Vaginal microbiota of American Indian women and associations with measures of psychosocial stress

Molecular-bacterial vaginosis (BV) is characterized by low levels of vaginal Lactobacillus species and is associated with higher risk of sexually transmitted infections (STI). Perceived psychosocial stress is associated with increased severity and persistence of infections, including STIs. American Indians have the highest rates of stress and high rates of STIs. The prevalence of molecular-BV among American Indian women is unknown. We sought to evaluate measures of psychosocial stress, such as historic loss (a multigenerational factor involving slavery, forced removal from one’s land, legally ratified race-based segregation, and contemporary discrimination) and their association with the vaginal microbiota and specific metabolites associated with BV, in 70 Northwestern Plains American Indian women. Demographics, perceived psychosocial stressors, sexual practices, and known BV risk factors were assessed using a modified version of the American Indian Service Utilization, Psychiatric Epidemiology, Risk and Protective Factors Project survey. Self-collected mid-vaginal swabs were profiled for bacterial composition by 16S rRNA gene amplicon sequencing and metabolites quantified by targeted liquid-chromatography mass spectrometry. Sixty-six percent of the participants were classified as having molecular-BV, with the rest being either dominated by L. crispatus (10%) or L. iners (24%). High levels of lifetime trauma were associated with higher odds of having molecular-BV (adjusted Odds Ratio (aOR): 2.5, 95% Credible Interval (CrI): 1.1–5.3). Measures of psychosocial stress, including historic loss and historic loss associated symptoms, were significantly associated with lifestyle and behavioral practices. Higher scores of lifetime trauma were associated with increased concentrations of spermine (aFC: 3.3, 95% CrI: 1.2–9.2). Historic loss associated symptoms and biogenic amines were the major correlates of molecular-BV. Historical loss associated symptoms and lifetime trauma are potentially important underlying factors associated with BV.

Lifetime trauma history and cognitive functioning in major depression and their role for cognitive-behavioral therapy outcome

Background While cognitive-behavioral therapy (CBT) is the gold-standard psychological treatment for major depression (MD), non-response and lacking stability of treatment gains are persistent issues. Potential factors influencing treatment outcome might be lifetime trauma history and possibly associated primarily prefrontal-cortex- and hippocampus-dependent cognitive alterations. Method We investigated MD and healthy control participants with (MD+T+, n = 37; MD-T+, n = 39) and without lifetime trauma history (MD+T-, n = 26; MD-T-, n = 45) regarding working memory, interference susceptibility, conflict adaptation, and autobiographical memory specificity. Further, MD+T+ (n = 21) and MD+T- groups (n = 16) were re-examined after 25 CBT sessions, with MD-T- individuals (n = 34) invited in parallel in order to explore the stability of cognitive alterations and the predictive value of lifetime trauma history, cognitive functioning, and their interaction for treatment outcome. Results On a cross-sectional level, MD+T+ showed the highest conflict adaptation, but MD+T- the lowest autobiographical memory specificity, while no group differences emerged for working memory and interference susceptibility. Clinical improvement did not differ between groups and cognitive functioning remained stable over CBT. Further, only a singular predictive association of forward digit span, but no other facets of baseline cognitive functioning, lifetime trauma history, or their interaction with treatment outcome emerged. Discussion These results indicate differential roles of lifetime trauma history and psychopathology for cognitive functioning in MD, and add to the emerging literature on considering cognitive, next to clinical remission as a relevant treatment outcome.

116Dementia risk in individuals with lifetime major trauma and post-traumatic stress disorder (PTSD) symptoms

