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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.

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.

Background Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress. Method Participants were 116 adolescent girls (M-age = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress. Results As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-alpha and interleukin-1 beta reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores. Discussion These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress.

Salivary markers of immune function are increasingly commonly used in studies of human health. Yet, few studies have examined the short-term or long-term reliability or stability of these biomarkers, making their measurement properties unclear. We addressed this issue in the present study by collecting two saliva samples, two hours apart, from 426 adolescent girls during a baseline laboratory visit. Then, eighteen months later, we collected the same samples again from a subset of these participants (n = 113). The correlations between the two samples collected at each session were generally high (mean r = 0.67). In contrast, although single saliva samples were only weakly correlated across 18 month (mean rs = 0.18), averaging the two quantifications within a session considerably improved the reliability (mean r = 0.27). In short, salivary immune markers exhibited strong short-term test-retest correlations, and averaging across multiple assessments notably improved long-term test-retest correlations. Additional research is needed to establish the health relevance and mechanisms underlying these potentially useful, non-invasive biomarkers.

Background Research has suggested that physical pain (e.g., caused by injury) and social pain (e.g., caused by social rejection) are modulated by some of the same biological systems. Consequently, it is possible that acetaminophen, which is commonly used to alleviate physical pain through neurochemical pathways, may have social pain-relieving effects that interact with forgiveness, which reduces social pain through psychological pathways. To date, however, only a few studies have examined how experiences of social pain change over time, and none have examined how acetaminophen and forgiveness interact to influence these effects. Purpose We addressed these issues by investigating how acetaminophen administration and daily forgiveness are associated with experiences of social pain over 21 days. We hypothesized that acetaminophen-related reductions in social pain across the 21-day study period would be greatest on days following high levels of forgiveness. Method To test this hypothesis, we conducted a double-blind, randomized, placebo-controlled trial in which we randomly assigned 42 healthy young adults to an acetaminophen condition (1,000 mg of acetaminophen daily), placebo-control condition (400 mg of potassium daily), or empty-control (no pill) condition. We then assessed their levels of forgiveness and social pain for 20 consecutive days. Results As hypothesized, acetaminophen reduced participants' social pain levels over time but only for those exhibiting high levels of forgiveness (i.e., 18.5% reduction in social pain over 20 days). Conclusions These data are the first to show that forgiveness and acetaminophen have interactive effects on experiences of social pain, which is one of the most common and impactful of all human experiences.

Background Prenatal life stress exposure is linked to dysregulated immune function and chronic inflammatory disease in offspring, but we know little about its effects on infant immune response during viral infection. Method To address this issue, we examined associations between prenatal life stress exposure and infant upper-airway inflammatory markers during acute respiratory infection (ARI) using data from a prospective, population-based birth-cohort study (N = 180). Infant inflammation was measured as a continuous latent factor within a structural equation modeling framework using nasal wash concentrations of interleukin-1β, interleukin-6, and tumor necrosis factor-α. We hypothesized that infants exposed to prenatal life stress would have greater levels of nasal inflammation during ARI and increased risk for ARI-related morbidity in early childhood. Results Our findings contradicted these hypotheses and provided evidence of sexually dimorphic effects of prenatal stress exposure on infant immune functioning during ARI. Among boys, but not girls, prenatal stress was negatively associated with nasal inflammation and indirectly associated with both lower ARI severity and reduced likelihood of subsequent ARI-related hospitalization in the 2nd and 3rd years of life. Conclusion These data suggest that prenatal stress exposure may be beneficial for infant boys in the context of respiratory viral infections; however, it will be critical to determine if these benefits are offset by increased risk for chronic inflammatory diseases in later childhood. As the participants in this cohort are being followed longitudinally through age 8, we will be able to evaluate long-term health outcomes in future studies.

IntroductionAlthough a considerable proportion of Asians in the USA experience depression, anxiety and poor sleep, these health issues have been underestimated due to the model minority myth about Asians, the stigma associated with mental illness, lower rates of treatment seeking and a shortage of culturally tailored mental health services. Indeed, despite emerging evidence of links between psychosocial risk factors, the gut microbiome and depression, anxiety and sleep quality, very few studies have examined how these factors are related in Chinese and Korean immigrants in the USA. The purpose of this pilot study was to address this issue by (a) testing the usability and feasibility of the study’s multilingual survey measures and biospecimen collection procedure among Chinese and Korean immigrants in the USA and (b) examining how stress, discrimination, acculturation and the gut microbiome are associated with depression, anxiety and sleep quality in this population.Method and analysisThis is a cross-sectional pilot study among first and second generations of adult Chinese and Korean immigrants in the greater Atlanta area (Georgia, USA). We collected (a) gut microbiome samples and (b) data on psychosocial risk factors, depression, anxiety and sleep disturbance using validated, online surveys in English, Chinese and Korean. We aim to recruit 60 participants (30 Chinese, 30 Korean). We will profile participants’ gut microbiome using 16S rRNA V3-V4 sequencing data, which will be analysed by QIIME 2. Associations of the gut microbiome and psychosocial factors with depression, anxiety and sleep disturbance will be analysed using descriptive and inferential statistics, including linear regression.Ethics and disseminationThis study has been approved by the Institutional Review Board at Emory University (IRB ID: STUDY00000935). Results will be made available to Chinese and Korean community members, the funder and other researchers and the broader scientific community.

OBJECTIVE: Although research has examined associations between socioeconomic status (SES), gender, and acute and chronic life stressors in depression, most studies have been conducted in WEIRD (Western, Educated, Industrialized, Rich, Democratic) populations. METHOD: We addressed this issue by interviewing 65 adults (55 women, M(age) = 37) living in Madagascar, a typical low- and middle-income country (LMIC). RESULTS: As hypothesized, women experienced more life stressors and depressive symptoms, on average, than men, as did those from lower (vs. higher) SES backgrounds. Additionally, lifetime stress exposure was associated with greater symptoms of depression, accounting for 19% of the variability in depressive symptom levels. These effects differed for acute vs. chronic and distal vs. recent stressors. Finally, stress exposure significantly mediated the relation between SES and gender on depressive symptoms, accounting for 24.0% to 70.8% of the SES/gender-depression association depending on stressor type. CONCLUSIONS: These data extend prior research by describing how social stratification and gender relate to lifetime stress exposure and depressive symptoms in a non-WEIRD population.

