Lifetime Stress Research Articles

Resilience, Mental Health, Sleep, and Smoking Mediate Pathways Between Lifetime Stressors and Multiple Sclerosis Severity

Introduction: Lifetime stressors (e.g., poverty, violence, discrimination) have been linked to features of multiple sclerosis (MS); yet mechanistic pathways and relationships with cumulative disease severity remain nebulous. Further, protective factors like resilience, that may attenuate the effects of stressors on outcomes, are seldom evaluated. Aim: To deconstruct pathways between lifetime stressors and cumulative severity on MS outcomes, accounting for resilience. Methods: Adults with MS (N = 924) participated in an online survey through the National MS Society listserv. Structural equation modeling was used to examine the direct and indirect effects of lifetime stressors (count/severity) on MS severity (self-reported disability, relapse burden, fatigue, pain intensity, and interference) via resilience, mental health (anxiety and depression), sleep disturbance, and smoking. Results: The final analytic model had an excellent fit (GFI = 0.998). Lifetime stressors had a direct relationship with MS severity (β = 0.27, p < 0.001). Resilience, mental health, sleep disturbance, and smoking significantly mediated the relationship between lifetime stressors and MS severity. The total effect of the mediation was significant (β = 0.45). Conclusions: This work provides foundational evidence to inform the conceptualization of pathways by which stress could influence MS disease burden. Resilience may attenuate the effects of stressors, while poor mental health, smoking, and sleep disturbances may exacerbate their impact. Parallel with usual care, these mediators could be targets for early multimodal therapies to improve the disease course.

Shared and unique lifetime stressor characteristics and brain networks predict adolescent anxiety and depression.

Exposure to major life stressors and aberrant brain functioning have been linked to anxiety and depression, especially during periods of heighted functional brain plasticity, such as adolescence. However, it remains unclear if specific characteristics of major life stressors and functional network disruptions differentially predict anxiety and depression symptoms over time and, if so, whether they act independently or jointly. We collected baseline lifetime stressor exposure data and resting-state functional magnetic resonance imaging data in a longitudinal sample of 107 adolescents enriched for anxiety and depressive disorders. We examined five stressor characteristics: physical danger, interpersonal loss, humiliation, entrapment, and role change/disruption. Anxiety and depression symptoms were assessed at baseline, 6-month and 12-month follow-ups. Linear mixed effect models tested if these stressor characteristics, functional connectivity within and between frontoparietal, default, and ventral attention networks, and their interactions differentially predicted anxiety and depression symptoms at 6-month and 12-month follow-ups. Greater lifetime severity of physical danger and humiliation prospectively predicted increased anxiety symptoms at both follow-ups, whereas greater lifetime entrapment severity prospectively predicted higher anxiety and depression symptoms. Only the effects of lifetime entrapment severity were robust to including within- and between-network functional connectivity metrics and other significantly predictive stressor characteristics. Lifetime entrapment severity more strongly predicted anxiety symptoms in youth with higher default network connectivity. Greater functional connectivity between frontoparietal and default networks prospectively predicted increased depression symptoms. Taken together, these results underscore the critical importance of using stressor characteristics and functional connectivity jointly to study predictors for adolescent anxiety and depression.

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.

Differential effects of lifetime stressors on major depressive disorder severity: a longitudinal community-based cohort study.

Stressors across the lifespan are associated with the onset of major depressive disorder (MDD) and increased severity of depressive symptoms. However, it is unclear how lifetime stressors are related to specific MDD subtypes. The present study aims to examine the relationships between MDD subtypes and stressors experienced across the lifespan while considering potential confounders. Data analyzed were from the Zone d'Épidémiologie Psychiatrique du Sud-Ouest de Montréal (N = 1351). Lifetime stressors included childhood maltreatment, child-parent bonding, and stressful life events. Person-centered analyses were used to identify the clusters/profiles of the studied variables and multinomial logistic regression analyses were performed to examine the relationships between stressors and identified MDD subtypes. Intersectional analysis was applied to further examine how distal stressors interact with proximal stressors to impact the development of MDD subtypes. There was a significant association between proximal stressors and melancholic depression, whereas severe atypical depression and moderate depression were only associated with some domains of stressful life events. Additionally, those with severe atypical depression and melancholic depression were more likely to be exposed to distal stressors such as childhood maltreatment. The combinations of distal and proximal stressors predicted a greater risk of all MDD subtypes except for moderate atypical depression. MDD was characterized into four subtypes based on depressive symptoms and severity. Different stressor profiles were linked with various MDD subtypes. More specific interventions and clinical management are called to provide precision treatment for MDD patients with unique stressor profiles and MDD subtypes.

