Lynn Ostrow

cortisol Secretion in Relation to Age in Major Depression1

&NA; Twenty‐five unmedicated hospitalized patients, ages 26‐64, with severe major depressive disorders, endogenous subtype, were evaluated both clinically and endocrinologically. Although measures reflecting cortisol secretion did not correlate with symptom dimensions and diagnostic subtypes, we did find a significant relationship between cortisol secretion and age during endogenous depressive illness; this included the mean 24 hour plasma cortisol, assessed by sampling every 30 minutes for 24 hours, as well as other single plasma cortisol assessments on other days. After clinical recovery, when plasma cortisol levels returned to normal, there was no significant relationship between cortisol secretion and age. Replication is required of this apparent interaction among age, depressive illness, and cortisol secretion. The result may relate to the proposed role of brain noradrenalin in tonically inhibiting cortisol secretion, the decline of hypothalamic noradrenalin with age, and the hypothesized deficit in depressive illness.

The dexamethasone suppression test in depressive illness: clinical correlates.

Abstract Clinical correlates of endogenous depression which may be associated with dexamethasone resistance have been evaluated by many investigators and found to be inconclusive. The authors investigated in 40 endogenously depressed patients the relationship of the dexamethasone suppression test (DST) and various clinical correlates - SADS scales, Research Diagnostic Criteria (RDC) depressive subtypes, family history from the FHRDC, responsivity to antidepressant treatment, etc. Dexamethasone resistance was found to be significantly associated with psychotic and bipolar depression but unrelated to the other clinical correlates examined. These findings are limited to the 2 mg DST; clinical correlates associated with non-suppression to dexamethasone may be related to the dose of dexamethasone.

Endocrine responses to thyrotropin-releasing hormone in major depressive disorders

The endocrine response to thyrotropin-releasing hormone (TRH) was studied in severely endogenously depressed patients during illness (n = 21) and after recovery (n = 18). The thyroid-stimulating hormone (TSH) response to TRH was blunted (deltaTSH less than 5 microIU/ml) in over one third of depressives during illness and remained blunted in most even after recovery. There was no correlation between multiple measures of cortisol secretion (the mean 24-hour plasma cortisol, dexamethasone suppression test, and plasma cortisol during the TRH procedure) and the TSH response during illness and after recovery. The TSH and prolactin (PRL) responses to TRH, as well as the baseline PRL, were significantly lower during illness. The role of possible abnormalities in dopamine and/or serotonin in depression contributing to these endocrine disturbances is discussed.

The prolactin-stimulating potency of reserpine in man

The prolactin (PRL) response to 0.5 mg i.m. of reserpine was compared to 0.5 mg i.m. of haloperidol in eight young men. The fact that reserpine was found to be a potent releaser of PRL--significantly greater than haloperidol--suggests a major role of storage pool dopamine in regulating PRL Secretion. Since the PRL response to neuroleptics is highly correlated with clinical potency, reserpine could be a potent antipsychotic, and further clinical trials are indicated.