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Background The 22q11.2 deletion (22q11Del) is among the strongest known genetic risk factors for psychosis. Stress, a known risk factor for psychosis in the general population, has seldom been studied in 22q11Del. We investigated how lifetime stressors related to symptomatic outcomes in patients with 22q11Del. We also explored this association in individuals with 22q11.2 duplications (22q11Dup), which may be potentially protective against psychosis. Method One hundred individuals (46 with 22q11Del, 30 with 22q11Dup, and 24 healthy controls; Mage = 17.30 years±10.15) were included. Logistic models were used to examine cross-sectional associations between lifetime acute and chronic stressors (severity and count) and the presence (score ⩾3) of positive, negative, and general symptoms, assessed via the Structured Interview for Psychosis-risk Syndromes (SIPS). Results The 22q11Dup group reported the greatest number and severity of acute lifetime stressors, but did not differ from 22q11Del in chronic stressor count or severity. Lifetime chronic and acute stressors were uniquely associated with positive symptoms in 22q11Del (chronic count: odds ratio [OR] = 2.35, p = 0.02; chronic severity: OR = 1.88, p = 0.03; acute count: OR = 1.78, p = 0.03), but not with negative or general symptoms (ps > 0.05). Conclusion Findings suggest that stress may play a role in psychotic symptoms in 22q1Del, while the 22q11Dup CNV appears protective against psychotic symptoms despite higher rates of stressors. Interventions that mitigate effects of stressors in 22qDel may reduce the odds of psychosis in this group. Prospective longitudinal research is needed to replicate these findings.

Objective Whether psychosocial adversity during pregnancy impacts fetal health outcomes at birth remains underexplored. This is a critical issue given significant social disadvantage and psychosocial stress faced by pregnant women worldwide. Study design Measures of social disadvantage and psychological factors, and medical/reproductive and nutritional health status in pregnant women were obtained at each trimester. Using Structural Equation Modeling (SEM), we investigated the relationship of forms of adversity to each other and to infant gestational age, and birthweight. Results Among 399 singletons, Social Disadvantage significantly predicted gestational age (p = 0.003), and residual birthweight (p = 0.006). There was a 0.4 week decrease in gestational age and a 3% decrease in birthweight for each standard deviation increase in Social Disadvantage. Conclusion Significant negative effects of social adversity on the developing fetus were found. Notably, these effects emerged despite good prenatal care and after accounting for maternal age and medical reproductive risk factors.

This study addressed whether lifetime stressor exposure was associated with psychophysiological reactivity and habituation to a novel laboratory-based stressor. Eighty-six participants (Mage = 23.31 years, SD = 4.94) reported their exposure to lifetime non-sport and sport-specific stressors before completing two consecutive trials of the Trier Social Stress Test, while cardiovascular (i.e., heart rate) and endocrine (i.e., salivary cortisol) data were recorded. Exposure to a moderate number of lifetime non-sport and sport-specific stressors was associated with adaptive cardiovascular reactivity, whereas very low or very high stressor exposure was related to maladaptive reactivity. Moreover, experiencing a very low number of lifetime non-sport (but not sport-specific) stressors was associated with poorer habituation. In contrast, lifetime stressor severity was unrelated to cardiovascular reactivity. Finally, greater lifetime non-sport and sport-specific stressor counts were associated with blunted cortisol reactivity and poorer habituation. These results suggest that lifetime stressor exposure may influence sport performers’ acute stress responses.

