Role of stress in functional gastrointestinal disorders. Evidence for stress-induced alterations in gastrointestinal motility and sensitivity.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing mechanistic animal research and observational human literature
PubMed 11752838 · doi:10.1159/000050681
What was done
This narrative review synthesized experimental animal and human literature on the physiological effects of acute psychological and physical stress on gastrointestinal motility and visceral sensitivity, focusing on irritable bowel syndrome and underlying pathways involving corticotropin-releasing factor, serotonin, and mucosal mast cells.
What was found
The abstract reports no numerical estimates or statistical effect sizes. It reports qualitative patterns: acute stress consistently inhibits gastric emptying and accelerates colonic transit, with exaggerated colonic motor responses observed in irritable bowel syndrome. Stress-induced visceral hypersensitivity is linked to central corticotropin-releasing factor (CRF-1 and CRF-2 receptors), amygdala pathways, peripheral serotonin action via 5-HT3 receptors, and mucosal mast cell activation.
Why it matters
It outlines how stress-induced neuroendocrine signaling directly modulates gut motility and sensory thresholds, providing a physiological basis for stress-related exacerbations in functional gastrointestinal disorders.
Limits
The abstract provides no quantitative data, sample sizes, or systematic search methodology. Direct human data clarifying whether altered motility responses stem from autonomic imbalance versus baseline stress susceptibility remain scarce, and much of the granular receptor mechanism is derived from animal studies.
Cited by
- supports Acute stressful thoughts evoking fear or anxiety cause stomach motility to slow down while simultaneously speeding up colonic motility.