Fleur E P van Dooren1, Miranda T Schram2, Casper G Schalkwijk2, Coen D A Stehouwer2, Ronald M A Henry2, Pieter C Dagnelie3, Nicolaas C Schaper4, Carla J H van der Kallen2, Annemarie Koster5, Simone J S Sep2, Johan Denollet6, Frans R J Verhey7, Frans Pouwer6. 1. Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands; CoRPS - Center of Research on Psychological and Somatic disorders, Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands; MHeNS - Alzheimer Centre Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. Electronic address: F.E.P.vanDooren@uvt.nl. 2. Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands; CARIM Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. 3. CARIM Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands; CAPHRI School for Public Health and Primary Care, Maastricht University, Maastricht, The Netherlands; Department of Epidemiology, Maastricht University, Maastricht, The Netherlands. 4. Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands; CARIM Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands; CAPHRI School for Public Health and Primary Care, Maastricht University, Maastricht, The Netherlands. 5. Department of Social Medicine, Maastricht University, Maastricht, The Netherlands; CAPHRI School for Public Health and Primary Care, Maastricht University, Maastricht, The Netherlands. 6. CoRPS - Center of Research on Psychological and Somatic disorders, Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands. 7. MHeNS - Alzheimer Centre Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands.
Abstract
BACKGROUND: The pathogenesis of depression may involve low-grade inflammation and endothelial dysfunction. We aimed to evaluate the independent associations of inflammation and endothelial dysfunction with depressive symptoms and depressive disorder, and the role of lifestyle factors in this association. METHODS: In The Maastricht Study, a population-based cohort study (n=852, 55% men, m=59.8±8.5years), depressive symptoms were assessed with the Patient Health Questionnaire-9 and (major and minor) depressive disorder with the Mini-International Neuropsychiatric Interview. Plasma biomarkers of inflammation (hsCRP, SAA, sICAM-1, IL-6, IL-8, TNF-α) and endothelial dysfunction (sVCAM-1, sICAM-1, sE-selectin, vWF) were measured with sandwich immunoassays and combined into two standardized sum scores. RESULTS: Biomarkers of inflammation (hsCRP, TNF-α, SAA, sICAM-1) and endothelial dysfunction (sICAM-1, sE-Selectin) were univariately associated with depressive symptoms and depressive disorder. The sum scores of inflammation and endothelial dysfunction were associated with depressive disorder after adjustment for age, sex, type 2 diabetes, kidney function and prior cardiovascular disease (OR 1.54, p=0.001 and 1.40, p=0.006). Both sum scores remained significantly associated with depressive disorder after additional adjustment for lifestyle factors smoking, alcohol consumption and body mass index. The sum score of inflammation was also independently associated with depressive symptoms, while the sum score of endothelial dysfunction was not. CONCLUSIONS: Inflammation and endothelial dysfunction are both associated with depressive disorder, independent of lifestyle factors. Our results might suggest that inflammation and endothelial dysfunction are involved in depression.
BACKGROUND: The pathogenesis of depression may involve low-grade inflammation and endothelial dysfunction. We aimed to evaluate the independent associations of inflammation and endothelial dysfunction with depressive symptoms and depressive disorder, and the role of lifestyle factors in this association. METHODS: In The Maastricht Study, a population-based cohort study (n=852, 55% men, m=59.8±8.5years), depressive symptoms were assessed with the Patient Health Questionnaire-9 and (major and minor) depressive disorder with the Mini-International Neuropsychiatric Interview. Plasma biomarkers of inflammation (hsCRP, SAA, sICAM-1, IL-6, IL-8, TNF-α) and endothelial dysfunction (sVCAM-1, sICAM-1, sE-selectin, vWF) were measured with sandwich immunoassays and combined into two standardized sum scores. RESULTS: Biomarkers of inflammation (hsCRP, TNF-α, SAA, sICAM-1) and endothelial dysfunction (sICAM-1, sE-Selectin) were univariately associated with depressive symptoms and depressive disorder. The sum scores of inflammation and endothelial dysfunction were associated with depressive disorder after adjustment for age, sex, type 2 diabetes, kidney function and prior cardiovascular disease (OR 1.54, p=0.001 and 1.40, p=0.006). Both sum scores remained significantly associated with depressive disorder after additional adjustment for lifestyle factors smoking, alcohol consumption and body mass index. The sum score of inflammation was also independently associated with depressive symptoms, while the sum score of endothelial dysfunction was not. CONCLUSIONS:Inflammation and endothelial dysfunction are both associated with depressive disorder, independent of lifestyle factors. Our results might suggest that inflammation and endothelial dysfunction are involved in depression.
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