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. 2016 Apr:83:33-9.
doi: 10.1016/j.jpsychores.2016.02.008. Epub 2016 Feb 26.

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

Paul A Dennis  1 , J Brice Weinberg  2 , Patrick S Calhoun  3 , Lana L Watkins  4 , Andrew Sherwood  4 , Michelle F Dennis  5 , Jean C Beckham  6
Affiliations

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

Paul A Dennis et al. J Psychosom Res. 2016 Apr.

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.

Keywords: Alcohol dependence; Cigarette smoking; Cytokines; Inflammation; Posttraumatic stress disorder; Vagal tone.

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Conflict of interest statement

Declaration of Interests

The authors have no competing interests to report.

Figures

Figure 1
Figure 1
Latent variable model of inflammation as a function of PTSD symptom severity. Estimates represent standardized coefficients. N = 164.
Figure 2
Figure 2
Latent variable model of inflammation as a function of PTSD symptom severity and RSA. Estimates represent standardized coefficients. N = 164.
Figure 3
Figure 3
Latent variable model of inflammation as a function of PTSD symptom severity and smoking status. Estimates represent standardized coefficients. N = 164.
Figure 4
Figure 4
Latent variable model of inflammation as a function of PTSD symptom severity and lifetime alcohol dependence. Estimates represent standardized coefficients. N = 164.
See this image and copyright information in PMC

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