Clinical anxiety, cortisol and interleukin-6: evidence for specificity in emotion-biology relationships.

Hdl Handle:
http://hdl.handle.net/10147/207678
Title:
Clinical anxiety, cortisol and interleukin-6: evidence for specificity in emotion-biology relationships.
Authors:
O'Donovan, Aoife; Hughes, Brian M; Slavich, George M; Lynch, Lydia; Cronin, Marie-Therese; O'Farrelly, Cliona; Malone, Kevin M
Affiliation:
Department of Psychiatry and Mental Health Research, St. Vincent's University, Hospital, University College Dublin, Ireland. aoife.odonovan@ucsf.edu
Citation:
Brain Behav Immun. 2010 Oct;24(7):1074-7. Epub 2010 Mar 18.
Journal:
Brain, behavior, and immunity
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207678
DOI:
10.1016/j.bbi.2010.03.003
PubMed ID:
20227485
Abstract:
Anxiety confers increased risk for inflammatory diseases, and elevated inflammatory activity in anxious individuals may contribute to this increased risk. One complication, however, is that anxiety could be associated with inflammatory activity either through a specific anxiety pathway or through a more general negative emotionality pathway. To investigate, we measured levels of the stress hormone cortisol, the pro-inflammatory cytokine interleukin-6 (IL-6), and the systemic inflammatory marker C-reactive protein (CRP), as well as depression and neuroticism, in clinically anxious and non-anxious adults. Compared with non-anxious participants, clinically anxious participants exhibited significantly lower levels of morning cortisol and significantly higher levels of IL-6, independent of age, sex, and depressive symptoms. These group differences were robust when controlling for neuroticism. Conversely, the groups had equivalent levels of CRP in all analyses. Results are indicative of anxiety-specific effects on inflammatory activity, and highlight a pathway by which anxiety may increase risk for inflammatory diseases.
Language:
eng
MeSH:
Adult; Anxiety/*metabolism/psychology; C-Reactive Protein/*metabolism; Depression/*metabolism/psychology; Female; Humans; Hydrocortisone/*metabolism; Interleukin-6/*blood; Male; Neurotic Disorders/*metabolism/psychology; Personality Inventory; Questionnaires; Saliva/metabolism
ISSN:
1090-2139 (Electronic); 0889-1591 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorO'Donovan, Aoifeen_GB
dc.contributor.authorHughes, Brian Men_GB
dc.contributor.authorSlavich, George Men_GB
dc.contributor.authorLynch, Lydiaen_GB
dc.contributor.authorCronin, Marie-Thereseen_GB
dc.contributor.authorO'Farrelly, Clionaen_GB
dc.contributor.authorMalone, Kevin Men_GB
dc.date.accessioned2012-02-01T10:34:43Z-
dc.date.available2012-02-01T10:34:43Z-
dc.date.issued2012-02-01T10:34:43Z-
dc.identifier.citationBrain Behav Immun. 2010 Oct;24(7):1074-7. Epub 2010 Mar 18.en_GB
dc.identifier.issn1090-2139 (Electronic)en_GB
dc.identifier.issn0889-1591 (Linking)en_GB
dc.identifier.pmid20227485en_GB
dc.identifier.doi10.1016/j.bbi.2010.03.003en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207678-
dc.description.abstractAnxiety confers increased risk for inflammatory diseases, and elevated inflammatory activity in anxious individuals may contribute to this increased risk. One complication, however, is that anxiety could be associated with inflammatory activity either through a specific anxiety pathway or through a more general negative emotionality pathway. To investigate, we measured levels of the stress hormone cortisol, the pro-inflammatory cytokine interleukin-6 (IL-6), and the systemic inflammatory marker C-reactive protein (CRP), as well as depression and neuroticism, in clinically anxious and non-anxious adults. Compared with non-anxious participants, clinically anxious participants exhibited significantly lower levels of morning cortisol and significantly higher levels of IL-6, independent of age, sex, and depressive symptoms. These group differences were robust when controlling for neuroticism. Conversely, the groups had equivalent levels of CRP in all analyses. Results are indicative of anxiety-specific effects on inflammatory activity, and highlight a pathway by which anxiety may increase risk for inflammatory diseases.en_GB
dc.language.isoengen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAnxiety/*metabolism/psychologyen_GB
dc.subject.meshC-Reactive Protein/*metabolismen_GB
dc.subject.meshDepression/*metabolism/psychologyen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshHumansen_GB
dc.subject.meshHydrocortisone/*metabolismen_GB
dc.subject.meshInterleukin-6/*blooden_GB
dc.subject.meshMaleen_GB
dc.subject.meshNeurotic Disorders/*metabolism/psychologyen_GB
dc.subject.meshPersonality Inventoryen_GB
dc.subject.meshQuestionnairesen_GB
dc.subject.meshSaliva/metabolismen_GB
dc.titleClinical anxiety, cortisol and interleukin-6: evidence for specificity in emotion-biology relationships.en_GB
dc.contributor.departmentDepartment of Psychiatry and Mental Health Research, St. Vincent's University, Hospital, University College Dublin, Ireland. aoife.odonovan@ucsf.eduen_GB
dc.identifier.journalBrain, behavior, and immunityen_GB
dc.description.provinceLeinster-

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