En-Young N Wagner1, Marie-Pierre F Strippoli2, Vladeta Ajdacic-Gross3, Mehdi Gholam-Rezaee2, Jennifer Glaus4, Caroline Vandeleur2, Peter Vollenweider5, Martin Preisig2, Roland von Känel6. 1. Department of Consultation-Liaison Psychiatry and Psychosomatic Medicine, University Hospital Zurich, and University of Zurich, Zurich, Switzerland; Department of BioMedical Research, Bern University Hospital, Bern, Switzerland. Electronic address: en-young.wagner@dbmr.unibe.ch. 2. Department of Psychiatry, Center for Research in Psychiatric Epidemiology and Psychopathology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. 3. Department of Psychiatry, Psychotherapy and Psychosomatics, Psychiatric Hospital, University of Zurich, Switzerland. 4. Department of Psychiatry, Service of Child and Adolescent Psychiatry, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. 5. Department of Medicine, Internal Medicine, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland. 6. Department of Consultation-Liaison Psychiatry and Psychosomatic Medicine, University Hospital Zurich, and University of Zurich, Zurich, Switzerland.
Abstract
BACKGROUND: Anxiety disorders have been related to cardiovascular diseases via low-grade inflammation, but longitudinal studies on the association between generalized anxiety disorder (GAD) and inflammatory biomarkers are sparse. Furthermore, no studies have examined the association between GAD and the "cardio-protective" adipocytokine adiponectin in this context so far. METHODS: In a Swiss population-based sample of 2,415 adults participating in baseline and follow-up exams (mean follow-up duration=5.5 years), we diagnosed a total of 55 persons (2.3%) with GAD using a validated semi-structured psychiatric interview. We prospectively examined the relation between GAD and circulating levels of inflammatory biomarkers (i.e., C-reactive protein, interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and adiponectin), in linear regression models, statistically controlled for the baseline inflammatory marker, socioeconomic status, cardiovascular risk factors, health behaviors, and psychiatric disorders. RESULTS: Compared to those without GAD, individuals with GAD had lower IL-6 (β=-0.249, 95%-CI -0.493-(-0.004), p=0.046), and adiponectin (β=-0.264, 95%-CI -0.482-(-0.045), p=0.018) levels at follow-up after adjustment for all covariates. Moreover, GAD was unrelated to several other inflammatory measures. CONCLUSION: Individuals with GAD do not seem to exhibit chronic low-grade inflammation, suggesting different underlying biobehavioral mechanisms to those from other anxiety disorders. Low adiponectin levels may be linked to symptoms of GAD through brain areas directly involved in the processing of fear and anxiety.
BACKGROUND:Anxiety disorders have been related to cardiovascular diseases via low-grade inflammation, but longitudinal studies on the association between generalized anxiety disorder (GAD) and inflammatory biomarkers are sparse. Furthermore, no studies have examined the association between GAD and the "cardio-protective" adipocytokine adiponectin in this context so far. METHODS: In a Swiss population-based sample of 2,415 adults participating in baseline and follow-up exams (mean follow-up duration=5.5 years), we diagnosed a total of 55 persons (2.3%) with GAD using a validated semi-structured psychiatric interview. We prospectively examined the relation between GAD and circulating levels of inflammatory biomarkers (i.e., C-reactive protein, interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and adiponectin), in linear regression models, statistically controlled for the baseline inflammatory marker, socioeconomic status, cardiovascular risk factors, health behaviors, and psychiatric disorders. RESULTS: Compared to those without GAD, individuals with GAD had lower IL-6 (β=-0.249, 95%-CI -0.493-(-0.004), p=0.046), and adiponectin (β=-0.264, 95%-CI -0.482-(-0.045), p=0.018) levels at follow-up after adjustment for all covariates. Moreover, GAD was unrelated to several other inflammatory measures. CONCLUSION: Individuals with GAD do not seem to exhibit chronic low-grade inflammation, suggesting different underlying biobehavioral mechanisms to those from other anxiety disorders. Low adiponectin levels may be linked to symptoms of GAD through brain areas directly involved in the processing of fear and anxiety.