Explaining The Last Post With Simpler Terms.

Coffee causes decreased blood glucose, and when glucose concentrations in the brain fall, there are interneurons that connect the brain’s cortex to its thalamus, causing increased epinephrine release. Increased plasma epinephrine (adrenaline) leads to upper GI motility. Microbial metabolism of dietary carbohydrates results mainly in the formation of SCFAs (short chain fatty acids) that initiate signals causing the release of factors that regulate neuronal excitability corresponding to increased pain. Colon pain project to the Po (posterior nucleus of the thalamus), so neck pain, thalamic activation, and colon pain might be additive in producing an adrenaline release. The primary somatosensory cortex (SI) is a major projection target of Po that increases sensory aspects of pain, (encodes stimulus intensity), such that normally non-noxious movements of the neck (application of the cervical traction), act to noxiously increase outflow to the adrenal glands. This activates the dorsal motor nucleus of the vagus, causing cecal relaxation, and an increased flow of carbohydrate-rich chyme through the cecum. In patients with chronic constipation there is an abnormally high rate of contraction of the small bowel. The enterochromaffin cell senses increased PO2, causing a decrease in 5-HT release, decreasing ileal contractions associated with c-IBS. This would increase SCFA at colon walls, activating colon projections to the somatosensory cortex, such that the cervical traction device function (to increase adrenaline) repeats.
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46-50, M
Dec 4, 2012