HPA axis genetic variation, cortisol and psychosis in major depression
Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psy...
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| Published in | Molecular psychiatry Vol. 19; no. 2; pp. 220 - 227 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.02.2014
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1359-4184 1476-5578 1476-5578 |
| DOI | 10.1038/mp.2013.129 |
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| Abstract | Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (
r
2
=0.288) and from 0100 to 0900 h (
r
2
=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. |
|---|---|
| AbstractList | Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (r2=0.288) and from 0100 to 0900 h (r2=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (r super(2)=0.288) and from 0100 to 0900 h (r super(2)=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (r(2)=0.288) and from 0100 to 0900 h (r(2)=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD);26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h ([r.sup.2] = 0.288) and from 0100 to 0900 h ([r.sup.2] = 0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h ( r 2 =0.288) and from 0100 to 0900 h ( r 2 =0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis over-activity in healthy controls and patients with severe forms of major depression has not been well explored but could explain risk for cortisol dysregulation. 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with nonpsychotic major depression (NPMD); and 29 healthy controls (HC). Collection of genetic material was added one third of the way into a larger study on cortisol, cognition, and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 6pm to 9am and for the assessment of alleles for 6 genes involved in HPA Axis regulation. Two of the 6 genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression, and psychosis, and medication status, only allelic variation for the glucocorticoid receptor gene (GR) accounted for significant variance for mean cortisol levels from 6pm to 1am (r 2 =.317) and from 1am to 9am (r 2 =.194). Interestingly, neither depression severity nor psychosis predicted cortisol variance. In addition, GR and corticotropin-releasing hormone receptor 1 (CRH-R1) contributed significantly to psychosis measures and CRH-R1 contributed significantly to depression severity rating. Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD);26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h ([r.sup.2] = 0.288) and from 0100 to 0900 h ([r.sup.2] = 0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. Molecular Psychiatry (2014) 19, 220-227;doi:10.1038/mp.2013.129; published online 29 October 2013 Keywords: cortisol; glucocorticoid genes; HPA axis; major depression; psychosis Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (r(2)=0.288) and from 0100 to 0900 h (r(2)=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating.Genetic variation underlying hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with severe forms of major depression has not been well explored, but could explain risk for cortisol dysregulation. In total, 95 participants were studied: 40 patients with psychotic major depression (PMD); 26 patients with non-psychotic major depression (NPMD); and 29 HCs. Collection of genetic material was added one third of the way into a larger study on cortisol, cognition and psychosis in major depression. Subjects were assessed using the Brief Psychiatric Rating Scale, the Hamilton Depression Rating Scale and the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Blood was collected hourly for determination of cortisol from 1800 to 0900 h and for the assessment of alleles for six genes involved in HPA axis regulation. Two of the six genes contributed significantly to cortisol levels, psychosis measures or depression severity. After accounting for age, depression and psychosis, and medication status, only allelic variation for the glucocorticoid receptor (GR) gene accounted for a significant variance for mean cortisol levels from 1800 to 0100 h (r(2)=0.288) and from 0100 to 0900 h (r(2)=0.171). In addition, GR and corticotropin-releasing hormone receptor 1 (CRHR1) genotypes contributed significantly to psychosis measures and CRHR1 contributed significantly to depression severity rating. |
| Audience | Academic |
| Author | Sarginson, J E Tennakoon, L Kraemer, F B Lembke, A Keller, J Williams, G Murphy, G M Schatzberg, A F Lazzeroni, L C |
| AuthorAffiliation | 3 VA Palo Alto Health Care System 2 Harvard Medical School and Brigham & Women’s Hospital 1 Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine |
| AuthorAffiliation_xml | – name: 3 VA Palo Alto Health Care System – name: 2 Harvard Medical School and Brigham & Women’s Hospital – name: 1 Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine |
| Author_xml | – sequence: 1 givenname: A F surname: Schatzberg fullname: Schatzberg, A F email: afschatz@stanford.edu organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 2 givenname: J surname: Keller fullname: Keller, J organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 3 givenname: L surname: Tennakoon fullname: Tennakoon, L organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 4 givenname: A surname: Lembke fullname: Lembke, A organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 5 givenname: G surname: Williams fullname: Williams, G organization: Department of Medicine, Harvard Medical School and Brigham & Women’s Hospital – sequence: 6 givenname: F B surname: Kraemer fullname: Kraemer, F B organization: Division of Endocrinology, Gerontology and Metabolism, VA Palo Alto Health Care System, Department of Medicine, Stanford University School of Medicine – sequence: 7 givenname: J E surname: Sarginson fullname: Sarginson, J E organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 8 givenname: L C surname: Lazzeroni fullname: Lazzeroni, L C organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine – sequence: 9 givenname: G M surname: Murphy fullname: Murphy, G M organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine |
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| Copyright | Macmillan Publishers Limited 2014 2015 INIST-CNRS COPYRIGHT 2014 Nature Publishing Group Copyright Nature Publishing Group Feb 2014 Macmillan Publishers Limited 2014. |
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| Keywords | cortisol HPA axis glucocorticoid genes major depression psychosis Mood disorder Corticosteroid Genetic variability Hypothalamohypophysoadrenal axis Steroid hormone Antiinflammatory agent Depression Cortisol Hydrocortisone Genetic determinism Glucocorticoid Psychosis Gene Adrenal hormone Genetics |
| Language | English |
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| PublicationTitle | Molecular psychiatry |
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| SubjectTerms | 631/208/726/649 631/378/1689/1761 631/378/340 692/699/476/1414 Adult Adult and adolescent clinical studies Affective Disorders, Psychotic - diagnosis Affective Disorders, Psychotic - genetics Affective Disorders, Psychotic - physiopathology Behavioral Sciences Biological and medical sciences Biological Psychology Brain research Cognition Corticotropin-releasing hormone Corticotropin-Releasing Hormone - genetics Depression Depression, Mental Depressive Disorder, Major - diagnosis Depressive Disorder, Major - genetics Depressive Disorder, Major - physiopathology Female Genes Genetic aspects Genetic diversity Genetic engineering Genetic variation Genotypes Glucocorticoids Hormones Humans Hydrocortisone Hydrocortisone - blood Hypothalamic-pituitary-adrenal axis Hypothalamo-Hypophyseal System - physiopathology Hypothalamus Identification and classification Interview, Psychological Linkage Disequilibrium Male Medical sciences Medicine Medicine & Public Health Mental depression Mental disorders Miscellaneous Mood disorders Neurosciences original-article Patients Pharmacotherapy Pituitary Pituitary-Adrenal System - physiopathology Psychiatric Status Rating Scales Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychosis Receptors, Corticotropin-Releasing Hormone - genetics Receptors, Glucocorticoid - genetics Receptors, Mineralocorticoid - genetics Stress Stress response Tacrolimus Binding Proteins - genetics |
| Title | HPA axis genetic variation, cortisol and psychosis in major depression |
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