Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion–biology relationships
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 t...
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| Veröffentlicht in: | Brain, behavior, and immunity behavior, and immunity, 2010-10, Vol.24 (7), p.1074-1077 |
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| creator | O’Donovan, Aoife Hughes, Brian M Slavich, George M Lynch, Lydia Cronin, Marie-Therese O’Farrelly, Cliona Malone, Kevin M |
| description | 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. |
| doi_str_mv | 10.1016/j.bbi.2010.03.003 |
| format | Article |
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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.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2010.03.003</identifier><identifier>PMID: 20227485</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adult ; Age ; Allergy and Immunology ; Anxiety ; Anxiety - metabolism ; Anxiety - psychology ; C-Reactive Protein - metabolism ; Cortisol ; Depression ; Depression - metabolism ; Depression - psychology ; Female ; Humans ; Hydrocortisone - metabolism ; Interleukin-6 ; Interleukin-6 - blood ; Male ; Neurotic Disorders - metabolism ; Neurotic Disorders - psychology ; Neuroticism ; Personality Inventory ; Psychiatry ; Saliva - metabolism ; Surveys and Questionnaires</subject><ispartof>Brain, behavior, and immunity, 2010-10, Vol.24 (7), p.1074-1077</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>Copyright © 2010 Elsevier Inc. All rights reserved.</rights><rights>2010 Elsevier Inc. All rights reserved 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-1a260e049d705e995571efe6d55b8ddc9c9536a3e47fdf1e498877c66299ba543</citedby><cites>FETCH-LOGICAL-c537t-1a260e049d705e995571efe6d55b8ddc9c9536a3e47fdf1e498877c66299ba543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbi.2010.03.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20227485$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>O’Donovan, Aoife</creatorcontrib><creatorcontrib>Hughes, Brian M</creatorcontrib><creatorcontrib>Slavich, George M</creatorcontrib><creatorcontrib>Lynch, Lydia</creatorcontrib><creatorcontrib>Cronin, Marie-Therese</creatorcontrib><creatorcontrib>O’Farrelly, Cliona</creatorcontrib><creatorcontrib>Malone, Kevin M</creatorcontrib><title>Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion–biology relationships</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>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.</description><subject>Adult</subject><subject>Age</subject><subject>Allergy and Immunology</subject><subject>Anxiety</subject><subject>Anxiety - metabolism</subject><subject>Anxiety - psychology</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cortisol</subject><subject>Depression</subject><subject>Depression - metabolism</subject><subject>Depression - psychology</subject><subject>Female</subject><subject>Humans</subject><subject>Hydrocortisone - metabolism</subject><subject>Interleukin-6</subject><subject>Interleukin-6 - blood</subject><subject>Male</subject><subject>Neurotic Disorders - metabolism</subject><subject>Neurotic Disorders - psychology</subject><subject>Neuroticism</subject><subject>Personality Inventory</subject><subject>Psychiatry</subject><subject>Saliva - metabolism</subject><subject>Surveys and Questionnaires</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1u1DAUhSMEotPCA7BB2bEhw7UdOzZIlapR-ZEqsQDWluPctHeaiQc7MyI73oE37JOQaIYKWMDK8vU5R7a_k2XPGCwZMPVqvaxrWnKY9iCWAOJBtmBgoOBMmIfZArQ2BZOGnWSnKa0BQAqmH2cnHDivSi0XGa066sm7Lnf9N8JhfJn7EAdKYZ40OfUDxg53t9QX6nV-uacGe495G2KetuipJU_DOOly3ISBQn_3_UdNoQvXYx6xc_Mo3dA2Pcketa5L-PS4nmVf3l5-Xr0vrj6--7C6uCq8FNVQMMcVIJSmqUCiMVJWDFtUjZS1bhpvvJFCOYFl1TYtw9JoXVVeKW5M7WQpzrLzQ-52V2-w8dgP0XV2G2nj4miDI_vnSU839jrsbSkUAy2ngBfHgBi-7jANdkPJY9e5HsMuWc0qBUJw9V9lJSXTwDWflOyg9DGkFLG9vw8DO7O0azuxtDNLC8JOLCfP898fcu_4BW8SvDkIcPrOPWG0ydNMp6GIfrBNoH_Gn__l9scq3OKIaR12sZ84WWYTt2A_zWWau8Rg7pGS4ifgQccG</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>O’Donovan, Aoife</creator><creator>Hughes, Brian M</creator><creator>Slavich, George M</creator><creator>Lynch, Lydia</creator><creator>Cronin, Marie-Therese</creator><creator>O’Farrelly, Cliona</creator><creator>Malone, Kevin M</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QG</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20101001</creationdate><title>Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion–biology relationships</title><author>O’Donovan, Aoife ; 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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adult Age Allergy and Immunology Anxiety Anxiety - metabolism Anxiety - psychology C-Reactive Protein - metabolism Cortisol Depression Depression - metabolism Depression - psychology Female Humans Hydrocortisone - metabolism Interleukin-6 Interleukin-6 - blood Male Neurotic Disorders - metabolism Neurotic Disorders - psychology Neuroticism Personality Inventory Psychiatry Saliva - metabolism Surveys and Questionnaires |
| title | Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion–biology relationships |
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