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

Department of Psychiatry and Mental Health Research, St. Vincent's University Hospital, University College Dublin, Ireland.
Brain Behavior and Immunity (Impact Factor: 5.89). 03/2010; 24(7):1074-7. DOI: 10.1016/j.bbi.2010.03.003
Source: PubMed


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.

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    • "In humans, the experience of chronic stress is associated with proinflammatory leukocytic phenotypes that are unresponsive to the anti-inflammatory actions of glucocorticoids (GCs) (Cohen et al., 2012) and a transcriptional profile that is consistent with the expansion and priming of myeloid-derived cells (Miller et al., 2008; Powell et al., 2013). The mechanistic association between inflammation and depression is particularly well-established (Raison et al., 2006; Dantzer et al., 2008; Miller et al., 2009; Norman et al., 2010; Capuron and Miller, 2011), while the case continues to build for the mechanistic association between inflammation and anxiety (Maes et al., 1998; Pitsavos et al., 2006; O'Donovan et al., 2010; Pace and Heim, 2012). The murine repeated social defeat (RSD) paradigm recapitulates many key immunological and behavioral features associated with psychosocial stress in humans. "
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