An investigation of vago-regulatory and health-behavior accounts for increased inflammation in posttraumatic stress disorder.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Dennis, PA; Weinberg, JB; Calhoun, PS; Watkins, LL; Sherwood, A; Dennis, MF; Beckham, JC

Published Date

  • April 2016

Published In

Volume / Issue

  • 83 /

Start / End Page

  • 33 - 39

PubMed ID

  • 27020074

Pubmed Central ID

  • PMC4813329

Electronic International Standard Serial Number (EISSN)

  • 1879-1360

Digital Object Identifier (DOI)

  • 10.1016/j.jpsychores.2016.02.008


  • eng

Conference Location

  • England