Paul A Dennis1, J Brice Weinberg2, Patrick S Calhoun3, Lana L Watkins4, Andrew Sherwood4, Michelle F Dennis5, Jean C Beckham6. 1. Durham Veterans Affairs Medical Center, Durham, NC 27705, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA. Electronic address: paul.dennis2@va.gov. 2. Durham Veterans Affairs Medical Center, Durham, NC 27705, USA; Department of Medicine, Duke University Medical Center, Durham, NC 27705, USA. 3. Durham Veterans Affairs Medical Center, Durham, NC 27705, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA; Veterans Affairs Mid-Atlantic Region Mental Illness Research, Education, and Clinical Center, Durham, NC 27705, USA; Veterans Affairs Center for Health Services Research in Primary Care, Durham, NC 27705, USA. 4. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA. 5. Durham Veterans Affairs Medical Center, Durham, NC 27705, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA. 6. Durham Veterans Affairs Medical Center, Durham, NC 27705, USA; Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27705, USA; Veterans Affairs Mid-Atlantic Region Mental Illness Research, Education, and Clinical Center, Durham, NC 27705, USA.
Abstract
OBJECTIVE: Posttraumatic stress disorder (PTSD) has been linked to chronic inflammation, a condition that poses a risk for cardiovascular disease. Attenuated vagal activity has been proposed as a potential mediator of PTSD and inflammation, although associated behavioral health risks-namely cigarette smoking and alcohol dependence-might also account for that link. METHODS: Inflammation was quantified by fasting serum concentrations of C-reactive protein (CRP), tumor necrosis factor (TNF)-α, interleukin (IL)-10, and thymus- and activation-regulated chemokine (TARC)/CCL17 collected from 85 participants with PTSD and 82 without PTSD. Latent variable modeling was used to assess the relationship between PTSD symptom severity and inflammation along with potential mediators vagal activity (respiratory sinus arrhythmia; RSA), smoking status, and lifetime alcohol dependence. RESULTS: PTSD symptom severity was associated with increased inflammation (β=.18, p=.02). However, this association was reduced in models that adjusted for RSA, smoking status, and lifetime alcohol dependence. Independent mediation effects were deemed significant via bootstrapping analyses. Together, RSA, smoking status, and lifetime alcohol dependence accounted for 95% of the effect of PTSD symptom severity on inflammation. CONCLUSION: Although RSA accounted for a modest proportion of the association between posttraumatic stress and pro-inflammatory responses, behavioral factors-specifically cigarette smoking and alcohol dependence-proved to be larger mediators. The benefits of PTSD treatment may be enhanced by additional interventions aimed at modifying these health behaviors. Published by Elsevier Inc.
OBJECTIVE:Posttraumatic stress disorder (PTSD) has been linked to chronic inflammation, a condition that poses a risk for cardiovascular disease. Attenuated vagal activity has been proposed as a potential mediator of PTSD and inflammation, although associated behavioral health risks-namely cigarette smoking and alcohol dependence-might also account for that link. METHODS:Inflammation was quantified by fasting serum concentrations of C-reactive protein (CRP), tumor necrosis factor (TNF)-α, interleukin (IL)-10, and thymus- and activation-regulated chemokine (TARC)/CCL17 collected from 85 participants with PTSD and 82 without PTSD. Latent variable modeling was used to assess the relationship between PTSD symptom severity and inflammation along with potential mediators vagal activity (respiratory sinus arrhythmia; RSA), smoking status, and lifetime alcohol dependence. RESULTS:PTSD symptom severity was associated with increased inflammation (β=.18, p=.02). However, this association was reduced in models that adjusted for RSA, smoking status, and lifetime alcohol dependence. Independent mediation effects were deemed significant via bootstrapping analyses. Together, RSA, smoking status, and lifetime alcohol dependence accounted for 95% of the effect of PTSD symptom severity on inflammation. CONCLUSION: Although RSA accounted for a modest proportion of the association between posttraumatic stress and pro-inflammatory responses, behavioral factors-specifically cigarette smoking and alcohol dependence-proved to be larger mediators. The benefits of PTSD treatment may be enhanced by additional interventions aimed at modifying these health behaviors. Published by Elsevier Inc.
Authors: B Spivak; B Shohat; R Mester; S Avraham; I Gil-Ad; A Bleich; A Valevski; A Weizman Journal: Biol Psychiatry Date: 1997-09-01 Impact factor: 13.382
Authors: Ania E Oddone; Paul A Dennis; Patrick S Calhoun; Lana L Watkins; Andrew Sherwood; Eric A Dedert; Kimberly T Green; Jacob N Stein; Michelle F Dennis; Jean C Beckham Journal: Psychol Trauma Date: 2014-11-10
Authors: Carsten Spitzer; Sven Barnow; Henry Völzke; Henri Wallaschofski; Ulrich John; Harald J Freyberger; Bernd Löwe; Hans Joergen Grabe Journal: J Psychiatr Res Date: 2009-07-22 Impact factor: 4.791
Authors: Paul A Dennis; Nathan A Kimbrel; Andrew Sherwood; Patrick S Calhoun; Lana L Watkins; Michelle F Dennis; Jean C Beckham Journal: Psychosom Med Date: 2017-06 Impact factor: 4.312
Authors: M W Miller; H Maniates; E J Wolf; M W Logue; S A Schichman; A Stone; W Milberg; R McGlinchey Journal: Brain Behav Immun Date: 2017-09-01 Impact factor: 7.217
Authors: Paul A Dennis; Julia M Neal; Emili Travis; Lana L Watkins; Patrick S Calhoun; Michelle F Dennis; Jean C Beckham Journal: J Psychophysiol Date: 2018-07-18 Impact factor: 1.333
Authors: M Bam; X Yang; E E Zumbrun; J P Ginsberg; Q Leyden; J Zhang; P S Nagarkatti; M Nagarkatti Journal: Transl Psychiatry Date: 2017-08-29 Impact factor: 6.222