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Cushing's disorder and depression present overlapping although not identical psychological symptomatology. In turn, a subset of patients with affective disorders present with hypercortisolemia and disturbances, specifically disinhibition, of the hypothalamic hypophysio adrenal axis (HHAA). Memory disturbances, in particular, biasing toward negative contents, overlapping sleep abnormalities (marked reduction of stages 3 and 4) increased fatigue and loss of energy, attentional deficits and irritability, are just part of the common symptomatology presented by patients with both Cushing's disorder and depression. All of these behavioral manifestations are known to be affected by adrenal steroid hormones. There is consensus that hippocampal structures are a main target for adrenal steroid hormones; hence, these neural regions are some of the most likely mediators of the effects of corticoadrenal steroids on behavior. This paper proposes that an imbalance of adrenal steroids and their metabolites may play a fundamental role in the psychophysiopathology of Cushing's and depressive disorders. The imbalance of these hormones, especially at limbic sites, could distort mood and memory content affecting cognition based on recollection and present experiences. Reestablishing an adrenal balance could therefore be considered as a therapeutic aid in a subset of depressive disorders.
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Post-natal development of plasma and urine osmolality, as well as plasma renin activity, aldosterone and cortisol levels were studied in calves between 1 and 9 months of age. The ratio of urine to plasma osmolality rose from 0.8 at an early post-natal age to 3.8 at the end of the study period. Plasma renin activity, plasma aldosterone and cortisol levels did not show any change during the post-natal development period. The plasma concentrations of these hormones were in the same range as is found in the adult.
Serum levels of progesterone, cortisol and phenytoin as well as the excretion of 17-OHCS were determined in 45 male epileptics before and during 24 months of the therapy. A significant decrease of the hormones was found in untreated patients. Phenytoin administration caused further decrease of cortisol and its metabolite 17-OHCS levels and a compensation of progesterone serum concentration.