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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.

Key Points Question Does estradiol mitigate the negative association of visceral fat with structural brain networks and cognitive health? Findings In this cross-sectional study of a German population-based cohort of 974 adults, higher estradiol levels were associated with increased structural brain network covariance and a reduction in the negative association of visceral fat with network covariance, but only for women. In women, higher estradiol levels were associated with better structural network covariance and cognitive performance during midlife. Meaning Assessing visceral adipose tissue and hormone profiles, particularly in women during midlife, may be essential for promoting a healthy brain aging trajectory., This cross-sectional study of a German population-based cohort assesses whether visceral adipose fat moderates the association between age and brain network structure and whether estradiol moderates the association between visceral adipose fat and brain network structure., Importance Changes in estradiol during aging are associated with increased dementia risk. It remains unclear how estradiol supports cognitive health and whether risk factors, such as midlife obesity, are exacerbated by estrogen loss. Objectives To assess whether visceral adipose tissue (VAT) moderates the association between age and brain network structure and to investigate whether estradiol moderates the association between VAT and brain network structure. Design, Setting, and Participants Cross-sectional study of data from 974 cognitively healthy adults in Germany who participated in the Health Study of the Leipzig Research Centre for Civilization Diseases, a previously described population-based cohort study. Two moderation analyses were performed, including VAT as the moderator variable between age and brain network structure and estradiol as the moderator variable between VAT and brain network structure. The study was conducted from August 1, 2011, to November 23, 2014. Analyses were conducted from August 2017 to September 2018. Exposures Serum estradiol levels from fasting blood and visceral adipose tissue volume from T1-weighted magnetic resonance imaging (MRI). Main Outcomes and Measures Brain network covariance (individual loading on structural network derived from T1-weighted MRI) and memory performance (composite score from the Consortium to Establish a Registry for Alzheimer Disease [CERAD] verbal episodic memory test on learning [score range, 0-30], recall [score range, 0-10], and recognition [score range, 0-20]). Results Final analyses included data from 473 women (mean [SD] age, 50.10 [15.63] years) and 501 men (mean [SD] age, 51.24 [15.67] years). Visceral adipose tissue was associated with an exacerbation of the negative association of aging with network covariance for women (interaction term β = −0.02; 95% bias-corrected bootstrap CI, −0.03 to −0.01; P = .001) and men (interaction term β = −0.02; 95% bias-corrected bootstrap CI, −0.03 to −0.01; P

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.

Psychoneuroimmunology (PNI) is the study of how psychological, neural, and immunologic processes interact and affect human health and behavior. Although once a relatively small field, some of the most exciting discoveries in psychopathology and mental health research have recently involved ideas and methods from PNI. In reviewing this work, I first summarize the structure and function of the human immune system, focusing primarily on inflammation. Second, I describe neural and physiologic pathways that link the brain and immune system, which give neurocognitive processes the ability to regulate the immune system and immunologic processes the ability to affect neural, cognitive-emotional, and behavioral outcomes. Third, I review studies examining associations between life stress and inflammation, and inflammation and mental health. Finally, I highlight several promising avenues for future research. Overall, despite the notable impact that PNI has already had on our understanding of mental and physical health, many important questions remain unanswered.