Background Psychosocial stressors characterized by social threat, such as interpersonal loss and social rejection, are associated with depression in adolescents. Few studies, however, have examined whether social threat affects fronto-cingulate-limbic systems implicated in adolescent depression. Methods We assessed lifetime stressor severity across several domains using the Stress and Adversity Inventory (STRAIN) in 57 depressed adolescents (16.15 ± 1.32 years, 34 females), and examined whether the severity of social threat and non-social threat stressors was associated with gray matter volumes (GMVs) in the anterior cingulate cortex (ACC), amygdala, hippocampus, and nucleus accumbens (NAcc). We also examined how lifetime social threat severity and GMVs in these regions related to depressive symptoms at baseline and over 9 months. Results General stressor severity was related to greater depression severity at baseline and over 9 months. Moreover, greater severity of social threat (but not non-social threat) stressors was associated with smaller bilateral amygdala and NAcc GMVs, and smaller bilateral surface areas of caudal and rostral ACC (all pFDR ⩽ 0.048). However, neither social threat nor non-social threat stressor severity was related to hippocampal GMVs (all pFDR ⩾ 0.318). All fronto-cingulate-limbic structures that were associated with the severity of social threat were negatively associated with greater depression severity over 9 months (all pFDR ⩽ 0.014). Post-hoc analyses suggested that gray matter morphometry of bilateral amygdala, NAcc, and rostral and caudal ACC mediated the association between social threat and depression severity in adolescents over 9 months (all pFDR < 0.048). Conclusions Social threat specifically affects fronto-cingulate-limbic pathways that contribute to the maintenance of depression in adolescents.

Despite considerable research documenting how stress affects brain and neurobehavioral outcomes, few studies have assessed stressor exposure occurring over the entire life span, and no studies have investigated these associations in people living with HIV (PLWH), despite the high stress and disease burden experienced by this population. To address this issue, we examined how cumulative lifetime chronic stressor exposure related to cognition and brain integrity (i.e., gray matter volume) in White and African American PLWH and HIV-uninfected (HIV-) adults.Participants were 91 community-dwelling adults (47.3% PLWH) who completed a comprehensive interview assessing lifetime stressor exposure using the Stress and Adversity Inventory and underwent neuropsychological testing and structural magnetic resonance imaging. Regional brain volumes were derived from T1-weighted images processed through Freesurfer.As hypothesized, greater lifetime chronic stressor exposure was related to worse global cognition ( b = -0.06, standard error [SE] = 0.03, p = .032), processing speed ( b = -0.04, SE = 0.14, p = .041), and executive functioning ( b = -0.06, SE = 0.02, p = .02), and smaller prefrontal cortex (PFC) volume ( b = -16.20, SE = 5.78, p = .007). HIV status did not moderate any of these associations. Moreover, results from mediation analyses demonstrated that the relationship between lifetime chronic stressor exposure and processing speed was fully mediated by PFC volume.These results highlight the critical role of the PFC in the maintenance of processing speed abilities and its vulnerability to cumulative stressor exposure. Specifically, the negative impact of lifetime chronic stressor exposure on cognition-particularly functions reliant on frontal lobe integrity-may be partly driven by smaller volumes in the PFC.

Although substantial research has separately investigated forgiveness, rumination, and depression in the United States, few studies have investigated all three constructs in the same sample and we know of no studies that have examined how forgiveness, rumination, and depression are interrelated across cultures.To address this issue, we conducted a cross-cultural study wherein 204 and 297 healthy young adults from Korea and the United States, respectively, completed the Heartland Forgiveness Scale, Ruminative Response Scale, and Beck Depression Inventory-II.Compared to US participants, Korean participants exhibited more forgiveness, similar levels of rumination, and slightly more depression. Two-group structural equation models revealed that forgiveness was directly related to depressive symptoms, and that forgiveness was indirectly related to depressive symptoms through rumination, in both the United States (proportion mediated = 0.363) and Korea (proportion mediated = 0.394). This indirect association did not differ across cultures.Considered together, these results suggest that forgiveness appears to have beneficial effects on depression that are mediated through forgiveness-related reductions in rumination, and, importantly, that these effects are similar across cultures.

Subjective stress severity appraisals have consistently emerged as better predictors of poor health than stressor exposure, but the reason for this is unclear. Subjective stress may better predict poor health for one of at least two reasons. First, because stressor exposure measures consider all stressors as equal, stress severity measures-which "weight" stressors by self-reported severity-might better predict poor health simply by not treating all stressors as being equally impactful. Second, subjective stress appraisals may index important individual differences in stress vulnerability. We tested these two possibilities in this preregistered, two-study manuscript. Across these two different studies, subjective stress severity was a better predictor of poor health than independently weighted stress severity or stressor exposure. These results demonstrate that, beyond weighting of stressful experiences, subjective stress severity indexes health-relevant individual differences. Moreover, the results suggest that subjective stress severity may be the preferred stress summary metric even when derived from imprecise stress assessment instruments.