Vicarious heterosexism-based stress induces alcohol, nicotine, and cannabis craving and negative affect among sexual minority young adults: An experimental study

PurposeSexual minority young adults are at increased risk for hazardous drinking and alcohol use disorder compared to heterosexual adults. Heterosexism-based stressors contribute and often explain inequities in alcohol outcomes. However, the extant research primarily relies on correlational designs, and often neglects the importance of alcohol craving, despite its foundational role in addiction. Leveraging a novel experimental mood induction paradigm, this study examined the effects of exposure to vicarious heterosexism-based stress on alcohol craving and negative affect among sexual minority young adults who drink heavily. We also examined its effects on cannabis and nicotine craving among participants who used cannabis and nicotine, respectively. Lastly, we examined moderating factors that could influence the impact of exposure to heterosexism-based stress on alcohol craving. MethodsParticipants were 101 heavy drinking sexual minority young adults, ages 20–35 (M = 26.46 years old; SD = 3.49), recruited from the community (51.5% female sex assigned at birth; 76.3% cisgender; 51.5% plurisexual; and 42.6% racial and ethnic minorities). They completed three mood induction trials counterbalanced over three visits on different days: heterosexism stress, general stress, and neutral. Structured interviews assessed criteria for DSM-5 alcohol use disorder (AUD) and substance use, and self-report measures assessed lifetime traumatic stressors. ResultsMost participants met criteria for past-year AUD (74.7%). Exposure to heterosexism stress produced more negative affect and substance craving than the neutral mood induction, even while controlling for demographic variables and lifetime exposure to traumatic and heterosexism stressors. Exposure to heterosexism-based stress had large effects on alcohol craving among participants who had greater drinking to cope motives and heterosexism-specific rejection sensitivity, whereas the effects were small for those who had lower drinking to cope motives and heterosexism-specific rejection sensitivity. Demographic, lifetime stress, prior alcohol use, and AUD symptom severity variables were not significant moderators. Greater substance craving induced by heterosexism-based stress in the laboratory was associated with greater recent and current substance use. ConclusionsThis study findings show that vicarious exposure to heterosexism elicits negative mood and alcohol, cannabis, and nicotine craving among sexual minority young adults who engaged in heavy drinking. The effects for alcohol craving were largest among those who endorse high levels of drinking to cope motives and heterosexism-based rejection sensitivity. These findings have implications for oppression-based stress and motivational models of addiction.

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.

Lifetime stressor exposure is associated with greater rewarding effects of stress-related eating

Acute stressors tend to shift preferences toward comfort foods, yet they do not ubiquitously increase the amount of food consumed. Moreover, although many individuals eat more under stress, others eat less or show no change. Although the precise mechanisms explaining this variability in stress-related eating are unknown, they may be driven by individual differences in the rewarding effects of comfort eating, which are enhanced by greater lifetime stressor exposure. To investigate this possibility, we examined whether differences in lifetime stressor exposure predicted reductions in negative affect following snacking (i.e., negative reinforcement) and if this effect was specific to stress-related snacking or snacking in general. Participants were 26 women (23 % non-White) between 20 and 45 years old (M = 31), with a mean body mass index of 26, who completed three laboratory visits. Participants completed an assessment of lifetime stressor exposure (i.e., STRAIN) on the first visit and, on two subsequent laboratory visits in counterbalanced order, were given snacks after an acute social stress task (i.e., TSST) or rest period. Greater lifetime stressor exposure was related to greater post-ingestive decreases in negative affect following the acute social stressor but not following the rest period. If stress-related eating is more comforting for women with greater lifetime stressors and contributes to a stronger stress-eating association, then this may inform obesity-related clinical treatments that target behaviors and cognitions related to reward-based learning.

