It is based on basic principles...back to the "wild days" on reading body language and displaying non verbal communication (ie. whispering). It is not a new concept, it has just been given a new name. I have been training dogs since I was a teenager and can easily get them (and the horses) to react accordingly with a glance or a motion...or as simple as my own demeanor.

I can't help much with the meds but can tell you I owned a miniature poodle that always had elevated alkphos (in the 600's) for years and one vet finally told me that it was just normal for my dog. He was diagnosed with Cushings in his final 2 years but I was never convinced the tests were accurate since my dog never had 'true' cushings symptoms. The symptoms he did have, and died from, were more indicative of a brain tumor. I wish you the best with your little gal.

Rocky had his x-rays yesterday and I'm very happy to report that the x-rays showed there is nothing wrong with his hips, knees or hocks. The vet said his hip/leg are seated (?) beautifully .. might be the beginning of some arthritis in the right ... but otherwise he looks like a normal young healthy dog. Her office is having a radiation clinic today, as part of their continuing education, so she's going to have them look at Rocky's films just to make sure she didn't miss anything ... she said she's not that comfortable looking at hock x-rays because they have too many parts (?). She did say that even when she manipulated his legs while he was sedated, that the right rear leg did not move as freely as the left one did. She says that's a puzzle ... I asked her if it could be a muscular injury left over from when he was young ... shortly after I got him, I asked the previous owner why Rocky didn't like riding in cars. He told me that Rocky had been in the front seat of his truck when he got hit head-on by a drunk driver. He also said that Rocky was thrown around quite a bit when they got hit. This guy never took Rocky to a vet ... he'd never had any shots or been neutered ... he didn't take him to a vet after the accident either. My vet agrees it could be something left over from that. So seems I have another male dog that is a puzzle ... my previous male dog had skin/eating issues that were a challenge for me and my vet. But we're very happy that we're not facing surgery at his young age!

