Psycho-neuro-endocrine-immune modulation through
the brain-gut axis likely has a key role in the pathogenesis
of inflammatory bowel disease (IBD). The brain-gut
axis involves interactions among the neural components,
including (1) the autonomic nervous system, (2)
the central nervous system, (3) the stress system (hypothalamic-pituitary-adrenal
axis), (4) the (gastrointestinal)
corticotropin-releasing factor system, and (5) the
intestinal response (including the intestinal barrier,
the luminal microbiota, and the intestinal immune
response). Animal models suggest that the cholinergic
anti-inflammatory pathway through an anti–tumor
necrosis factor effect of the efferent vagus nerve could
be a therapeutic target in IBD through a pharmacologic,
nutritional, or neurostimulation approach. In
addition, the psychophysiological vulnerability of patients
with IBD, secondary to the potential presence of
any mood disorders, distress, increased perceived
stress, or maladaptive coping strategies, underscores
the psychological needs of patients with IBD. Clinicians
need to address these issues with patients because
there is emerging evidence that stress or other
negative psychological attributes may have an effect
on the disease course. Future research may include
exploration of markers of brain-gut interactions, including
serum/salivary cortisol (as a marker of the
hypothalamic-pituitary-adrenal axis), heart rate variability
(as a marker of the sympathovagal balance), or
brain imaging studies. The widespread use and potential
impact of complementary and alternative medicine
and the positive response to placebo (in clinical
trials) is further evidence that exploring other psychointerventions
may be important therapeutic adjuncts
to the conventional therapeutic approach in IBD.
the brain-gut axis likely has a key role in the pathogenesis
of inflammatory bowel disease (IBD). The brain-gut
axis involves interactions among the neural components,
including (1) the autonomic nervous system, (2)
the central nervous system, (3) the stress system (hypothalamic-pituitary-adrenal
axis), (4) the (gastrointestinal)
corticotropin-releasing factor system, and (5) the
intestinal response (including the intestinal barrier,
the luminal microbiota, and the intestinal immune
response). Animal models suggest that the cholinergic
anti-inflammatory pathway through an anti–tumor
necrosis factor effect of the efferent vagus nerve could
be a therapeutic target in IBD through a pharmacologic,
nutritional, or neurostimulation approach. In
addition, the psychophysiological vulnerability of patients
with IBD, secondary to the potential presence of
any mood disorders, distress, increased perceived
stress, or maladaptive coping strategies, underscores
the psychological needs of patients with IBD. Clinicians
need to address these issues with patients because
there is emerging evidence that stress or other
negative psychological attributes may have an effect
on the disease course. Future research may include
exploration of markers of brain-gut interactions, including
serum/salivary cortisol (as a marker of the
hypothalamic-pituitary-adrenal axis), heart rate variability
(as a marker of the sympathovagal balance), or
brain imaging studies. The widespread use and potential
impact of complementary and alternative medicine
and the positive response to placebo (in clinical
trials) is further evidence that exploring other psychointerventions
may be important therapeutic adjuncts
to the conventional therapeutic approach in IBD.
Last edited by a moderator: