Pathways of risk, resilience, and recovery: impact of stress and trauma on women and girls

Introduction Stress and trauma are ubiquitous experiences that have been identified as transdiagnostic factors associated with a higher risk for disproportionately detrimental physical and mental health outcomes for women and girls, including posttraumatic and affective disorders (1, 2). The underlying mechanisms of this increased risk likely involve complex biopsychosocial processes that have yet to be fully identified (3). Furthermore, the role of protective and resilience factors buffering these associations remain relatively unexamined. In this Research Topic, we aim to address this complexity from various interdisciplinary perspectives and discuss the biological, psychological, and social factors that may underpin both risk and resilience in the face of stressful and traumatic experiences. This collection of research includes biological substrates of risk, such as neural (Eder-Moreau et al.), genetic (Carvalho et al.) and endocrine (Brouillard et al.) factors. It also addresses potential social determinants of poor health, such as economic precarity and social isolation (Pazderka et al.) as well as the co-occurrence among mental health, risky behavior, and infectious disease among women released from incarceration (Johnson et al.). Social determinants also hold the potential for buffering potentially negative impact, through resources accessed in the face of adversity (Zamir et al.). The psychological underpinnings that may help explain the associations between stressful experience and compromised outcomes are also explored. These include interpretation of stressors from a social perspective (Azoulay and Gilboa-Schechtman) as well as from a psychological perspective, such as mentalizing (Ensink et al.). Finally, this Research Topic considers potential mechanisms for familial, intergenerational effects of maternal stress, such as parenting (Ahmad et al.)

Greater hippocampal volume is associated with PTSD treatment response

Previous research associates smaller hippocampal volume with posttraumatic stress disorder (PTSD). It is unclear, however, whether treatment affects hippocampal volume or vice versa. Seventy-six subjects, 40 PTSD patients and 36 matched trauma-exposed healthy resilient controls, underwent clinical assessments and magnetic resonance imaging (MRI) at baseline, and 10 weeks later, during which PTSD patients completed ten weeks of Prolonged Exposure (PE) treatment. The resilient controls and treatment responders (n=23) had greater baseline hippocampal volume than treatment non-responders (n=17) (p=0.012 and p=0.050, respectively), perhaps due to more robust fear-extinction capacity in both the initial phase after exposure to trauma and during treatment

Curtailing the communicability of psychiatric disorders

Although psychiatric disorders are classified as non-communicable diseases, we believe this classification is too rigid and limiting. We present evidence of the communicability of psychiatric disorders through three major pathways: infectious and ecological, familial, and sociocultural communicability. Successful strategies developed to control the spread of communicable infectious diseases are relevant to curtailing the communicability of psychiatric disorders, thereby reducing their burden. Current interventions and policies that conceptualise psychiatric illnesses as non-communicable mostly focus on the individual. By applying strategies from infectious disease and chronic illness prevention models within a socioecological framework, we posit a broad communicable chronic disease psychiatric illness control plan for effectively treating the patient with the psychiatric disorder (host) as early as possible, providing benefits to their family and the community, and preventing transmission to others

PTSD remission after prolonged exposure treatment is associated with anterior cingulate cortex thinning and volume reduction

Background: Brain structures underlying posttraumatic stress disorder (PTSD) have been a focus of imaging studies, but associations between treatment outcome and alterations in brain structures remain largely unexamined. We longitudinally examined the relation of structural changes in the rostral anterior cingulate cortex (rACC), a previously identified key region in the PTSD fear network, to outcome of prolonged exposure (PE) treatment. Method: The sample included 78 adults (53 women): 41 patients with PTSD and 37 trauma-exposed healthy volunteers (TE-HCs). Patients underwent a 10-week course of PE treatment and completed pre- and posttreatment assessments and magnetic resonance imaging (MRI) structural scans. TE-HCs also underwent assessment and MRI at baseline and 10 weeks later. PE remitters (n = 11), nonremitters (n = 14), and TE-HCs, were compared at baseline on demographic and clinical characteristics and ACC structure. Remitters, nonremitters, and TE-HCs were compared for pre- to posttreatment clinical and structural ACC change, controlling for potential confounding variables. Results: There were no baseline differences in structure between PTSD and TE-HCs or remitters and nonremitters. Following treatment, PTSD remitters exhibited cortical thinning and volume decrease in the left rACC compared with PTSD nonremitters and TE-HCs. Conclusions: These results, while in need of replication, suggest that PE treatment for PTSD, by extinguishing maladaptive trauma associations, may promote synaptic plasticity and structure change in rACC. Future research should explore possible underlying mechanisms