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

Recent estimates suggest that more than 50% of all deaths worldwide are currently attributable to inflammation-related diseases. Psychosocial interventions may represent a potentially useful strategy for addressing this global public health problem, but which types of interventions reliably improve immune system function, under what conditions, and for whom are unknown.To address this issue, we conducted a systematic review and meta-analysis of randomized clinical trials (RCTs) in which we estimated associations between 8 different psychosocial interventions and 7 markers of immune system function, and examined 9 potential moderating factors.PubMed, Scopus, PsycInfo, and ClinicalTrials.gov databases were systematically searched from February 1, 2017, to December 31, 2018, for all relevant RCTs published through December 31, 2018.Eligible RCTs included a psychosocial intervention, immune outcome, and preintervention and postintervention immunologic assessments. Studies were independently examined by 2 investigators. Of 4621 studies identified, 62 were eligible and 56 included.Data were extracted and analyzed from January 1, 2019, to July 29, 2019. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guideline was followed. Data were extracted by 2 investigators who were blind to study hypotheses and analyses, and were then analyzed using robust variance estimation. Analysis included 8 psychosocial interventions (behavior therapy, cognitive therapy, cognitive behavior therapy [CBT], CBT plus additive treatment or mode of delivery that augmented the CBT, bereavement or supportive therapy, multiple or combined interventions, other psychotherapy, and psychoeducation), 7 immune outcomes (proinflammatory cytokine or marker levels, anti-inflammatory cytokine levels, antibody levels, immune cell counts, natural killer cell activity, viral load, and other immune outcomes), and 9 moderating factors (intervention type, intervention format, intervention length, immune marker type, basal vs stimulated markers, immune marker measurement timing, disease state or reason for treatment, age, and sex).The primary a priori outcomes were pretest-posttest-control (ppc) group effect sizes (ppc g) for the 7 immunologic outcomes investigated.Across 56 RCTs and 4060 participants, psychosocial interventions were associated with enhanced immune system function (ppc g = 0.30, 95% CI, 0.21-0.40; t50.9 = 6.22; P .001). Overall, being randomly assigned to a psychosocial intervention condition vs a control condition was associated with a 14.7% (95% CI, 5.7%-23.8%) improvement in beneficial immune system function and an 18.0% (95% CI, 7.2%-28.8%) decrease in harmful immune system function over time. These associations persisted for at least 6 months following treatment and were robust across age, sex, and intervention duration. These associations were most reliable for CBT (ppc g = 0.33, 95% CI, 0.19-0.47; t27.2 = 4.82; P .001) and multiple or combined interventions (ppc g = 0.52, 95% CI, 0.17-0.88; t5.7 = 3.63; P = .01), and for studies that assessed proinflammatory cytokines or markers (ppc g = 0.33, 95% CI, 0.19-0.48; t25.6 = 4.70; P .001).These findings suggest that psychosocial interventions are reliably associated with enhanced immune system function and may therefore represent a viable strategy for improving immune-related health.

The purpose of the present chapter is to provide an overview of key issues involving the definition and assessment of major life events for researchers interested in the effects of life stress on a wide range of disorders. General conceptual and definitional issues are addressed initially, and a conceptual heuristic is proposed for guiding inquiry on major life stress and human disorder. This heuristic is drawn upon to develop principled practices for assessing, operationalizing, and finally quantifying major life events. Throughout the chapter, contemporary approaches for research on major life events are evaluated, their relative merits and shortcomings discussed, and their psychometric credentials formally compared. In closing, we consider future directions for research on major life events and their implications for health and disease.

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.

Adolescence is a developmental period during which time individuals adopt health behaviors that affect their lifelong health and disease risk. Socioeconomic status, social–cultural values, and stress have all been hypothesized to play a role in this association, but very few studies have examined how these factors interrelate and explain differences in health behaviors in adolescence. To address this issue, we assessed youths’ socioeconomic status, social–cultural values, life stress levels across seven domains, and health behaviors in a national sample of 1,830 high school seniors living in the four largest cities in Croatia. Structural equation modelling examined the extent to which stress mediates the effects of socioeconomic status and social– cultural values on positive and negative health behaviors. As hypothesized, stress levels significantly mediated associations between youths’ socioeconomic status, social–cultural values, and healthy and unhealthy habits. Additionally, whereas better socioeconomic status predicted less stress, greater social–cultural value on achieving a “good life” predicted more stress. More stress, in turn, was associated with engaging in fewer healthy behaviors for both males and females, and more unhealthy behaviors for males. Socioeconomic status and social–cultural values thus appear to influence stress levels, which may in turn affect adolescents’ health behaviors and, potentially, their lifespan health.

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)

Socially disadvantaged individuals are at greater risk for simultaneously being exposed to severe psychosocial stress in childhood as well as poor air quality across the life span. Recent evidence ...

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

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.

