBTT and positive LBT may be useful in identifying those patients with SIBO diagnosed by LBT and potentially target therapeutic options for those refractory to standard therapy. Interestingly, patients with positive LBT did not necessarily have a generalized gastrointestinal motility (similar [Gastric Emptying Times] among groups), suggesting that small bowel transit specifically predisposes to the development of SIBO. Future, prospective studies are needed to further characterize intestinal dysmotility and other contributing pathophysiological mechanisms in SIBO and to investigate the potential benefits of prokinetics in this challenging patient population.

(emphasis added)


Although this paper demonstrates a correlation between slow gastrointestinal motility and SIBO, it can't prove that slow gastrointestinal motility causes SIBO. What do you think? Feel free to look through the many SIBO discussions we've had here:

• https://forums.phoenixrising.me/threads/small-intestinal-bacteria-overgrowth-sibo.79399/
• https://forums.phoenixrising.me/threads/different-causes-of-sibo-and-high-hydrogen.80291/
• https://forums.phoenixrising.me/threads/sibo-how-to-clear-small-intestine-fix-motility.80196/
• https://forums.phoenixrising.me/threads/treating-sibo.80548/

Reference:
[1] https://pubmed.ncbi.nlm.nih.gov/25319735/

 

[ljimbo423]

Although this paper demonstrates a correlation between slow gastrointestinal motility and SIBO, it can't prove that slow gastrointestinal motility causes SIBO. What do you think?

I think slow gut motility could cause SIBO. I also think SIBO can cause slow gut motility. My feeling is, in most cases SIBO causes the slow gut motility. Probably the biggest reason I have for this view is because so many things that most people are exposed to on a regular if not daily basis can cause SIBO.

This is a list I've saved of potential things that could cause or contribute to SIBO-

"Antibiotics, bad diet, food poisoning, food allergies or sensitivities, parasites, viral or bacterial gut infections, excessive drinking, excessive exercise, non steroidal anti-inflammatory drugs, excessive or chronic stress, pesticides.

Heavy metals, many other toxins, chemotherapy, concussions, many general viral infections, because they often effect the gut too."

I've read recently that 50% of covid 19 patients have had gastrointestinal symptoms and that the virus directly effects the small intestine.

 

[kangaSue]

I think we will get some better answers once the the 'human gas capsule' gets to market . At the moment, there's no way of knowing which gas is coming from which part of the GI tract.
https://www.gastrojournal.org/article/S0016-5085(15)01513-9/pdf
http://www.australasianscience.com....2016/capsule-look-inside-irritable-bowel.html

If I were to try rifaxamin (or other antibiotics) though, I'd be coupling it with partially hydrogenised guar gum.
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2036.2010.04436.x

Then again, I'm a cheapskate so I'd just take the partially hydrogenised guar gum (eg Sunfiber) and just do a colon cleanse which can also remove a bacterial overgrowth.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852716/

 

[Pyrrhus]

I think slow gut motility could cause SIBO. I also think SIBO can cause slow gut motility.

Yes, it's always important to make sure we're not accidentally reversing cause and effect. I've read that some of the intestinal gas produced in SIBO physically blocks the movement of food in the small intestine. But perhaps the gas wouldn't be there in the first place if the small intestine was moving food through it fast enough.

This is a list I've saved of potential things that could cause or contribute to SIBO-

"Antibiotics, bad diet, food poisoning, food allergies or sensitivities, parasites, viral or bacterial gut infections, excessive drinking, excessive exercise, non steroidal anti-inflammatory drugs, excessive or chronic stress, pesticides.

Heavy metals, many other toxins, chemotherapy, concussions, many general viral infections, because they often effect the gut too."

Wow, that's quite a list. I wonder if low-grade intestinal inflammation would slow down the movement of food in the intestines. If so, then anything that triggers such inflammation could be a contributing factor to SIBO?

I think we will get some better answers once the the 'human gas capsule' gets to market . At the moment, there's no way of knowing which gas is coming from which part of the GI tract.
https://www.gastrojournal.org/article/S0016-5085(15)01513-9/pdf
http://www.australasianscience.com....2016/capsule-look-inside-irritable-bowel.html

That's a good point. Gas is perfectly normal for the large intestine (colon), but not for the small intestine. And thanks for those articles, I had fun looking through them. They reminded me of some of the biosensors we studied back in my PhD program.

 

[Pyrrhus]

Then again, I'm a cheapskate so I'd just take the partially hydrogenised guar gum (eg Sunfiber) and just do a colon cleanse which can also remove a bacterial overgrowth.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852716/

That's an interesting article. I'm going to post an excerpt from that paper for the benefit of others:

The Relationship between Small-Intestinal Bacterial Overgrowth and Intestinal Permeability in Patients with Irritable Bowel Syndrome

Background/Aims: Small-intestinal bacterial overgrowth (SIBO) is a frequent finding in patients with irritable bowel syndrome (IBS). Many patients with IBS also have abnormal intestinal permeability, which is probably due to low-grade inflammation in the intestinal mucosa. Our aim was to verify the relationship between SIBO and small-intestinal permeability in IBS patients.

