Vanuytsel · Gut 2014 · controlled experimental crossover study · n=36

Psychological stress and corticotropin-releasing hormone increase intestinal permeability in humans by a mast cell-dependent mechanism.

Cited 608 times in the scientific literature.

Level 3 - non-randomized controlled study

Controlled experimental human crossover challenge studies without reported randomization details in the abstract

PubMed 24153250 · doi:10.1136/gutjnl-2013-305690 · record verified 2026-08-28

What was done

Small intestinal permeability was measured using a 2-hour urinary lactulose-mannitol excretion test across two human challenge experiments. In Study 1, 23 healthy volunteers were tested across four conditions: baseline control, indomethacin (positive control), public speaking stress, and anticipation of electroshocks, alongside salivary cortisol measurements. In Study 2, 13 healthy volunteers were evaluated across five conditions: control, pretreatment with the mast cell stabilizer disodium cromoglycate (DSCG), administration of corticotropin-releasing hormone (CRH), DSCG plus CRH, and DSCG plus public speech.

What was found

Indomethacin increased the lactulose-mannitol ratio from 0.030 ± 0.022 to 0.071 ± 0.040 (p < 0.0001). Public speaking increased permeability to 0.059 ± 0.040 (p < 0.01), whereas anticipation of electroshocks did not. Salivary cortisol rose only after public speaking, and subgroup analysis showed the permeability increase was present only in subjects with a significant elevation of cortisol. CRH administration increased the lactulose-mannitol ratio from 0.028 ± 0.009 to 0.042 ± 0.021 (p = 0.02). Pretreatment with DSCG blocked both the CRH-induced and public speech-induced increases in permeability.

Why it matters

This study provides direct experimental evidence in humans that acute psychological stress elevates intestinal permeability via CRH and mast cell activation. This helps explain the mechanistic bridge between central nervous system stress and gut barrier dysfunction relevant to irritable bowel syndrome and inflammatory bowel disease.

Limits

Sample sizes were very small (23 and 13 participants), and the study tested acute laboratory stressors in healthy volunteers rather than chronic real-world stress or patients with clinical bowel disease. The abstract does not report whether sequence allocation was randomized or blinded.

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