Introduction: Major depressive disorder (MDD) is often precipitated by life stress and growing evidence suggests that stress-induced alterations in reward processing may contribute to such risk. However, no human imaging studies have examined how recent life stress exposure modulates the neural systems that underlie reward processing in depressed and healthy individuals. Methods: In this proof-of-concept study, 12 MDD and 10 psychiatrically healthy individuals were interviewed using the Life Events and Difficulties Schedule (LEDS) to assess their perceived levels of recent acute and chronic life stress exposure. Additionally, each participant performed a monetary incentive delay task under baseline (no-stress) and stress (social-evaluative) conditions during functional MRI. Results: Across groups, medial prefrontal cortex (mPFC) activation to reward feedback was greater during acute stress versus no-stress conditions in individuals with greater perceived stressor severity. Under acute stress, depressed individuals showed a positive correlation between perceived stressor severity levels and reward-related mPFC activation (r¼0.79, p¼0.004), whereas no effect was found in healthy controls. Moreover, for depressed (but not healthy) individuals, the correlations between the stress (r¼0.79) and no-stress (r ¼� 0.48) conditions were significantly different. Finally, relative to controls, depressed participants showed significantly reduced mPFC gray matter, but functional findings remained robust while accounting for structural differences. Limitation: Small sample size, which warrants replication. Conclusion: Depressed individuals experiencing greater recent life stress recruited the mPFC more under stress when processing rewards. Our results represent an initial step toward elucidating mechanisms underlying stress sensitization and recurrence in depression. & 2015 Published by Elsevier B.V.

BACKGROUND The impact of psychological well-being on the physiologic processes involved in cancer progression remains unclear. Prior research has implicated adrenergic signaling in tumor growth and metastasis. Given that adrenergic signaling is influenced by both positive and negative factors, the authors examined how 2 different aspects of well-being (eudaimonic and positive affect) and psychological distress were associated with tumor norepinephrine (NE) in patients with ovarian cancer. METHODS A total of 365 women with suspected ovarian cancer completed psychosocial assessments before surgery and clinical information was obtained from medical records. Study inclusion was confirmed after histological diagnosis. Tumor NE was measured in frozen tissue samples using high-performance liquid chromatography with electrochemical detection. Confirmatory factor analysis was used to model eudaimonic well-being, positive affect, and psychological distress, and structural equation modeling was used to examine associations between these factors and tumor NE. RESULTS Eudaimonic well-being, positive affect, and psychological distress, modeled as distinct but correlated constructs, best fit the data (ie, compared with unitary or 2-factor models) (root mean square error of approximation, 0.048; comparative fit index, 0.982; and standardized root-mean-squared residual, 0.035). Structural equation modeling analysis that included physical well-being, stage of disease, histology, psychological treatment history, beta-blocker use, and caffeine use as covariates was found to have good model fit (root mean square error of approximation, 0.052; comparative fit index, 0.955; and standardized root-mean-squared residual, 0.036) and demonstrated that eudaimonic well-being was related to lower tumor NE (β = -.24 [P = .045]). In contrast, no effects were found for positive affect or psychological distress. CONCLUSIONS Eudaimonic well-being was found to be associated with lower tumor NE, independent of positive affect and psychological distress. Because adrenergic signaling is implicated in tumor progression, increasing eudaimonic well-being may improve both psychological and physiologic resilience in patients with ovarian cancer. Cancer 2015;121:3435–43. © 2015 American Cancer Society.

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

Although exposure to a recent major life event is one of the strongest known risk factors for depression, many people who experience such stress do not become depressed. Moreover, the biological mechanisms underlying differential emotional reactions to social adversity remain largely unknown. To investigate this issue, we examined whether the endogenous opioid system, which is known to influence sensitivity to physical pain, is also implicated in differential risk for depression following socially painful targeted rejection versus non-targeted rejection life events. Adolescents (n = 420) enrolled in a large longitudinal birth cohort study had their recent stress exposure and current mental health status assessed using self-report and interview-based methods. Participants were also genotyped for the A118G polymorphism in the μ-opioid receptor gene (OPRM1, rs1799971), which has been found to influence neural and psychological responses to rejection, likely by affecting opioid receptor expression and signaling efficiency. As hypothesized, G allele carriers, who are known to exhibit less opioid receptor expression and signaling efficiency, were more severely depressed and twice as likely to meet criteria for major depressive disorder following a recent targeted rejection major life event (e.g., being broken up with, getting fired) relative to A/A homozygotes who experienced such stress. However, A118G genotype did not moderate the effects of other similarly severe major life events on depression. These data thus elucidate a biological pathway that may specifically influence sensitivity to social pain and rejection, which in turn has implications for understanding differential risk for depression and several other social stress-related disorders.

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.

