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Abstract Several studies have reported the factor structure of posttraumatic stress disorder (PTSD) using confirmatory factor analysis (CFA). The results show models with different number of factors, high correlations between factors, and symptoms that belong to different factors in different models without affecting the fit index. These elements could suppose the existence of considerable item cross-loading, the overlap of different factors or even the presence of a general factor that explains the items common source of variance. The aim is to provide new evidence regarding the factor structure of PTSD using CFA and exploratory structural equation modeling (ESEM). In a sample of 1,372 undergraduate students, we tested six different models using CFA and two models using ESEM and ESEM bifactor analysis. Trauma event and past-month PTSD symptoms were assessed with Life Events Checklist for DSM-5 (LEC–5) and PTSD Checklist for DSM-5 (PCL–5). All six tested CFA models showed good fit indexes (RMSEA = .051–.056, CFI = .969–.977, TLI = .965–.970), with high correlations between factors ( M = .77, SD = .09 to M = .80, SD = .09). The ESEM models showed good fit indexes (RMSEA = .027–.036, CFI = .991–.996, TLI = .985–.992). These models confirmed the presence of cross-loadings on several items as well as loads on a general factor that explained 76.3% of the common variance. The results showed that most of the items do not meet the assumption of dimensional exclusivity, showing the need to expand the analysis strategies to study the symptomatic organization of PTSD.
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Epigenetic research in post-traumatic stress disorder (PTSD) is essential, given that environmental stressors and fear play such a crucial role in its development. As such, it may provide a framework for understanding individual differences in the prevalence of the disorder and in treatment response. This paper reviews the epigenetic markers associated with PTSD and its treatment, including candidate genes and epigenome-wide studies. Because the etiopathogenesis of PTSD rests heavily on learning and memory, we also draw upon animal neuroepigenetic research on the acquisition, update and erasure of fear memory, focusing on the mechanisms associated with memory reconsolidation. Reconsolidation blockade (or impairment) treatment in PTSD has been studied in clinical trials and, from a neurological perspective, may hold promise for identifying epigenetic markers of successful therapy. We conclude this paper by discussing several key considerations and challenges in epigenetic research on PTSD in humans.