Adversity Inventory Research Articles

Cumulative stressor exposure predicts menstrual cycle affective changes in a transdiagnostic outpatient sample with past-month suicidal ideation.

Affective responses to the menstrual cycle vary widely. Some individuals experience severe symptoms like those with premenstrual dysphoric disorder, while others have minimal changes. The reasons for these differences are unclear, but prior studies suggest stressor exposure may play a role. However, research in at-risk psychiatric samples is lacking. In a large clinical sample, we conducted a prospective study of how lifetime stressors relate to degree of affective change across the cycle. 114 outpatients with past-month suicidal ideation (SI) provided daily ratings (n = 6187) of negative affect and SI across 1-3 menstrual cycles. Participants completed the Stress and Adversity Inventory (STRAIN), which measures different stressor exposures (i.e. interpersonal loss, physical danger) throughout the life course, including before and after menarche. Multilevel polynomial growth models tested the relationship between menstrual cycle time and symptoms, moderated by stressor exposure. Greater lifetime stressor exposure predicted a more pronounced perimenstrual increase in active SI, along with marginally significant similar patterns for negative affect and passive SI. Additionally, pre-menarche stressors significantly increased the cyclicity of active SI compared to post-menarche stressors. Exposure to more interpersonal loss stressors predicted greater perimenstrual symptom change of negative affect, passive SI and active SI. Exploratory item-level analyses showed that lifetime stressors moderated a more severe perimenstrual symptom trajectory for mood swings, anger/irritability, rejection sensitivity, and interpersonal conflict. These findings suggest that greater lifetime stressor exposure may lead to heightened emotional reactivity to ovarian hormone fluctuations, elevating the risk of psychopathology.

Cumulative lifetime stressor exposure impairs stimulus–response but not contextual learning

Greater exposure to stressors over the life course is believed to promote striatum-dependent over hippocampus-dependent learning and memory processes under stressful conditions. However, little research in this context has actually assessed lifetime stressor exposure and, moreover, it remains unknown whether greater cumulative lifetime stressor exposure exerts comparable effects on striatum-dependent learning and hippocampus-dependent learning in non-stressful contexts. To investigate this issue, we used the Stress and Adversity Inventory for Adults (Adult STRAIN) and Multicued Search Task to investigate the relation between cumulative lifetime stressor exposure and striatum-dependent stimulus–response learning and hippocampus-dependent contextual learning under non-stressful conditions among healthcare professionals (N = 205; 157 females, 48 males; Age: M = 34.23, SD 9.3, range 20–59 years). Individuals with moderate, but not low, cumulative lifetime stressor exposure exhibited impaired learning for stimulus–response associations. In contrast, learning for context associations was unrelated to participants' lifetime stressor exposure profiles. These results thus provide first evidence that cumulative lifetime stressor exposure may have negative consequences on human striatum-dependent stimulus–response learning under non-stressful environmental conditions.

Preliminary validation of the Stress and Adversity Inventory for Adults (Adult STRAIN) in Dutch and its associations with in‐vivo locus coeruleus integrity

