The neurobiology of stress and gastrointestinal disease

Learned Fear of Gastrointestinal Sensations in Healthy Adults

“…Together, these results convincingly demonstrate that fear for innocuous gastrointestinal sensations can arise from temporal contingencies between gastrointestinal events, giving rise to associative learning. This in turn can be linked to earlier hypotheses on the generation of gastrointestinal symptom-specific fear, which attribute an important role to associative learning processes by which initially relatively 'neutral' bodily sensations start provoking fear through activation of fear circuits in the brain [10][11][12] .…”

“…interoceptive, this is referred to as interoceptive conditioning 9 . Homoreflexive interoceptive fear conditioning is an interesting candidate mechanism in the development and maintenance of gastrointestinal symptom-specific fear, but to the best of our knowledge, this has not been directly studied [10][11][12] .…”

A sustained hypothalamic–pituitary–adrenal axis response to acute psychosocial stress in irritable bowel syndrome

“…Taken together, this indicates a total greater cortisol output in response to acute psychosocial stress in IBS that is largely reflective of both a failure to adequately shut off the HPA axis following stress and a generalized elevation in HPA axis activity in IBS, rather than a difference in the intensity of the response. Despite the well-recognized role of HPA axis dysfunction in the pathophysiology of IBS (Mayer, 2000), results of HPA challenge tests have been inconsistent between studies, with many reports that patients with IBS do not differ in the neuroendocrine response to various stressors including a dichotomous listening task (Murray et al 2004), the Stroop task (Posserud et al 2004) and a short (3-min) unstandardized public-speaking task (Elsenbruch et al 2006). However, in accordance with our findings, it has previously been shown that pharmacological challenge of the HPA axis using a corticotrophin-releasing factor (CRF) infusion, in a large well-characterized and carefully phenotyped population of patients with IBS, caused an exaggerated release of serum adrenocorticotrophic-releasing hormone (ACTH) and cortisol, with a normal response to the dexamethasone (DEX) suppression test (Dinan et al 2006).…”

Psychological Comorbidity and Chronic Heartburn: Which Is the Chicken and Which Is the Egg?

“…Vital exhaustion, a measure of sustained stress, is the most common parameter that correlates with heartburn [15]. Furthermore, prolonged stress can lead to hypervigilance and thus the over-reporting of symptoms [16]. Acute stress can exacerbate heartburn symptoms by enhancing perceptive responses to intra-esophageal acid [15].…”