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BACKGROUND: Exposure to traumatic events is a necessary but not a sufficient condition for the development of posttraumatic stress disorder (PTSD). Pretrauma, peritrauma and posttrauma factors interact to impact on symptom severity. The aim of the present study is to determine risk factors for PTSD symptoms in Brazilian police officers. METHOD: In a cross-sectional sample of active duty officers (n = 212), participants were asked to complete a socio-demographic questionnaire and self-report scales on affective traits, cumulative critical incident exposure, peritraumatic distress and dissociation, PTSD symptoms, and social support. Hierarchical linear regression analysis was conducted to examine predictors of PTSD symptoms. RESULTS: Variables related to negative affect, job duration, frequency of critical incident exposure, peritraumatic dissociation, and lack of social support remained significant in the final model and explained 55% of the variance in PTSD symptoms. When interaction terms were evaluated, a synergistic effect between negative affect and peritraumatic dissociation was found. CONCLUSIONS: The risk factors found in this study provide clues on how to elaborate primary prevention strategies regarding PTSD symptoms in police officers. Such initiatives may lessen the impact of repeated exposure to traumatic events on police officers over the course of their careers.INTRODUÇÃO: A exposição a eventos traumáticos é uma condição necessária, porém não única, para o desenvolvimento de transtorno de estresse pós-traumático (TEPT). Fatores individuais pré, peri e pós-trauma exercem impacto sobre a gravidade dos sintomas. O objetivo do presente estudo é determinar os fatores de risco para o desenvolvimento de sintomas de TEPT em policiais brasileiros. MÉTODO: Uma amostra transversal de policiais em atividade (n = 212) foi convidada a responder um questionário sóciodemográfico e escalas autoaplicáveis sobre afeto positivo e negativo, frequência de incidentes críticos, sofrimento e dissociação peritraumáticos, sintomas de TEPT e apoio social. Regressão linear hierárquica foi utilizada para avaliar fatores de risco. RESULTADOS: Afeto negativo, tempo de trabalho, frequência de exposição a eventos traumáticos, dissociação peritraumática e apoio social diminuído permaneceram no modelo final e explicaram 55% das variações dos sintomas de TEPT. Foi observado efeito sinérgico entre dissociação peritraumática e afeto negativo. CONCLUSÃO: Baseados nos achados os autores discutem estratégias de prevenção que visam diminuir o impacto da exposição a eventos traumáticos em policiais ao longo de suas carreiras.

INTRODUCTION:It has been reported that posttraumatic stress disorder (PTSD) is associated with secondary spouse/partner (S/P) emotional distress and relationship violence. OBJECTIVE:To investigate the relationships between PTSD, S/P emotional distress and relationship violence among police recruits using a prospective design. METHODS:Two hypotheses were tested in 71 S/Ps: (1) Police officer reports of greater PTSD symptoms after 12 months of police service will be associated with greater secondary trauma symptoms among S/Ps; (2) Greater secondary trauma symptoms among S/Ps at 12 months will be associated with S/P reports of greater relationship violence. METHODS:71 police recruits and their S/Ps were assessed at baseline and 12 months after the start of police officer duty. Using linear and logistic regression, we analyzed explanatory variables for 12 month S/P secondary traumatic stress symptoms and couple violence, including baseline S/P variables and couple violence, as well as exposure and PTSD reports from both S/P and officer. RESULTS:S/P perception of officer PTSD symptoms predicted S/P secondary traumatic stress. OS/P secondary trauma was significantly associated with both total couple violence (.34, p = .004) and S/P to officer violence (.35, p = .003). CONCLUSIONS:Although results from this relatively small study of young police officers and their S/Ps must be confirmed by larger studies in general populations, findings suggest that S/P perception of PTSD symptoms may play a key role in the spread of traumatic stress symptoms across intimate partner relationships and intimate partner violence in the context of PTSD.

Posttraumatic stress disorder (PTSD) is associated with impaired major domains of psychology and behavior. Individuals with PTSD also have increased co-morbidity with several serious medical conditions, including autoimmune diseases, cardiovascular disease, and diabetes, raising the possibility that systemic pathology associated with PTSD might be identified by metabolomic analysis of blood. We sought to identify metabolites that are altered in male combat veterans with PTSD. In this case-control study, we compared metabolomic profiles from age-matched male combat trauma-exposed veterans from the Iraq and Afghanistan conflicts with PTSD (n = 52) and without PTSD (n = 51) ('Discovery group'). An additional group of 31 PTSD-positive and 31 PTSD-negative male combat-exposed veterans was used for validation of these findings ('Test group'). Plasma metabolite profiles were measured in all subjects using ultrahigh performance liquid chromatography/tandem mass spectrometry and gas chromatography/mass spectrometry. We identified key differences between PTSD subjects and controls in pathways related to glycolysis and fatty acid uptake and metabolism in the initial 'Discovery group', consistent with mitochondrial alterations or dysfunction, which were also confirmed in the 'Test group'. Other pathways related to urea cycle and amino acid metabolism were different between PTSD subjects and controls in the 'Discovery' but not in the smaller 'Test' group. These metabolic differences were not explained by comorbid major depression, body mass index, blood glucose, hemoglobin A1c, smoking, or use of analgesics, antidepressants, statins, or anti-inflammatories. These data show replicable, wide-ranging changes in the metabolic profile of combat-exposed males with PTSD, with a suggestion of mitochondrial alterations or dysfunction, that may contribute to the behavioral and somatic phenotypes associated with this disease.