This study examined changes in salivary cortisol levels pre-to-post-treatment in adult female rape victims diagnosed with post traumatic stress disorder (PTSD) randomly assigned to be treated with either Prolonged Exposure Therapy or Eye Movement Desensitization and Reprocessing. Salivary cortisol was collected at baseline, session 3, and session 9. A significant decrease in salivary cortisol levels was observed in individuals classified as treatment responders in both treatment conditions. Findings suggest that successful exposure-based treatments for PTSD which result in trauma-related and depressive symptom reduction may impact the action of the hypothalamic-pituitary-adrenal axis as measured by changes in level of salivary cortisol from pre-to-post-treatment.
Background: Despite concerns over measurement error, self-report continues to be the most common measure of adolescent alcohol use used by researchers. Objective measures of adolescent alcohol use continue to advance; however, they tend to be cost prohibitive for larger studies. By combining appropriate statistical techniques and validation subsamples, the benefits of objective alcohol measures can be made more accessible to a greater number of researchers. Objectives: To compare three easily implemented methods to correct for measurement error when objective measures of alcohol use are available for a subsample of participants, regression calibration, multiple imputation for measurement error (MIME), and probabilistic sensitivity analysis (PSA), and provide guidance regarding the use of each method in scenarios likely to occur in practice. Methods: This simulation experiment compared the performance of each method across different sample sizes, both differential and non-differential error, and differing levels of sensitivity and specificity of the exposure measure. Results: Failure to adjust for measurement error led to substantial bias across all simulated scenarios ranging from a 35% to 208% change in the log-odds. For non-differential misclassification, regression calibration reduced this bias to between a 1% and 23% change in the log-odds regardless of sample size. At higher sample sizes, MIME produced approximately unbiased (between a 0% and 9% change in the log-odds) and relatively efficient corrections for both non-differential and differential misclassification. PSA provided little utility for correcting misclassification due to the inefficiency of its estimates. Conclusion: Concern over measurement error resulting from self-reported adolescent alcohol use persists in research. Where appropriate, methods involving validity subsamples provide an efficient avenue for addressing these concerns.
Knowledge about the transmission, prevention, and treatment of HIV remains a critical element in psychosocial models of HIV risk behavior and is commonly used as an outcome in HIV prevention interventions. However, most HIV knowledge questions have not undergone rigorous psychometric testing such as using item response theory. The current study used data from six studies of men who have sex with men (MSM; n = 3565) to (1) examine the item properties of HIV knowledge questions, (2) test for differential item functioning on commonly studied characteristics (i.e., age, race/ethnicity, and HIV risk behavior), (3) select items with the optimal item characteristics, and (4) leverage this combined dataset to examine the potential moderating effect of age on the relationship between condomless anal sex (CAS) and HIV knowledge. Findings indicated that existing questions tend to poorly differentiate those with higher levels of HIV knowledge, but items were relatively robust across diverse individuals. Furthermore, age moderated the relationship between CAS and HIV knowledge with older MSM having the strongest association. These findings suggest that additional items are required in order to capture a more nuanced understanding of HIV knowledge and that the association between CAS and HIV knowledge may vary by age.
The role of deviant peers in adolescent antisocial behavior has been well documented, but less is known about individual differences in susceptibility to negative peer influence. This study examined whether specific temperament dimensions moderate the prospective relationship between peer deviance and delinquent behavior in early adolescence. Participants included 704 adolescents recruited from the community. At baseline, parents provided information on adolescents' temperament and youth reported on their own and their friends' delinquent behavior. Selfreports of adolescents' delinquent behavior were collected again 16 months later. Peer deviance was related to delinquent behavior over time more strongly for adolescents with low levels of task orientation, flexibility, and positive mood, compared to youth with high levels of task orientation, flexibility, and positive mood. Analyses of gender differences indicated that low flexibility increased susceptibility to negative peer influence only for males, but not females. General activity level and sleep rhythmicity did not moderate the effect of peer behavior on delinquency.
by
Monica Uddin;
Shun-Chiao Chang;
Chao Zhang;
Kerry Ressler;
Kristina B. Mercer;
Sandro Galea;
Katherine M. Keyes;
Katie A. McLaughlin;
Derek E. Wildman;
Allison E. Aiello;
Karestan C. Koenen
Background: A growing literature indicates that genetic variation, in combination with adverse early life experiences, shapes risk for later mental illness. Recent work also suggests that molecular variation at the ADCYAP1R1 locus is associated with posttraumatic stress disorder (PTSD) in women. We sought to test whether childhood maltreatment (CM) interacts with ADCYAP1R1 genotype to predict PTSD in women.