Background Life stress and blunted reward processing each have been associated with the onset and maintenance of major depressive disorder. However, much of this work has been cross-sectional, conducted in separate lines of inquiry, and focused on recent life stressor exposure, despite the fact that theories of depression posit that stressors can have cumulative effects over the lifespan. To address these limitations, we investigated whether acute and chronic stressors occurring over the lifespan interacted with blunted reward processing to predict increases in depression over time in healthy youth. Method Participants were 245 adolescent girls aged 8–14 years old (Mage = 12.4, s.d. = 1.8) who were evaluated at baseline and two years later. The reward positivity (RewP), an event-related potential measure of reward responsiveness, was assessed at baseline using the doors task. Cumulative lifetime exposure to acute and chronic stressors was assessed two years later using the Stress and Adversity Inventory for Adolescents (Adolescent STRAIN). Finally, depressive symptoms were assessed at both baseline and follow-up using the Children's Depression Inventory. Results As hypothesized, greater lifetime acute stressor exposure predicted increases in depressive symptoms over two years, but only for youth exhibiting a blunted RewP. This interaction, however, was not found for chronic stressors. Conclusions Lifetime acute stressor exposure may be particularly depressogenic for youth exhibiting a blunted RewP. Conversely, a robust RewP may be protective in the presence of greater acute lifetime stressor exposure.

Psychiatry stands to benefit from brief non-pharmacological treatments that effectively reduce depressive symptoms. To address this need, we conducted a single-blind randomized clinical trial assessing how a 6-day immersive psychosocial training program, followed by 10-min daily psychosocial exercises for 30 days, improves depressive symptoms. Forty-five adults were block-randomized by depression score to two arms: (a) the immersive psychosocial training program and 10-min daily exercise group (36 days total; total n=23; depressed at baseline n=14); or (b) a gratitude journaling control group (36 days total; total n=22; depressed at baseline n=13). The self-report PHQ-9 was used to assess depression levels in both groups at three time points: baseline, study week one, and study week six. Depression severity improved over time, with a significantly greater reduction in the psychosocial training program group (-82.7%) vs. the control group (-23%), p=0.02 for baseline vs. week six. The effect size for this reduction in depression symptoms was large for the intervention group (d=-1.3; 95% CI, -2.07, -0.45; p&nbsp

Although Black American mothers and infants are at higher risk for morbidity and mortality than their White counterparts, the biological mechanisms underlying these phenomena remain largely unknown. To investigate the role that lifetime stressor exposure, perceived stressor severity, and systemic inflammatory markers might play, we studied how these factors were interrelated in 92 pregnant Black American women. We also compared inflammatory marker levels for women who did versus did not go on to give birth preterm. During the early third trimester, women completed the Stress and Adversity Inventory for Adults to assess the stressors they experienced over their lifetime. Women also provided blood samples for plasma interleukin (IL)-6, IL-8, IL-1β, and tumor necrosis factor (TNF)-α quantification. Preterm births were identified by medical record review. Controlling for relevant covariates, there were significant positive associations between average levels of both overall and acute perceived stressor severity and plasma IL-1β levels. Controlling for perceived stress at assessment and exposure to racial discrimination did not affect these results. Mediation models revealed that exposure to more chronic stressors was related to higher plasma IL-1β levels, as mediated by higher average levels of overall perceived stressor severity. Exposure to fewer acute stressors was related to higher plasma IL-1β levels, as mediated by higher average levels of acute perceived stressor severity. Finally, women who went on to give birth preterm had higher levels of plasma IL-6. These data thus highlight the potential importance of assessing and addressing lifetime stressor exposure among mothers before and during maternal-infant care.