Maternal lifetime stress and psychological functioning in pregnancy is associated with preschoolers' temperament: Exploring effect modification by race and ethnicity

BackgroundPsychosocial stress and psychopathology frequently co-occur, with patterns differing by race and ethnicity. We used statistical mixtures methodology to examine associations between prenatal stress and child temperament in N = 382 racially and ethnically diverse maternal-child dyads to disentangle associations among maternal stressful life events, maternal psychological functioning in pregnancy, childhood neurobehavior, and maternal race and ethnicity. MethodsThis study utilized data from a longitudinal pregnancy cohort, PRogramming of Intergenerational Stress Mechanisms (PRISM). Mothers completed the Lifetime Stressor Checklist-Revised, Edinburgh Postnatal Depression Scale, and Spielberger State-Trait Anxiety Scale during pregnancy. When their children were 3–5 years of age, they completed the Children's Behavior Questionnaire, which yields three temperament dimensions: Negative Affectivity (NA), Effortful Control (EC), and Surgency (S). We used weighted quantile sum regression to derive a weighted maternal stress index encompassing lifetime stress and depression and anxiety symptoms and examined associations between the resulting stress index and child temperament. Differential contributions of individual stress domains by race and ethnicity also were examined. ResultsMothers self-identified as Black/Black Hispanic (46.1 %), non-Black Hispanic (31.9 %), or non-Hispanic White (22 %). A higher maternal stress index was significantly associated with increased child NA (β = 0.72 95 % CI = 0.35, 1.10). Lifetime stress was the strongest contributor among Hispanic (36.7 %) and White (17.8 %) mothers, whereas depressive symptoms in pregnancy was the strongest contributor among Black (16.7 %) mothers. ConclusionPrenatal stress was most strongly associated with negative affectivity in early childhood. Consideration of multiple stress measures as a mixture accounted for differential contributions of individual stress domains by maternal race and ethnicity. These findings may help elucidate the etiology of racial/ethnic disparities in childhood neurobehavior.

372. Investigating the Effects of Acute and Lifetime Stress on Decisions Involving Uncertainty

372. Investigating the Effects of Acute and Lifetime Stress on Decisions Involving Uncertainty

Lifetime stressors relate to invisible symptoms of multiple sclerosis

Aim: Childhood stressors can increase adult stress perception and may accumulate over the lifespan to impact symptoms of multiple sclerosis (MS). Growing evidence links childhood stressors (e.g., abuse, neglect) to fatigue, pain, and psychiatric morbidity in adults with MS; yet literature in this area is lacking a comprehensive lifespan approach. The aim of this cross-sectional study was to examine contributions of childhood and adulthood stressor characteristics (i.e., count, severity), on three individual outcomes: fatigue, pain interference, and psychiatric morbidity in People with MS (PwMS). Methods: An online survey was distributed through the National MS Society. Hierarchical block regression modeling was used to sequentially assess baseline demographics, childhood stressors, and adult stressors per outcome. We hypothesized that child and adult stressors would significantly contribute to fatigue, pain interference, and psychiatric morbidity. Results: Overall, 713 PwMS informed at least one final analytic model. Both childhood and adult stressors significantly contributed to pain interference and psychiatric morbidity. Adult stressor severity independently correlated with psychiatric morbidity (P < 0.0001). Childhood stressors significantly contributed to fatigue (LR test P < 0.0001). Childhood stressor severity independently significantly correlated with both fatigue likelihood (P = 0.03) and magnitude (P < 0.001). Conclusions: This work supports a relationship between stressors across the lifespan and fatigue, pain, and psychiatric morbidity in PwMS. Stressor severity may have an important role which may not be captured in count-based trauma measurement tools. Clinicians and researchers should consider lifetime stress when addressing fatigue, pain, and psychiatric morbidity among PwMS.

Lifetime adversity predicts depression, anxiety, and cognitive impairment in a nationally representative sample of older adults in the United States.

