A potential mediator and treatment target.
What is perhaps more surprising is that the presence of glucocorticoids in the ENS was associated with a delay in colonic transit time. This delay appears to be due to a decrease in mature neurons and an increase in immature neurons, presumably because of increased cell death due to greater susceptibility to injury. Mature neurons are responsible for the production of acetylcholine, a neurotransmitter that is critical for muscle movements and contractions in the intestinal tract.
To put it a bit more simply, as concentrations of stress hormones accumulate in the ENS, it drives a process through which mature neurons are prematurely replaced. These prematurely replaced neurons include those that produce acetylcholine, a neurotransmitter that helps stimulate the muscles to move waste through the colon. Consequently, a decrease in acetylcholine leads to delays in colonic transit times.
Finally, an investigation using human subjects found an association between stress and dysmotility, as well as an association linking elevated levels of perceived stress. This leads to increased levels of specific proteins, inflammatory markers, and inflammatory bowel disease severity. This indicates that psychological stress contributes to symptomology in those who are susceptible, and sets the stage for severe flareups of intestinal inflammation.
It is becoming increasingly clear that problematic inflammation doesn’t respect our neatly contrived definitions separating the CNS and PNS. As thestudy shows, psychological stress is not merely a subjective phenomenon; it can and does have a significant impact on one’s mental health, gut health, and overall health.
If reducing the perception of stress can reduce the levels of circulating glucocorticoids, then it’s possible that psychiatry and psychology can help patients with symptom management through the use of stress mitigation techniques. These techniques may include
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