Although stress is a strong risk factor for poor health, especially for women, it remains unclear how stress affects the key neurohormones cortisol and oxytocin, which influence stress-related risk and resilience. Whereas cortisol mediates energy mobilization during stress, oxytocin has anti-inflammatory, anxiolytic, and analgesic effects that support social connection and survival across the lifespan. However, how these neurohormones interrelate and are associated with cognitive control of emotional information during stress remains unclear. To address these issues, we recruited 37 college-aged women (M(age) = 19.19, SD = 1.58) and randomly assigned each to a one-hour experimental session consisting of either an acute stress (emotionally stressful video) or control (non-stressful video) condition in a cross-sectional manner across the semester. Salivary cortisol and oxytocin samples were collected at baseline and after the video, at which point participants also completed measures assessing affect and an emotional Stroop task. As hypothesized, the emotional stressor induced negative emotions that were associated with significant elevations in cortisol and faster Stroop reaction times. Moreover, higher baseline oxytocin predicted greater positive affect after the stressor and also better cognitive accuracy on the Stroop. Analyses examining the naturalistic stress effects revealed that basal oxytocin levels rose steeply three weeks before the semester’s end, followed by rising cortisol levels one week later, with both neurohormones remaining elevated through the very stressful final exam period. Considered together, these data suggest that women’s collective experiences of stress may be potentially buffered by a synchronous oxytocin surge that enhances cognitive accuracy and reduces stress “when the going gets tough”.

Life stress increases risk for multiple forms of psychopathology, in part by altering neural processes involved in performance monitoring. However, the ways in which these stress-cognition effects are influenced by the specific timing and types of life stressors experienced remains poorly understood. To address this gap, we examined how different social-psychological characteristics and developmental timing of stressors are related to the error-related negativity (ERN), a negative-going deflection in the event-related potential (ERP) waveform that is observed from 0 to 100 ms following error commission. A sample of 203 emerging adults performed an ERN-eliciting arrow flanker task and completed an interview-based measure of lifetime stress exposure. Adjusting for stress severity during other developmental periods, there was a small-to-medium effect of stress on performance monitoring, such that more severe total stress exposure, as well as more severe social-evaluative stress in particular, experienced during early adolescence significantly predicted an enhanced ERN. These results suggest that early adolescence may be a sensitive developmental period during which stress exposure may result in lasting adaptations to neural networks implicated in performance monitoring.

Losing a spouse is considered one of the most stressful life events a person can experience. Particularly in the immediate weeks and months after the loss, bereavement is associated with a significantly increased risk of morbidity and mortality. Despite an abundance of research aimed at identifying risk factors for adverse health outcomes following marital death, the mechanisms through which mental and physical health problems emerge following bereavement remain poorly understood. To address this issue, the present review examines several pathways that may link bereavement and health, including inflammation and immune dysregulation, genetic and epigenetic changes, gut microbiota activity, and biological aging. We then describe how these processes may be viewed from the perspective of the Social Signal Transduction Theory of Depression to provide a novel framework for understanding individual differences in long-term trajectories of adjustment to interpersonal loss. Finally, we discuss several avenues for future research on psychobiological mechanisms linking bereavement with mental and physical health outcomes.

This study examined how lifetime stress exposure and race are associated with first-birth intendedness, and whether these associations differ based on stress exposure timing. Greater lifetime stress exposure was related to increased first-birth intendedness for black women but was unrelated or even associated with decreased first-birth intendedness for white women, depending on stress exposure timing. These effects were robust while controlling for age, partner status, household income, and education, and they differed based on the timing of participants’ stress exposure. These data thus provide evidence that first-birth intendedness is influenced by both lifetime stress exposure and race in the United States.

Despite having an initial verbal memory advantage over men, women have greater rates of Alzheimer’s disease and more rapid cognitive decline once diagnosed. Moreover, although Alzheimer’s disease is influenced by inflammation, which itself has known sex differences, no study has investigated whether sex differences in memory are moderated by peripheral inflammatory activity. To address this issue, we analyzed data from 109 individuals (50 women, Mage = 71.62, range = 55–87) diagnosed as cognitively normal, or having mild cognitive impairment or Alzheimer’s disease dementia. We then followed the sample for 12 months, as part of a longitudinal study of aging and Alzheimer’s disease. At baseline, we assessed levels of the inflammatory cytokines interleukin (IL)-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) in plasma. At baseline and 12 months, we assessed verbal memory using the Rey Auditory Verbal Learning Test and nonverbal memory using the Brief Visuospatial Memory Test-Revised. As hypothesized, for the full sample, women exhibited stronger verbal (but not nonverbal) memory than men. In women, but not men, higher IL-1β at baseline related to poorer verbal learning across both time points and delayed recall at 12 months. The effect of sex on memory also differed by IL-1β level, with women exhibiting a memory advantage both at baseline and 12 months, but only for those with low-to-moderate IL-1β levels. Therefore, high peripheral inflammation levels may lead to a sex-specific memory vulnerability relevant for Alzheimer’s disease.

Significant childhood adversity and chronic life stress are highly prevalent in patients with severe obesity. Such stress has been found to increase risk of adulthood obesity by up to 50% and it can also substantially degrade the effectiveness of evidence-based treatments for this chronic disease condition. Despite general appreciation of these facts, though, stress is not frequently measured in obesity research or routinely assessed during treatment for obesity or obesity-related complications. To address this important issue, we describe several validated tools that can be used for assessing life stress and discuss how information obtained from these instruments can be integrated into obesity treatment and research. Given the ease with which stress can be assessed, we argue that stress assessment and management should be widely included in clinical treatments for obesity, and that stress should be routinely measured in studies examining the long-term effects of obesity and obesity treatment.

OBJECTIVE: Both lower subjective social status (SSS)—or viewing oneself as having lower status relative to others—and greater early life stress consistently relate to poorer health in adolescence. Early life stress can also negatively influence one’s social relationships and may thereby shape social status. The present studies investigated how early life stress relates to the development of SSS and how SSS relates to health across the transition to college. DESIGN: In Study 1, 91 older adolescents (M(age) = 18.37) reported early life stress, society SSS, and school SSS, and they reported their society SSS and school SSS again 2 years later. In Study 2, 94 first-year college students (M(age) = 18.20) reported early life stress and society SSS at study entry and reported their dorm SSS, university SSS, and mental health monthly throughout the year. RESULTS: Greater early life stress was related to lower society SSS, but not school SSS, in both studies. In Study 2, dorm and university SSS and early life stress were uniquely related to mental health, although associations weakened over time. CONCLUSION: Early life stress may predispose people to have low society SSS, and both low school SSS and high early life stress may increase risk for poorer health during transition periods.