Methods: A cohort of 38 IBS patients (20 women and 18 men; age range 16-70 years; mean age 40.2 years) with symptoms that fulfilled Rome-II criteria, and 12 healthy controls (5 women and 7 men; age range 25-52 years; mean age: 37.8 years) were recruited. All subjects underwent lactulose breath tests (LBTs) and intestinal permeability tests using the polyethylene glycol (PEG) 3350/400 retrieval ratio.

Results: A positive LBT was found in 18.4% (7/38) of patients with IBS and 8.3% (1/12) of control subjects. Intestinal permeability was significantly increased in patients with IBS compared with the normal controls (0.82±0.09 vs 0.41±0.05 [mean±SD], respectively; p<0.05). However, the intestinal permeability did not differ significantly between IBS patients with a positive LBT and those with a negative LBT (0.90±0.13 and 0.80±0.11, respectively; p>0.05).

Conclusions: Intestinal permeability was increased in patients with IBS, but this finding did not correlated with the occurrence of SIBO.

Here are what I see as some points made in this article:

• Patients with Irritable Bowel Syndrome (IBS) have increased intestinal permeability, which may theoretically be due to low-grade inflammation in the intestines.
• SIBO appears to be somewhat more common in patients with IBS than in healthy controls.
• However, there was no difference in intestinal permeability between IBS patients with SIBO and IBS patients without SIBO. So, SIBO itself may not have an impact on intestinal permeability.

 

[Pyrrhus]

Another interesting discussion on this topic can be found here:

Treatment for SIBO, leaky gut and general gut dysbiosis
https://forums.phoenixrising.me/thr...bo-leaky-gut-and-general-gut-dysbiosis.81532/

 

[Wolfcub]

I have been wondering if one big key to SIBO is in fact the dysfunction of the Migrating Motor Complex (MMC) in a fasting state.
(Cholinergic influence on the Enteric Nervous System ) -so a combination of hormonal and electrical activity.
https://www.sciencedirect.com/topics/medicine-and-dentistry/migrating-motor-complex

cholinergic involves the use of neurotransmitter Acetylcholine. (parasympathetic nervous system.)


It seems a healthy gut which goes through full phases 1, 2. and 3 of this "clean sweeping" nightly, and during fasting states in daytime too, are kept clear of small intestinal bacterial overgrowth.

So anything dysregulating the autonomic nervous system, with a sympathetic NS bias could disrupt the MMC

This really interests me.

 

[Daffodil]

When I got fusion of C3-C6, I had A LOT of gas exit my body about 3 or 4 days after the surgery. Since then, I have been experiencing normal flatulence when before, I had all but stopped having any. I noticed this disappearing as my ME/CFS progressed. I wonder if the stenosis was affecting my gut motility via pressure on the vagus nerve or something? Anyway, I am still sick so .....after 27 yrs my gut it beyond repair perhaps. It is also possible I am imagining the whole thing and the flatulence was because my diet was changed.

But as you know, there have been many who are in remission after (cranio)cervical fusion

 

[mitoMAN]

Ive read that a good portion of CFS Patients has SFN. And SFN causes dismobility of the gut and is linked to SIBO and IBS.

 

[Flnn]

Ive read that a good portion of CFS Patients has SFN. And SFN causes dismobility of the gut and is linked to SIBO and IBS.

Can you share what SFN stands for, please?

 

[Dubitat]

I think slow gut motility could cause SIBO. I also think SIBO can cause slow gut motility.

I agree. There is potential for a self-reinforcing feedback loop if SIBO impairs gut motility and gut motility worsens SIBO.

Among probiotic options, Lactobacillus Rhamnosus (marketed as Culturelle) has been shown to improve gut motility in mice.

Two medications commonly used in CFS or POTS treatment are also known to increase gut motility: Pyridostigmine (Mestinon) and LDN (Low dose naltrexone).

 

[minimus]

Can you share what SFN stands for, please?

Small fiber neuropathy

 

[Daffodil]

neck issues might also cause SIBO which in turn would cause LPS/inflammation which in turn could impact ligaments which in turn could worsen spinal issues

 

[Daffodil]

ebv, norovoris, and some others can damage neuromodulatory cells in the gut, leading to gastroperisis too

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7479810/

 

[kangaSue]

https://www.nih.gov/news-events/new...fy-nutrient-helps-prevent-bacterial-infection
NIH scientists identify nutrient that helps prevent bacterial infection (2021)

I thought I had posted this article here before but obviously not.

One measure that can be tried for suspected SIBO is to take a taurine supplement.