Classic theories of stress and health are largely based on assumptions regarding how different psychosocial stressors influence biological processes that, in turn, affect human health and behavior. Although theoretically rich, this work has yielded little consensus and led to numerous conceptual, measurement, and reproducibility issues. Social Safety Theory aims to address these issues by using the primary goal and regulatory logic of the human brain and immune system as the basis for specifying the social-environmental situations to which these systems should respond most strongly to maximize reproductive success and survival. This analysis gave rise to the integrated, multi-level formulation described herein, which transforms thinking about stress biology and provides a biologically based, evolutionary account for how and why experiences of social safety and social threat are strongly related to health, well-being, aging, and longevity. In doing so, the theory advances a testable framework for investigating the biopsychosocial roots of health disparities as well as how health-relevant biopsychosocial processes crystalize over time and how perceptions of the social environment interact with childhood microbial environment, birth cohort, culture, air pollution, genetics, sleep, diet, personality, and self-harm to affect health. The theory also highlights several interventions for reducing social threat and promoting resilience.

Although many emerging adults struggle to gain status and develop social relationships, particularly during the college transition, it remains unclear whether certain personality traits facilitate this transition. Using a longitudinal design, we investigated whether status-related traits-namely, entitlement, intrasexual competitiveness, and dominance-related to the development of status in 91 first-year college students (

Atypically elevated inflammation is a transdiagnostic risk factor for a number of psychiatric (e.g., depression, psychosis) and somatic conditions (e.g., ulcerative colitis, osteoarthritis, rheumatoid arthritis). Inflammation can be influenced by a variety of psychosocial processes, such as emotion regulation. Characterization of which emotion regulation characteristics impact inflammatory biology could help refine psychosocial interventions aimed at normalizing health-harming inflammatory activity for individuals with psychiatric and somatic illnesses. To realize this aim, we systematically reviewed the extant literature on associations between a variety of emotion regulation traits and inflammatory biology. A total of 804 articles were identified, 36 of which were included in the final review. Of these 36 articles, 28 (78%) found that (a) poor emotion regulation is associated with higher levels of inflammatory proteins and/or (b) strong emotion regulation skills are associated with lower levels of inflammatory proteins. The consistency of these results differed as a function of both the emotion regulation construct investigated and methodological characteristics. Results were most consistent for studies testing positive coping/social support seeking or broadly defined emotion regulation/dysregulation. Methodologically, studies testing inflammatory reactivity to an acute stressor, adopting a vulnerability-stress framework, or using longitudinal data most consistently supported study hypotheses. Implications for integrated, transdiagnostic psychoimmunological theories are discussed, as well as recommendations for clinical research.

Although race/ethnicity is associated with substantial differences in risk for depression and other diseases of aging in the United States, the processes underlying these health disparities remain poorly understood. We addressed this issue by examining how levels of a robust marker of inflammatory activity, C-reactive protein (CRP), and depression symptoms varied across racial/ethnic groups. Additionally, we tested whether the inflammation-depression association differed across groups. Data were drawn from the Chicago Community Adult Health Survey, an epidemiological survey examining biopsychosocial factors affecting health and well-being. Participants were 3105 Chicago community adults, of which 610 provided blood samples and were included in analyses. C-reactive protein was assayed from blood samples, and depression symptoms were assessed using the 11-item Center for Epidemiologic Studies-Depression scale. Race/ethnicity was self-reported and consisted of Black, Hispanic, White, and other racial/ethnic groups. Results revealed that these racial/ethnic groups differed in terms of both their CRP and depression levels. Specifically, Black Americans exhibited higher levels of CRP as compared to White and other race/ethnicity Americans. Moreover, Black Americans exhibited more depression symptoms than Hispanic Americans. Finally, we found that inflammatory levels were strongly related to depression symptoms but only for Black Americans, with CRP alone accounting for 8% of the variance in depression symptoms in this subgroup. These data thus point to a biological process that may help to explain disparities in mental health outcomes across race/ethnicity in the United States. At the same time, additional research is needed to understand the social and structural factors driving these effects.

