Background The objective of this study is to investigate the association between childhood trauma and lipid profiles in adults from a highly traumatized population at-risk for cardiovascular disease. Method We recruited 452 participants, primarily African American, low socioeconomic status from general medical clinics in a large urban hospital. We performed direct comparisons, univariate ANOVA and regression analyses together and separated by sex, examining the associations of child abuse, BMI, lipid lowering drug use, blood pressure, age, and substance use to HDL levels and HDL/LDL ratios. Results A history of moderate to severe levels of childhood trauma and abuse was associated with a significant decrease in HDL levels (p≤0.01) and HDL/LDL ratios (p≤0.001) relative to males with low levels of abuse. This relationship held when the status of lipid-lowering drugs was considered. When controlling for age, substance abuse, tobacco use, and adult trauma, the effects of childhood trauma remained significant. We found a significant child abuse by sex interaction on HDL/LDL ratios (F(1, 369)=13.0, p≤0.0005) consistent with a differential effect of trauma on dyslipidemia in male but not female subjects Conclusions Our data suggest that childhood trauma exposure, obtained with self-report measures, may contribute to increased risk of cardiovascular disease by way of stress-mediated alterations of lipid concentration and composition in male, but not female, subjects.

Dissociative disorders affect 29% of the clinical population, with women diagnosed 9 times more often than men. For this study, the authors used a phenomenological approach to uncover experiences of 5 men with dissociative identity disorder. Findings revealed 5 themes: history, alters, male gender expectations and identity, challenges, and strengths and support. Implications for practitioners are discussed.

Posttraumatic stress disorder (PTSD) is often conceptualized from a fear conditioning perspective given individuals with PTSD demonstrate a reduced ability to inhibit fear even under safe conditions as compared to those without PTSD. The self-medication hypothesis suggests that individuals with PTSD often develop substance use disorders (SUDs) as an attempt to mitigate trauma-related distressing emotions. This investigation examined this hypothesis in a sample 214 participants, of which 81 did not meet criteria for either PTSD or SUDs (No diagnosis Control group); 33 met criteria for lifetime PTSD, but not SUDs (PTSD only group); 54 met criteria for lifetime SUDs, but not PTSD (SUDs only group); and 46 met lifetime criteria for both disorders (PTSD+SUDs group). PTSD was assessed using the modified PTSD Symptoms Scale (mPSS), SUDs were assessed using the Structured Clinical Interview for DSM-IV-TR (SCID). The startle magnitude was assessed using electromyography (EMG) of the eyeblink muscle in response to an acoustic startle probe. Fear-potentiated startle (FPS) was analyzed by comparing startle magnitude at baseline to startle during a fear conditioned stimulus. Results showed that PTSD significantly increased startle responses. However, there was a significant effect of SUDs on fear-potentiated startle to the danger signal, in that those who met criteria for SUDs had reduced fear compared to those who did not. The individuals who had co-morbid PTSD and SUDs did not differ from the Control group. Findings indicate that SUDs may attenuate exaggerated fear responses associated with PTSD. Consistent with the self-medication hypothesis, results suggest that substance use may co-occur with PTSD because it reduces heightened fear load and may allow normalized function in traumatized individuals.

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