Since having cushing's disease is a permanent ovedose of steroids, I am copying the drug information for glucocorticoids from a veterinary drug handbook. By looking at the effects glucocorticoids have, you may better be able to understand your dog's condition. EFFECRS OF GLUCOCORTICOIDS Cardiovascular System: Glucocorticoids can reduce capillary permeability and enhance vasoconstriction. A relatively clinically insignificant positive inotropic effect can occur after glucocorticoid administration. Increased blood pressure can result from both the drugs' vasoconstrictive properties and increased blood volume that may be produced. Cells: Glucocorticoids inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes and the cellular response to mediators of inflammation. Glucocorticoids stabilize lysosomal membranes. CNS/Autonomic Nervous System: Glucocorticoids can lower seizure threshold, alter mood and behavior, diminish the response to pyrogens, stimulate appetite and maintain alpha rhythm. Glucocorticoids are necessary for normal adrenergic receptor sensitivity. Endocrine System: When animals are not stressed, glucocorticoids will suppress the release of ACTH from the anterior pituitary, thereby reducing or preventing the release of endogenous corticosteroids. Stress factors (e.g., renal disease, liver disease, diabetes) may sometimes nullify the suppressing aspects of exogenously administered steroids. Release of thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), prolactin and luteinizing hormone (LH) may all be reduced when glucocorticoids are administered at pharmacological doses. Conversion of thyroxine (T4) to triiodothyronine (T3) may be reduced by glucocorticoids; and plasma levels of parathyroid hormone increased. Glucocorticoids may inhibit osteoblast function. Vasopressin (ADH) activity is reduced at the renal tubules and diuresis may occur. Glucocorticoids inhibit insulin binding to insulin-receptors and the post-receptor effects of insulin. Hematopoietic System: Glucocorticoids can increase the numbers of circulating platelets, neutrophils and red blood cells, but platelet aggregation is inhibited. Decreased amounts of lymphocytes (peripheral), monocytes and eosinophils are seen as glucocorticoids can sequester these cells into the lungs and spleen and prompt decreased release from the bone marrow. Removal of old red blood cells is diminished. Glucocorticoids can cause involution of lymphoid tissue. GI Tract and Hepatic System: Glucocorticoids increase the secretion of gastric acid, pepsin and trypsin. They alter the structure of mucin and decrease mucosal cell proliferation. Iron salts and calcium absorption are decreased while fat absorption is increased. Hepatic changes can include increased fat and glycogen deposits within hepatocytes, increased serum levels of alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (GGT). Significant increases can be seen in serum alkaline phosphatase levels. Glucocorticoids can cause minor increases in BSP (bromosulfophthalein) retention time. Immune System (also see Cells and Hematopoietic System): Glucocorticoids can decrease circulating levels of T-lymphocytes; inhibit lymphokines; inhibit neutrophil, macrophage, and monocyte migration; reduce production of interferon; inhibit phagocytosis and chemotaxis; antigen processing; and diminish intracellular killing. Specific acquired immunity is affected less than nonspecific immune responses. Glucocorticoids can also antagonize the complement cascade and mask the clinical signs of infection. Mast cells are decreased in number and histamine synthesis is suppressed. Many of these effects only occur at high or very high doses and there are species differences in response. Metabolic effects: Glucocorticoids stimulate gluconeogenesis. Lipogenesis is enhanced in certain areas of the body (e.g., abdomen) and adipose tissue can be redistributed away from the extremities to the trunk. Fatty acids are mobilized from tissues and their oxidation is increased. Plasma levels of triglycerides, cholesterol and glycerol are increased. Protein is mobilized from most areas of the body (not the liver). Musculoskeletal: Glucocorticoids may cause muscular weakness (also caused if there is a lack of glucocorticoids), atrophy, and osteoporosis. Bone growth can be inhibited via growth hormone and somatomedin inhibition, increased calcium excretion and inhibition of vitamin D activation. Resorption of bone can be enhanced. Fibrocartilage growth is also inhibited. Ophthalmic: Prolonged corticosteroid use (both systemic or topically to the eye) can cause increased intraocular pressure and glaucoma, cataracts and exophthalmos. Renal, Fluid, & Electrolytes: Glucocorticoids can increase potassium and calcium excretion; sodium and chloride reabsorption and extracellular fluid volume. Hypokalemia and/or hypocalcemia occur rarely. Diuresis may occur following glucocorticoid administration. Skin: Thinning of dermal tissue and skin atrophy can be seen with glucocorticoid therapy. Hair follicles can become distended and alopecia may occur. Adverse effects are generally associated with long-term administration of these drugs, especially if given at high dosages or not on an alternate day regimen. Effects generally are manifested as symptoms of hyperadrenocorticism. Many of the potential effects, adverse and otherwise, are outlined above in the Pharmacology section. In dogs, polydipsia (PD), polyphagia (PP) and polyuria (PU), may all be seen with short-term "burst" therapy as well as with alternate-day maintenance therapy on days when the drug is given. Adverse effects in dogs can include dull, dry haircoat, weight gain, panting, vomiting, diarrhea, elevated liver enzymes, pancreatitis, GI ulceration, lipidemias, activation or worsening of diabetes mellitus, muscle wasting and behavioral changes (depression, lethargy, viciousness). With the exception of PU/PD/PP, adverse effects associated with antiinflammatory therapy are relatively uncommon. Adverse effects associated with immunosuppressive doses are more common and potentially more severe. As far as evaluating quality of like, ask yourself what are 5 things your dog used to love (food, walks, swimming, whatever). Then ask yourself if she is still able to enjoy those things. If not, then her quality of life is diminished. I don't believe that dogs with Cushings are painful, but I think they can become uncomfortable. Cushings makes animals more prone to other conditions which can be painful, such as UTIs, pancreatitis, etc. I hope this helps a bit. Personally I think if you are questioning her quality of life, then it is probably diminished. But whether or not it has diminished to an unacceptable level is a decision only you and your family can make, since you know your dog better than anyone else.