Peer-Reviewed Journal Details
Mandatory Fields
O'Donovan, A,Hughes, BM,Slavich, GM,Lynch, L,Cronin, MT,O'Farrelly, C,Malone, KM
2010
October
Brain Behavior And Immunity
Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion-biology relationships
Published
()
Optional Fields
Anxiety Depression Cortisol Interleukin-6 Neuroticism CORONARY-HEART-DISEASE C-REACTIVE PROTEIN PSYCHOLOGICAL STRESS DEPRESSION SCALE HOSPITAL ANXIETY INFLAMMATION ASSOCIATION ACTIVATION DISORDERS SYMPTOMS
24
1074
1077
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. (C) 2010 Elsevier Inc. All rights reserved.
DOI 10.1016/j.bbi.2010.03.003
Grant Details
Publication Themes