AbstractBackgroundThe Stress and Adversity Inventory (STRAIN) systematically assesses lifetime stressor exposure, but its validity has yet to be established in The Netherlands. This work aims to validate the Dutch translation of STRAIN and its association with key biological correlates: cortisol measures and the locus coeruleus (LC), a brainstem nucleus involved in stress responses and accumulating phosphorylated tau early in adulthood.MethodsEighty‐seven cognitively unimpaired Dutch participants (31‐81 years; ∼45% female; Table 1) completed stress‐ and affective‐related questionnaires, cognitive testing, salivary and plasma cortisol measurements, and 7T‐MRI. The STRAIN was administered after translation into Dutch. LC MRI signal intensity was extracted from an MT‐TFL sequence by normalizing LC signal against the pontine tegmentum (reference region) and creating a sample‐specific LC template. Pearson correlation models assessed associations between STRAIN summary scores (total stressor count and severity), and stress‐related (MIA‐Anxiety, PSS, DASS‐Stress, NEO PI‐R‐Neuroticism), affective (DASS‐Anxiety‐Depression, HDRS), cognitive (WLTDR, LDST, STR3), stress‐related biological (salivary‐, plasma cortisol), and LC measures (Table 1). HDRS models employed Spearman correlations. Age and sex were included as covariates, additionally including education for cognitive measures. Analyses were FDR‐corrected and conducted based on complete cases.ResultsOverall, the sample had relatively low lifetime stressor counts (M = 14.08; Figure 1A). When assessing concurrent validity, the STRAIN was positively associated with other stress measures (r = .21,.36; pFDR <.05; Figure 1B,C). Models including cortisol revealed that less stressor exposure and severity were associated with higher cortisol levels (r = ‐.22,‐.23; pFDR <.05). Affective and cognitive measures were investigated for discriminant validity. STRAIN was not associated with DASS, but was positively associated with HDRS (r = .17,.28; pFDR <.05). Generally, greater stressor exposure was related to poorer cognitive performance (r = .13,‐.19; pFDR <.05), except for a positive association between WLTDR and stressor severity (r = .18; pFDR <.05). No significant associations were found with LC MRI signal intensity (Figure 1B).ConclusionThis study demonstrates preliminary good concurrent and discriminative validity for the Dutch STRAIN translation, even among individuals with low‐to‐moderate self‐reported stress levels. We found no direct associations between LC integrity and lifetime stressors. Future research will investigate associations with other STRAIN domains and potential moderating effects of Alzheimer’s Disease‐related biomarkers on the relationship between cumulative stressor exposure and LC integrity.

Greater stress and trauma mediate race-related differences in epigenetic age between Black and White young adults in a community sample

Black Americans suffer lower life expectancy and show signs of accelerated aging compared to other Americans. While previous studies observe these differences in children and populations with chronic illness, whether these pathologic processes exist or how these pathologic processes progress has yet to be explored prior to the onset of significant chronic illness, within a young adult population. Therefore, we investigated race-related differences in epigenetic age in a cross-sectional sample of young putatively healthy adults and assessed whether lifetime stress and/or trauma mediate those differences. Biological and psychological data were collected from self-reported healthy adult volunteers within the local New Haven area (399 volunteers, 19.8% Black, mean age: 29.28). Stress and trauma data was collected using the Cumulative Adversity Inventory (CAI) interview, which assessed specific types of stressors, including major life events, traumatic events, work, financial, relationship and chronic stressors cumulatively over time. GrimAge Acceleration (GAA), determined from whole blood collected from participants, measured epigenetic age. In order to understand the impact of stress and trauma on GAA, exploratory mediation analyses were then used. We found cumulative stressors across all types of events (mean difference of 6.9 p = 2.14e-4) and GAA (β = 2.29 years [1.57–3.01, p = 9.70e-10] for race, partial η2 = 0.091, model adjusted R2 = 0.242) were significantly greater in Black compared to White participants. Critically, CAI total score (proportion mediated: 0.185 [0.073–0.34, p = 6e-4]) significantly mediated the relationship between race and GAA. Further analysis attributed this difference to more traumatic events, particularly assaultive traumas and death of loved ones. Our results suggest that, prior to development of significant chronic disease, Black individuals have increased epigenetic age compared to White participants and that increased cumulative stress and traumatic events may contribute significantly to this epigenetic aging difference.

Religious Attendance, Religious Coping, and Systemic Inflammation among Older African American Adults

Older African Americans bear a disproportionate burden of cardiovascular disease risk. One factor underlying these effects may be lifetime stressors exposure. Prior research has shown that religious attendance and positive religious coping, exhibiting a trusting relationship with God, are positively related to health outcomes. Mixed results emerged for negative religious coping. We examined whether these factors interacted with stress in predicting systemic inflammation, a key mechanism in stress-related chronic disease risk. Data was collected from the Health among Older Adults Living in Detroit study (N= 211, M= 67.6 yrs., 73.3% female). Measures included the number and severity of life stressors (measured via the Adult Stress and Adversity Inventory), religious attendance, positive/negative religious coping, and C-Reactive Protein (CRP). Number of participants (N= 114-119) varied in different analyses because of listwise deletion. Religious attendance and negative religious coping did not interact with any lifetime stressor indicators in predicting CRP. However, a significant interaction was found between stress severity and positive religious coping. A significant negative association emerged between positive religious coping and CRP for participants at -1.5 SD (but not +1.5 SD) from average stress severity. At very high levels of stress severity (~+2 SD), a positive link was found between positive religious coping and CRP. Positive religious coping may help to buffer against inflammation for older African American adults reporting low levels of lifetime stress severity. For participants reporting very high levels of stress, religious coping might have deleterious effects on inflammation.