Methods: Data were obtained from 495 adult female participants from the Detroit Neighborhood Health Study. Genotyping of rs2267735, an ADCYAP1R1 variant, was conducted via TaqMan assay. PTSD, depression, and CM exposure were assessed via structured interviews. Main and interacting effects of ADCYAP1R1 and CM levels on past month PTSD and posttraumatic stress (PTS) severity were examined using logistic regression and a general linear model, respectively. As a secondary analysis, we also assessed main and interacting effects of ADCYAP1R1 and CM variation on risk of past-month depression diagnosis and symptom severity.
Results: No significant main effects were observed for ADCYAP1R1 genotype on either PTSD/PTS severity. In contrast, a significant ADCYAP1R1 × CM interaction was observed for both past month PTSD and PTS severity, with carriers of the "C" allele showing enhanced risk for these outcomes among women exposed to CM. No significant main or interaction effects were observed for past month depression/depression severity.
Conclusions: Genetic variation at the ADCYAP1R1 locus interacts with CM to shape risk of later PTSD, but not depression, among women. The molecular mechanisms contributing to this interaction require further investigation.
Elucidating whether PTSD symptoms predict poorer social connectedness over time (i.e. social erosion) and/or that poor social connectedness contributes to maintenance of PTSD (i.e. social causation) has implications for PTSD treatment and relapse prevention. Most extant research has been cross-sectional and examined overall PTSD symptoms. Evidence of longitudinal associations among heterogeneous PTSD symptom clusters and social connectedness could provide insight into more nuanced targets for intervention. Using data from 1,491 U.S. military veterans in residential treatment for PTSD at 35 Department of Veterans Affairs facilities, we evaluated a two-wave cross-lagged panel model including a five-factor model of PTSD and two aspects of social connectedness. PTSD, quality of connectedness (i.e. degree of distress related to interpersonal conflict), and structural social support (i.e. number of days of contact with supportive loved ones) in the past 30 days were assessed at baseline and 4 months after discharge. The largest effect was greater severity of PTSD dysphoric arousal symptoms (i.e. irritability/anger, poor concentration, and sleep problems) at baseline predicting more conflict-related distress at follow-up (β = 0.43). Post-hoc symptom-level analyses indicated that irritability/anger drove this association. In addition, conflict-related distress predicted greater PTSD symptom severity across all five clusters (β’s = 0.10 to 0.14, p’s < 0.01). More days of contact predicted lower severity of avoidance and numbing symptoms (β’s = −.05 and −.07, p’s < 0.01), along with individual symptoms within these clusters, plus flashbacks. Results support both social erosion and social causation models. Engaging loved ones in veterans’ treatment and targeting dysphoric arousal symptoms, particularly anger and irritability, may improve long-term PTSD and relationship outcomes, respectively.
A multidisciplinary expert review of key issues and future directions from the conference “Controversial labels and clinical uncertainties: psychogenic disorders, conversion disorder, and functional symptoms.”
On October 9 and 10, 2015, a conference entitled “Controversial labels and clinical uncertainties: psychogenic disorders, conversion disorder, and functional symptoms” was held at the Center for Ethics, Emory University, Atlanta, GA, USA. This conference brought together a select group of 30 distinguished thought leaders and practitioners, including ethicists, researchers, clinicians, humanities scholars, and advocates to discuss the unique challenges and controversies related to the diagnosis, treatment, and stigma for patients with what is currently recognized as functional (“psychogenic”) neurological disorders. Our group of experts explored the conflicts and ethical tensions within health care that must be addressed in order to advance care for these disorders. What follows is a reflection on the conversations between conference attendees outlining key challenges and value conflicts in the diagnosis and treatment of patients with functional disorders. With this report, we aim to provide a roadmap for reducing stigma and improving care for functional neurological disorders (FND). A path forward would involve (1) setting a multifactorial research agenda that equally prioritized access to effective psychotherapy as well as identification of novel biomarkers; (2) empowering patients with FND to be heard and to drive changes in care; and (3) reducing isolation for clinicians by providing formal training and setting up multidisciplinary care teams and support networks.