Diagnosis and treatment for a life threatening illness such as cancer are known to be psychologically impactful. However, little is known about the influence that non-cancer life stressors have on the quality of life (QOL) of ovarian cancer patients. The goal of the present study was to examine associations between non-cancer life stressors and QOL in 123 women with invasive epithelial ovarian cancer who were followed prospectively and longitudinally for one year.Mixed models for repeated measures were used to examine the relationship between life stressors and QOL pre-surgery and one year later, while adjusting for age, cancer stage, depressive symptoms, anxiety, and chemotherapy status (at one year). Prospective associations between QOL pre-surgery and one-year QOL were also examined.Number and severity of life stressors were unrelated to QOL of participants before surgery. At one year, however, participants experiencing a greater number of life stressors reported poorer concurrent physical well-being (PWB) (p=0.015), functional well-being (FWB) (p0.0001), social well-being (SWB) (p=0.0003), and total QOL (p0.0001). Similar effects were found for life event severity. Finally, experiencing a greater number of life stressors pre-surgery predicted poorer overall QOL one year post-diagnosis (p0.0001).Non-cancer life stressors can substantially impact long-term QOL of ovarian cancer patients, adjusting for medical variables such as chemotherapy and cancer stage, thus highlighting the importance of evaluating the stress burden of patients in ongoing cancer care.

The ability to measure cumulative stress exposure is important for research and teaching in stress and health, but until recently, no structured system has existed for assessing exposure to stress over the lifespan. Here, we report the results of two experimental studies that examined the pedagogical efficacy of using an automated system for assessing life stress, called the Stress and Adversity Inventory (STRAIN), for teaching courses on stress and health. In Study 1, a randomized, wait-list controlled experiment was conducted with 20 college students to test whether the STRAIN, coupled with a related lecture and discussion, promoted learning about stress and health. Results showed that this experiential lesson led to significant learning gains. To disentangle the effects of completing the STRAIN from participating in the lecture and discussion, we subsequently conducted Study 2 on 144 students using a 2 (STRAIN versus control activity) by 2 (STRAIN-specific lecture versus general stress lecture) repeated-measures design. Although the STRAIN-specific lecture was sufficient for promoting learning, completing the STRAIN also generated significant learning gains when paired with only the general stress lecture. Together, these studies suggest that the STRAIN is an effective tool for promoting experiential learning and teaching students about stress and health.

BACKGROUND Sleep disturbance is a common clinical complaint of oncology patients and contributes to substantial morbidity. However, because most sleep studies have been cross-sectional, associations between sleep quality and distress in patients with ovarian cancer over time remain unclear. This prospective longitudinal study examined rates of sleep disturbance; contributions of depression, anxiety, and medication use in sleep disturbance; and associations between sleep quality and quality of life (QOL) during the first year after diagnosis among women with ovarian cancer. METHODS Women with a pelvic mass completed measures of sleep quality, depression, anxiety, and QOL before surgery. Those diagnosed with primary epithelial ovarian, fallopian tube, or peritoneal cancer repeated surveys at 6 months and 1 year after diagnosis. Mixed modeling was used to examine trajectories of psychosocial measures over time, as well as associations between changes in distress and sleep quality. Relationships between changes in sleep and QOL were also examined. RESULTS The majority of patients reported disturbed global sleep (Pittsburgh Sleep Quality Index > 5) at all 3 time points. Medications for sleep and pain were associated with worse sleep at all time points. Greater increases in depression were associated with increased disturbances in sleep quality over time (P

Dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis is believed to play a role in the pathophysiology of depression. To investigate mechanisms that may underlie this effect, we examined several indices of HPA axis function – specifically, diurnal cortisol slope, cortisol awakening response, and suppression of cortisol release following dexamethasone administration – in 26 pre-menopausal depressed women and 23 never depressed women who were matched for age and body mass index. Salivary cortisol samples were collected at waking, 30 min after waking, and at bedtime over three consecutive days. On the third day, immediately after the bedtime sample, participants ingested a 0.5 mg dexamethasone tablet; they then collected cortisol samples at waking and 30 min after waking the following morning. As predicted, depressed women exhibited flatter diurnal cortisol rhythms and more impaired suppression of cortisol following dexamethasone administration than non-depressed women over the three sampling days. In addition, flatter diurnal cortisol slopes were associated with reduced cortisol response to dexamethasone treatment, both for all women and for depressed women when considered separately. Finally, greater self-reported depression severity was associated with flatter diurnal cortisol slopes and with less dexamethasone-related cortisol suppression for depressed women. Depression in women thus appears to be characterized by altered HPA axis functioning, as indexed by flatter diurnal cortisol slopes and an associated impaired sensitivity of cortisol to dexamethasone. Given that altered HPA axis functioning has been implicated in several somatic conditions, the present findings may be relevant for understanding the pathophysiology of both depression and depression-related physical disease.