The Association Between Parent and Child Self-Reported Stress and Child Hair Cortisol in Internationally-Adopted and Comparison Youth

Biological embedding occurs when children’s physiology is shaped by caregiving context, but how such embedding occurs is still being explored. The hypothalamic-adrenal-axis (HPA) and its end product, cortisol, is a target for biological embedding. Here, we explore whether parents’ stressful experiences are reflected in their child’s HPA function, and whether this is dependent on shared genetics and/or shared experience. As part of an ongoing study, 67 youth (54% female, M age=14.9 years) and a parent completed the Stress and Adversity Inventory (STRAIN), which indexed physical and mental health symptoms, count of stressful events, and severity of stressful events for parent and child. Youth provided a 3 cm hair sample for cortisol determination (HCC). 32 youth (21 female) were adopted from institutional care before age 5. Parent STRAIN is unrelated to child: sex, group, or age; Parent and Child STRAIN are uncorrelated. Child STRAIN is related to age, sex, group such that older, female, and adopted youth show higher STRAIN; it does not predict Child HCC. Parent STRAIN is reflected in Child HCC: a regression predicting HCC from adoption status, parent STRAIN, and their interaction is significant, R²=.13, p=<.05, with parent STRAIN contributing significantly, β=.42, t=2.66, p<.05. Youth living with parents under greater strain demonstrate greater HCC. These early findings demonstrate evidence of biological embedding of parent strain into child HPA functioning. The study is ongoing and longitudinal: a larger sample will provide power to detect patterns and change over time.

How do early and recent life stress shape cortisol reactivity and decision making in middle-to-older adulthood?

Greater lifetime stressor exposure and acute stress are both related to greater risky decision making; however, lifetime stressor exposure is also associated with blunted physiological response to acute stress, implying nuanced relations among life stress, acute stress, and decision making. In support of this, some work suggests that specific timings of stressor exposure (e.g., childhood vs. adulthood) may differentially relate to both physiology and decision making. To date, however, no work has concurrently examined lifetime and acute stressor exposure in relation to risky decision making. To address this issue, we examined how lifetime stressor exposure as assessed with the Stress and Adversity Inventory for Adults (STRAIN) is related to cortisol reactivity to the Trier Social Stress Test (TSST) and risky decision making in 63 middle-to-older aged adults (age range: 45-81 years). In the decision making task, participants made decisions about gambles framed as either gains or losses before and after the TSST. Regardless of age, participants with greater early and recent life stressor exposure exhibited lower cortisol reactivity than those with less of those exposures. Also regardless of age, participants made riskier decisions on loss trials than on gain trials. Finally, older adults reporting more early life and recent life stressor exposures showed the riskiest decision making after the TSST than younger adults who reported lower life stressor exposure. Early and recent life stressor exposure are associated with stress-related changes in physiology and decision making. These changes may lead to risky decision making in older age.

Instruments for assessing stress in Brazilians: an integrative review

Numerous instruments have been developed around the world to assess stress. This study aimed to identify instruments with validation studies that mapping stress in Brazil. an integrative review was carried out on databases and the Testing System of the Federal Council of Psychology (SATEPSI) in June 2017 and updated this year. Two independent judges participated in analyzing the results. Of the 6,377 articles, 47 articles were selected from the Index Psi, SciELO, LILACS and PubMed databases, and 35 instruments made up the sample, two of which were from SATEPSI. Nine of these tools map stress in a more general way, nine are aimed at specific clinical contexts, 12 are aimed at occupational stress, three at the sports context and another two at other contexts. Numerous health problems are associated with early and chronic stressors, however it was identified that most instruments access stress in a more recent period of time (last year, month or week). A more accurate analysis of the relationships between longitudinal stress and health outcomes appears limited in this sense. The Stress and Adversity Inventory (STRAIN) appears as an alternative for studying stress throughout life in the Brazilian reality.