Background Increasing evidence suggests that stress may be a risk factor for dementia, however further investigation is required particularly in community-dwelling individuals. This study investigated whether lifetime major trauma with and without re-experiencing of PTSD symptoms is associated with dementia risk. Methods Participants were 1,700 community-dwelling men and women enrolled in the ESPRIT study of later-life neuropsychiatric disorders. Lifetime major trauma and PTSD were assessed using Watson’s PTSD Inventory. Cognitive function was measured using tests of global cognition, visual memory, verbal fluency, psychomotor speed and executive function. Fourteen-year incident dementia was diagnosed according to DSM-IV criteria. The association between lifetime trauma and cognition, as well as incident dementia was determined by multivariate logistic regression and Cox-proportional hazards regression, respectively. Results An unexpected, yet consistent finding was the association between lifetime major trauma without re-experiencing symptoms, and better baseline cognition (global OR: 0.67 [95% CI: 0.52-0.87], executive function OR: 0.69 [95% CI: 0.51-0.93]). Furthermore, lifetime trauma without re-experiencing symptoms was associated with a decreased risk of dementia (HR: 0.63, 95% CI: 0.44-0.91), particularly for females (HR: 0.49, 95% CI: 0.29-0.80). Conclusions Lifetime major trauma without re-experiencing symptoms may be protective for later-life cognitive function and could reduce dementia risk, especially in females. The mechanisms and moderating factors underlying these association requires further investigation. Key messages This study presents novel findings, and suggests that in some instances, experiencing traumatic events may be beneficial in later-life health.

The impact of lifetime interpersonal and intentional trauma on cognition and vulnerability to psychosis in bipolar disorder

Background Studies have shown that over half of individuals with bipolar disorder experience early-life trauma, which may influence clinical outcomes, including suicidality and presence of psychotic features. However, studies report inconsistent findings regarding the effect of trauma on cognitive outcomes in bipolar disorder. Aims Our study explores the effect of lifetime trauma on the level of vulnerability to psychosis and cognitive performance in participants with bipolar disorder. Method We evaluated lifetime trauma history in 236 participants with a diagnosis of bipolar disorder type 1 or 2, using the Structured Clinical Interview for DSM-IV and the Childhood Trauma Questionnaire. We classified trauma types based on the Substance Abuse and Mental Health Services Administration's concept of trauma, which characterises the type of experienced trauma (e.g. interpersonal and intentional, accidental or naturally occurring). Our primary outcome measures of interest were vulnerability to psychosis (Schizotypal Personality Questionnaire), cognitive performance (MATRICS Consensus Cognitive Battery) and social functioning (Social Adjustment Scale Self-Report). Results Multivariate analysis of covariance showed a significant effect of trauma type on the Schizotypal Personality Questionnaire cognitive–perceptual domain (F(3) = 6.7, P < 0.001). The no-trauma group had lower cognitive–perceptual schizotypal features compared with the accidental and intentional trauma (P < 0.001) and interpersonal and intentional trauma (P = 0.01) groups. Conclusions Our results highlight the need for careful trauma inquiry in patients with bipolar disorder, and consideration of how trauma-focused or -informed treatments may be an integral part of treatment planning to improve outcomes in bipolar disorder.

Abstract P080: Lifetime Trauma Is Associated With Elevated Blood Pressure In Middle-aged And Older Latinas

Introduction: Latina women are more likely than non-Latina White women to have uncontrolled and undertreated hypertension. Prior research suggests greater exposure to traumatic experiences (such as interpersonal violence) is associated with elevated blood pressure and higher cardiovascular disease risk in women. However, few studies have investigated these associations among Latina women, a population that is at increased risk for hypertension. The purpose of this pilot study was to fill knowledge gaps by examining the associations of lifetime trauma (including childhood and adulthood) with blood pressure in middle-aged and older Latinas. Hypothesis: We assessed the hypothesis that lifetime trauma is associated with elevated blood pressure in middle-aged and older Latinas. Methods: Participants were recruited from an existing study in New York City called the Washington Heights/Inwood Comparative Effectiveness Research Project. Data collection consisted of a questionnaire administered by a research coordinator and in-office assessment of two blood pressure readings using recommended guidelines. The average systolic and diastolic blood pressures were calculated from these two measurements. Lifetime trauma was assessed with the Life Events Checklist which assesses 17 potentially traumatic experiences. We summed responses to the Life Events Checklist to create a count of lifetime trauma. Posttraumatic stress disorder (PTSD) symptoms were assessed with the PTSD Checklist-Civilian Version that assess presence and severity of 17 PTSD symptoms in the last month. We used linear regression models to separately examine the associations of lifetime trauma with systolic and diastolic blood pressure adjusted for demographic characteristics, health behaviors, PTSD symptoms, sociocultural factors (such as discrimination and acculturation). Results: The final sample included 50 Latina women (ages 42-77, mean=63.1 [9.7]). All women reported at least one traumatic experience with an average of 4.8 traumatic experiences in their lifetimes (range 1-10). A higher count of lifetime trauma (B [SE] = 5.56 [2.63], p = 0.04) was positively associated with greater systolic blood pressure in adjusted regression models. Although women who reported a higher count of lifetime trauma had higher diastolic blood pressure, this association was not statistically significant (B [SE] = 2.14 [1.67], p = 0.21). Conclusion: Findings indicate a higher count of lifetime trauma is associated with elevations in systolic blood pressure among Latina women. This is consistent with results of studies that have examined associations of lifetime trauma with blood pressure among women in the general population. There is a need for larger studies that incorporate longitudinal designs to investigate the associations of trauma and other sociocultural factors with blood pressure among Latina women.