Social Safety Theory hypothesizes that developing and maintaining friendly social bonds is a fundamental organizing principle of human behavior and that threats to social safety are a critical feature of psychological stressors that increase risk for disease. Central to this formulation is the fact that the human brain and immune system are principally designed to keep the body biologically safe, which they do by continually monitoring and responding to social, physical, and microbial threats in the environment. Because situations involving social conflict, isolation, devaluation, rejection, and exclusion historically increased risk for physical injury and infection, anticipatory neural–immune reactivity to social threat was likely highly conserved. This neurocognitive and immunologic ability for humans to symbolically represent and respond to potentially dangerous social situations is ultimately critical for survival. When sustained, however, this multilevel biological threat response can increase individuals’ risk for viral infections and several inflammation-related disease conditions that dominate present-day morbidity and mortality.

BACKGROUND Social isolation has shown robust associations with clinical outcomes in the general population and in patients with cancer. In patients with ovarian cancer, social isolation has been found to be related to decreased survival and multiple biomarkers supporting tumor progression. However, to the authors' knowledge, little is known regarding the relationship between social isolation and the molecular characteristics of ovarian tumors. Herein, the authors have used genome-wide transcriptional profiling to quantify associations between social isolation and epithelial-mesenchymal transition (EMT) polarization in ovarian tumors and transcriptome-driven, promoter-based bioinformatics analyses to identify gene regulatory pathways that may potentially underlie these changes. METHODS Tumor was sampled during primary surgical resection and immediately frozen in liquid nitrogen. After RNA extraction, microarray analysis of the transcriptome was performed and samples were analyzed to assess associations between EMT-related gene transcripts and social isolation (as indicated by a Social Provisions Scale Attachment subscale score

Stress can influence health throughout the lifespan, yet there is little agreement about what types and aspects of stress matter most for human health and disease. This is in part because “stress” is not a monolithic concept but rather, an emergent process that involves interactions between individual and environmental factors, historical and current events, allostatic states, and psychological and physiological reactivity. Many of these processes alone have been labeled as “stress.” Stress science would be further advanced if researchers adopted a common conceptual model that incorporates epidemiological, affective, and psychophysiological perspectives, with more precise language for describing stress measures. We articulate an integrative working model, highlighting how stressor exposures across the life course influence habitual responding and stress reactivity, and how health behaviors interact with stress. We offer a Stress Typology articulating timescales for stress measurement – acute, event-based, daily, and chronic – and more precise language for dimensions of stress measurement.

Background: During adolescence, peer victimization is a potent type of social stressor that can confer enduring risk for poor mental and physical health. Given recent research implicating inflammation in promoting a variety of serious mental and physical health problems, this study examined the role that peer victimization and cognitive vulnerability (i.e. negative cognitive styles and hopelessness) play in shaping adolescents' pro-inflammatory cytokine responses to an acute social stressor.Methods: Adolescent girls at risk for psychopathology (n = 157; Mage = 14.73 years; SD = 1.38) were exposed to a laboratory-based social stressor before and after which we assessed salivary levels of three key pro-inflammatory cytokines - interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α).Results: As hypothesized, adolescents with greater peer victimization exposure exhibited greater increases in IL-6 and IL1-β in response to the laboratory-based social stressor. Moreover, for all three cytokines individually, as well as for a combined latent factor of inflammation, peer victimization predicted enhanced inflammatory responding most strongly for adolescents with high levels of hopelessness.Conclusions: The findings reveal a biological pathway by which peer victimization may interact with cognitive vulnerability to influence health in adolescence.

Background Social factors in the patient macroenvironment have been shown to influence molecular events in the tumor microenvironment and thereby influence cancer progression. However, biomarkers providing a window into the longitudinal effects of biobehavioral factors on tumor biology over time are lacking. Exosome analysis is a novel strategy for in vivo monitoring of dynamic changes in tumor cells. This study examined exosomal profiles from patients with low or high levels of social support for epithelial-mesenchymal transition (EMT) polarization and gene expression related to inflammation and β-adrenergic signaling. Methods Exosomes were isolated from plasma sampled from a series of 40 women before primary surgical resection of advanced-stage, high-grade ovarian carcinoma. Samples were selected for analysis on the basis of extremes of low and high levels of social support. After exosomal isolation and RNA extraction, a microarray analysis of the transcriptome was performed. Results Primary analyses identified significant upregulation of 67 mesenchymal-characteristic gene transcripts and downregulation of 63 epithelial-characteristic transcripts in patients with low social support; this demonstrated increased EMT polarization (P = .0002). Secondary analyses using promoter sequence bioinformatics supported a priori hypotheses linking low social support to 1) increased activity of cyclic adenosine monophosphate response element binding protein (CREB)/activating transcription factor (ATF) family transcription factors that mediate the β-adrenergic response to catecholamines via the cyclic adenosine monophosphate/protein kinase A signaling pathway (mean fold change for CREB: 2.24 ± 0.65; P = .0019; mean fold change for ATF: 2.00 ± 0.55; P = .0049) and 2) increased activity of the proinflammatory nuclear factor κB/Rel family of transcription factors (mean fold change: 2.10 ± 0.70; P = .0109). Conclusions These findings suggest the possibility of leveraging exosomes as a noninvasive assessment of biobehavioral factors to help to direct personalized treatment approaches. Cancer 2018;124:580-6. © 2017 American Cancer Society.

Fatigue is a challenge in ovarian cancer survivorship and greatly impacts quality of life. In other cancer populations, fatigue has been associated with abnormal diurnal cortisol patterns. However, little is known about biological and behavioral factors in 5+-year ovarian cancer survivors and potential mechanisms underlying persistent fatigue have not been investigated in this population. Moreover, relationships between neuroendocrine and psychosocial factors in 5+-year ovarian cancer survivors have not been studied. We addressed these issues by examining relationships between diurnal cortisol rhythms, fatigue, life stress, and social support in 30 survivors of ovarian cancer who were assessed at least 5 years (mean = 6.20 years) following their primary diagnosis. Flatter diurnal cortisol slopes were associated with higher levels of fatigue, suggesting a role for HPA-axis dysregulation in sustained fatigue experienced by survivors. Moreover, greater cumulative lifetime stressor exposure (p = 0.023) and stressor severity (p = 0.004) were associated with flatter diurnal cortisol slopes, while higher social attachment (p = 0.001) was associated with steeper diurnal cortisol slopes. These findings suggest that ovarian cancer survivors with greater lifetime stress exposure or lower social attachment may be at increased risk for circadian rhythm disruption, which in turn is associated with fatigue. Future research should examine relationships of clinical stage and inflammatory cytokines to cortisol rhythms and fatigue in long-term ovarian cancer survivors, as well as investigating the clinical significance of abnormal diurnal cortisol profiles in this population.

