In my previous blogposts I have hypothesized that activation of TRPA1 is somehow involved in ME comorbidities. And I have found research about central fatigue and serotonin:
Transient Receptor Potential in Multiple Chemical Sensitivity
TRPA1/TRPV4/PAR in inflammation/pain
TRPA1 involvement in autonomic dysfunction in ME?
ME, neuropathy, TRPA1
Exercise and...TRPA1 and TRPV1
Mitochondrial dysfunction - influence on TRPA1
TRPA1, Hypoxia and ME?
Central fatigue and serotonin
Now I will continue my speculations to find connections in the biochemistry and ME comorbidities:
Gastroparesis, also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for a longer time than normal.
Gastric emptying is slow in chronic fatigue syndrome
Many patients with gastroparesis have had their gallbladders removed. Cholecystectomy is the surgical removal of the gallbladder.
A study showed that "Patients with cholecystectomy had more comorbidities, particularly chronic fatigue syndrome, fibromyalgia, depression, and anxiety."
What is the biochemistry behind delayed gastric emptying? Could TRPA1 be involved?
Serotonin (5-hydroxytryptamine (5-HT) is a neurostransmitter. Biochemically derived from tryptophan, serotonin is primarily found in the gastrointestinal tract. Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the alimentary canal (gut), where it is used to regulate intestinal movements.
TRPA1 is highly expressed in human and rat enterochromaffin (EC) cells, and TRPA1 agonists enhance the release of serotonin from EC cells in vitro. Reference
And now my favorite part: TRPA1 agonists delay gastric emptying in rats through serotonergic pathways
And this one: TRPA1 regulates gastrointestinal motility through serotonin release from enterochromaffin cells
This is one of those moments where I think science is beautiful! :-))