Although life stress and adversity are well-known risk factors for mental health problems and cognitive impairment among older adults, limited research has comprehensively examined the impact of both childhood and adulthood adversity on psychiatric and cognitive impairment symptoms over a prolonged period. To address this issue, we investigated how lifetime adversity exposure is related to symptoms of depression, anxiety, and cognitive impairment in a nationally representative, longitudinal sample of older adults in the United States. We analyzed data from the Health and Retirement Study (1992-2016). The sample included 3496 individuals (59.9% female), aged ≥64 years old (Mage = 76.0 ± 7.6 years in 2016). We used the individual-level panel data and ordinary least squares regressions to estimate associations between childhood and adulthood adversities, and later-life depression, anxiety, and cognitive impairment. Many participants experienced a significant early life (38%) or adulthood (79%) stressor. Moreover, experiencing one childhood adversity (vs. none) was associated with a 17.4% increased risk of adulthood adversity. Finally, as hypothesized, childhood adversity exposure was related to experiencing more depression and anxiety symptoms in later life, whereas adulthood stressor exposure predicted more cognitive impairment as well as more depression and anxiety symptoms. These findings demonstrate significant associations between lifetime adversity and symptoms of depression, anxiety, and cognitive impairment in older adults. Screening for lifetime stressors may thus help healthcare professionals and policymakers identify individuals who could potentially benefit from interventions designed to reduce stress and enhance resilience.

Alcohol and stress exposure across the lifespan are key risk factors for Alzheimer's Disease and cognitive decline

Alzheimer's Disease and related dementias (ADRD) are an increasing threat to global health initiatives. Efforts to prevent the development of ADRD require understanding behaviors that increase and decrease risk of neurodegeneration and cognitive decline, in addition to uncovering the underlying biological mechanisms behind these effects. Stress exposure and alcohol consumption have both been associated with increased risk for ADRD in human populations. However, our ability to understand causal mechanisms of ADRD requires substantial preclinical research. In this review, we summarize existing human and animal research investigating the connections between lifetime stress and alcohol exposures and ADRD.

Looking Upstream to Understand Race/Ethnicity as a Moderator for Poststroke Neuroinflammation and a Social Determinant for Poststroke Aphasia Outcomes.

Over the past decade, the stroke literature has begun to acknowledge and explore explanations for longstanding racial/ethnic differences in stroke outcomes. Poststroke cognitive impairment (PSCI) and poststroke aphasia are two such negative poststroke outcomes where racial/ethnic differences exist. Physiological differences, such as stroke type and lesion size, have been used to partially explain the variation in PSCI and aphasia. However, there is some evidence, although limited, that suggests neuroinflammatory processes as part of allostatic load may be a key contributor to the observed disparities. In this tutorial, we explore the influence of race differences in inflammation on poststroke cognitive outcomes. We suggest lifetime stress and other external determinants of health such as neighborhood environment and discriminatory practices through "weathering" explain differences in inflammation. While using an allostatic load framework, we explore the literature focusing specifically on the role of neuroinflammation on poststroke outcomes. Examination of the immune response poststroke provides a foundation for understanding the mechanisms of PSCI and poststroke aphasia and the potential contributions of neuroinflammatory processes on poststroke cognitive outcomes. Furthermore, understanding of racial differences in those processes may contribute to a better understanding of racial disparities in general stroke outcomes as well as poststroke aphasia.

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.

Early life stress aggravates disease pathogenesis in mice with experimental autoimmune encephalomyelitis: Support for a two-hit hypothesis of multiple sclerosis etiology

Vision problems are one of the earliest diagnosed symptoms of multiple sclerosis (MS). The onset and progression of vision loss and the underlying pathogenesis in MS may be influenced by cumulative psychophysiological stress. Here, we used a two-hit model of stress in female mice to determine if early life stress (ELS, the first hit) influences the response to an immunization that induces experimental autoimmune encephalomyelitis (EAE, the second hit) later in life. We hypothesized that ELS caused by animal transportation from a vendor during early postnatal development represents a co-factor which can exacerbate the clinical severity of EAE. Indeed, adult EAE mice with a history of ELS displayed more severe clinical signs and delayed recovery compared to non-stressed EAE mice. ELS also diminished visual acuity measured by optokinetic responses, as well as locomotion and exploratory behaviours in EAE mice. Notably, ELS accelerated vision loss and caused earlier onset of visual impairments in EAE. Exacerbated functional impairments in stressed EAE mice were highly correlated with circulating corticosterone levels. The findings show that the progression of induced EAE in adulthood can be significantly impacted by adverse early life experiences. These observations emphasize the importance of comprehensive behavioural testing, including non-motor functions, to enhance the translational value of preclinical animal models of MS. Moreover, shipment stress of laboratory animals should be considered a necessary variable in preclinical MS research. The consideration of cumulative lifetime stresses provides a new perspective of MS pathogenesis within a personalized medicine framework.

