Put you on HC without tests??? Thats crazy. Stop taking it,,, period. Find another doctor.
.wikipedia.org/wiki/Cortisol
Cortisol is released in response to stress, acting to restore homeostasis. However, prolonged cortisol secretion (which may be due to chronic stress or the excessive secretion seen in Cushing's syndrome) results in significant physiological changes.[12]
Insulin
Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis[13] and inhibits the peripheral utilization of glucose (insulin resistance) [13] by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane.[14][15] However, cortisol increases glycogen synthesis (glycogenesis) in the liver.[16] The permissive effect of cortisol on insulin action in liver glycogenesis is observed in hepatocyte culture in the laboratory, although the mechanism for this is unknown.
Collagen
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than in any other tissue.[17][18] Cortisol (as opticortinol) may inversely inhibit IgA precursor cells in the intestines of calves.[19] Cortisol also inhibits IgA in serum, as it does IgM; however, it is not shown to inhibit IgE.[20]
Gastric and renal secretion
Cortisol stimulates gastric-acid secretion.[21] Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme.[22] Net chloride secretion in the intestines is inversely decreased by cortisol in vitro (methylprednisolone).[23][disambiguation needed]
Sodium
Cortisol inhibits sodium loss through the small intestine of mammals.[24] Sodium depletion, however, does not affect cortisol levels[25] so cortisol cannot be used to regulate serum sodium. Cortisol's original purpose may have been sodium transport. This hypothesis is supported by the fact that freshwater fish utilize cortisol to stimulate sodium inward, while saltwater fish have a cortisol-based system for expelling excess sodium.[26]
Potassium
A sodium load augments the intense potassium excretion by cortisol; corticosterone is comparable to cortisol in this case.[27] In order for potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell.[28] This should make pH regulation much easier (unlike the normal potassium-deficiency situation, in which two sodium ions move in for each three potassium ions that move out—closer to the deoxycorticosterone effect). Nevertheless, cortisol consistently causes serum alkalosis; in a deficiency, serum pH does not change. The purpose of this may be to reduce serum pH to an optimum value for some immune enzymes during infection, when cortisol declines. Potassium is also blocked from loss in the kidneys by a decline in cortisol (9 alpha fluorohydrocortisone).[29]
Water
Cortisol acts as a diuretic hormone, controlling one-half of intestinal diuresis;[24] it has also been shown to control kidney diuresis in dogs. The decline in water excretion following a decline in cortisol (dexamethasone) in dogs is probably due to inverse stimulation of antidiuretic hormone (ADH or arginine vasopressin), which is not overridden by water loading.[30] Humans and other animals also use this mechanism.[31]
Copper
Cortisol stimulates many copper enzymes (often to 50% of their total potential), probably to increase copper availability for immune purposes.[32] This includes lysyl oxidase, an enzyme which is used to cross-link collagen and elastin.[33] Especially valuable for immune response is cortisol's stimulation of the superoxide dismutase,[34] since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria. Cortisol causes an inverse four- or fivefold decrease of metallothionein (a copper storage protein) in mice;[35] however, rodents do not synthesize cortisol themselves. This may be to furnish more copper for ceruloplasmin synthesis or to release free copper. Cortisol has an opposite effect on aminoisobuteric acid than on the other amino acids.[36] If alpha-aminoisobuteric acid is used to transport copper through the cell wall, this anomaly might be explained.
Immune system
Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor.[37] Cortisol also has a negative-feedback effect on interleukin-1.[38] IL-1 must be especially useful in combating some diseases; however, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of CRH hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor (GRMF),[39] so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone (the endogenous Type I and Type II receptor agonist) or RU28362 (a specific Type II receptor agonist) to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are not affected by cortisol.[40]
Bone metabolism
Cortisol reduces bone formation, favoring long-term development of osteoporosis. It transports potassium out of cells in exchange for an equal number of sodium ions (see above).[41] This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine.[42]
Memory
Cortisol works with epinephrine (adrenaline) to create memories of short-term emotional events; this is the proposed mechanism for storage of flash bulb memories, and may originate as a means to remember what to avoid in the future. However, long-term exposure to cortisol damages cells in the hippocampus;[43] this damage results in impaired learning. Furthermore, it has been shown that cortisol inhibits memory retrieval of already stored information.[44][45]
Additional effects
Increases blood pressure by increasing the sensitivity of the vasculature to epinephrine and norepinephrine; in the absence of cortisol, widespread vasodilation occurs[citation needed]
Inhibits secretion of corticotropin-releasing hormone (CRH), resulting in feedback inhibition of ACTH (Adrenocorticotropic hormone or corticotropin) secretion. Some researchers believe that this normal feedback system may become dysregulated when animals are exposed to chronic stress[citation needed]
Causes the kidneys to produce hypotonic urine[citation needed]
Shuts down the reproductive system, resulting in an increased chance of miscarriage and (in some cases) temporary infertility. Fertility returns after cortisol levels return to normal[46]
Has anti-inflammatory properties, reducing histamine secretion and stabilizing lysosomal membranes. Stabilization of lysosomal membranes prevents their rupture, preventing damage to healthy tissues[citation needed]
Stimulates hepatic detoxification by inducing tryptophan oxygenase (reducing serotonin levels in the brain), glutamine synthase (reducing glutamate and ammonia levels in the brain), cytochrome P-450 hemoprotein (mobilizing arachidonic acid), and metallothionein (reducing heavy metals in the body)[citation needed]
In addition to cortisol's effects in binding to the glucocorticoid receptor, because of its molecular similarity to aldosterone it also binds to the mineralocorticoid receptor. Aldosterone and cortisol have a similar affinity for the mineralocorticoid receptor; however, glucocorticoids circulate at roughly 100 times the level of mineralocorticoids. An enzyme exists in mineralocorticoid target tissues to prevent overstimulation by glucocorticoids and allow selective mineralocorticoid action. This enzyme—11-beta hydroxysteroid dehydrogenase type II (Protein:HSD11B2)—catalyzes the deactivation of glucocorticoids to 11-dehydro metabolites[citation needed]
There are potential links between cortisol, appetite and obesity.[47]