Self-regulation is a fundamental human process that refers to multiple complex methods by which individuals pursue goals in the face of distractions. Whereas superior self-regulation predicts better academic achievement, relationship quality, financial and career success, and lifespan health, poor self-regulation increases a person’s risk for negative outcomes in each of these domains and can ultimately presage early mortality. Given its centrality to understanding the human condition, a large body of research has examined cognitive, emotional, and behavioral aspects of self-regulation. In contrast, relatively little attention has been paid to specific biologic processes that may underlie self-regulation. We address this latter issue in the present review by examining the growing body of research showing that components of the immune system involved in inflammation can alter neural, cognitive, and motivational processes that lead to impaired self-regulation and poor health. Based on these findings, we propose an integrated, multilevel model that describes how inflammation may cause widespread biobehavioral alterations that promote self-regulatory failure. This immunologic model of self-regulatory failure has implications for understanding how biological and behavioral factors interact to influence self-regulation. The model also suggests new ways of reducing disease risk and enhancing human potential by targeting inflammatory processes that affect self-regulation.

Life stress is central to many contemporary theories of human health and behavior. Despite this fact, numerous conceptual and measurement issues remain unresolved. The present article explores these topics by first summarizing several key definitional and conceptual matters that are important for life stress research. Second, I introduce stressnology, defined herein as the fictitiously named, but otherwise very real and problematic approach to studying life stress exposure that involves measuring only the superficial contours of this very complex construct. Finally, I review some recent methodological advancements that have the potential to move us past primitive approaches to conceptualizing and assessing life stress. Ultimately, although the influence that life stress has on human health and behavior is profound, our understanding of this construct-and how it affects wellbeing, functioning, and development-is still very limited. Using state-of-the-art instruments for assessing life stress exposure, especially across the entire life course, should therefore be a top scientific and clinical priority.

It has been widely hypothesized that stressors occurring over the lifespan exert a cumulative impact on health, but little work has directly tested these theories given the difficulty associated with measuring cumulative stress exposure over the lifespan. We addressed this issue in Brazil by translating the Stress and Adversity Inventory for Adults (Adult STRAIN) into Brazilian Portuguese. We then examined the instrument’s usability and acceptability; concurrent, discriminant, predictive, and incremental validity; and test-retest reliability. Participants were 330 Brazilian adults (238 women; Mage = 32.16; range: 18-76 years old) who completed the Adult STRAIN in Brazilian Portuguese, Childhood Trauma Questionnaire-Short Form (CTQ-SF), and Perceived Stress Scale (PSS). They also completed measures of socioeconomic status, personality, social desirability, negative affect, physical and mental health complaints, sleep quality, executive function, and doctor-diagnosed general health problems and autoimmune disorders. The STRAIN exhibited excellent usability and acceptability and was completed in 16 minutes and 27 seconds, on average. It showed good concurrent validity relative to the CTQ-SF and PSS (r ≥ .377) and good discriminant validity, both with and without adjusting for covariates. In addition, the STRAIN significantly predicted all of the health outcomes assessed except for executive function and explained substantial variance in these outcomes over and above the CTQ-SF, PSS, and covariates assessed. Finally, the test-retest reliability indices for total lifetime stressor count and severity were outstanding (ricc = .936 and .953, respectively, over M = 34.86 days). The Adult STRAIN in Brazilian Portuguese thus exhibits excellent usability and acceptability, good concurrent and discriminant validity, strong predictive and incremental validity across a variety of health outcomes, and outstanding test-retest reliability. We therefore conclude that the STRAIN is a practical, valid, and reliable instrument for researchers and clinicians looking to efficiently assess cumulative lifetime stress exposure in Brazilian Portuguese.

Social Signal Transduction Theory of Depression hypothesizes that social stress upregulates inflammatory activity, which in turn contributes to depression for some individuals. However, the specific cognitive processes underlying social stress-induced increases in inflammatory activity remain unclear. We addressed this issue by examining two separate relations: (1) between executive control measured following a laboratory-based social stress induction and individuals’ pro-inflammatory cytokine responses to the same stress induction and (2) between pro-inflammatory cytokine responses and participants’ depressive symptom levels. Healthy young participants (M(age) = 18.58 years old) were randomly assigned to either a stress condition or control condition. Executive control, and the inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α, were measured before and after the social stress induction or control task. Regression analyses (stress condition, n = 20; control condition, n = 16) demonstrated that in the stress condition only, greater increases in interleukin-6 were associated with more depressive symptoms. Additional analyses in the stress condition (n = 16) indicated that greater impairment in executive control following the social stress induction was related to greater social stress-induced increases in interleukin-6. These findings are consistent with Social Signal Transduction Theory of Depression and with the hypothesis that impairment in executive control during times of stress may be one process that contributes to stress-induced inflammatory activity, which may in turn increase risk for depression.

Exposure to social stress is a well-established risk factor for the development and recurrence of depression. Reduced neural responsiveness to monetary reward has been associated with greater symptoms following stress exposure. However, it remains unclear whether reduced reward responsiveness serves as a mediator or moderator of the effects of stress on internalizing symptoms or whether similar patterns emerge with responses to social reward. We addressed this issue by measuring lifetime stress exposure and event-related potentials (ERPs) to social reward in 231 emerging adults (M = 18.16, SD = 0.41 years old). Participants completed the Stress and Adversity Inventory (STRAIN) to assess severity of lifetime stressors and self-report measures of current internalizing symptoms. In addition, participants completed the Island Getaway task in which the reward positivity (RewP) ERP was recorded in response to social acceptance, adjusting for responses to rejection (RewP residual). In this task, participants vote to accept or reject peers and receive reward/acceptance and rejection feedback. Stressors were divided into social and non-social stress severity scores. Analyses were conducted to test social reward responsiveness as a mediator or moderator of the effects of social and non-social stress on internalizing symptoms. Both social and non-social stress exposure over the life course predicted symptoms of depression (ps < 0.001) and social anxiety (ps < 0.002). The effect of social stress on depression was moderated by the residual RewP to social reward, adjusting for responses to social rejection (p =0.024), such that greater lifetime social stress exposure and a relatively blunted RewP to social reward were associated with greater depressive symptoms. Social reward responsiveness did not mediate effects of stress on internalizing symptoms. Reduced processing of social reward may be a vulnerability for depression that increases risk for symptoms following exposure to social stress. Blunted social reward responsiveness appears to be a relatively unique vulnerability for depression, rather than social anxiety. Results support the utility of ERP measures in measuring individual differences in social reward processing that can be applied to better understand neural processes involved in the development of depression, and highlight the importance of considering specific dimensions of stressful life experiences.