779 Effects of lifetime trauma exposure on the association between neighborhood safety and sleep

Introduction Greater perceived neighborhood safety (PNS) has been linked to better sleep quality and longer sleep duration. There is also evidence that past exposure to traumatic events may be associated with lower perceived personal safety and poor mental health. Yet, the moderating effects of lifetime trauma exposure on the association between PNS and sleep (duration & latency), has not been assessed. Methods We used cross-sectional data from 190 healthy NYC Latino adults. Lifetime trauma exposure was measured using the Life Events Checklist [LEC] (a count of traumatic events that happened to or were witnessed). In the first set of models, we regressed self-reported sleep duration in minutes (continuous), on PNS (safe vs. not safe), a single item scale, with three covariates (i.e. age, gender, education). In the second set, self-reported sleep latency in minutes, replaced sleep duration. To test for moderation, interaction terms—LEC x PNS—were added to covariate-adjusted models. In sensitivity analyses, regression models were re-run with adjustment for PTSD symptoms, and with short sleep duration (&lt;7hours) as the outcome. Results On average, participants were 37.9 years old (SE= 1.02), 65.8% female, 59.5% foreign-born, and 33.2% completed &lt; Bachelor’s degree. Overall, 43.68% slept &lt;7 hours and 83.68% were exposed to &gt;1 traumatic event in their lifetime. In adjusted models, each traumatic event (b= -2.95, SE = 1.34, p=0.03) was negatively associated with sleep duration. When PTSD symptoms was added, trauma was no longer statistically significant (b=-1.08, SE=1.02, p=0.18). However, each traumatic event exposure was associated with a 10% higher odds of short sleep duration (OR= 1.10, CI=1.02, 1.15), and this association remained significant with adjustment for PTSD symptoms. No interaction terms were significant. In models for sleep latency, there were no statistically significant main effects for LEC or interaction terms. Conclusion We found a dose response in the negative association between lifetime exposure to trauma and sleep duration, but not sleep latency. Trauma history did not moderate the association between PNS and sleep. These results suggest that short sleep duration may be particularly sensitive to lifetime exposure to trauma independent of neighborhood safety. Future studies should replicate these results in population-based samples. Support (if any):

Traumatic life events and risk of post-traumatic stress disorder among the Indigenous population of regional, remote and metropolitan Central-Eastern Australia: a cross-sectional study

