Endogenous concentrations of DHEA and DHEA-S Decrease with remission of depression in older adults

Fabian, Tanya J.; Dew, Mary Amanda; Pollock, Bruce G.; Reynolds, Charles F.; Mulsant, Benoit H.; Butters, Meryl A.; Zmuda, Michelle; Linares, Ana María; Trottini, Mario; Kroboth, Patricia D.

doi:10.1016/s0006-3223(01)01198-2

Cited by 79 publications

(58 citation statements)

References 45 publications

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“…For example, plasma DHEA is higher in drug-free panic disorder patients than in control subjects (Brambilla et al, 2005). Patients with major depression have increased diurnal plasma DHEA (Heuser et al, 1998); notably, DHEA and DHEA-S have been reported to decrease with remission of depression in older adults (Fabian et al, 2001). One study identified a positive correlation between morning serum DHEA-S concentration and anxiety ratings in drug-free major depressive patients, but no relationship to depression ratings (Hsiao, 2006).…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of neurosteroids in obsessive compulsive disorder

Bigos

Folan

Jones

et al. 2009

Journal of Psychiatric Research

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Alterations in hormone concentrations, including adrenocorticotropin, corticotropin releasing hormone, and cortisol have been reported in patients with obsessive compulsive disorder (OCD). Dehydroepiandrosterone (DHEA) and its sulfated metabolite, DHEA-S, have not been assessed in patients with OCD. We report 24-hour serum DHEA, DHEA-S, and cortisol concentrations in a young man with OCD and 15 healthy young men. Circadian patterns of DHEA and cortisol were markedly different in the subject with OCD than in the control subjects. DHEA and DHEA-S concentrations were substantially higher in the OCD subject than in the control subjects. In contrast, cortisol concentrations were similar in the OCD subject and the control subjects. Future clinical studies are needed to evaluate the significance of DHEA and DHEA-S in OCD. To the EditorAlterations in hormone concentrations have been reported in patients with obsessive compulsive disorder (OCD). Studies have reported differences in concentrations of cortisol (Catapano et al., 1992;Monteleone et al., 1994), melatonin (Catapano et al., 1992;Monteleone et al., 1994), corticotropin releasing hormone (Altemus et al., 1992), adrenocorticotropin (ACTH) (Bailly et al., 1994), arginine vasopressin (Altemus et al., 1992, and oxytocin (Leckman et al., 1994). Some patients with OCD demonstrate a lack of inhibition of cortisol secretion after a dexamethasone suppression test (Catapano et al., 1990;Cottraux et al., 1984), indicating hyperactivity of the hypothalamic-pituitary-adrenal axis. ContributorsKristin Bigos was involved with data acquisition, data analysis, and manuscript writing. Mary Folan was involved with data acquisition and data analysis, and manuscript revisions. Mark Jones was the social worker and therapist for the patients in this study and was involved with recruitment. Gretchen Haas completed all the psychiatric evaluations (SCID). Frank Kroboth completed all the medical histories and physicals. Patricia Kroboth was involved with funding, data analysis, and manuscript writing.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Two important steroids, dehydroepiandrosterone (DHEA) and its sulfated metabolite DHEA-S, have not been assessed in patients with OCD. DHEA is secreted synchronously with cortisol from the adrenal cortex in response to ACTH. DHEA and DHEA-S are also neurosteroids, which are both synthesized and active in the brain. DHEA-S, and to a lesser extent DHEA, is a potent noncompetitive antagonist of γ-aminobutyric acid type A (GABA A ) receptors (Majewska, 1992;Majewska et al., 1990), and induces anxiogen...

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Section: Discussionmentioning

confidence: 99%

Dysregulation of neurosteroids in obsessive compulsive disorder

Bigos

Folan

Jones

et al. 2009

Journal of Psychiatric Research

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“…A dysregulation of DHEA and DHEA-S has also been reported in other mood and anxiety disorders (Eser et al 2006;Baker 2002, 2004). For example, subjects with major depression show increased diurnal plasma DHEA (Heuser et al 1998) and both DHEA and DHEA-S have been found to decrease with the remission of depression (Fabian et al 2001). The relative amounts of DHEA and/or DHEA-S appear to be maintained between blood and brain (Bernardi et al 2005;Guazzo et al 1996).…”

Section: Hormonal Abnormalities In Ocdmentioning

confidence: 99%

Circadian rhythms in obsessive–compulsive disorder

Lange

Hauser

et al. 2012

J Neural Transm

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The etiopathology and neurobiology of obsessive-compulsive disorder (OCD) are not fully understood. As for altered circadian rhythms associated with OCD, hormonal dysregulation and a delayed sleep phase have come into the focus of research. The novel antidepressant agomelatine is able to resynchronize circadian rhythms and the augmentative administration of this compound has been shown to be of benefit in some OCD patients who are refractory to common forms of pharmacotherapy. Adjunctive chronotherapy might also enhance the outcome in treatment-refractory OCD. The present review summarises the findings regarding circadian abnormalities in OCD.

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“…However, these studies revealed inconsistent results. In patients suffering from depression, decreased DHEAS plasma levels [26, 27] and DHEA salivary concentrations [28] have been observed. In contrast, other studies reported significant elevations of DHEAS 24-hour urinary levels [29] and diurnal minimal and mean DHEA plasma concentrations [30].…”

Section: Neuroactive Steroids As Endogenous Modulators Of Depression mentioning

confidence: 99%

Neuroactive Steroids in Depression and Anxiety Disorders: Clinical Studies

et al. 2006

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Certain neuroactive steroids modulate ligand-gated ion channels via non-genomic mechanisms. Especially 3α-reduced pregnane steroids are potent positive allosteric modulators of the γ-aminobutyric acid type A (GABA_A) receptor. During major depression, there is a disequilibrium of 3α-reduced neuroactive steroids, which is corrected by clinically effective pharmacological treatment. To investigate whether these alterations are a general principle of successful antidepressant treatment, we studied the impact of nonpharmacological treatment options on neuroactive steroid concentrations during major depression. Neither partial sleep deprivation, transcranial magnetic stimulation, nor electroconvulsive therapy affected neuroactive steroid levels irrespectively of the response to these treatments. These studies suggest that the changes in neuroactive steroid concentrations observed after antidepressant pharmacotherapy more likely reflect distinct pharmacological properties of antidepressants rather than the clinical response. In patients with panic disorder, changes in neuroactive steroid composition have been observed opposite to those seen in depression. However, during experimentally induced panic induction either with cholecystokinine-tetrapeptide or sodium lactate, there was a pronounced decline in the concentrations of 3α-reduced neuroactive steroids in patients with panic disorder, which might result in a decreased GABAergic tone. In contrast, no changes in neuroactive steroid concentrations could be observed in healthy controls with the exception of 3α,5α-tetrahydrodeoxycorticosterone. The modulation of GABA_A receptors by neuroactive steroids might contribute to the pathophysiology of depression and anxiety disorders and might offer new targets for the development of novel anxiolytic compounds.

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Endogenous concentrations of DHEA and DHEA-S Decrease with remission of depression in older adults

Cited by 79 publications

References 45 publications

Dysregulation of neurosteroids in obsessive compulsive disorder

Dysregulation of neurosteroids in obsessive compulsive disorder

Circadian rhythms in obsessive–compulsive disorder

Neuroactive Steroids in Depression and Anxiety Disorders: Clinical Studies

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