Precision health relies on the ability to assess disease risk at an individual level, detect early preclinical conditions and initiate preventive strategies. Recent technological advances in omics and wearable monitoring enable deep molecular and physiological profiling and may provide important tools for precision health. We explored the ability of deep longitudinal profiling to make health-related discoveries, identify clinically relevant molecular pathways and affect behavior in a prospective longitudinal cohort (n = 109) enriched for risk of type 2 diabetes mellitus. The cohort underwent integrative personalized omics profiling from samples collected quarterly for up to 8 years (median, 2.8 years) using clinical measures and emerging technologies including genome, immunome, transcriptome, proteome, metabolome, microbiome and wearable monitoring. We discovered more than 67 clinically actionable health discoveries and identified multiple molecular pathways associated with metabolic, cardiovascular and oncologic pathophysiology. We developed prediction models for insulin resistance by using omics measurements, illustrating their potential to replace burdensome tests. Finally, study participation led the majority of participants to implement diet and exercise changes. Altogether, we conclude that deep longitudinal profiling can lead to actionable health discoveries and provide relevant information for precision health. Personalized omics profiling can lead to actionable health discoveries and stimulate lifestyle changes.

BACKGROUND: Numerous theories have posited that stressors occurring over the lifespan may exert a cumulative effect on psychological and biological processes that increase individuals’ risk for a variety of mental and physical health problems. Given the difficulty associated with assessing lifetime stress exposure, however, few empirical studies have directly tested these cumulative risk models of psychopathology and human health. METHOD: To address this issue, we examined the usability, acceptability, concurrent validity, and predictive validity of the recently developed Stress and Adversity Inventory for Adolescents (Adolescent STRAIN) in 338 youth (M(age) = 15.64; 229 females) seeking mental health treatment. RESULTS: The Adolescent STRAIN achieved high acceptability and was completed in approximately 25 min (interquartile range: 20–32 min). Concurrent associations with other measures of early adversity (Childhood Trauma Questionnaire-Short Form) and interpersonal stress (Revised Peer Experiences Questionnaire) were very good (rs = .50−.59). In analyses that adjusted for participants’ age, sex, and race, the STRAIN was significantly associated with depression, anxiety, and anhedonia severity; general mental and physical health complaints; risky behavior engagement; and number of interviewer-based psychiatric diagnoses (βs = .16−.52; risk ratios = 1.006–1.014). Contrary to classic theories of stress which assume that different stressors exert similar effects on health, substantial differences were observed across the two stressor types, twelve life domains, and five core social-psychological characteristics assessed by the Adolescent STRAIN. CONCLUSIONS: These data confirm the relevance of lifetime stress exposure for multiple health outcomes in adolescence, which can in turn inform existing theories of lifespan health. Because stress is a common presenting problem in hospitals and clinics, these data also suggest the possibility of using the Adolescent STRAIN to generate stress exposure profiles for case conceptualization and treatment planning purposes.

Stress research typically emphasizes the toxic effects of stress, but recent evidence has suggested that stress exposure, in moderation, can facilitate resilience. To test whether moderate stress exposure promotes psychological resilience to cancer, we examined the relationship between lifetime stress exposure prior to cancer diagnosis and postdiagnosis psychological functioning among 122 breast cancer survivors. Lifetime acute and chronic stress was assessed using an interview-based measure, and psychological functioning was assessed using measures of cancer-related intrusive thoughts and positive and negative affect. Results indicated that acute stress exposure was associated with cancer-related intrusive thoughts in a quadratic fashion (p = .016), such that participants with moderate acute stress reported fewer intrusive thoughts compared to those with low or high acute stress. Similarly, a quadratic relationship emerged between acute stress exposure and positive affect (p = .009), such that individuals with moderate acute stress reported the highest levels of positive affect. In contrast, acute and chronic stress were related to negative affect in a positive, linear fashion (ps < .05). In conclusion, moderate stress exposure was associated with indicators of psychological resilience among breast cancer survivors, supporting stress exposure as a key factor influencing adjustment to breast cancer and providing evidence for stress-induced resilience in a novel population.

Executive function is a neuropsychological construct that enables controlled cognitive processing, which has been hypothesized to enhance individuals’ resilience to stress. However, little empirical work has directly examined how executive function under different conditions mitigates the negative effects of stress exposure on health. To address this issue, we recruited 110 healthy young adults and assessed their recent life stress exposure, executive function in either a stressful or non-stressful context, and current health complaints. Based on existing research, we hypothesized that individuals exhibiting better executive function following a laboratory-based stressor (but not a control task) would demonstrate weaker associations between recent stress exposure and health because they perceived recent life stressors as being less severe. Consistent with this hypothesis, better executive function during acute stress, but not in the absence of stress, was associated with an attenuated link between participants’ recent life stress exposure and their current health complaints. Moreover, this attenuating effect was mediated by lesser perceptions of stressor severity. Based on these data, we conclude that better executive function under stress is associated with fewer health complaints and that these effects may occur by reducing individuals’ perceptions of stressor severity. The data thus suggest the possibility of reducing stress-related health problems by enhancing executive function.

Life stress is a central construct in many models of human health and disease. The present article reviews research on stress and health, with a focus on (a) how life stress has been conceptualized and measured over time, (b) recent evidence linking stress and disease, and (c) mechanisms that might underlie these effects. Emerging from this body of work is evidence that stress is involved in the development, maintenance, or exacerbation of several mental and physical health conditions, including asthma, rheumatoid arthritis, anxiety disorders, depression, cardiovascular disease, chronic pain, human immunodeficiency virus/AIDS, stroke, and certain types of cancer. Stress has also been implicated in accelerated biological aging and premature mortality. These effects have been studied most commonly using self-report checklist measures of life stress exposure, although interview-based approaches provide a more comprehensive assessment of individuals’ exposure to stress. Most recently, online systems like the Stress and Adversity Inventory (STRAIN) have been developed for assessing lifetime stress exposure, and such systems may provide important new information to help advance our understanding of how stressors occurring over the life course get embedded in the brain and body to affect lifespan health.

