Model of Post-traumatic Growth in Newly Traumatized vs. Retraumatized Adolescents

Background: In our analysis of adolescents affected by the 2016 Fort McMurray wildfire, we observed many negative mental health effects in individuals with a prior history of psychological trauma. Elevated rates of depression and markers of post-traumatic stress disorder (PTSD) were observed, consistent with the hypothesis that prior trauma may reduce sensitivity thresholds for later psychopathology (stress sensitization). Surprisingly, levels of anxiety did not differ based on prior trauma history, nor were retraumatized individuals at increased risk for recent (past month) suicidal ideation. These results are more suggestive of inoculation by prior trauma than stress sensitization. This led us to consider whether individuals with a prior trauma history showed evidence of Post-Traumatic Growth (PTG), a condition in which the experience of a previous trauma leads to areas of sparing or even improvement.Method: To investigate this issue, we generated a structural equation model (SEM) exploring the role of anxiety in previously traumatized (n = 295) and wildfire trauma alone (n = 740) groups. Specifically, models were estimated to explore the relationship between hopelessness, anxiety, PTSD symptoms, self-efficacy and potential protective factors such as friend and family support in both groups. The model was tested using a cross-sectional sample of affected youth, comparing effects between the two groups.Results: While both models produced relatively good fit, differences in the effects and chi-squared values led us to conclude that the groups are subject to different causal specifications in a number of areas, although details warrant caution pending additional investigation.Discussion: We found that adolescents with a prior trauma history appear to have a more realistic appraisal of potential difficulties associated with traumatic events, and seem less reactive to potentially unsettling PTSD symptoms. They also seemed less prone to overconfidence as they got older, an effect seen in the adolescents without a history of trauma. Our findings provide preliminary evidence that the construct of anxiety may work differently in newly traumatized and retraumatized individuals, particularly in the context of mass trauma events.

Sensitization or inoculation: Investigating the effects of early adversity on personality traits and stress experiences in adulthood

Cumulative evidence has been found for the associations between personality traits and stress experiences in adulthood. However, less is known about the moderating mechanisms underlying these associations. The present study tested whether the stress sensitization and stress inoculation hypotheses could be applied to the relationship between early adversity and personality in adulthood. Specifically, we tested the linear and curvilinear relations between early adversity (measured retrospectively) and adulthood personality traits, as well as the linear and curvilinear moderating effects of early adversity on the associations between adulthood stress and personality traits. Samples of older adults from the Health and Retirement Study (HRS; N = 6098) and middle-aged adults from the Midlife in the United States Survey (MIDUS; N = 6186) were used. Across the two samples, positive linear associations were found between retrospective early adversity and neuroticism. The results also suggested significant linear effects of early adversity on the association between ongoing chronic stressors and neuroticism such that individuals with moderate exposure to early adversity showed stronger associations between ongoing chronic stressors and neuroticism. Results from the current research were more in line with the stress sensitization model. No support was found for the stress inoculation effects on personality.

Emotion regulation deficits mediate childhood sexual abuse effects on stress sensitization and depression outcomes

Child sexual abuse (CSA) is a notable risk factor for depressive disorders. Though multiply determined, increased sensitivity to stress (stress sensitization) and difficulty managing distress (emotion regulation) may reflect two pathways by which CSA confers depression risk. However, it remains unclear whether stress sensitization and emotion regulation deficits contribute to depression risk independently or in a sequential manner. That is, the frequent use of maladaptive emotion regulation responses and insufficient use of those that attenuate distress (adaptive emotion regulation) may lead to stress sensitization. We tested competing models of CSA, stress sensitization, and emotion regulation to predict depression symptoms and depressive affects in daily life among adults with and without histories of CSA. Results supported a sequential mediation: CSA predicted greater maladaptive repertoires that, in turn, exacerbated the effects of stress on depression symptoms. Maladaptive responses also exacerbated the effects of daily life stress on contemporaneous negative affect (NA) levels and their increase over time. Independent of stress sensitization, emotion regulation deficits also mediated CSA effects on both depressive outcomes, though the effect of maladaptive strategies was specific to NA, and adaptive responses to positive affect. Our findings suggest that emotion regulation deficits and stress sensitization play key intervening roles between CSA and risk for depression.

