tag:blogger.com,1999:blog-6761513370150878848.post2375183230894555068..comments2023-10-30T05:48:26.367-04:00Comments on Feasting on Research: Cortisol and eating disordersCarrie Arnoldhttp://www.blogger.com/profile/02569839838912988783noreply@blogger.comBlogger1125tag:blogger.com,1999:blog-6761513370150878848.post-19880651183898761072015-05-04T14:46:44.248-04:002015-05-04T14:46:44.248-04:00I suspect that you will find interesting the artic...I suspect that you will find interesting the article below, which discusses the function of cortisol in the body as a hormone that inversely mobilizes the body against potassium wasting intestinal diseases, and in http://charles_w.tripod.com/cortisol.html with the references and links. If you see anything that can be improved please let me know. You may see a journal article that discusses this briefly in the 1998 vol. 51 issue of Medical Hypotheses, p 289-2<br />It is proposed that the primary purpose of the glucocorticoids, including cortisol (hydrocortisone), is to mobilize the body to resist infection. They do so by normally altering processes which increase pathogens' growth or their adverse effects and then declining when under attack. Cortisol is for intestinal disease (diarrhea) and corticosterone serum disease. Glucocorticoid mobilization for fight or flight is an adjunct, made possible because most processes which resist infection impair fight or flight. A different hormone controls those which do not. <br />Potassium loss is the most serious aspect of intestinal diseases, so the electrolyte capabilities of cortisol, but not corticosterone, are oriented toward conserving potassium. Low cell potassium reduces adrenal synthesis of cortisol, but not corticosterone. Sodium, water, glucose, amino acids, chloride, hydrogen ion, copper , and numerous others are controlled by cortisol in such a way as to survive during intestinal disease.<br />Some gram negative bacteria have an endotoxin which subverts this strategy by forcing the secretion of huge amounts of ACTH, which is the chief mediator of cortisol. A glucocorticoid response modifying factor (GRMF) and interleukin-1, raises the effective set point of cortisol. The immune cells thus take over their own regulation, using interleukin-1 to mediate production of cortisol via ACTH.<br />Scroll down to INTRODUCTION below.<br /> If you wish to see the whole article, please let me know, no charge.<br />Anonymousnoreply@blogger.com