Neuroendocrinological studies on depression with special reference to research at the Max-Planck-Institute of Psychiatry.

Hypercortisolism due to Cushing's syndrome or glucocorticoid therapy induces disturbances in several other endocrine systems and may also cause mental changes, predominantly depression of various degrees. On the other hand, it has repeatedly been shown that endogenous depression is often accompanied by hypercortisolemia, usually of a modest degree, and/or by changes in other hormonal systems similar to those observed in Cushing's syndrome and during treatment with glucocorticoids. Research performed at the MPIP on 327 psychiatric patients and 103 healthy subjects has demonstrated that, in contrast to Cushing's syndrome, the circadian rhythm in depression is usually well preserved, and that diurnal variation in mood is correlated with that rhythm. Furthermore, it was found that a modest hyperactivity of the HPA system, as indicated by enhanced UFC excretion and nonsuppression in the DST, is not specific for depression in general or its endogenous subtype. It can also be observed in many other psychiatric disorders and seems to mirror stress and the influence of other factors, such as weight loss due to anorexia, rather than a particular nosology. TSH blunting in the TRH test appears as a consequence of hypercortisolemia in psychiatric disorders as is the case in Cushing's syndrome and in the course of glucocorticoid therapy. Differences in the patterns of neuroendocrine abnormalities in depressives and other psychiatric patients probably reflect differences in the individual responsiveness of the various hormonal axes to stress rather than nosological subtypes of the disorder. A comparison of these results with the past and current literature reveals remarkable changes in the concepts of neuroendocrine dysfunctions in depression and leads to suggestions of new strategies for research on this subject.