Stress sensitization to depression following childhood adversity: Moderation by HPA axis and serotonergic multilocus profile scores

Childhood adversity appears to sensitize youth to stress, increasing depression risk following stressful life events occurring throughout the lifespan. Some evidence suggests hypothalamic–pituitary–adrenal (HPA) axis-related and serotonergic genetic variation moderates this effect, in a “gene-by-environment-by-environment” interaction (G × E × E). However, prior research has tested single genetic variants, limiting power. The current study uses a multilocus genetic profile score (MGPS) approach to capture polygenic risk relevant to HPA axis and serotonergic functioning. Adolescents (N = 241, Mage = 15.90) completed contextual-threat-based interviews assessing childhood adversity and acute life events, and diagnostic interviews assessing depression. Established MGPSs indexed genetic variation linked to HPA axis (10 single nucleotide polymorphisms [SNPs]) and serotonergic (five SNPs) functioning. Results showed significant MGPS × Childhood Adversity × Recent Life Stress interactions predicting depression for both HPA axis and serotonergic MGPSs, with both risk scores predicting stronger Childhood Adversity × Recent Stress interactions. Serotonergic genetic risk specifically predicted sensitization to major interpersonal stressors. The serotonergic MGPS G × E × E was re-tested in an independent replication sample of early adolescent girls, with comparable results. Findings support the notion that genetic variation linked to these two neurobiological symptoms alters stress sensitization, and that gene-by-environment (G × E) interactions may be qualified by environmental exposures occurring at different points in development.

S225. STRESS SENSITIZATION IN INDIVIDUALS WITH SUBCLINICAL SYMPTOMS INDICATIVE OF PSYCHOPATHOLOGY

Background Repeated exposure to stressors can sensitize the stress system and in turn propel the development of various psychiatric disorders. Stress sensitization can be identified through stress reactivity patterns. Individuals at risk of developing psychosis for example, already show aberrant patterns of daily stress reactivity prior to clinical diagnosis, with blunted physiological responses to mild stressors that could be indicative of a dysregulation of the hypothalamic pituitary adrenocortical axis. In parallel, while they do not show significant physiological responses to the stressor, they report significant increases in negative affect (NA) ensuing from it. This study aims to test whether sensitization can already be observed in healthy volunteers exhibiting only subclinical symptoms. Methods Thirty, first year students took part in two laboratory sessions where stress was induced using a modified version of the Montreal Imaging Stress Task (MIST), one week apart. Baseline measures of psychopathology were collected using the Symptom Checklist 90 (SCL-90). During the laboratory sessions, continuous ECG signals were collected, as well as five subjective stress measures per session. We calculated average heart rate (HR) and heart rate variability (HRV) per condition. Multilevel models testing the three-way interaction between psychopathology, session, and condition with individual data points nested within days were used to assess overall psychopathology and more specifically subclinical symptoms of psychosis in repeated stress reactivity. Results Mixed models investigating repeated stress in overall psychopathology indicates a significant three way interaction for HR (β = -.15, SE=.01, p< .01), and HRV (β = -.01, SE=.04, p= .02), with individuals scoring lower on the scl-90 exhibiting comparable increases in HR and decreases in HRV on both sessions. In contrast, individuals scoring higher on the scale show a blunted response on the second session compared to the first. Analyses with stress (β = .03, SE= .01, p= .01), and NA (β = .06, SE=.29, p= .03) show that generally the stressor elicited a mild negative subjective response with a decrease in stress and NA that was comparable on both sessions for individuals scoring lower on the scl-90. No subjective reactivity was reported on the second session for participants scoring high on the scale. Likewise, models that focused on subclinical psychotic symptoms found similar significant interactions. In the same way as in the analyses with psychopathology we find significant interactions for stress (β = .36, SE= .11, p< .01), NA (β = .06, SE=.03, p= .03) HR (β = -1.08, SE=.13 p< .01), and HRV (β = 3.72, SE=.39, p< .01). Analyses show the same comparable patterns of reactivity in both sessions for participants low in psychosis, and a blunted response on the second session for participants high in psychosis. Discussion Symptoms of psychopathology and more specifically psychosis are related to blunted stress reactivity during a second exposure to the same stressor. Psychopathological vulnerability may be reflected in a blunting response to repeated stress in healthy individuals with subclinical symptoms. Findings suggest that dysregulation in the stress system may be present long before individual complaints, further highlighting the need for early intervention.