OBJECTIVE: The present study investigated the contribution of health risk factors (using the Charlson Comorbidity Index [CCI]) on cognitive outcomes in a sample of 380 HIV-positive (HIV+; n = 221) and HIV-seronegative (HIV−; n = 159) African American and European American adults aged 50+. METHODS: Participants were recruited from HIV clinics and community advertisements. HIV status was confirmed by serological testing. Self-report and chart history review was used to gather information about medical sss-comorbidities. The Charlson Comorbidity Index (CCI) was used to create a comorbidity score. Participants were administered a brief cognitive test battery. RESULTS: As expected, health risks were greater among those with HIV. There was a HIV × Race interaction on CCI scores, such that in the HIV + group, European Americans had significantly higher CCI scores (M = 3.74; SD = 2.1) than African American HIV + participants (M = 2.70; SD = 1.9). However, in the HIV − group, African Americans had significantly higher CCI scores (M = 2.20; SD = 1.1) than HIV − European American participants (M = 1.80; SD = 1.2). Also, consistent with hypotheses, across the entire sample CCI score was significantly associated with global cognition (β = −.24, p = .02). CONCLUSIONS: Study results underscore the importance of considering HIV serostatus in studies examining racial disparities in health, and how multiple medical risks relate to cognitive outcomes. Neuropsychologists evaluating patients living with HIV should consider how the presence of multiple medical comorbidities may contribute to the course of cognitive decline as people age.

BACKGROUND: Although characterizing associations between inflammation and depression may prove critical for informing theory, research, and treatment decisions, extant research has been limited by ignoring the possibility that inflammation may be simultaneously associated with depression broadly and with a subset of symptoms. This lack of direct comparison has hampered attempts to understand inflammatory phenotypes of depression and critically fails to consider that inflammation might be uniquely associated with both depression broadly and individual symptoms. METHODS: We used moderated nonlinear factor analysis in 5 NHANES (National Health and Nutrition Examination Survey) cohorts (N = 27,730, 51% female, mean age = 46 years). RESULTS: C-reactive protein (CRP) is simultaneously associated with latent depression, appetite, and fatigue. Specifically, CRP was associated with latent depression in all 5 samples (rs: 0.044–0.089; ps: < .001–.002) and was associated with both appetite (significant rs: 0.031–0.049, significant ps: .001–.007) and fatigue (significant rs: 0.030–0.054, significant ps: < .001–.029) in 4 samples. These results were largely robust to covariates. CONCLUSIONS: Methodologically, these models indicate that the Patient Health Questionnaire-9 is scalar non-invariant as a function of CRP (i.e., identical Patient Health Questionnaire-9 scores may represent different constructs in those with high vs. low CRP levels). Therefore, mean comparisons of depression total scores and CRP might be misleading without accounting for symptom-specific associations. Conceptually, these findings indicate that studies investigating inflammatory phenotypes of depression should examine how inflammation is simultaneously related both to depression broadly and to specific symptoms, and whether these relations function via different mechanisms. This has the potential to yield new theoretical insights and may lead to the development of novel therapies for reducing inflammation-related symptoms of depression.

Biobehavioral factors such as social isolation and depression have been associated with disease progression in ovarian and other cancers. Here, the authors developed a noninvasive, exosomal RNA profile for predicting ovarian cancer disease progression and subsequently tested whether it increased in association with biobehavioral risk factors.Exosomes were isolated from plasma samples from 100 women taken before primary surgical resection or neoadjuvant (NACT) treatment of ovarian carcinoma and 6 and 12 months later. Biobehavioral measures were sampled at all time points. Plasma from 76 patients was allocated to discovery analyses in which morning presurgical/NACT exosomal RNA profiles were analyzed by elastic net machine learning to identify a biomarker predicting rapid (≤6 months) versus more extended disease-free intervals following initial treatment. Samples from a second subgroup of 24 patients were analyzed by mixed-effects linear models to determine whether the progression-predictive biomarker varied longitudinally as a function of biobehavioral risk factors (social isolation and depressive symptoms).An RNA-based molecular signature was identified that discriminated between individuals who had disease progression in ≤6 months versus6 months, independent of clinical variables (age, disease stage, and grade). In a second group of patients analyzed longitudinally, social isolation and depressive symptoms were associated with upregulated expression of the disease progression propensity biomarker, adjusting for covariates.These data identified a novel exosome-derived biomarker indicating propensity of ovarian cancer progression that is sensitive to biobehavioral variables. This derived biomarker may be potentially useful for risk assessment, intervention targeting, and treatment monitoring.

