Irritable Bowel Syndrome (IBS): Summary of discussions

[Pyrrhus]

Since Irritable Bowel Syndrome (IBS) is a common comorbidity/symptom of ME, I thought I'd start a thread to try to summarize discussions on IBS.

First, note that IBS is not to be confused with Inflammatory Bowel Disorder (IBD), a separate diagnosis based on diagnostic markers of inflammation.

Many people have different ideas about what IBS is and what the symptoms are, so I'll first summarize the main diagnostic criteria used to diagnose IBS:

• The Rome Criteria are the diagnostic criteria used to diagnose IBS. These criteria focus on the principal symptom of abdominal pain or discomfort and how the pain or discomfort changes with defecation. (Although the latest version of the criteria removed the word "discomfort" as it seemed too ambiguous.)

• IBS-C vs. IBS-D vs. IBS-M: The Rome Criteria also looks at the symptoms of constipation/gastroparesis versus diarrhea/cramping. If the IBS mainly consists of constipation/gastroparesis, it is referred to as "constipation-predominant IBS" or IBS-C. If the IBS mainly consists of diarrhea/cramping, is is referred to as "diarrhea-predominant IBS" or IBS-D. If the IBS alternates between IBS-C and IBS-D, it is referred to as "mixed IBS" or IBS-M.

 

[Pyrrhus]

Here is a discussion that looks at the overlap between ME and IBS:


CFS & IBS? (2014)
https://forums.phoenixrising.me/threads/cfs-ibs.31497/

Anyway, it seems like there's some confusion over the relationship between CFS and IBS. For example, some resources say "exclude IBS" when diagnosing CFS, which implies you can't have CFS if you have IBS. However other resources list IBS (and its pain) as a symptom of CFS, implying you can definitely have both.

So do I have CFS? If so, do I have IBS and CFS or IBS because of CFS?

I am not quite sure what the CDC mean by "irritable bowel" in their definition of CFS. There is no such medical condition as irritable bowel, but there is a medical condition called irritable bowel syndrome (IBS).

IBS and ME/CFS are independent conditions, and you can have either on their own, or both together.

However, although IBS is not part of ME/CFS, there is a high statistical prevalence of IBS in ME/CFS patients (ie, IBS is a common comorbidity of ME/CFS). Studies of IBS among patients with chronic fatigue syndrome have reported a prevalence ranging from 35-92%.†

 

[Pyrrhus]

Here is a discussion of a study that suggested that autonomic dysfunction (dysautonomia) could cause IBS:


"Is there any association between irritable bowel syndrome subgroups and autonomous dysfunction" (2016)
https://forums.phoenixrising.me/thr...e-subgroups-and-autonomous-dysfunction.44302/

http://www.ncbi.nlm.nih.gov/pubmed/27097952
Eur Rev Med Pharmacol Sci. 2016 Apr;20(7):1315-22.
Is there any association between irritable bowel syndrome subgroups and autonomous dysfunction.
Yildirim AE1, Korkmaz M, Altun R, Sandikçi SC, Ocal S, Selçuk H.

OBJECTIVE:
Irritable bowel syndrome (IBS) is a common functional intestinal disorder. Although there are marked improvements in the conceptualization of IBS pathophysiology in brain-intestinal interaction disorder, there is no definite consensus in the role of autonomic dysfunction (AD) in disease development and symptom progression. The aim of this study was to evaluate autonomous dysfunction in IBS subgroups.

PATIENTS AND METHODS:
A total of 50 patients and 49 healthy controls were included. IBS subgroup types and demographic characteristics of patients were recorded. AD investigations were made up of parasympathetic and sympathetic tests.
[...]
RESULTS:
Three parasympathetic and one sympathetic autonomic neuropathy tests were found significantly different (respectively p < 0.001, p = 0.001, p = 0.016, p < 0.001, p = 0.375). There were significant decreases in parasympathetic tests in IBS-C patients; however, in the control group, there were significant decreases in sympathetic tests when compared with IBS-D patients (p < 0.001). The severity of AD in IBS-C subgroup was more pronounced than the IBS-D subgroup. No correlation was determined between dysautonomia and disease duration (p > 0.05).

CONCLUSIONS:
AD may have a role in IBS pathophysiology. Deterioration of the autonomous system not only affects the gastrointestinal system but also other systems including the cardiovascular system. Patients may also be susceptible to more diverse problems.

Thanks, I found that quite interesting as I have extremely severe autonomic dysfunction (its causing me to end up in hospital a lot) and have had severe IBS-C too (I had my bowel prolapse due to it). So its not surprising for me to read that these things correspond

 

[Pyrrhus]

Here is a discussion of an article that suggests that autonomic neuropathy (dysautonomia) could lead to a diagnosis of IBS:


Autonomic and peripheral neuropathy with reduced intraepidermal nerve fiber density can be observed in patients with gastrointestinal dysmotility (2020)
https://forums.phoenixrising.me/thr...ents-with-gastrointestinal-dysmotility.79113/

Autonomic and peripheral neuropathy with reduced intraepidermal nerve fiber density can be observed in patients with gastrointestinal dysmotility
Dec 2019

Abstract

Neuropathy should be considered as a possible etiological factor in patients with severe gastrointestinal symptoms, without signs of disease on routine investigations. Examinations of the autonomic and peripheral nervous systems may be helpful to select the patients who should be investigated with full‐thickness intestinal biopsy, and to give appropriate care.


