Disorders of brain-gut interaction

The wiki’s cardiac bias has a cost, and this page is where it shows. Nearly all the interoceptive evidence held here is cardiac, for methodological reasons Petzschner et al. make explicit (the heart is the one internal signal fast and countable enough to build a task around). The gut is the other major interoceptive channel, it has its own clinical literature, and Bonaz et al. (2021) — with Emeran Mayer, whose programme this is — bring it in.

IBS as the exemplar

Irritable bowel syndrome is “the most common disorder of brain–gut interactions,” affecting 5–20% of people worldwide with significant socioeconomic burden. In the absence of generally agreed biomarkers or overt organic pathology it is still diagnosed by symptom criteria: abdominal pain associated with defecation and/or accompanied by a change in bowel habits.

The reframing from “functional gastrointestinal disorder” to “disorder of brain-gut interaction” is not cosmetic. It asserts that the condition is a failure of a regulatory loop — and therefore has a mechanism — rather than a symptom cluster left over after organic disease is excluded. See functional-disorders for that distinction and its history.

The biopsychosocial formulation established a close link with stress and emotion (Pellissier & Bonaz 2017), and altered connectivity in brain networks for attention, emotion and pain processing is implicated in the maladaptive gut-brain interactions producing visceral pain, altered bowel habits, raised stress reactivity and anxiety.

The discrepancy profile, reached independently

The finding on this page that matters most for the rest of the wiki:

Deficits in interoceptive processing increase the risk for IBS: IBS patients typically score high on subjective measures of interoceptive sensibility, consistent with a strong focus on their gastrointestinal symptoms and likely indicative of altered functional processing within interoceptive brain networks.

That is the accuracy-low / sensibility-high signature — impaired processing paired with elevated self-reported bodily attention — which the wiki holds under ITPE on the strength of Garfinkel’s autism and anxiety work, and which functional-disorders reports for functional motor disorders. Gastroenterology is a separate measurement tradition with separate instruments and separate patients, and it lands on the same shape.

This is worth recording as convergent evidence, with one honest caveat: the “deficits in interoceptive processing” here are inferred from a mixed literature (Fournier et al. 2020; Longarzo et al. 2017 on interoceptive awareness and functional connectivity), not from a heartbeat task, so the two profiles are the same description arrived at with different measures rather than the same measurement replicated. That is a strength for generality and a weakness for precision. See interoceptive-taxonomy.

Where the signals come from

Two channels feed this loop, and only one of them is neural in the ordinary sense:

• Vagal and spinal afferents from the gut, converging with all other interoceptive traffic at the NTS — the standard CAN route.
• The microbiota-gut-brain-axis — bacterial metabolites acting on enteroendocrine cells and directly on vagal afferent receptors. Dysbiosis is hypothesized as an IBS mechanism, though Bonaz et al. concede establishing causality “is elusive” and microbiome-targeted therapy (prebiotics, probiotics, synbiotics, antibiotics) has “generally mixed results.”

Overlap, and what it suggests

Two overlaps in the review are suggestive rather than conclusive but worth keeping:

• Around 60% of women with pelvic floor disorders present with overlapping bladder and bowel symptoms, and experimental bladder filling and rectal distension both activate the insula (Halani et al. 2020) — offered as a partial anatomical account of why visceral symptom syndromes co-occur across organs that have little else in common.
• IBS sits inside the review’s larger comorbidity cluster with chronic-pain, fibromyalgia, anxiety and depression, with early adversity as the shared upstream determinant. The rat maternal-deprivation model is the mechanistic case: one early perturbation, and the adult animal shows visceral hypersensitivity, mucosal dysfunction, colitis susceptibility, raised HPA response and anxiety together.

Why this page is thin, and should be

The wiki holds no primary gastroenterology source. Everything here comes through one review section written by the two authors whose programme it is — which is a reason to hold the framing loosely, not a reason to omit it. If a Mayer or Bonaz primary paper reaches raw/, this page should be rewritten first-hand. See emeran-mayer, bruno-bonaz.