Objective Ovarian cancer is characterized by poor prognosis, high levels of distress, disturbed sleep, and compromised quality of life (QOL). Although life stressors have been shown to significantly impact physical and psychological health in cancer populations, no studies have used a high-resolution stress assessment to differentiate effects of acute versus chronic stressors among women with ovarian cancer. We addressed this issue in the present prospective longitudinal study by examining how acute and chronic stress exposure in the year pre-diagnosis relate to depressive symptoms, sleep quality, and QOL over the first year post-diagnosis in women with ovarian cancer. Methods One hundred thirty-seven women completed the Life Events and Difficulties Schedule within a month of initial treatment for suspected ovarian cancer. Depressive symptoms, sleep, and QOL were measured pre-treatment, at six months, and one-year post-diagnosis. Mixed models were used to examine associations of acute and chronic stress pre-diagnosis with (a) change in psychosocial outcomes over the first year post-diagnosis and (b) levels of psychosocial outcomes across all time points. Results Both the number and severity of chronic difficulties (but not acute life events) were related to significantly greater depression, and poorer sleep quality and QOL, across all time-points. In contrast, these stress indices were unrelated to changes in psychosocial functioning over time. Conclusions Chronic but not acute stress exposure predicted average levels of depression, sleep, and QOL in the first year post-diagnosis among women with ovarian cancer. Assessing stressors and designing interventions for reducing stress may thus be beneficial for ovarian cancer patients.

Research has shown that sexual minority people of color experience pervasive and sometimes severe life stressors that increase their risk of experiencing mental health problems, and that can contribute to lifelong health disparities. However, no studies in this population have investigated stressor exposure occurring over the entire lifespan. Moreover, it remains unknown whether these stressor-health effects differ based on the timing or types of stressors experienced.The purpose of this study is to examine how cumulative lifetime stressor exposure is associated with mental health among Black, Latinx, and biracial Black-Latinx sexual minority persons.Participants were 285 ethnic/racial minority young adults (MMultiple regression analyses indicated that experiencing more-and more severe-stressors across the lifespan was related to greater anxiety, depressive, and somatization symptoms. These effects were robust while controlling for race/ethnicity, sexual orientation, education, and employment status, and they differed based on stressor exposure timing, type, primary life domain, and core social-psychological characteristic.Greater cumulative lifetime stressor exposure is related to poorer mental health among sexual minority people of color. Screening for lifetime stressors may thus help identify at-risk persons and provide an opportunity to intervene to help mitigate or prevent mental health disparities in multiply stigmatized adults.

Background Takotsubo syndrome (TTS) is an acute heart failure syndrome characterized by transient left ventricular dysfunction, increased myocardial biomarkers, and electrocardiographic changes. Symptoms of TTS are similar to those of acute coronary syndromes, but there is often no significant coronary stenosis. Although emotional and physical stressors are often reported as having triggered TTS, the pathogenesis is largely unknown. To address this issue, we comprehensively characterized a monozygous pair of twin sisters, one of whom experienced TTS. Case summary The 60-year-old Caucasian monozygotic female twins with and without TTS were examined at the University Hospital Zurich in Switzerland. The twins completed questionnaires and clinical interviews assessing several sociopsychological factors. The twin sister with TTS exhibited higher levels of anxiety, vital exhaustion, social inhibition, and alexithymia, and lower levels of quality of and meaning in life. She was given the diagnoses of social phobia, adjustment disorder, specific anxiety disorder, obsessive–compulsive personality disorder, and an accentuated anxiety-avoidant personality disorder. Additionally, the twin with TTS experienced more—and also more severe—stressors involving life-threatening and dangerous situations over the life course. Discussion These monozygous female twins with and without TTS differed in several notable aspects of their psychological functioning, psychiatric status, personality, and lifetime stressor exposure. The results thus highlight several factors, besides genetic components, that may play an important role in the pathogenesis of TTS. Looking forward, larger studies using experimental and longitudinal designs are needed to elucidate the role that psychosocial factors play in TTS.