1 INTRODUCTION

Severe gastrointestinal (GI) dysmotility in the form of chronic intestinal pseudo‐obstruction (CIPO) and enteric dysmotility (ED) are rare diseases, which are difficult to diagnose.1 Enteric neuropathy, leading to dysmotility, is seldom studied, since there are few centers available for evaluation of GI motility. Furthermore, there are difficulties to get access to myenteric plexus of the enteric nervous system, and the histopathological examination of tissue samples is time‐consuming.

Subsequently, most patients with GI dysmotility and pain are diagnosed to have irritable bowel syndrome (IBS), or the neuropathy diagnosis is delayed for several years.2, 3

I suspect I have some ancient SFN with early involvement of small autonomic fibers that spread progressively to small sensory fibers to muscle and that small sensory fibers to skin got involved only recently, which could explain why I was not aware of this disease before I suddenly felt the tingling/numbness/warm in my hands and feet.
It's only an hypothesis though, as I have no idea if the course of the SFN can go down this progressive road!
But it would match with my progressive symptoms, starting in the stomach/gut dyscomfort, spreading to muscles/pain then spine/pain, then arriving many years later to sensory skin disturbance….

 

[Pyrrhus]

Here is a discussion of a study that found that a genetic defect led to poor regulation of gastrointestinal motility in a small subset of IBS patients:


Mayo Clinic Researchers Find Genetic Clue to Irritable Bowel Syndrome (2014)
https://forums.phoenixrising.me/thr...netic-clue-to-irritable-bowel-syndrome.29085/

Mayo Clinic Researchers Find Genetic Clue to Irritable Bowel Syndrome

ROCHESTER, Minn. — March 20, 2014 —Is irritable bowel syndrome (IBS) caused by genetics, diet, past trauma, anxiety? All are thought to play a role, but now, for the first time, researchers have reported a defined genetic defect that causes a subset of IBS. The research was published in the journal Gastroenterology.

Researchers found that patients with a subset of IBS have a specific genetic defect, a mutation of the SCN5A gene. This defect causes patients to have a disruption in bowel function, by affecting the Nav1.5 channel, a sodium channel in the gastrointestinal smooth muscle and pacemaker cells.

Researchers studied the sodium channel of 584 people with IBS and 1,380 control subjects. The analysis demonstrated that a defect in the SCN5A gene was found in 2.2 percent of IBS patients. The results were confirmed in a genome-wide association study and replicated in 1,745 patients in four independent cohorts of patients with IBS and control subjects.

The Farrugia et al (2014) study in question is this one:

Loss-of-function of the Voltage-gated Sodium Channel NaV1.5 (Channelopathies) in Patients with Irritable Bowel Syndrome

The study concluded that: "About 2% of patients with IBS carry mutations in SCN5A. Most of these are loss-of-function mutations that disrupt NaV1.5 channel function. These findings provide a new pathogenic mechanism for IBS and possible treatment options."

2% of IBS patients seems like a pretty small IBS subgroup. If you have IBS, it's a 1 in 50 chance you are in this subgroup.

Incidentally, this earlier study by Farrugia et al (2009) concluded that: "the G298S-SCN5A missense mutation caused a marked reduction of whole cell Na+ current and loss of function of Nav1.5, suggesting SCN5A as a candidate gene in the pathophysiology of IBS."

 

[Pyrrhus]

Possibly related discussion:

Is SIBO caused by dysautonomic gastrointestinal motility?
https://forums.phoenixrising.me/thr...dysautonomic-gastrointestinal-motility.81362/

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...

 

[Pyrrhus]

Another study mentioning dysautonomia:

Pattern Of Dysautonomia In Patients With Functional Gastrointestinal Disorders (Ruffle et al., 2015)
https://doi.org/10.1016/j.autneu.2015.07.208

Background & Aims:
Functional gastrointestinal disorders (FGIDs) are a major health problem, and include disorders such as irritable bowel syndrome. Previous research has shown that patients with FGIDs have abnormal neuromuscular and brain-gut interactions. The autonomic nervous system (ANS) encompasses numerous integrations within the gut, and thus is thought implicated in these disorders. Our study aim was therefore to characterize the pattern of autonomic disturbances in FGIDs using validated neurophysiological techniques.

