HPA axis genetic variation, cortisol and psychosis in major depression
Open accessAbstract
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.
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- Authors
- Schatzberg, A. F., Keller, J., Tennakoon, L., Lembke, A., Williams, G., Kraemer, F. B., Sarginson, J. E., Lazzeroni, L. C., & Murphy, G. M.
- Affiliations
- Stanford Medicine (US)
- Brigham and Women's Hospital (US)
- VA Palo Alto Health Care System (US)
- Corresponding author
- Schatzberg, A F
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2013-10-29
- Volume
- 19
- Issue
- 2
- Pages
- 220-227
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC4339288
- OpenAlex
- W2031403268
- Cited by
- 131
- References
- 68
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 11 · 2023: 6 · 2022: 7 · 2021: 7 · 2020: 10 · 2019: 12 · 2018: 15 · 2017: 11 · 2016: 20 · 2015: 11 · 2014: 6
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Update notices
- erratum (2014-05-27)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- U.S. Department of Veterans Affairs (I01 BX000398)
- National Institutes of Health (UL1TR001085)
- National Institute of Mental Health (R01MH050604, MH-19938, MH50604, R01MH086135, T32MH019938)
- National Center for Research Resources (UL1RR025744)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- hypothalamic-pituitary-adrenal axis, major depressive disorder, psychosis, cortisol, glucocorticoid receptor gene, CRHR1, corticotropin-releasing hormone receptor 1, genetic polymorphism, cortisol dysregulation, depression severity, diurnal cortisol rhythm
- MeSH terms
- CRF Receptor, Type 1, Tacrolimus Binding Protein 5, Adult, Affective Disorders, Psychotic, Corticotropin-Releasing Hormone, Major Depressive Disorder, Female, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Interview, Psychological, Male, Pituitary-Adrenal System, Psychiatric Status Rating Scales, Receptors, Glucocorticoid, Linkage Disequilibrium, Receptors, Corticotropin-Releasing Hormone, Receptors, Mineralocorticoid, Tacrolimus Binding Proteins
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