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There is a direct association of symptoms of Irritable Bowel Syndrome (IBS) and stress.
There is the hypothalamo-pituitary-adrenal axis that plays an important role in the stress response. Stress leads to secretions of various hormones and chemical mediators from these organs that include the hypothalamus and the pituitary glands in the brain as well as the adrenal glands that lie over the kidney. The sress response is vital for living.
The response of an organism to stressors from outside is mediated by the integration of the hypothalamo-pituitary-adrenal (HPA) axis along with the sympathetic branch of the autonomic nervous system. This is supported by the immune system as well.
In the HPA axis in the hypothalamus, paraventricular nucleus neurones release corticotropin releasing factor (CRF), which stimulates anterior pituitary secretion of adrenocorticotropin hormone (ACTH). This in turn acts on the adrenal medulla, resulting in cortisol secretion into the blood circulation.
Release of CRF is dependent on input from the structures in the brain and from feedback by ACTH and cortisol circulating in blood. The production and release of CRF is therefore under multiple control systems.
It has been hypothesized that stress may play a role in exacerbations as well as onset of symptoms of IBS.
Classically IBS patients tend to have high levels of anxiety and in addition there is a considerable overlap of symptoms of IBS with other functional disorders including fibromyalgia and chronic fatigue syndrome.
These predisposed individuals may have altered central stress circuits that are triggered by external stressors resulting in the development of gut and non-intestinal symptoms.
Along with the HPA axis, the immune system also plays a role in IBS exacerbation. The persistence of chronic inflammatory changes in the gut mucosa after an infection and the persistence of the enterochromaffin cell hyperplasia or proliferation that remains even after the eradication of the infectious organism, are associated with the inadequate response to acute gut inflammation resulting from inadequate cortisol or altered sympathetic response which are controlled by the stress response circuits and the HPA axis.
Studies have shown that life stressors that have occurred years earlier or childhood abuse predispose to the risk of developing IBS in later life.
Psychiatric illness episodes or anxiety-provoking situations usually precede onset and exacerbation of IBS symptoms in two thirds of IBS patients. Furthermore IBS patients report significantly more negative life events than other stressed patients like those with peptic ulcers.
Those with anxiety and depression as well as those with increased stress have a higher risk of developing IBS.
Due to the positive association of IBS with stress, the treatment approaches to IBS management aim at reducing stress.
Potential mechanisms include non-specific approaches, such as with tricyclic antidepressants or the use of selective compounds, such as the CRF antagonists.