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Brain Behav Immun. 2010 Oct;24(7):1074-7. doi: 10.1016/j.bbi.2010.03.003. Epub 2010 Mar 18.

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

Author information

1
Department of Psychiatry and Mental Health Research, St. Vincent's University Hospital, University College Dublin, Ireland. aoife.odonovan@ucsf.edu

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.

PMID:
20227485
PMCID:
PMC4361085
DOI:
10.1016/j.bbi.2010.03.003
[Indexed for MEDLINE]
Free PMC Article

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