Pathophysiology

Enteric nerves control intestinal smooth muscle action and are connected to the brain by the autonomic nervous system. IBS is thought to result from dysregulation of this "brain-gut axis." The enteric nervous system is composed of two ganglionated plexuses that control gut innervation: the submucous plexus (Meissner's plexus) and the myenteric plexus (Auerbach's plexus). The enteric nervous system and the CNS are interconnected and interdependent. A number of neurochemicals mediate their func tion, including serotonin (5-hydroxytryptamine or 5-HT), acetylcholine, substance P, and nitric oxide, among others.

Two 5-HT receptor subtypes, 5-HT3 and 5-HT4, are involved in gut motility, visceral sensitivity, and gut secretion. The 5-HT3 receptors slow colonic transit and increase fluid absorption, whereas 5-HT4 receptor stimulation results in accelerated colonic transit.

Although no single pathologic defect has been found to account for the pattern of exacerbations and remissions seen in IBS, CNS abnormalities, dysmotility, visceral hypersensitivity, and a number of other factors have been implicated.14

The passage of fluids into and out of the colon is regulated by epithelial cells. In IBS, the colonic lining (epithelium) appears to work properly. However, increased movement of the contents in the colon can overwhelm its absorptive capacity. Disturbed intestinal motility appears to be a central feature of IBS, which leads to altered stool consistency. Studies suggest that the colon of IBS sufferers is abnormally sensitive to normal stimuli.15 This enhanced visceral sensitivity manifests as pain, especially related to gut distention.

IBS activity may be affected by the immune system. Some IBS patients have been found to have antibodies that may indicate food hypersensitivity that might be involved in symptom production.16 Specifically, sensitivity has been demonstrated to common foods such as wheat, beef, pork, soy, and eggs.

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