Anxiety disorders increase risk for the early development of several diseases of aging. Elevated inflammation, a common risk factor across diseases of aging, may play a key role in the relationship between anxiety and physical disease. However, the neurobiological mechanisms linking anxiety with elevated inflammation remain unclear. In this review, we present a neurobiological model of the mechanisms by which anxiety promotes inflammation. Specifically we propose that exaggerated neurobiological sensitivity to threat in anxious individuals may lead to sustained threat perception, which is accompanied by prolonged activation of threat-related neural circuitry and threat-responsive biological systems including the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system (ANS), and inflammatory response. Over time, this pattern of responding can promote chronic inflammation through structural and functional brain changes, altered sensitivity of immune cell receptors, dysregulation of the HPA axis and ANS, and accelerated cellular aging. Chronic inflammation, in turn, increases risk for diseases of aging. Exaggerated neurobiological sensitivity to threat may thus be a treatment target for reducing disease risk in anxious individuals.

BackgroundPsychological stress is a well-known risk factor for poor health, and recent research has suggested that the emotion-focused coping process of forgiveness may help mitigate these effects. To date, however, no studies have examined how levels of forgiveness, stress, and health fluctuate and interrelate over time.PurposeWe addressed this issue by examining how forgiveness, stress, and mental and physical health symptoms change and relate to one another over 5weeks. We hypothesized that increases in state levels of forgiveness would be associated with decreases in perceptions of stress, which would in turn be related to decreases in mental and physical health symptoms. A reverse effects model was also tested.MethodsWe recruited a large, community-based sample of 332 young, middle-aged, and older adults (16-79years old; M age = 27.9). Each week for 5weeks, participants reported on their levels of state forgiveness, perceived stress, and mental and physical health symptoms.ResultsLevels of forgiveness, stress, and mental and physical health symptoms each showed significant change and individual variability in change over time. As hypothesized, increases in forgiveness were associated with decreases in stress, which were in turn related to decreases in mental (but not physical) health symptoms (i.e., forgiveness → stress → health). The reverse effects model (i.e., health → stress → forgiveness) provided a relatively poorer fit.ConclusionsThis study is the first to provide prospective, longitudinal evidence showing that greater forgiveness is associated with less stress and, in turn, better mental health. Strategies for cultivating forgiveness may thus have beneficial effects on stress and health.

We propose that the domain general process of categorization contributes to the perception\ud of stress. When a situation contains features associated with stressful experiences, it is\ud categorized as stressful. From the perspective of situated cognition, the features used to\ud categorize experiences as stressful are the features typically true of stressful situations. To\ud test this hypothesis, we asked participants to evaluate the perceived stress of 572 imagined\ud situations, and to also evaluate each situation for how much it possessed 19 features\ud potentially associated with stressful situations and their processing (e.g., self-threat,\ud familiarity, visual imagery, outcome certainty). Following variable reduction through\ud factor analysis, a core set of 8 features associated with stressful situations—expectation\ud violation, self-threat, coping efficacy, bodily experience, arousal, negative valence, positive\ud valence, and perseveration—all loaded on a single Core Stress Features factor. In a\ud multilevel model, this factor and an Imagery factor explained 88% of the variance in\ud judgments of perceived stress, with significant random effects reflecting differences in how\ud individual participants categorized stress. These results support the hypothesis that people\ud categorize situations as stressful to the extent that typical features of stressful situations are\ud present. To our knowledge, this is the first attempt to establish a comprehensive set of\ud features that predicts perceived stress.

Although research has shown that certain aspects of personality can change over time, the determinants of such change remain unclear. Stress alters neural dynamics and precipitates disorders that shape personality traits involving negative affectivity. In this study, therefore, we assessed the perceived stress and pessimism levels of 332 young, middle-aged, and older adults for five weeks to examine how levels of stress and pessimism change and interrelate over time. The best fitting longitudinal model was a bivariate latent growth curve model, which indicated that stress and pessimism both changed and exhibited significant variability in change over time. Moreover, changes in stress were associated with changes in pessimism. Pessimism thus changes over time, with alterations in stress potentially structuring these changes.

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.

