Ole Köhler-Forsberg1, Henriette N Buttenschøn2, Katherine E Tansey3, Wolfgang Maier4, Joanna Hauser5, Mojca Zvezdana Dernovsek6, Neven Henigsberg7, Daniel Souery8, Anne Farmer3, Marcella Rietschel9, Peter McGuffin3, Katherine J Aitchison10, Rudolf Uher11, Ole Mors12. 1. Aarhus University Hospital, Risskov, Psychosis Research Unit, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark. Electronic address: karkoe@rm.dk. 2. iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark; Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Denmark. 3. MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, UK. 4. Department of Psychiatry, University of Bonn, Germany. 5. Laboratory of Psychiatric Genetics, Department of Psychiatry, Poznan University of Medical Sciences, Poland. 6. University Psychiatric Clinic, Ljubljana, Slovenia. 7. Croatian Institute for Brain Research, Medical School, University of Zagreb, Croatia. 8. Laboratoire de Psychologie Médicale, Université Libre de Bruxelles; Psy Pluriel - Centre Européen de Psychologie Médicale, Belgium. 9. Department of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. 10. MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, UK; Departments of Psychiatry and Medical Genetics, University of Alberta, Edmonton, AB, Canada. 11. Department of Psychiatry, Dalhousie University, Halifax, N.S., Canada. 12. Aarhus University Hospital, Risskov, Psychosis Research Unit, Aarhus, Denmark; iPSYCH, The Lundbeck Foundation Initiative for Integrative Psychiatric Research, Aarhus, Denmark.
Abstract
INTRODUCTION: Population-based studies have associated inflammation, particularly higher C-reactive protein (CRP), with depressive severity, but clinical trials in major depressive disorder were rather non-specific without examining the role of gender. We aimed to investigate the association between CRP and overall depression severity including specific depressive symptoms and to examine potential gender differences. METHODS: We included 231 individuals with major depressive disorder from the Genome-Based Therapeutics Drugs for Depression (GENDEP) study. At baseline, we assessed high-sensitivity CRP levels and psychopathology with the Montgomery Aasberg Depression Rating Scale (MADRS). We performed linear regression analyses to investigate the association between baseline CRP levels with overall MADRS severity and specific symptoms at baseline and adjusted for age, gender, anti-inflammatory and psychotropic drug treatment, body mass index, smoking, inflammatory diseases, and recruitment center. RESULTS: Higher CRP levels were significantly associated with greater overall MADRS symptom severity (p=0.02), which was significant among women (p=0.02) but not among men (p=0.68). Among women, higher CRP was associated with increased severity on observed mood, cognitive symptoms, interest-activity, and suicidality, but we found no significant associations among men. Interaction analyses showed no significant gender differences on the overall MADRS score or specific symptoms. DISCUSSION: Our results support the sickness syndrome theory suggesting that chronic low-grade inflammation may be associated with a subtype of depression. The potential gender differences in psychopathology may be explained by biological and/or psychosocial factors, e.g. differential modulation of immune responses by sex hormones. Clinical studies should investigate symptom-specific and/or gender-specific treatment guided by peripheral inflammatory markers.
INTRODUCTION: Population-based studies have associated inflammation, particularly higher C-reactive protein (CRP), with depressive severity, but clinical trials in major depressive disorder were rather non-specific without examining the role of gender. We aimed to investigate the association between CRP and overall depression severity including specific depressive symptoms and to examine potential gender differences. METHODS: We included 231 individuals with major depressive disorder from the Genome-Based Therapeutics Drugs for Depression (GENDEP) study. At baseline, we assessed high-sensitivity CRP levels and psychopathology with the Montgomery Aasberg Depression Rating Scale (MADRS). We performed linear regression analyses to investigate the association between baseline CRP levels with overall MADRS severity and specific symptoms at baseline and adjusted for age, gender, anti-inflammatory and psychotropic drug treatment, body mass index, smoking, inflammatory diseases, and recruitment center. RESULTS: Higher CRP levels were significantly associated with greater overall MADRS symptom severity (p=0.02), which was significant among women (p=0.02) but not among men (p=0.68). Among women, higher CRP was associated with increased severity on observed mood, cognitive symptoms, interest-activity, and suicidality, but we found no significant associations among men. Interaction analyses showed no significant gender differences on the overall MADRS score or specific symptoms. DISCUSSION: Our results support the sickness syndrome theory suggesting that chronic low-grade inflammation may be associated with a subtype of depression. The potential gender differences in psychopathology may be explained by biological and/or psychosocial factors, e.g. differential modulation of immune responses by sex hormones. Clinical studies should investigate symptom-specific and/or gender-specific treatment guided by peripheral inflammatory markers.
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