Research suggests that elite athletes are at increased risk of poor mental health, partly due to the intense demands associated with top-level sport. Despite growing interest in the topic, the factors that influence the mental health and well-being of elite athletes remain unclear. From a theoretical perspective, the accumulation of stress and adversity experienced over the life course may be an important factor. To investigate this possibility, we employed a mixed-method design to: (a) examine whether cumulative lifetime stress predicted depression, anxiety, and well-being in elite athletes; and (b) help explain why cumulative lifetime stress exposure might have resulted in poor mental health and well-being. Ninety-five elite athletes (M age = 29.81, SD = 10.88) completed the Stress and Adversity Inventory, Patient Health Questionnaire, Generalized Anxiety Disorder 7-item scale, and the Scales of General Well-Being. Hierarchical regression analyses revealed that total count and severity of lifetime stressor exposure significantly predicted greater depression (β =.42, p

Background Evidence suggests that behavioral, social, and environmental factors may modify the effects of life stress on health and performance of new nurses as they transition to hospitals. Objectives The aim of this study was to describe the methods of a project designed to investigate the role of social, behavioral, and environmental factors in modifying the adverse effects of stress on new nurses and to discuss demographic, health, and life stress characteristics of the cohort at baseline. Methods A prospective cohort design was used to conduct a comprehensive assessment of health endpoints, life stress, behaviors, personal traits, social factors, indicators of engagement and performance, and environmental exposures in nursing students. Adjusted odds ratios and analyses of covariance were used to examine associations between these factors at baseline. Results Health indicators in the cohort were comparable or better than in the broader United States population, and lifetime stress exposure was lower than among students from other majors. Exposure to more lifetime stressors was associated with greater risk for various health conditions, including hypertension, diabetes, and depression. Conversely, better social, environmental, behavioral, and personal profiles were associated with protective effects for the same health conditions. Discussion These data comprehensively summarize the lives of predominately Hispanic nursing students and highlight risk and resilience factors associated with their health and well-being. The findings are timely, as the nursing field diversifies in preparation to care for a diverse and aging population. Comprehensively assessing stress-health relationships among student nurses ought to inform the policies, practices, and curricula of nursing schools to better prepare nurses to thrive in the often-strenuous healthcare environment.

Prior research has found that recent life stress exposure is related to poorer working memory performance, but it remains unclear which aspects of working memory are related to stress. To address this important issue, we examined the extent to which recent life stress exposure was associated with working memory capacity (i.e., the number of items that can be held in working memory) and working memory precision (i.e., the quality of representations of items held within working memory) in a sample of 260 healthy young adults (Mage = 19.95 years old; range = 18–33). Recent life stress exposure and working memory were assessed with the Stress and Adversity Inventory for Daily Stress (Daily STRAIN) and color wheel task, respectively. We found that recent life stress was selectively associated with lower working memory capacity; moreover, the association of recent life stress with capacity was significantly stronger in magnitude than the non-significant association of recent life stress with precision. These associations were robust while controlling for potential confounds, including demographic factors, negative affect, and cumulative lifetime stress exposure. These results thus suggest that stress-related degradations in working memory capacity may help explain how recent life stress exposure affects working memory performance.

Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774-815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuations modulate women's susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.

Life stress is a well-established risk factor for a variety of mental and physical health problems, including anxiety disorders, depression, chronic pain, heart disease, asthma, autoimmune diseases, and neurodegenerative disorders. The purpose of this article is to describe emerging approaches for assessing stress using speech, which we do by reviewing the methodological advantages of these digital health tools, and the validation, ethical, and privacy issues raised by these technologies. As we describe, it is now possible to assess stress via the speech signal using smartphones and smart speakers that employ software programs and artificial intelligence to analyze several features of speech and speech acoustics, including pitch, jitter, energy, rate, and length and number of pauses. Because these digital devices are ubiquitous, we can now assess individuals’ stress levels in real time in almost any natural environment in which people speak. These technologies thus have great potential for advancing digital health initiatives that involve continuously monitoring changes in psychosocial functioning and disease risk over time. However, speech-based indices of stress have yet to be well-validated against stress biomarkers (e.g., cortisol, cytokines) that predict disease risk. In addition, acquiring speech samples raises the possibility that conversations intended to be private could one day be made public; moreover, obtaining real-time psychosocial risk information prompts ethical questions regarding how these data should be used for medical, commercial, and personal purposes. Although assessing stress using speech thus has enormous potential, there are critical validation, privacy, and ethical issues that must be addressed. Keywords: Life stress; voice; speech; privacy; ethics; digital health, Brain and Behavior Research Foundation (Grant NARSAD 23958)

BACKGROUND: Stress exposure occurring across the lifespan increases risk for disease, potentially involving telomere length shortening. Stress exposure during childhood and adulthood has been cross-sectionally linked with shorter telomere length. However, few longitudinal studies have examined telomere length attrition over time, and none have investigated how stressor duration (acute life events vs. chronic difficulties), timing (childhood vs. adulthood), and perceived severity may be uniquely related to telomere length shortening. METHODS: To address these issues, we administered a standardized instrument for assessing cumulative lifetime stress exposure (Stress and Adversity Inventory; STRAIN) to 175 mothers of children with Autism Spectrum Disorder or neurotypical children and measured their leukocyte telomere length (LTL) at baseline and 2 years later. RESULTS: Greater count of lifetime stressors was associated with shorter LTL at baseline and greater LTL attrition over time. When separating lifetime stressors into acute life events and chronic difficulties, only greater count of chronic difficulties significantly predicted shorter baseline LTL and greater LTL attrition. Similarly, when examining timing of stressor exposure, only greater count of chronic childhood difficulties (age < 18) significantly predicted shorter baseline LTL and greater LTL attrition over the 2-year period in mid-life. Importantly, these results were robust while controlling for stressors occurring during the interim 2-year period. Post-hoc analyses suggested that chronic difficulties occurring during earlier childhood (0–12 years) were associated with greater LTL attrition. Cumulative stressor severity predicted LTL attrition in a parallel manner, but was less consistently associated with baseline LTL. CONCLUSIONS: These data are the first to examine the effects of different aspects of cumulative lifetime stress exposure on LTL attrition over time, suggesting that accumulated chronic difficulties during childhood may play a unique role in shaping telomere shortening in midlife.

