Psychosocial factors influence gut physiology, the symptom experience, health behavior, and outcome. The gut is physiologically responsive to emotional and environmental stimuli. Research has shifted from etiology that is a unidirectional relationship between psychosocial events and gastrointestinal function to the reciprocal interaction of physiologic and psychosocial processes in these conditions. A unifying hypothesis to explain the FGIDs is that they result from dysregulation of brain—gut neuroenteric systems, much like anovulatory bleeding is a dysregulation of hypothalamic— pituitary—ovarian function rather than a disease of these structures. The brain—gut neurotransmitters associated with these symptoms are not site specific; they have varied influences on gastrointestinal, endocrine and immune function, and human behavior.
The role of the central nervous system in modulating motility is supported by evidence that: (1) the motility disturbances in FGID disappear during sleep2; (2) the frequency of the migrating motor complex decreases and propagating velocity increases progressively with alertness and arousal; (3) patients with FGID have a different electroencephalography sleep pattern than healthy subjects; and (4) positron emission tomography (PET) studies suggest that the CNS response to rectal distension is altered in patients with FGID compared with controls. The varied influences of environmental stress, thought, and emotions on gut function help explain the variation in symptoms of patients with these disorders. Like patients with other medical disorders patients with FGID, specially Irritable bowel disease (IBS) have higher trait anxiety and neuroticism scores than people without health problems or the non-clinical population with similar gastrointestinal complaints.
The Karolinska Scales of Personality (KSP) inventory has been used for explore and understand the complicated relationships between individual differences in behavior and FGID symptom which might help to identify individuals at risk and understand interaction between symptom-patterns and personality.