Greater lifetime stressor exposure is associated with poorer mental health among sexual minoritypeople of color.

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 (Mage = 25.18 years old, SD = 1.94, age range = 19-29 years), who completed the Stress and Adversity Inventory for Adultsto assess for retrospective reports of lifetime stressor count and severity. The Brief Symptom Inventory was used to assess participants' symptoms of anxiety, depression, and somatization, which were the main outcomes. Most participants identified as cisgender male (94.7%) and gay (74.2%), with the remaining participants identifying as transgender or genderqueer/nonbinary for gender and bisexual/pansexual, queer, or another sexual orientation. Multiple 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.

Corporal Punishment Is Uniquely Associated With a Greater Neural Response to Errors and Blunted Neural Response to Rewards in Adolescence

BackgroundAlthough 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. MethodsTo address this issue, we examined how corporal punishment affected neural measures of error and reward processing in 149 adolescent boys and girls of ages 11 to 14 years (mean age [SD] = 11.02 [1.16]). Corporal punishment experienced over the lifetime was assessed using the Stress and Adversity Inventory. In addition, participants completed a flankers task and a reward task to measure the error-related negativity and reward positivity, respectively, as well as measures of anxiety and depressive symptoms. ResultsAs hypothesized, participants who experienced lifetime corporal punishment reported more anxiety and depressive symptoms. Experiencing corporal punishment was also related to a larger error-related negativity and blunted reward positivity. Importantly, corporal punishment was independently related to a larger error-related negativity and a more blunted reward positivity beyond the impact of harsh parenting and lifetime stressors. ConclusionsCorporal punishment appears to potentiate neural response to errors and decrease neural response to rewards, which could increase risk for anxiety and depressive symptoms.

Social threat, fronto-cingulate-limbic morphometry, and symptom course in depressed adolescents: a longitudinal investigation.

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. 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. 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). Social threat specifically affects fronto-cingulate-limbic pathways that contribute to the maintenance of depression in adolescents.

Prefrontal Cortex Volume Mediates the Relationship Between Lifetime Chronic Stressor Exposure and Cognition in People Living With and Without HIV.

ABSTRACTObjectiveDespite 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.MethodParticipants 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.ResultsAs 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.ConclusionsThese 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.

Intergenerational transmission of lifetime stressor exposure in adolescent girls at differential maternal risk for depression.

Adolescent girls who grow up with mothers who are depressed are themselves highly vulnerable to developing depression (i.e., "intergenerational transmission of depression"). Stressor exposure is a strong risk factor for depression, and the transmission of depression risk from mothers to daughters is partly due to mothers experiencing more stressors, increasing daughters' stressor burden. However, research in this area has only assessed recent stressors, making the role of cumulative lifetime stressors unclear. To address this issue, we recruited 52 dyads of mothers and adolescent daughters, of which 22 daughters were at high maternal risk for depression. Participants completed diagnostic interviews, and daughters additionally self-reported their depressive symptoms. Participants also completed the Stress and Adversity Inventory, a new-generation instrument for assessing cumulative lifetime history of acute and chronic stressors based on the contextual threat approach. We tested moderated mediation models evaluating the conditional indirect effects of mothers' lifetime stressors on high- versus low-risk daughters' depressive symptoms through daughters' lifetime stressors. As hypothesized, mothers of high-risk (but not low-risk) adolescent daughters who reported more lifetime acute stressors had daughters who reported more lifetime acute stressors and current depressive symptoms. Moreover, this finding was driven specifically by mothers' stressors occurring after their daughters' births. There was also tentative evidence that high-risk daughters' lifetime chronic stressors potentiated the impact of daughters' acute stressors on their depressive symptoms. These findings provide new insights into how stressful contexts are transmitted intergenerationally.

Cumulative lifetime acute stressor exposure interacts with reward responsiveness to predict longitudinal increases in depression severity in adolescence.

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. 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. 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. 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.

