Article

Steroids and depression

Psychoendocrinology Unit, Research and Training Building, McGill University, Montreal, Canada
The Journal of Steroid Biochemistry and Molecular Biology (Impact Factor: 4.05). 06/1991; DOI: 10.1016/0960-0760(91)90312-S

ABSTRACT Patients with endogenous depression (major affective disorder) frequently have high cortisol levels, but the diurnal rhythm is usually maintained and they do not develop the physical signs of Cushing's syndrome. On the other hand, depression is a frequent feature of Cushing's syndrome regardless of etiology, and it is often relieved when the cortisol levels are reduced, by whatever means. The mechanisms of the hypercortisolemia and resistance to dexamethasone suppression commonly found in endogenous depression are poorly understood; contrary to expectations, ACTH levels are not clearly elevated. There is striking difference in the psychiatric features seen in endogenous hypercorticism compared to those seen after exogenous administration of glucocorticoids or ACTH. This suggests that either there are other stimulating or modifying factors besides ACTH or that the steroids stimulated by ACTH or other peptides differ from those in control subjects, i.e. there may be an alteration in the metabolism of steroids in depression. Little is known about the metabolic changes or the many steroids besides glucocorticoids produced by the hyperactive steroid-producing tissue. Preliminary studies suggest that major depression may be improved by steroid suppression. It is hypothesized that steroids themselves may be important in causing and perpetuating depression.

0 Followers
 · 
50 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: There is considerable interest in the possible antidepressant properties of antiglucocorticoids. Studies of the hypothalamic-pituitary-adrenal (HPA) axis in depression, coupled with increasing recognition of the importance of glucocorticoids in brain function, strongly support such interest. Psychiatric symptomatology in Cushing’s syndrome (a disorder involving hypersecretion of cortisol), the adverse cognitive effects of glucocorticoids, and the suppressive effects of conventional antidepressants on HPA function all suggest that HPA abnormalities could cause or contribute to depression. However, the psychiatrie effects of glucocortieoids and glucocorticoid withdrawal suggest that HPA hyperactivity compensates for some other defect. While preliminary clinical studies suggest that both glucocorticoids and antiglucocorticoids may have efficacy in depression, the toxicity and loss of efficacy of available drugs during long term administration will probably necessitate the development of new agents to advance this field.
    CNS Drugs 05/1996; 5(5). DOI:10.2165/00023210-199605050-00001 · 4.38 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mood disorders have been recognised by the World Health Organization (WHO) as the leading cause of disability worldwide. Notwithstanding the established efficacy of conventional mood agents, many treated individuals continue to remain treatment refractory and/or exhibit clinically significant residual symptoms, cognitive dysfunction, and psychosocial impairment. Therefore, a priority research and clinical agenda is to identify pathophysiological mechanisms subserving mood disorders to improve therapeutic efficacy. During the past decade, inflammation has been revisited as an important etiologic factor of mood disorders. Therefore, the purpose of this synthetic review is threefold: 1) to review the evidence for an association between inflammation and mood disorders, 2) to discuss potential pathophysiologic mechanisms that may explain this association and 3) to present novel therapeutic options currently being investigated that target the inflammatory-mood pathway. Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of mood disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces 'sickness behaviour' resembling depressive symptomatology. Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity and structural and functional brain changes. Anti-inflammatory agents, such as acetyl-salicylic acid (ASA), celecoxib, anti-TNF-α agents, minocycline, curcumin and omega-3 fatty acids, are being investigated for use in mood disorders. Current evidence shows improved outcomes in mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy; however, further research is needed to establish the therapeutic benefit and appropriate dosage.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 01/2014; DOI:10.1016/j.pnpbp.2014.01.013 · 4.03 Impact Factor
  • Irish Journal of Medical Science 10/1999; 167(1). DOI:10.1007/BF02937557 · 0.57 Impact Factor