Citation

Michopoulos V, Vester A, Neigh G. Exp. Neurol. 2016; 284(Pt B): 220-229.

Affiliation

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia; Yerkes National Primate Research Center, Atlanta, Georgia; Department of Physiology, Emory University School of Medicine, Atlanta, Georgia. Electronic address: gretchen.mccandless@vcuhealth.org.

Copyright

(Copyright © 2016, Elsevier Publishing)

DOI

10.1016/j.expneurol.2016.05.038

PMID

27246996

Abstract

Posttraumatic stress disorder (PTSD) is a heterogeneous psychiatric disorder that affects individuals exposed to trauma and is highly co-morbid with other adverse health outcomes, including cardiovascular disease and obesity. The unique pathophysiological feature of PTSD is the inability to inhibit fear responses, such that individuals suffering from PTSD re-experience traumatic memories and are unable to control psychophysiological responses to trauma-associated stimuli. However, underlying alterations in sympathetic nervous system activity, neuroendocrine systems, and metabolism associated with PTSD are similar to those present in traditional metabolic disorders, such as obesity and diabetes. The current review highlights existing clinical, translational, and preclinical data that support the notion that underneath the primary indication of impaired fear inhibition, PTSD is itself also a metabolic disorder and proposes altered function of inflammatory responses as a common underlying mechanism. The therapeutic implications of treating PTSD as a whole-body condition are significant, as targeting any underlying biological system whose activity is altered in both PTSD and metabolic disorders, (i.e. HPA axis, sympathetic nervous systems, inflammation) may elicit symptomatic relief in individuals suffering from these whole-body adverse outcomes.

Copyright © 2015. Published by Elsevier Inc.

Language: en