Mindfulness meditation represents a mental training framework for cultivating the state of mindful awareness in daily life. Recently, there has been a surge of interest in how mindfulness meditation improves human health and well-being. Although studies have shown that mindfulness meditation can improve self-reported measures of disease symptomatology, the effect that mindfulness meditation has on biological mechanisms underlying human aging and disease is less clear. To address this issue, we conducted the first comprehensive review of randomized controlled trials examining the effects of mindfulness meditation on immune system parameters, with a specific focus on five outcomes: (1) circulating and stimulated inflammatory proteins, (2) cellular transcription factors and gene expression, (3) immune cell count, (4) immune cell aging, and (5) antibody response. This analysis revealed substantial heterogeneity across studies with respect to patient population, study design, and assay procedures. The findings suggest possible effects of mindfulness meditation on specific markers of inflammation, cell-mediated immunity, and biological aging, but these results are tentative and require further replication. On the basis of this analysis, we describe the limitations of existing work and suggest possible avenues for future research. Mindfulness meditation may be salutogenic for immune system dynamics, but additional work is needed to examine these effects.

© 2016 Taylor & Francis. Stress is strongly associated with several mental and physical health problems that involve inflammation, including asthma, cardiovascular disease, certain types of cancer, and depression. It has been hypothesized that better cognitive control of emotional information may lead to reduced inflammatory reactivity to stress and thus better health, but to date no studies have examined whether differences in cognitive control predict pro-inflammatory cytokine responses to stress. To address this issue, we conducted a laboratory-based experimental study in which we randomly assigned healthy young-adult females to either an acute emotional stress (emotionally evocative video) or no-stress (control video) condition. Salivary levels of the key pro-inflammatory cytokines IL-1β, IL-6, and IL-8 were measured before and after the experimental manipulation, and following the last cytokine sample, we assessed participants’ cognitive control of emotional information using an emotional Stroop task. We also assessed participants’ cortisol levels before and after the manipulation to verify that documented effects were specific to cytokines and not simply due to increased nonwater salivary output. As hypothesized, the emotional stressor triggered significant increases in IL-1β, IL-6, and IL-8. Moreover, even in fully adjusted models, better cognitive control following the emotional (but not control) video predicted less pronounced cytokine responses to that stressor. In contrast, no effects were observed for cortisol. These data thus indicate that better cognitive control specifically following an emotional stressor is uniquely associated with less pronounced pro-inflammatory cytokine reactivity to such stress. These findings may therefore help explain why superior cognitive control portends better health over the lifespan.

Although substantial research has examined the effects of stress on cognition, much of this research has focused on acute stress (e.g. manipulated in the laboratory) or chronic stress (e.g. persistent interpersonal or financial difficulties). In contrast, the effects of recent life stress on cognition have been relatively understudied. To address this issue, we examined how recent life stress is associated with long-term, working memory, and self-reported memory in a sample of 142 healthy young adults who were assessed at two time points over a two-week period. Recent life stress was measured using the newly-developed Stress and Adversity Inventory for Daily Stress (Daily STRAIN), which assesses the frequency of relatively common stressful life events and difficulties over the preceding two weeks. To assess memory performance, participants completed both long-term and working memory tasks. Participants also provided self-reports of memory problems. As hypothesized, greater recent life stress exposure was associated with worse performance on measures of long-term and working memory, as well as more self-reported memory problems. These associations were largely robust while controlling for possible confounds, including participants' age, sex, and negative affect. The findings indicate that recent life stress exposure is broadly associated with worse memory. Future studies should thus consider assessing recent life stress as a potential predictor, moderator, or covariate of memory performance.

Supplemental digital content is available in the text., Objective Numerous theories have proposed that acute and chronic stressors may exert a cumulative effect on life-span health by causing biological “wear and tear,” or allostatic load, which in turn promotes disease. Very few studies have directly tested such models, though, partly because of the challenges associated with efficiently assessing stress exposure over the entire life course. To address this issue, we developed the first online system for systematically assessing lifetime stress exposure, called the Stress and Adversity Inventory (STRAIN), and describe its initial validation here. Methods Adults recruited from the community (n = 205) were administered the STRAIN, Childhood Trauma Questionnaire—Short Form, and Perceived Stress Scale, as well as measures of socioeconomic status, personality, social desirability, negative affect, mental and physical health complaints, sleep quality, computer-assessed executive function, and doctor-diagnosed general health problems and autoimmune disorders. Results The STRAIN achieved high acceptability and was completed relatively quickly (mean = 18 minutes 39 seconds; interquartile range = 12–23 minutes). The structure of the lifetime stress data best fit two latent classes overall and five distinct trajectories over time. Concurrent associations with the Childhood Trauma Questionnaire—Short Form and Perceived Stress Scale were good (r values = .147–.552). Moreover, the STRAIN was not significantly related to personality traits or social desirability characteristics and, in adjusted analyses, emerged as the measure most strongly associated with all six of the health and cognitive outcomes assessed except current mental health complaints (β values = .16–.41; risk ratios = 1.02–1.04). Finally, test-retest reliability for the main stress exposure indices over 2–4 weeks was excellent (r values = .904–.919). Conclusions The STRAIN demonstrated good usability and acceptability; very good concurrent, discriminant, and predictive validity; and excellent test-retest reliability.

There has been a long-standing interest in better understanding how social factors contribute to racial disparities in health, including birth outcomes. A recent emphasis in this context has been on identifying the effects of stress exposure and protective factors experienced over the entire lifetime. Yet despite repeated calls for a life course approach to research on this topic, very few studies have actually assessed how stressors and protective factors occurring over women’s lives relate to birth outcomes. We discuss this issue here by describing how challenges in the measurement of lifetime stress exposure and protective factors have prevented researchers from developing an empirically-based life course perspective on health. First, we summarize prevailing views on racial inequality and birth outcomes; second, we discuss measurement challenges that exist in this context; and finally, we describe both new tools and needed tools for assessing lifetime stress exposure and suggest opportunities for integrating information on stress exposure and psychosocial protective factors. We conclude that more studies are needed that integrate information about lifetime stress exposures and the protective factors that promote resilience against such exposures to inform policy and practice recommendations to reduce racial disparities in birth outcomes.

Exposure to stress throughout life can cumulatively influence later health, even among young adults. The negative effects of high cumulative stress exposure are well-known, and a shift from episodic to stimulus–response memory has been proposed to underlie forms of psychopathology that are related to high lifetime stress. At the other extreme, effects of very low stress exposure are mixed, with some studies reporting that low stress leads to better outcomes, while others demonstrate that low stress is associated with diminished resilience and negative outcomes. However, the influence of very low lifetime stress exposure on episodic and stimulus–response memory is unknown. Here we use a lifetime stress assessment system (STRAIN) to assess cumulative lifetime stress exposure and measure memory performance in young adults reporting very low and moderate levels of lifetime stress exposure. Relative to moderate levels of stress, very low levels of lifetime stress were associated with reduced use and retention (24 h later) of stimulus–response (SR) associations, and a higher likelihood of using context memory. Further, computational modeling revealed that participants with low levels of stress exhibited worse expression of memory for SR associations than those with moderate stress. These results demonstrate that very low levels of stress exposure can have negative effects on cognition.

