• F Saverio Bersani, Synthia H Mellon, Daniel Lindqvist, Jee In Kang, Ryan Rampersaud, Pramod Rajaram Somvanshi, Francis J Doyle, Rasha Hammamieh, Marti Jett, Rachel Yehuda, Charles R Marmar, and Owen M Wolkowitz.
• Department of Human Neurosciences, Sapienza University of Rome, Viale dell'Università 30, Rome 00185, Italy.
• Mil Med. 2020 Jan 7; 185 (Suppl 1): 311-318.

IntroductionCurrent pharmacological treatments of post-traumatic stress disorder (PTSD) have limited efficacy. Although the diagnosis is based on psychopathological criteria, it is frequently accompanied by somatic comorbidities and perhaps "accelerated biological aging," suggesting widespread physical concomitants. Such physiological comorbidities may affect core PTSD symptoms but are rarely the focus of therapeutic trials.MethodsTo elucidate the potential involvement of metabolism, inflammation, and mitochondrial function in PTSD, we integrate findings and mechanistic models from the DOD-sponsored "Systems Biology of PTSD Study" with previous data on these topics.ResultsData implicate inter-linked dysregulations in metabolism, inflammation, mitochondrial function, and perhaps the gut microbiome in PTSD. Several inadequately tested targets of pharmacological intervention are proposed, including insulin sensitizers, lipid regulators, anti-inflammatories, and mitochondrial biogenesis modulators.ConclusionsSystemic pathologies that are intricately involved in brain functioning and behavior may not only contribute to somatic comorbidities in PTSD, but may represent novel targets for treating core psychiatric symptoms.© Association of Military Surgeons of the United States 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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