Stress and the gastrointestinal tract.
Level 5 - mechanism / opinion, no new human data
Narrative review describing physiological mechanisms and animal models without systematic methodology.
PubMed 15740474 · doi:10.1111/j.1440-1746.2004.03508.x
What was done
This is a narrative review outlining the physiological, neuroendocrine, and cellular mechanisms through which acute and chronic stress impacts gastrointestinal function via the bidirectional brain-gut axis.
What was found
The abstract provides a qualitative overview of biological mechanisms without reporting quantitative human data or effect sizes. Corticotropin-releasing factor (CRF) acts as a primary central mediator: CRF-R1 stimulates colonic motor activity, whereas CRF-R2 slows gastric emptying. Mechanistically, stress increases intestinal permeability to large antigenic molecules, triggers mast cell degranulation, depletes colonic mucin, reverses small bowel water and electrolyte absorption via cholinergic pathways, and increases vulnerability to colonic inflammation.
Why it matters
It outlines the biological pathways linking central nervous system stress circuits to peripheral gut dysfunction, helping frame the pathophysiology of conditions like functional bowel disorders and inflammatory bowel disease.
Limits
The abstract describes a narrative review reliant largely on preclinical and animal model mechanisms rather than primary human clinical trial data. No systematic search criteria, sample sizes, or numerical effect estimates are provided.
Cited by
- supports Acute stressful thoughts evoking fear or anxiety cause stomach motility to slow down while simultaneously speeding up colonic motility.