Lifetime and Acute Stress Predict Functional Outcomes Following Stroke: Findings From the Longitudinal STRONG Study.

Stroke is a sudden-onset, uncontrollable event; stroke-related stress may impede rehabilitation and recovery. Lifetime stress may sensitize patients to experiencing greater stroke-related stress and indirectly affect outcomes. We examine lifetime stress as predictor of poststroke acute stress and examine lifetime and acute stress as predictors of 3- and 12-month functional status. We also compare acute stress and baseline National Institutes of Health Stroke Scale as predictors of poststroke functional status. Between 2016 and 2020 the STRONG Study (Stroke, Stress, Rehabilitation, and Genetics) enrolled adults with new radiologically confirmed stroke 2 to 10 days poststroke onset at 28 acute care US hospitals. Participants were interviewed 3 times: acute admission (acute stress; Acute Stress Disorder Interview), 3 months (Fugl-Meyer Upper Extremity motor impairment [Fugl-Meyer Upper Arm Assessment; N=431], modified Rankin Scale [3 months; N=542], Stroke Impact Scale-Activities of Daily Living [3 months; N=511], Lifetime Stress Exposure Inventory), and 12 months (modified Rankin Scale, N=533; Stroke Impact Scale 3.0 Activities of Daily Living; N=485; Telephone Montreal Cognitive Assessment; N=484) poststroke. Structural equation models examined whether acute stress predicted 3- and 12-month functional outcomes, and mediated an association between lifetime stress and outcomes controlling for demographics and initial National Institutes of Health Stroke Scale. Standardized betas are reported. Sample (N=763) was 19 to 95 years old (mean=63; SD=14.9); 448 (58.7%) were male. Acute stress scores ranged from 0 to 14 (mean, 3.52 [95% CI, 3.31-3.73]). Controlling for age, gender, baseline National Institutes of Health Stroke Scale, and race and ethnicity, higher lifetime stress predicted higher acute stress (β=0.18, P<0.001), which predicted lower 3-month Fugl-Meyer Upper Arm Assessment scores (β=-0.19, P<0.001), lower Stroke Impact Scale 3.0 Activities of Daily Living scores at 3 months (β=-0.21, P<0.001) and 12 months (β=-0.21, P<0.001), higher modified Rankin Scale scores at 3 months (β=0.23, P<0.001) and 12 months (β=0.22, P<0.001), and lower 12-month Telephone Montreal Cognitive Assessment scores (β=-0.20, P<0.001). Acute stress predicted 12-month tMoCA (χ2[1]=5.29, P=0.022) more strongly, 3-month and 12-month modified Rankin Scale and SIS scores as strongly (all Ps>0.18), but Fugl-Meyer scores (χ2[1]=7.01, P=0.008) less strongly than baseline National Institutes of Health Stroke Scale. Lifetime stress/trauma is associated with more poststroke acute stress, which is associated with greater motor and cognitive impairment and disability 3 and 12 months poststroke. Poststroke interventions for acute stress may help mitigate stroke-related disability.

Maternal steroids during pregnancy and their associations with exposure to lifetime stressful life events, prenatal stress appraisal and psychological functioning