Greater Cumulative Lifetime Stressor Exposure Predicts Blunted Reward Positivity in Adolescent Girls Followed for 2 Years

BackgroundAlthough research has found that life stress is associated with reward-related brain activity, few studies have examined how cumulative stressors occurring over the entire lifetime affect reward processing during adolescence. MethodsTo address this issue, we investigated how lifetime stressor exposure related to reward processing, indexed by the reward positivity, in 240 adolescent girls between ages 8 and 14 years (mean age = 12.4). Participants were followed for 2 years. They completed a reward task at baseline and follow-up and the Stress and Adversity Inventory at follow-up. ResultsAs hypothesized, greater lifetime stressor exposure was related to a blunted reward positivity at the follow-up session while controlling for baseline age, baseline reward positivity, and time between assessments. Furthermore, this association was evident for acute but not chronic lifetime stressors. ConclusionsThese data suggest that the development of adaptive reward processing may be adversely affected by experiencing major life stressors. The results may thus have implications for understanding how stressors increase risk for psychopathology, such as major depressive disorder.

Association of Prenatal Exposure to Early-Life Adversity With Neonatal Brain Volumes at Birth

Exposure to early-life adversity alters the structural development of key brain regions underlying neurodevelopmental impairments. The association between prenatal exposure to adversity and brain structure at birth remains poorly understood. To examine whether prenatal exposure to maternal social disadvantage and psychosocial stress is associated with neonatal global and regional brain volumes and cortical folding. This prospective, longitudinal cohort study included 399 mother-infant dyads of sociodemographically diverse mothers recruited in the first or early second trimester of pregnancy and their infants, who underwent brain magnetic resonance imaging in the first weeks of life. Mothers were recruited from local obstetric clinics in St Louis, Missouri from September 1, 2017, to February 28, 2020. Maternal social disadvantage and psychosocial stress in pregnancy. Confirmatory factor analyses were used to create latent constructs of maternal social disadvantage (income-to-needs ratio, Area Deprivation Index, Healthy Eating Index, educational level, and insurance status) and psychosocial stress (Perceived Stress Scale, Edinburgh Postnatal Depression Scale, Everyday Discrimination Scale, and Stress and Adversity Inventory). Neonatal cortical and subcortical gray matter, white matter, cerebellum, hippocampus, and amygdala volumes were generated using semiautomated, age-specific, segmentation pipelines. A total of 280 mothers (mean [SD] age, 29.1 [5.3] years; 170 [60.7%] Black or African American, 100 [35.7%] White, and 10 [3.6%] other race or ethnicity) and their healthy, term-born infants (149 [53.2%] male; mean [SD] infant gestational age, 38.6 [1.0] weeks) were included in the analysis. After covariate adjustment and multiple comparisons correction, greater social disadvantage was associated with reduced cortical gray matter (unstandardized β = -2.0; 95% CI, -3.5 to -0.5; P = .01), subcortical gray matter (unstandardized β = -0.4; 95% CI, -0.7 to -0.2; P = .003), and white matter (unstandardized β = -5.5; 95% CI, -7.8 to -3.3; P < .001) volumes and cortical folding (unstandardized β = -0.03; 95% CI, -0.04 to -0.01; P < .001). Psychosocial stress showed no association with brain metrics. Although social disadvantage accounted for an additional 2.3% of the variance of the left hippocampus (unstandardized β = -0.03; 95% CI, -0.05 to -0.01), 2.3% of the right hippocampus (unstandardized β = -0.03; 95% CI, -0.05 to -0.01), 3.1% of the left amygdala (unstandardized β = -0.02; 95% CI, -0.03 to -0.01), and 2.9% of the right amygdala (unstandardized β = -0.02; 95% CI, -0.03 to -0.01), no regional effects were found after accounting for total brain volume. In this baseline assessment of an ongoing cohort study, prenatal social disadvantage was associated with global reductions in brain volumes and cortical folding at birth. No regional specificity for the hippocampus or amygdala was detected. Results highlight that associations between poverty and brain development begin in utero and are evident early in life. These findings emphasize that preventive interventions that support fetal brain development should address parental socioeconomic hardships.