Methods:
29 patients with a diagnosis of a FGID (21 female, mean age 40 years, range 13-69) were screened for autonomic dysfunction or ‘dysautonomia’ using target-organ orientated neurophysiological examinations of the ANS. The brainstem was examined at rest by monitoring cardiac vagal tone (CVT) using validated NeuroScope methods. Similarly, respiratory modulation of cardiovagal motor neurons, baroreflex central gain and baroreceptor outputs were other parasympathetic functions measured using these methods. Cardioaccelerator function, vasoconstrictor function in muscles and vasoconstrictor function in the splanchnic vascular bed were the sympathetic functions measured. ANS dysfunction was identified by comparison with published laboratory standards.

Results:
Numerous autonomic disturbances amongst our patient cohort were demonstrable. 93% of patients had sympathetic dysautonomia in splanchnic vasoconstriction, 83% had dysautonomia of sympathetic cardioaccelerator tone, 82% had dysautonomia of resting cardiac sensitivity to the baroreflex and 72% had dysautonomia to carotid vasodepressor function.

Conclusion:
Our results suggest that the FGIDs are likely to be associated with autonomic dysfunction in the gut.

 

[Pyrrhus]

And a newer study, also mentioning dysautonomia:

Dysautonomia in children with irritable bowel syndrome and inflammatory bowel disease (Geljic et al., 2021)
http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.227

Abstract
To evaluate the presence of autonomic nervous system abnormalities (ANS) in children with irritable bowel syndrome (IBS) and quiescence inflammatory bowel disease (IBD) comparing to controls.

Consecutive children with quiescence IBD, IBS and aged and sex matched healthy controls (HC) were referred for the evaluation of dysautonomia.

N=24, mean age 15.7 yrs, 16 females; IBS: N=18, mean age 14.8 yrs, 9 females; HC: N=18, mean age 14.2 yrs, 9 females). Dysautonomia was evaluated subjectively with the Composite Autonomic Symptom Score (COMPASS 31), and objectively with the following autonomic tests: heart rate (HR) and blood pressure (BP) responses to the Valsalva maneuver, heart rate response to deep breathing (RSA), blood pressure response to passive tilt, and quantitative sudomotor axon reflex test (QSART). Additionally, heart rate variability (HRV) analysis was performed by Kubios HRV 2.2. Following HRV parameters were compared between the groups in supine and tilted positions: total power of low (LF) and high frequency domain components (HF), normalized HF (HFnu), low-to-high frequency ratio (LF/HF), standard deviation of normal-to-normal intervals (SDNN) and percentage of successive RR intervals that differ by more than 50 ms (PNN50).

Children with IBS scored highest on COMPASS-31, followed by patients with IBD and HC (median 15.6, 8.7 and 2.3, respectively, p<0.001). Similar differences were observed in the orthostatic intolerance and gastrointestinal domains of the COMPASS-31. No differences between groups were observed in HR and BP responses to the Valsalva maneuver, RSA and BP response to passive tilt. Children with IBS had higher sweat volumes on proximal lower leg on QSART (median IBD 0.9, IBS 1.5, HC 0.8 µL; p=0.039).

There was no difference in the HRV parameters between groups. However, children with IBS had significantly higher drop in LF (p=0.01) and SDNN (p=0.03) and lowest drop in PNN50 (p=0.01) during tilt test compared to children with IBD and HC.

We found significant subjective and objective ANS abnormalities in children with IBS compared to children with IBD and HC.

 

[ljimbo423]

Previous research has shown that patients with FGIDs have abnormal neuromuscular and brain-gut interactions. The autonomic nervous system (ANS) encompasses numerous integrations within the gut, and thus is thought implicated in these disorders.

I wonder if dysautonomia might be why SIBO is so hard to treat for many people. Sibo specialists often talk about the underlying cause of SIBO being poor migrating motor complex.

 

[YippeeKi YOW !!]

@Pyrrhus
I really value the various threads you've posted, with summaries of links to issues affecting, or affected by, ME/CFS .... you seem to have bravely shouldered the slack left after @PatJ left us, and you post thoughtful, valuable information in one single place that would take some of us, depending on our severity, a verrrrrrrry long time to dig up on our own.

Thank you !!! You're a gem !!!!

 

[Pyrrhus]

Thank you !!! You're a gem !!!!

Aw shucks... thanks for the thanks!

 

[YippeeKi YOW !!]

Aw shucks... thanks for the thanks!

 

[Rufous McKinney]

you post thoughtful, valuable information in one single place that would take some of us, depending on our severity, a verrrrrrrry long time to dig up on our own.

Yes, incredibly grateful to you @Pyrrhus for the remarkable job you've been doing keeping our threads up to date on important research, helping us understand it, summarizing it.

I just cannot tell you how much I value this!

And others, who keep topics updated, and hang in there despite our many challenges. Thank you thank you.

 

[Pyrrhus]

And here is an interesting discussion about possible overlap between IBS and food intolerances:

Histamine as an inducer of symptoms in IBS
https://forums.phoenixrising.me/threads/histamine-as-an-inducer-of-symptoms-in-ibs.88349/