The study investigated whether lifetime stress exposure is associated with greater impulsivity and addictive behavior. We also examined whether stress and impulsivity interactively predicted food addiction and alcohol-related behavior. Greater lifetime stress exposure was related to more impulsivity and food addictive behaviors, but not alcohol-related consequences. There were no interactions between lifetime stress exposure and impulsivity in predicting addictive behaviors. Exploratory analyses revealed that early and adulthood stress exposure predicted food addiction, whereas only adulthood stress predicted alcohol-related consequences. Therefore, lifetime stress exposure is related to impulsivity and addiction, but these effects differ by addiction outcome and specific timing of stress exposure.

Anxiety disorders are often preceded by interpersonal stress; however, most individuals who experience stress do not develop anxiety, making it difficult to predict who is most susceptible to stress. One proposed trans-diagnostic neural risk marker for anxiety is the error-related negativity (ERN), a negative deflection in the event-related potential waveform occurring within 100 ms of error commission. The present study sought to investigate whether interpersonal stress experienced over the course of a year interacts with ERN magnitude to prospectively predict anxiety symptoms. A sample of 57 emerging adults performed an arrow flanker task to elicit the ERN at the start of the academic school year (time one). Toward the end of the academic year (time two), participants reported on past-year interpersonal stress and anxiety symptoms. Stress interacted with ERN magnitude to predict anxiety symptoms, whereby, for individuals with an enhanced ERN at time one, greater interpersonal stress over the course of a year was significantly associated with increased anxiety symptoms at time two, even controlling for anxiety symptoms at time one. These findings suggest that enhanced performance monitoring may render individuals more susceptible to the adverse effects of interpersonal stress, thereby increasing risk for heightened anxiety.

Prenatal health behaviors can strongly influence risk of poor pregnancy birth outcomes. Although stress has been implicated in structuring the likelihood that individuals will engage in various prenatal health behavior patterns, no studies to date have examined life stress exposure occurring across the entire lifespan, and few have investigated how different types of stressors are comparatively associated with these outcomes. To address these issues, we interviewed 164 women at one of two large Midwestern, urban hospitals after delivering their first infant. We used the Stress and Adversity Inventory (STRAIN) to assess women's lifetime stress exposure severity and ordinary least squares regression models to examine associations between participants' life stress exposure and prenatal health behaviors. As hypothesized, greater lifetime stress exposure was associated with engaging in more negative prenatal health behaviors and fewer positive prenatal health behaviors while controlling for relevant sociodemographic factors and current perceived stress levels. These effects were stronger for negative versus positive health behaviors, and they differed substantially as a function of stressor type, exposure timing, and primary life domain. Stressors occurring over the life course thus have negative consequences for prenatal health behaviors, but these effects are not uniform across different types of life stress exposure.

Although corporal punishment is a common form of punishment with known negative impacts on health and behavior, how such punishment affects neurocognitive systems is relatively unknown.To address this issue, we examined how corporal punishment affects neural measures of error and reward processing in 149 adolescent boys and girls from 11- to 14-year-olds (MAs hypothesized, participants who experienced lifetime corporal punishment reported more anxiety and depressive symptoms. Experiencing corporal punishment also was related to a larger ERN and blunted RewP. Importantly, corporal punishment was independently related to a larger ERN and a more blunted RewP beyond the impact of harsh parenting and lifetime stressors.Corporal punishment appears to potentiate neural response to errors and decrease neural response to rewards, which could increase risk for anxiety and depressive symptoms.