ObjectiveTrauma is reported by 70% of the global population and 4% of those exposed develop post-traumatic stress disorder (PTSD), but data from Indigenous populations are limited. We aimed to determine the prevalence, types and age of occurrence of traumatic events among community-living Indigenous Australians and associations with PTSD.DesignLifetime trauma and PTSD were quantified among a broadly representative sample of 544 Indigenous participants using a diagnostic clinical interview. Logistic regression examined predictors of PTSD.SettingMetropolitan, regional and remote areas of Southern Queensland and Northern New South Wales.ParticipantsIndigenous Australians 18 years and older.Outcome measuresPrevalence of traumatic life events and risk of PTSD.Results64.9% of participants (standardised prevalence 62.6%) reported lifetime trauma, with more than one trauma category in 62.3%. Females reported 2.3 times more sexual violence, otherwise no gender differences existed. The prevalence of four common trauma categories were 1.7–3.0 times higher than in the Australian population; physical violence being the highest relative risk. Although overall childhood trauma was not increased, sexual or physical violence before age 15 was twice more common than in the Australian population.The standardised prevalence of 12-month PTSD was 13.3% (95% CI 10.4 to 16.1), 16.1% (95% CI 12.2 to 19.9) in females and 8.2% (95% CI 5.3 to 11.1) in males, three times the Australian rates. In multiple regression analysis, independent predictors of PTSD were female gender (OR 2.1), rural residence (OR 3.0), trauma under age 10 (OR 2.2), sexual (without physical) violence (OR 2.5), physical (without sexual) violence (OR 2.3), and both sexual and physical violence (OR 5.0).ConclusionIndigenous Australians are more likely to experience potentially harmful traumas and develop PTSD than other Australians. Mitigation of trauma among Indigenous Australians, particularly childhood exposure and sexual or physical violence, is essential to reduce their high burden of PTSD.

Volumetric trajectories of hippocampal subfields and amygdala nuclei influenced by adolescent alcohol use and lifetime trauma

Alcohol use and exposure to psychological trauma frequently co-occur in adolescence and share many risk factors. Both exposures have deleterious effects on the brain during this sensitive developmental period, particularly on the hippocampus and amygdala. However, very little is known about the individual and interactive effects of trauma and alcohol exposure and their specific effects on functionally distinct substructures within the adolescent hippocampus and amygdala. Adolescents from a large longitudinal sample (N = 803, 2684 scans, 51% female, and 75% White/Caucasian) ranging in age from 12 to 21 years were interviewed about exposure to traumatic events at their baseline evaluation. Assessments for alcohol use and structural magnetic resonance imaging scans were completed at baseline and repeated annually to examine neurodevelopmental trajectories. Hippocampal and amygdala subregions were segmented using Freesurfer v6.0 tools, followed by volumetric analysis with generalized additive mixed models. Longitudinal statistical models examined the effects of cumulative lifetime trauma measured at baseline and alcohol use measured annually on trajectories of hippocampal and amygdala subregions, while controlling for covariates known to impact brain development. Greater alcohol use, quantified using the Cahalan scale and measured annually, was associated with smaller whole hippocampus (β = −12.0, pFDR = 0.009) and left hippocampus tail volumes (β = −1.2, pFDR = 0.048), and larger right CA3 head (β = 0.4, pFDR = 0.027) and left subiculum (β = 0.7, pFDR = 0.046) volumes of the hippocampus. In the amygdala, greater alcohol use was associated with larger right basal nucleus volume (β = 1.3, pFDR = 0.040). The effect of traumatic life events measured at baseline was associated with larger right CA3 head volume (β = 1.3, pFDR = 0.041) in the hippocampus. We observed an interaction between baseline trauma and within-person age change where younger adolescents with greater trauma exposure at baseline had smaller left hippocampal subfield volumes in the subiculum (β = 0.3, pFDR = 0.029) and molecular layer HP head (β = 0.3, pFDR = 0.041). The interaction also revealed that older adolescents with greater trauma exposure at baseline had larger right amygdala nucleus volume in the paralaminar nucleus (β = 0.1, pFDR = 0.045), yet smaller whole amygdala volume overall (β = −3.7, pFDR = 0.003). Lastly, we observed an interaction between alcohol use and baseline trauma such that adolescents who reported greater alcohol use with greater baseline trauma showed smaller right hippocampal subfield volumes in the CA1 head (β = −1.1, pFDR = 0.011) and hippocampal head (β = −2.6, pFDR = 0.025), yet larger whole hippocampus volume overall (β = 10.0, pFDR = 0.032). Cumulative lifetime trauma measured at baseline and alcohol use measured annually interact to affect the volume and trajectory of hippocampal and amygdala substructures (measured via structural MRI annually), regions that are essential for emotion regulation and memory. Our findings demonstrate the value of examining these substructures and support the hypothesis that the amygdala and hippocampus are not homogeneous brain regions.