Jennifer A Sumner1, Qixuan Chen2, Andrea L Roberts3, Ashley Winning4, Eric B Rimm5, Paola Gilsanz4, M Maria Glymour6, Shelley S Tworoger7, Karestan C Koenen8, Laura D Kubzansky4. 1. Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, NY, United States. Electronic address: js4456@cumc.columbia.edu. 2. Department of Biostatistics, Columbia University Mailman School of Public Health, New York, NY, United States. 3. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, United States. 4. Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, United States. 5. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States. 6. Department of Epidemiology and Biostatistics, University of California San Francisco School of Medicine, San Francisco, CA, United States. 7. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States. 8. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, United States; Psychiatric and Neurodevelopmental Genetics Unit and Department of Psychiatry, Massachusetts General Hospital, Boston, MA, United States; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, United States.
Abstract
BACKGROUND: Research has linked posttraumatic stress disorder (PTSD) with higher circulating levels of inflammatory and endothelial function (EF) biomarkers, and effects may be bidirectional. We conducted the first investigation of new-onset PTSD and changes in inflammatory and EF biomarkers. METHODS: Data were from women in the Nurses' Health Study II. Biomarkers obtained at two blood draws, 10-16 years apart, included C-reactive protein (CRP), tumor necrosis factor-alpha receptor-II (TNFRII), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). PTSD was assessed via interview. Analyses compared biomarker levels in women with PTSD that onset between draws (n = 175) to women with no history of trauma (n = 175) and to women with history of trauma at draw 1 and no PTSD at either draw (n = 175). We examined if PTSD onset was associated with biomarker change over time and if pre-PTSD-onset biomarker levels indicated risk of subsequent PTSD using linear mixed models and linear regression, respectively. Biomarkers were log-transformed. RESULTS: Compared to women without trauma, women in the PTSD onset group had larger increases in VCAM-1 over time (b = 0.003, p = .068). They also had higher TNFRII (b = 0.05, p = .049) and ICAM-1 (b = 0.04, p = .060) levels at draw 1 (prior to trauma and PTSD onset). However, pre-PTSD-onset biomarker levels did not predict onset of more severe PTSD. CONCLUSIONS: PTSD onset (vs. no trauma) was associated with increases in one inflammation-related biomarker. Effects may be small and cumulative; longer follow-up periods with larger samples are needed. We did not observe strong support that pre-PTSD-onset biomarkers predicted risk of subsequent PTSD.
BACKGROUND: Research has linked posttraumatic stress disorder (PTSD) with higher circulating levels of inflammatory and endothelial function (EF) biomarkers, and effects may be bidirectional. We conducted the first investigation of new-onset PTSD and changes in inflammatory and EF biomarkers. METHODS: Data were from women in the Nurses' Health Study II. Biomarkers obtained at two blood draws, 10-16 years apart, included C-reactive protein (CRP), tumor necrosis factor-alpha receptor-II (TNFRII), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). PTSD was assessed via interview. Analyses compared biomarker levels in women with PTSD that onset between draws (n = 175) to women with no history of trauma (n = 175) and to women with history of trauma at draw 1 and no PTSD at either draw (n = 175). We examined if PTSD onset was associated with biomarker change over time and if pre-PTSD-onset biomarker levels indicated risk of subsequent PTSD using linear mixed models and linear regression, respectively. Biomarkers were log-transformed. RESULTS: Compared to women without trauma, women in the PTSD onset group had larger increases in VCAM-1 over time (b = 0.003, p = .068). They also had higher TNFRII (b = 0.05, p = .049) and ICAM-1 (b = 0.04, p = .060) levels at draw 1 (prior to trauma and PTSD onset). However, pre-PTSD-onset biomarker levels did not predict onset of more severe PTSD. CONCLUSIONS:PTSD onset (vs. no trauma) was associated with increases in one inflammation-related biomarker. Effects may be small and cumulative; longer follow-up periods with larger samples are needed. We did not observe strong support that pre-PTSD-onset biomarkers predicted risk of subsequent PTSD.
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