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SaltZookeepergame691 t1_jddc88t wrote

That’s not what this study is suggesting. And we already know IBS is a syndrome related to disordered gut-brain interaction - that’s why the umbrella terminology for these conditions is literally “disorders of gut-brain interaction”.

This study shines a closer light on the specific cellular mechanisms that might be involved in IBS discomfort/pain, which provides targets for specific therapies at the level of the gut - they are specifically looking at hyperactivation of enterochromaffin cells, which are neuronal cells embedded in the gut wall, that then signal to gut neurons and ultimately produce visceral pain reactions.

Edit: the serotonin signalling modulator they use as proof-of-principle in the model is alosetron, which is only used in very severe IBS in women (it was withdrawn from all other indications due to side effects). Trust me - they are not suggesting that everyone take systemic alosetron, they are not stupid:

>Data presented here also support a role for local, rather than systemic serotonergic signalling at the interface between EC cells and mucosal afferents, consistent with recent suggestions that primary afferent nerve fibres form synapse-like associations with enteroendocrine cells. Alosetron, which is approved for the treatment of severe IBS with diarrhoea in women39, has been proposed to exert its analgesic effect centrally or through inhibition of high-threshold nociceptors in the gut wall. We propose an alternative or further mechanism to account for this sex-biased analgesic effect, namely one involving modulation of serotonergic signalling at EC cell–mucosal afferent circuits.


Former_Maybe_8437 t1_jdeb7xv wrote

> And we already know IBS is a syndrome related to disordered gut-brain interaction

I respectfully have to take issue with this statement.

We know that modulation of neurochemicals can modulate GI symptoms, and/or perception of GI symptoms in certain patients and we know that there is a connection between certain kinds of gut-brain signaling, but to say that this is the original causal mechanism behind IBS isn’t founded. It’s one proposed model of IBS, one of many.

Just proving the concept that these pathways are active in GI symptom perception doesn’t prove that this is the root cause. It merely proves that these pathways can be leveraged as potential treatments.


SaltZookeepergame691 t1_jdeezz7 wrote

You’re right that “know” is being overworked in my initial statement. But, insofar as DGBI is a broad church of mechanisms from stimuli to neuronal function to the brain, and DGBI is the terminology employed by the body defining IBS, there really aren’t any major competing theories any more.


DeathRebirth t1_jdexjvu wrote

Except that IBS is a big pot doctors throw people into when they don’t have any other easy answers. Some studies suggest a massive overlap with SIBO which really puts into question if this isn’t a mine field of misdiagnosis and lack of fundamental understanding of what’s going on in these patients.

I experienced exactly this first hand until now.


SaltZookeepergame691 t1_jdgrqm4 wrote

I agree to some extent in practice, but recent changes to diagnostic criteria (ie Rome IV, and shortly Rome V) and a shift towards positive diagnosis are reducing the number of patients defined as having IBS.

There is certainly an overlap with conditions like SIBO, but as I said to another commenter, these are mechanisms within the DGBI umbrella given the need for visceral overreactivity to convey symptoms.


Former_Maybe_8437 t1_jdexkv4 wrote

>there really aren’t any major competing theories any more.

This is false. Food intolerances, medication side effects, SIBO and motility issues are all potential underlying causes of IBS other that neurochemical imbalances.

Where is your source of a major medical body declaring that DGBI is the sole cause of IBS to the exclusion of all others?