Depressive symptoms and hopelessness as mediators of the daily hassles-suicidal ideation link in low-income African American women exposed to intimate partner violence (n = 100) were investigated. As hypothesized, daily hassles, depressive symptoms, and hopelessness were each significantly and positively associated with suicidal ideation. Moreover, the relation between daily hassles and suicidal ideation was, in part, accounted for by depressive symptoms and hopelessness. This study demonstrates the importance of assessing for the presence of these risk factors when determining the likelihood that an abused African American woman will consider suicide. The findings further highlight the value of designing and implementing interventions that target the reduction in depressive symptoms and hopelessness in abused African American women exposed to daily hassles to reduce their suicide risk.
Background Molecular mechanisms underlying psychological sequelae of exposure to stressful experiences, such as posttraumatic stress disorder (PTSD) and depression, are not well understood. Methods Using convergent evidence from animal and human transcriptomic and genomic studies, we aimed to identify genetic mechanisms underlying depression and anxiety after traumatic experiences. Results From a transcriptome-wide analysis in mice, we found the Ppm1f gene to be differentially expressed in the amygdala and medial prefrontal cortex (mPFC) a week after immobilization stress. Next, we found that PPM1F messenger RNA levels in human blood were downregulated in cases with symptoms of comorbid PTSD and depression and consistently in cases with anxiety symptoms in a separate human dataset. Furthermore, we showed that a genetic variant of PPM1F, rs17759843, was associated with comorbid PTSD and depression and with PPM1F expression in both human brain and blood. Given prior reported mechanistic links between PPM1F and CAMK2 (CAMKII), we examined blood messenger RNA level of CAMK2G in humans and found it to be lower in cases with comorbid PTSD and depression. We also found that PPM1F protein levels and colocalization with CAMK2G were altered in amygdala and mPFC of male mice. Additionally, we found that a systemic dose of corticosterone blocked the depressive-like phenotype elicited by stress in female mice. Lastly, corticosterone rescued the anxiety-like phenotype and messenger RNA levels of Ppm1f in amygdala and mPFC in male mice and in mPFC of female mice. Conclusions Taken together, our data suggest a mechanistic pathway involving PPM1F and CAMK2G in stress- and trauma-related manifestation of anxiety and depression across species.
Stress and trauma profoundly influence psychiatric biobehavioral outcomes. The identification of treatment and biomarker targets would be accelerated by a broad understanding of the biological responses to these events. The goal of this study was to determine genes responsive to auditory fear conditioning (FC), a well-characterized amygdala-dependent rodent model of threat-exposure, in the presence or absence of prior stress history, providing insight into the physiological processes underlying response to trauma. RNA-sequencing was performed in blood and amygdala from mice that underwent fear conditioning with (Immo+FC) and without (FC) prior immobilization stress, a paradigm that induces HPA axis, and behavioral stress sensitization. In the amygdala, 607 genes were regulated by FC vs. home-cage (HC) controls, and 516 genes differed in stress-sensitized mice (Immo+FC vs. FC). In the former, we observed an enhancement of specific biological processes involved in learning and synaptic transmission, and in the latter processes associated with cell proliferation and the cellular response to drugs. In the blood of stress-sensitized animals, 468 genes were dynamically regulated when compared to FC, and were enriched for the biological pathways of inflammation and cytokine signaling. This study identified genes and pathways that respond to threat in the amygdala and blood of mice with and without a prior stress history and reveals the impact of stress history on subsequent inflammation. Future studies will be needed to examine the role of these dynamically regulated genes may play in human clinical stress and trauma-related disorders.