Taurine produces hydrogen sulfide and this can prevent bacterial colonisation but the scientists in this article believe that low levels of taurine can be the issue, resulting in an insufficient level of hydrogen sulfide to prevent colonisation.

There's probably more to it than just that though. Bile composition has effect on gastric motility and taurine makes bile more hydrophilic (water soluble). Ursodeoxycholic acid which has similar effect has been found to be beneficial for SIBO in those with functional dyspepsia (FD), and there's significant crossover in symptoms between IBS and FD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7284594/
https://acpinternist.org/archives/2...disorders-become-clearer-as-models-emerge.htm

 

[Pyrrhus]

Here's another interesting paper, which raises the possibility that dysautonomia of the ileocecal valve (ileo-cecal reflux) might also contribute to SIBO.

The ileocecal valve allows food to pass from the small intestine into the large intestine, while preventing bacteria from flowing backwards from the large intestine into the small intestine. (Although bacteria is normally found in the large intestine, bacteria are usually not found in the small intestine.) Like other valves in the gastrointestinal system, the ileocecal valve is controlled by the autonomic nervous system.

Ileocecal valve dysfunction in small intestinal bacterial overgrowth: A pilot study (Miller et al., 2012)
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3520169/pdf/WJG-18-6801.pdf

Excerpt:

The literature regarding the ileocecal valve (ICV) and its relationship to small intestinal bacterial overgrowth (SIBO) is limited. [...] Surgical removal of the ICV maximizes reflux ultimately leading to bacterial overgrowth.
[...]
In the current study, we aimed to explore whether patients with a positive lactulose breath test (indicative of SIBO) may have an incompetent ICV leading to reflux of [large intestine] contents into the small intestine[10]. To test this hypothesis we measured pressures within the ICV during cecal distension and compared these pressures with the results of lactulose breath tests.

 

[motorhead]

@Pyrrhus can I ask your opinion on this interview on SIBO: https://www.thesibodoctor.com/2017/12/20/sibo-and-hydrogen-sulfide/#dr-greg-nigh

 

[Pyrrhus]

@Pyrrhus can I ask your opinion on this interview on SIBO: https://www.thesibodoctor.com/2017/12/20/sibo-and-hydrogen-sulfide/#dr-greg-nigh

The interview talks about hydrogen sulfide, which is a gas that can be naturally produced by bacteria in the intestines, giving farts their "rotten egg" odor. If inhaled, hydrogen sulfide can be harmful, but I don't know if the amount of hydrogen sulfide normally produced in the intestines is sufficient to cause any harm.

I don't think that hydrogen sulfide is tested for in standard SIBO breath tests - perhaps it should be. But its strong "rotten egg" odor should be easily recognizable.

They also talk about so-called "sulfur intolerance", which is a concept that doesn't make much sense as sulfur is not a molecule, just an atom. The human body is full of natural molecules that happen to contain sulfur and our diet is full of important nutrients that happen to contain sulfur. We simply couldn't live without these important nutrients that happen to contain sulfur.

In any case, it's not directly relevant to dysautonomia or gastrointestinal motility.

 

[motorhead]

I was more curious about those patients' remission without intervening on the autonomic nervous system, I mean that approach isn't targeting motility.
By sulfur intolerance you mean sulfur sensitivity such as having a reaction to eating eggs for example? That's a known reaction afaik.

 

[Pyrrhus]

I was more curious about those patients' remission without intervening on the autonomic nervous system, I mean that approach isn't targeting motility.

I'm sorry, I didn't see that part of the transcript. But yes, SIBO can certainly be treated without targeting motility. The problem is that it might return after the treatment...

you mean sulfur sensitivity such as having a reaction to eating eggs for example?

There are a few ways that people might have bad reactions to foods which they might characterize as "sulfur intolerance":

1. First, there's sulfite sensitivity, where about 1% of the population have allergic reactions to certain added preservatives, which are not naturally found in food.
2. Second, as mentioned in the interview, there is the idea that certain bacteria (or archaea) in the intestines might produce excessive hydrogen sulfide in response to ingesting methionine or cysteine, which are the two amino acids that happen to contain sulfur. I don't think there has been much research into this idea.
3. Third, if you have a glutathione deficiency or methylfolate trap in some key cells, you may experience start-up effects when consuming methionine or cysteine, epecially in the form of supplemental N-acetyl-cysteine (NAC). For me, these start-up effects were almost intolerable, but faded after about 8-12 weeks of supplementing with NAC: https://forums.phoenixrising.me/threads/glutathione-causing-anxiety-irritability.81246/#post-2304206

But none of these phenomena could technically be called "sulfur intolerance", although I certainly see why it is a tempting phrase to use. A better phrase might be "methionine/cysteine sensitivity".

Here's a good link that discusses this further:
https://deannaminich.com/is-there-really-such-a-thing-as-sulfur-intolerance/

Hope this helps.