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      Cortisol and antidepressant effects of yoga

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          Abstract

          Context:

          Hypercortisolemia is well-known in depression and yoga has been demonstrated earlier to reduce the parameters of stress, including cortisol levels.

          Aim:

          We aimed to find the role of yoga as an antidepressant as well as its action on lowering the serum cortisol levels.

          Settings and Design:

          An open-labeled study consisting of three groups (yoga alone, yoga along with antidepressant medication and antidepressant medication alone) was conducted at a tertiary care psychiatry hospital.

          Methodology:

          Out-patient depressives who were not suicidal were offered yoga as a possible antidepressant therapy. A validated yoga module was used as therapy taught over a month and to be practiced at home daily. Patients were free to choose the drugs if their psychiatrist advised. Patients ( n=54) were rated on Hamilton Depression Rating Scale (HDRS) with serum cortisol measurements at baseline and after 3 months. In 54 patients, assessments and blood test results were both available. 19 each received yoga alone or with drugs and 16 received drugs only. Healthy comparison subjects ( n=18) too underwent morning cortisol measurements once.

          Results:

          Serum cortisol was higher in depressives compared with controls. In the total sample, the cortisol level dropped significantly at the end of treatment. More patients in the yoga groups had a drop in cortisol levels as compared to drug-only group. In the yoga-only group, the cortisol drop correlated with the drop in HDRS score (antidepressant effect).

          Conclusion:

          The findings support that yoga may act at the level of the hypothalamus by its ‘anti-stress’ effects (reducing the cortisol), to bring about relief in depression.

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          Most cited references19

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          Diagnostic and statistical manual of mental disorders.

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            Cortisol levels during human aging predict hippocampal atrophy and memory deficits.

            Elevated glucocorticoid levels produce hippocampal dysfunction and correlate with individual deficits in spatial learning in aged rats. Previously we related persistent cortisol increases to memory impairments in elderly humans studied over five years. Here we demonstrate that aged humans with significant prolonged cortisol elevations showed reduced hippocampal volume and deficits in hippocampus-dependent memory tasks compared to normal-cortisol controls. Moreover, the degree of hippocampal atrophy correlated strongly with both the degree of cortisol elevation over time and current basal cortisol levels. Therefore, basal cortisol elevation may cause hippocampal damage and impair hippocampus-dependent learning and memory in humans.
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              When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders.

              Previous theories have emphasized the role of excessive glucocorticoid activity in the pathology of chronic stress. Nevertheless, insufficient glucocorticoid signaling (resulting from decreased hormone bioavailability or reduced hormone sensitivity) may have equally devastating effects on bodily function. Such effects may be related in part to the role of glucocorticoids in restraining activation of the immune system and other components of the stress response, including the sympathetic nervous system (SNS) and corticotropin-releasing hormone (CRH). The literature on neuroendocrine function and glucocorticoid-relevant pathologies in stress-related neuropsychiatric disorders, including posttraumatic stress disorder and major depression, was reviewed. Although not occurring together, both hypocortisolism and reduced responsiveness to glucocorticoids (as determined by dexamethasone challenge tests) were reliably found. Stress-related neuropsychiatric disorders were also associated with immune system activation/inflammation, high SNS tone, and CRH hypersecretion, which are all consistent with insufficient glucocorticoid-mediated regulation of stress hyperresponsiveness. Finally, antidepressants, a mainstay in the treatment of stress-related disorders, were regularly associated with evidence of enhanced glucocorticoid signaling. Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders. Impaired feedback regulation of relevant stress responses, especially immune activation/inflammation, may, in turn, contribute to stress-related pathology, including alterations in behavior, insulin sensitivity, bone metabolism, and acquired immune responses. From an evolutionary perspective, reduced glucocorticoid signaling, whether achieved at the level of the hormone or its receptor, may foster immune readiness and increase arousal. Emphasis on insufficient glucocorticoid signaling in stress-related pathology encourages development of therapeutic strategies to enhance glucocorticoid signaling pathways.
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                Author and article information

                Journal
                Indian J Psychiatry
                Indian J Psychiatry
                IJPsy
                Indian Journal of Psychiatry
                Medknow Publications & Media Pvt Ltd (India )
                0019-5545
                1998-3794
                July 2013
                : 55
                : Suppl 3
                : S405-S408
                Affiliations
                [1]Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
                [1 ]Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India
                Author notes
                Address for correspondence: Dr. Jagadisha Thirthalli, Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bangalore - 560 029, Karnataka, India. E-mail: jagatth@ 123456yahoo.com
                Article
                IJPsy-55-405
                10.4103/0019-5545.116315
                3768222
                24049209
                1cea36f4-a5ab-4341-99b3-40fa124ed44a
                Copyright: © Indian Journal of Psychiatry

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Original Article

                Clinical Psychology & Psychiatry
                cortisol,depression,hypercortisolemia,stress,yoga
                Clinical Psychology & Psychiatry
                cortisol, depression, hypercortisolemia, stress, yoga

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