BackgroundDuring pregnancy, steroids enable physiological adaptations in response to many factors, including maternal stress or psychological functioning. While stress and psychological dysfunction can have endocrine-disrupting effects beyond cortisol disruption, associations between prenatal maternal stress or related psychological dysfunction and the broader steroid milieu remain understudied. AimTo assess associations between independent and joint maternal stress and psychological functioning measures and steroid profiles in pregnancy (22–40 gestational weeks) in the Programming of Intergenerational Stress Mechanisms (PRISM) birth cohort (n = 334). MethodsSerum metabolomics detected 42 steroids and their metabolites, which were grouped into five classes (pregnenolone, androgens, estrogens, progestin, and corticosteroids). The Perceived Stress Scale, Life Stressor Checklist-Revised, and Edinburgh Postnatal Depression Scale indexed lifetime traumatic/non-traumatic stressors, global prenatal stress appraisal, and depressive symptoms during pregnancy, respectively. Exposures were categorized as high-low using the corresponding 3rd quartiles. We assessed associations between both individual and joint stress exposures with steroid classes using linear mixed effect models and with individual steroids using linear regressions. We also examined fetal sex-specific effects. ResultsHigh prenatal perceived stress was independently associated with lower levels of androgens and estrogens in the overall sample [β (95%CI): androgens: −0.13 (−0.25;−0.01); estrogens: −0.16 (−0.31;−0.01)], particularly among women carrying males [androgens: −0.22 (−0.39;−0.05); estrogens: −0.28 (−0.50;−0.07)]. Results on estrogens were consistent when considering joint exposure to both greater lifetime stressors and higher prenatal perceived stress. We also found a single testosterone metabolite—5alpha-androstan-3alpha,17alpha-diol disulfate—negatively associated with both individual high perceived stress and joint exposure to high lifetime stressors and high perceived stress among women carrying males. ConclusionsIncreased maternal perceived stress experienced in pregnancy was independently associated with lower maternal androgen and estrogen levels during pregnancy in the overall sample, particularly among women carrying males. Results on estrogens were consistent when we considered the joint exposure of increased lifetime stressors and higher prenatal perceived stress.

A qualitative exploration of how lifetime stressor exposure influences sport performers’ health, well-being, and performance

ABSTRACT Background and objectives Recent research has shown that lifetime stressor exposure can negatively impact sport performers. However, this work has predominantly relied on quantitative methods, which has provided limited information regarding how stressors occurring over the life course affect health, well-being, and performance. This study aimed to explore how relatively high levels of lifetime (non-sport and sport-specific) stressor exposure influenced sport performers’ health, well-being, and performance. Methods and Design To identify participants who had experienced high lifetime (non-sport and sport-specific) stressors, we used criterion-based purposeful sampling from a prior study. Subsequently, semi-structured interviews, complemented by timelining, were conducted with 22 sport performers (17 female; Mage = 25.89, SD = 10.20). Results We used reflexive thematic analysis to develop three overarching themes that illustrate how high lifetime (non-sport and sport-specific) stressor exposure influences sport performers’ health, well-being, and performance. These were: psychological (e.g., maladaptive coping strategies), social (e.g., difficulties in building relationships), and behavioral (e.g., risky behaviors) factors. Conclusions These findings can help practitioners identify sport performers at risk of developing stress-related health, well-being, and performance problems, and may aid the development of effective interventions.

A creative nonfiction story of male elite athletes’ experiences of lifetime stressor exposure, performance, and help-seeking behaviors.

A creative nonfiction story of male elite athletes’ experiences of lifetime stressor exposure, performance, and help-seeking behaviors.

Characterizing experiential elements of early-life stress to inform resilience: Buffering effects of controllability and predictability and the importance of their timing.

Key theoretical frameworks have proposed that examining the impact of exposure to specific dimensions of stress at specific developmental periods is likely to yield important insight into processes of risk and resilience. Utilizing a sample of N = 549 young adults who provided a detailed retrospective history of their lifetime exposure to numerous dimensions of traumatic stress and ratings of their current trauma-related symptomatology via completion of an online survey, here we test whether an individual's perception of their lifetime stress as either controllable or predictable buffered the impact of exposure on trauma-related symptomatology assessed in adulthood. Further, we tested whether this moderation effect differed when evaluated in the context of early childhood, middle childhood, adolescence, and young adulthood stress. Consistent with hypotheses, results highlight both stressor controllability and stressor predictability as buffering the impact of traumatic stress exposure on trauma-related symptomatology and suggest that the potency of this buffering effect varies across unique developmental periods. Leveraging dimensional ratings of lifetime stress exposure to probe heterogeneity in outcomes following stress - and, critically, considering interactions between dimensions of exposure and the developmental period when stress occurred - is likely to yield increased understanding of risk and resilience following traumatic stress.