© 2017 Elsevier Inc. Purpose Long-term survival of women with advanced-stage ovarian cancer is relatively rare. Little is known about quality of life (QOL) and survivorship concerns of these women. Here, we describe QOL of women with advanced-stage ovarian cancer surviving for 8.5 years or longer and compare women with 0–1 recurrence to those with multiple recurrences. Methods Participants (n = 56) recruited from 5 academic medical centers and the Ovarian Cancer Research Fund Alliance completed surveys regarding QOL (FACT-O), mood (CESD), social support (SPS), physical activity (IPAQ-SF), diet, and clinical characteristics. Median survival was 14.0 years (range 8.8–33.3). Results QOL and psychological adjustment of long-term survivors was relatively good, with mean FACT-G scores (multiple recurrences: 80.81 ± 13.95; 0–1 recurrence: 89.05 ± 10.80) above norms for healthy community samples (80.1 ± 18.1). Survivors with multiple recurrences reported more compromised QOL in domains of physical and emotional well-being (p

To examine risk and resilience factors that affect health, lifetime stress exposure histories, dispositional forgiveness levels, and mental and physical health were assessed in 148 young adults. Greater lifetime stress severity and lower levels of forgiveness each uniquely predicted worse mental and physical health. Analyses also revealed a graded Stress × Forgiveness interaction effect, wherein associations between stress and mental health were weaker for persons exhibiting more forgiveness. These data are the first to elucidate the interactive effects of cumulative stress severity and forgiveness on health, and suggest that developing a more forgiving coping style may help minimize stress-related disorders.

Social stratification has important implications for health and well-being, with individuals lower in standing in a hierarchy experiencing worse outcomes than those higher up the social ladder. Separate lines of past research suggest that alterations in inflammatory processes and neural responses to threat may link lower social status with poorer outcomes. This study was designed to bridge these literatures to investigate the neurocognitive mechanisms linking subjective social status and inflammation. Thirty-one participants reported their subjective social status, and underwent a functional magnetic resonance imaging scan while they were socially evaluated. Participants also provided blood samples before and after the stressor, which were analysed for changes in inflammation. Results showed that lower subjective social status was associated with greater increases in inflammation. Neuroimaging data revealed lower subjective social status was associated with greater neural activity in the dorsomedial prefrontal cortex (DMPFC) in response to negative feedback. Finally, results indicated that activation in the DMPFC in response to negative feedback mediated the relation between social status and increases in inflammatory activity. This study provides the first evidence of a neurocognitive pathway linking subjective social status and inflammation, thus furthering our understanding of how social hierarchies shape neural and physiological responses to social interactions.

Although extensive research has documented a relationship between depression and inflammation, links between anxiety and inflammation are less well-characterized. Among ovarian cancer patients, who generally have a poor prognosis, 29%–38% have significant anxiety at diagnosis. However, little is known about the relationship of anxiety with inflammation, which often supports tumor progression in ovarian cancer. To address this issue, we examined changes in anxiety over time in ovarian cancer patients following primary treatment, and associations of anxiety with inflammation and inflammatory control. Participants ( n = 373) completed questionnaires assessing anxiety symptoms (POMS-SF anxiety subscale), and had blood draws pre-surgery, following chemotherapy (6-months), and 12-months post-diagnosis. Linear-mixed models assessed associations between changes in anxiety and changes in IL-6 and nocturnal cortisol over time, with age and cancer stage as covariates. Self-reported anxiety decreased significantly from pre-surgery ( M = 9.51, S.D. = 5.65) to 6 months ( M = 4.58, S.D. = 4.70, p p = 0.006) and nocturnal cortisol (beta = 0.092, p = 0.04) over time. These findings do not address directionality or possible causality between anxiety and inflammation. However, as elevations in both IL-6 and nocturnal cortisol have been related to shorter survival in ovarian cancer, patients with increasing anxiety during the first year following diagnosis may be at risk for more rapid disease progression. Further examination of mechanisms underlying these results is warranted.

The dorsal anterior cingulate cortex (dACC) is recruited when a person is socially rejected or negatively evaluated. However, it remains to be fully understood how this region responds to repeated exposure to personally-relevant social evaluation, in both healthy populations and those vulnerable to Major Depressive Disorder (MDD), as well as how responding in these regions is associated with subsequent clinical functioning. To address this gap in the literature, we recruited 17 young women with past history of MDD (previously depressed) and 31 healthy controls and exposed them to a social evaluative session in a neuroimaging environment. In two bouts, participants received an equal amount of positive, negative, and neutral feedback from a confederate. All participants reported increases in feelings of social evaluation in response to the evaluative task. However, compared to healthy controls, previously depressed participants tended to show greater increases in depressed mood following the task. At the neural level, in response to negative (vs. positive) feedback, no main effect of group or evaluation periods was observed. However, a significant interaction between group and evaluation periods was found. Specifically, over the two bouts of evaluation, activity in the dACC decreased among healthy participants while it increased among previously depressed individuals. Interestingly and unexpectedly, in the previously depressed group specifically, this increased activity in dACC over time was associated with lower levels of depressive symptoms at baseline and at 6-months following the evaluation session (controlling for baseline levels). Thus, the subset of previously depressed participants who showed increases in the recruitment of the dACC over time in response to the negative evaluation seemed to fair better emotionally. These findings suggest that examining how the dACC responds to repeated bouts of negative evaluation reveals a new dimension to the role of the dACC in processing exclusion and contributing to mental health outcomes in a population vulnerable to MDD. Further, investigation of the dynamics of the dACC response to negative social evaluation is warranted.

Introduction Hypothalamic-pituitary-adrenal (HPA) deregulation is commonly observed in cancer patients, but its clinical significance is not well understood. We prospectively examined the association between HPA activity, tumor-associated inflammation, and survival in ovarian cancer patients prior to treatment. Materials and Methods Participants were 113 women with ovarian cancer who provided salivary cortisol for three days prior to treatment for calculation of cortisol slope, variability, and night cortisol. Cox proportional hazard regression analyses were used to examine associations between cortisol and survival in models adjusting for disease stage, tumor grade, cytoreduction and age. On a subsample of 41 patients with advanced disease ascites fluid was assayed for levels of interleukin-6 (IL-6) and correlated with cortisol variables. Results Each cortisol measure was associated with decreased survival time, adjusting for covariates (all p.36, all p