Abstract

Post-traumatic stress disorder (PTSD) and metabolic syndrome (MetS) frequently coexist and share neurobiological and clinical features. In particular, the results of meta-analyses indicate a higher prevalence of MetS in patients with PTSD compared to the general population. PTSD is also a recognized risk factor for MetS. This synchronicity can be partially explained by pathogenetic pathways present in both conditions. These include genetic factors, dysfunction of the hypothalamic-pituitary-adrenal axis, chronic low-grade inflammation, oxidative stress, insulin resistance, and immune dysregulation. Thus, similar mechanisms are involved in the clinical worsening of PTSD and the development of adverse cardiovascular events associated with MetS. Dyssomnias are one of the characteristic clinical features of PTSD. Today, it is believed that posttraumatic circadian rhythm disorders are the core and not a secondary feature of PTSD, which mediate the neurobiological correlates of disorders due to homeostasis imbalance. At the same time, dyssomnias, chronodestruction, and depressive disorders are part of the pathogenesis of insulin resistance, obesity, and MetS. Thus, treatment of dyssomnias is one of the key tasks in the prevention and treatment of comorbid PTSD and MetS. Regulation of sleep processes and circadian rhythms through exogenous intervention, especially with melatonergic drugs, is likely to be a key part of preventing and treating dyssomnias in people who have both PTSD and MetS. The purpose of this review is to analyze the specifics of the relationships between PTSD and MetS, PTSD and dyssomnias, MetS and sleep disorders. We conducted the search in Scopus, Science Direct (from Elsevier), and PubMed, including Medline databases. The key words used were “post-traumatic stress disorder,” “dyssomnias,” “chronodestruction,” and “metabolic syndrome”. The identification of research findings that were not found during online searches involved manual searching of the bibliography of publications.

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