Cumulative lifetime stressor exposure assessed by the STRAIN predicts economic ambiguity aversion

Uncertainty is inherent in most decisions humans make. Economists distinguish between two types of decision-making under non-certain conditions: those involving risk (i.e., known outcome probabilities) and those that involve ambiguity (i.e., unknown outcome probabilities). Prior research has identified individual differences that explain risk preferences, but little is known about factors associated with ambiguity aversion. Here, we hypothesized that cumulative exposure to major psychosocial stressors over the lifespan might be one factor that predicts individuals’ ambiguity aversion. Across two studies (Study 1: n = 58, Mage = 25.7; Study 2: n = 188, Mage = 39.81), we used a comprehensive lifetime stressor exposure inventory (i.e., the Stress and Adversity Inventory for Adults, or STRAIN) and a standard economic approach to quantify risk and ambiguity preferences. Greater lifetime stressor exposure as measured by the STRAIN, particularly in early life, was associated with higher aversion to ambiguity but not risk preferences.

Lifetime stressor exposure, systemic inflammation during pregnancy, and preterm birth among Black American women

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.

Assessing lifetime stressor exposure in sport performers: Associations with trait stress appraisals, health, well-being, and performance

Research has found that greater lifetime stressor exposure increases the risk for mental and physical health problems. Despite this, few studies have examined how stressors occurring over the entire lifespan affect sport performers’ health, well-being, and performance, partly due to the difficulty of assessing lifetime stressor exposure. To address this issue, we developed a sport-specific stress assessment module (Sport SAM) for the Stress and Adversity Inventory (STRAIN) and then analyzed the instrument’s usability, acceptability, validity, and test-retest reliability. Furthermore, we examined whether trait-like tendencies to appraise stressful situations as a challenge or threat mediated the association between lifetime stressor exposure and health, well-being, and performance. Participants were 395 sport performers (Mage = 22.50 years, SD = 5.33) who completed an online survey. Results revealed that the Sport SAM demonstrated good usability and acceptability, good concurrent validity in relation to the Adult STRAIN (rs = 0.23 to 0.29), and very good test-retest reliability (ricc = 0.87 to 0.89). Furthermore, the Sport SAM was significantly associated with symptoms of depression (β = 0.21 to 0.24, ps ≤ .001) and anxiety (β = 0.13 to 0.19, ps ≤ .012), and general physical (β = 0.24 to 0.27, ps = ≤ 0.001) and mental (β = 0.23 to 0.32, p ≤ .001) health complaints. Finally, we found that associations between total lifetime non-sport and sport-specific stressor severity and health were mediated by trait stress appraisals. Consequently, these findings may help practitioners better identify sport performers who are at risk of developing stress-related health problems.

Lifetime and perceived stress, social support, loneliness, and health in autistic adults.

Although the health consequences of life stress exposure in the general population are well known, how different stressors occurring over the lifetime cause morbidity and mortality in autism is unclear, as are the factors that moderate and mediate these associations. The few studies that have compared autistic and nonautistic individuals have used instruments that yield few stress exposure indices and assess stressors occurring over short time periods. To address these issues, we used the Stress and Adversity Inventory to assess lifetime stressor exposure and perceived stressor severity in 127 autistic and 104 nonautistic adults. Moderated mediation analysis examined associations between stressor exposure and physical and mental ill-health with respect to the hypothesized mediating role of stressor perception, and moderation effects of loneliness and social support. Autistic adults experienced more lifetime stressors and generally perceived stressors as being more severe. Greater perceived stressor severity was related to poorer physical and mental health and to greater loneliness and lower social support for both groups. An additional post hoc analysis of the association between diagnostic status and mental ill-health revealed that loneliness mediated the relation between being autistic and having poorer mental health. Autistic individuals experienced more lifetime stressors, and their impact on physical and mental health was mediated by perceived stressor severity. Moreover, loneliness and low social support were associated with greater negative impact of lifetime stress exposure on mental health. Interventions that reduce cognitive-perceptual stress appraisals, and that target loneliness and social support, may help reduce risk for stress-related disease in autistic individuals. (PsycInfo Database Record (c) 2021 APA, all rights reserved).