Despite decades of research examining diathesis-stress models of emotional disorders, it remains unclear whether dysfunctional attitudes interact with stressful experiences to shape affect on a daily basis and, if so, how clinical and genetic factors influence these associations. To address these issues, we conducted a multi-level daily diary study that examined how dysfunctional attitudes and stressful events relate to daily fluctuations in negative and positive affect in 104 young adults. Given evidence that clinical and genetic factors underlie stress sensitivity, we also examined how daily affect is influenced by internalizing and externalizing symptoms and brain-derived neurotrophic factor (BDNF) genotype, which have been shown to influence neural, endocrine, and affective responses to stress. In multivariate models, internalizing symptoms and BDNF Val66Met genotype independently predicted heightened negative affect on stressful days, but dysfunctional attitudes did not. Specifically, the BDNF Met allele and elevated baseline internalizing symptomatology predicted greater increases in negative affect in stressful circumstances. These data are the first to demonstrate that BDNF genotype and stress are jointly associated with daily fluctuations in negative affect, and they challenge the assumption that maladaptive beliefs play a strong independent role in determining affective responses to everyday stressors. The results may thus inform the development of new multi-level theories of psychopathology and guide future research on predictors of affective lability.

Purpose Previous research has demonstrated relationships of social support with disease-related biomarkers in patients with ovarian cancer. However, the clinical relevance of these findings to patient outcomes has not been established. This prospective study examined how social support relates to long-term survival among consecutive patients with ovarian cancer. We focused on two types of social support: social attachment, a type of emotional social support reflecting connections with others, and instrumental social support reflecting the availability of tangible assistance. Patients and Methods Patients were prospectively recruited during a presurgical clinic visit and completed surveys before surgery. One hundred sixty-eight patients with histologically confirmed epithelial ovarian cancer were observed from the date of surgery until death or December 2010. Clinical information was obtained from medical records. Results In a Cox regression model, adjusting for disease stage, grade, histology, residual disease, and age, greater social attachment was associated with a lower likelihood of death (hazard ratio [HR], 0.87; 95% CI, 0.77 to 0.98; P = .018). The median survival time for patients with low social attachment categorized on a median split of 15 was 3.35 years (95% CI, 2.56 to 4.15 years). In contrast, by study completion, 59% of patients with high social attachment were still alive after 4.70 years. No significant association was found between instrumental social support and survival, even after adjustment for covariates. Conclusion Social attachment is associated with a survival advantage for patients with ovarian cancer. Clinical implications include the importance of screening for deficits in the social environment and consideration of support activities during adjuvant treatment.

Approaches to classroom instruction have evolved considerably over the past 50 years. This progress has been spurred by the development of several learning principles and methods of instruction, including active learning, student-centered learning, collaborative learning, experiential learning, and problem-based learning. In the present paper, we suggest that these seemingly different strategies share important underlying characteristics and can be viewed as complimentary components of a broader approach to classroom instruction called transformational teaching. Transformational teaching involves creating dynamic relationships between teachers, students, and a shared body of knowledge to promote student learning and personal growth. From this perspective, instructors are intellectual coaches who create teams of students who collaborate with each other and with their teacher to master bodies of information. Teachers assume the traditional role of facilitating students’ acquisition of key course concepts, but do so while enhancing students’ personal development and attitudes toward learning. They accomplish these goals by establishing a shared vision for a course, providing modeling and mastery experiences, challenging and encouraging students, personalizing attention and feedback, creating experiential lessons that transcend the boundaries of the classroom, and promoting ample opportunities for preflection and reflection. We propose that these methods are synergistically related and, when used together, maximize students’ potential for intellectual and personal growth.

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.

Although exposure to early adversity and prior experiences with depression have both been associated with lower levels of precipitating life stress in depression, it is unclear whether these stress sensitization effects are similar for all types of stress or whether they are specific to stressors that may be particularly depressogenic, such as those involving interpersonal loss. To investigate this issue, we administered structured, interview-based measures of early adversity, depression history, and recent life stress to one hundred adults who were diagnosed with major depressive disorder. As predicted, individuals who experienced early parental loss or prolonged separation (i.e., lasting one year or longer) and persons with more lifetime episodes of depression became depressed following lower levels of life stress occurring in the etiologically-central time period of three months prior to onset of depression. Importantly, however, additional analyses revealed that these effects were unique to stressors involving interpersonal loss. These data highlight potential stressor-specific effects in stress sensitization and demonstrate for the first time that individuals exposed to early parental loss or separation, and persons with greater histories of MDD, may be selectively sensitized to stressors involving interpersonal loss.