PTSD and suPAR: A multicohort investigation of chronic inflammation.

dc.contributor.author

Bourassa, Kyle J

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Moffitt, Terrie E

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Arseneault, Louise

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Barrett-Young, Ashleigh

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Danese, Andrea

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Garrett, Melanie E

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Houts, Renate

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Matthews, Timothy

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Poulton, Richie G

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Ramrakha, Sandhya

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Sprinckmoller, Stefan

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Sugden, Karen

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Williams, Benjamin

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Beckham, Jean C

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Ashley-Koch, Allison E

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Kimbrel, Nathan A

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Fisher, Helen L

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Theodore, Reremoana F

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Caspi, Avshalom

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Rasmussen, Line JH

dc.date.accessioned

2025-12-01T14:27:14Z

dc.date.available

2025-12-01T14:27:14Z

dc.date.issued

2025-10

dc.description.abstract

Posttraumatic stress disorder (PTSD) is associated with poor health. Prior research has shown stressful events are associated with inflammatory biomarkers, such as soluble urokinase plasminogen activator receptor (suPAR), suggesting systemic chronic inflammation could be a mechanism linking adversity to poor health. In this study, we examined associations of PTSD and suPAR in two research cohorts-the E-Risk Study (United Kingdom; n = 1,389) and the Dunedin Multidisciplinary Health and Development Study (New Zealand; n = 927)-and a clinical cohort of medical patients (Denmark; n = 29,285). We also present results from two commonly assessed inflammatory biomarkers: C-reactive protein (CRP) and interleukin-6 (IL-6). People with a lifetime history of PTSD had higher suPAR at age 18 in E-Risk (β = 0.21, p = 0.046) and age 38 in the Dunedin Study (β = 0.23, p = 0.025), but not age 45 in the Dunedin Study (β = 0.18, p = 0.050). Individuals who developed PTSD in the year prior to age 45 in Dunedin had significant increases in suPAR from age 38 to 45 (β = 0.45, p = 0.034). Danish patients with a recent diagnosis of PTSD or a stress-related psychiatric disorder had higher levels of suPAR compared to propensity score-matched patients without such diagnoses (0.10 < βs < 0.24, ps < 0.05). CRP and IL-6 did not show consistent associations with PTSD. These results suggest that PTSD is associated with suPAR and that systemic chronic inflammation could help explain how trauma and PTSD might result in poor health.

dc.identifier

S0889-1591(25)00401-5

dc.identifier.issn

0889-1591

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1090-2139

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https://hdl.handle.net/10161/33574

dc.language

eng

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Elsevier BV

dc.relation.ispartof

Brain, behavior, and immunity

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10.1016/j.bbi.2025.106159

dc.rights.uri

https://creativecommons.org/licenses/by-nc/4.0

dc.subject

CRP

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IL-6

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Inflammation

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PTSD

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Trauma

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suPAR

dc.title

PTSD and suPAR: A multicohort investigation of chronic inflammation.

dc.type

Journal article

duke.contributor.orcid

Bourassa, Kyle J|0000-0001-9372-2309

duke.contributor.orcid

Moffitt, Terrie E|0000-0002-8589-6760|0000-0002-9834-2011

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Beckham, Jean C|0000-0001-8746-8949

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Ashley-Koch, Allison E|0000-0001-5409-9155

duke.contributor.orcid

Kimbrel, Nathan A|0000-0001-7218-1005

duke.contributor.orcid

Caspi, Avshalom|0000-0003-0082-4600

pubs.begin-page

106159

pubs.organisational-group

Duke

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Sanford School of Public Policy

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School of Medicine

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Trinity College of Arts & Sciences

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Duke Population Research Institute

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Affiliate

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Basic Science Departments

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Clinical Science Departments

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Institutes and Centers

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Biostatistics & Bioinformatics

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Molecular Genetics and Microbiology

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Medicine

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Psychiatry & Behavioral Sciences

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Medicine, Nephrology

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Psychology & Neuroscience

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University Institutes and Centers

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Duke Institute for Brain Sciences

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Duke Molecular Physiology Institute

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Psychiatry, Child & Family Mental Health & Community Psychiatry

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Center for Population Health & Aging

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Duke Population Research Center

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Psychiatry & Behavioral Sciences, Behavioral Medicine & Neurosciences

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Biostatistics & Bioinformatics, Division of Integrative Genomics

pubs.publication-status

Published

pubs.volume

131

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