Showing papers on "Social stress published in 2020"

Emotional distress in young adults during the COVID-19 pandemic: evidence of risk and resilience from a longitudinal cohort study.

Abstract: Background The coronavirus disease 2019 (COVID-19) pandemic and associated lockdown could be considered a 'perfect storm' for increases in emotional distress Such increases can only be identified by studies that use data collected before and during the pandemic Longitudinal data are also needed to examine (1) the roles of previous distress and stressors in emotional distress during the pandemic and (2) how COVID-19-related stressors and coping strategies are associated with emotional distress when pre-pandemic distress is accounted for Methods Data came from a cohort study (N = 768) Emotional distress (perceived stress, internalizing symptoms, and anger), COVID-19-related stressors, and coping strategies were measured during the pandemic/lockdown when participants were aged 22 Previous distress and stressors were measured before COVID-19 (at age 20) Results On average, participants showed increased levels of perceived stress and anger (but not internalizing symptoms) during the pandemic compared to before Pre-COVID-19 emotional distress was the strongest predictor of during-pandemic emotional distress, followed by during-pandemic economic and psychosocial stressors (eg lifestyle and economic disruptions) and hopelessness, and pre-pandemic social stressors (eg bullying victimization and stressful life events) Most health risks to self or loved ones due to COVID-19 were not uniquely associated with emotional distress in final models Coping strategies associated with reduced distress included keeping a daily routine, physical activity, and positive reappraisal/reframing Conclusions In our community sample, pre-pandemic distress, secondary consequences of the pandemic (eg lifestyle and economic disruptions), and pre-pandemic social stressors were more consistently associated with young adults' emotional distress than COVID-19-related health risk exposures

Molecular adaptations of the blood–brain barrier promote stress resilience vs. depression

Abstract: Preclinical and clinical studies suggest that inflammation and vascular dysfunction contribute to the pathogenesis of major depressive disorder (MDD). Chronic social stress alters blood–brain barrier (BBB) integrity through loss of tight junction protein claudin-5 (cldn5) in male mice, promoting passage of circulating proinflammatory cytokines and depression-like behaviors. This effect is prominent within the nucleus accumbens, a brain region associated with mood regulation; however, the mechanisms involved are unclear. Moreover, compensatory responses leading to proper behavioral strategies and active resilience are unknown. Here we identify active molecular changes within the BBB associated with stress resilience that might serve a protective role for the neurovasculature. We also confirm the relevance of such changes to human depression and antidepressant treatment. We show that permissive epigenetic regulation of cldn5 expression and low endothelium expression of repressive cldn5-related transcription factor foxo1 are associated with stress resilience. Region- and endothelial cell-specific whole transcriptomic analyses revealed molecular signatures associated with stress vulnerability vs. resilience. We identified proinflammatory TNFα/NFκB signaling and hdac1 as mediators of stress susceptibility. Pharmacological inhibition of stress-induced increase in hdac1 activity rescued cldn5 expression in the NAc and promoted resilience. Importantly, we confirmed changes in HDAC1 expression in the NAc of depressed patients without antidepressant treatment in line with CLDN5 loss. Conversely, many of these deleterious CLDN5-related molecular changes were reduced in postmortem NAc from antidepressant-treated subjects. These findings reinforce the importance of considering stress-induced neurovascular pathology in depression and provide therapeutic targets to treat this mood disorder and promote resilience.

Extending the Minority Stress Model to Understand Mental Health Problems Experienced by the Autistic Population

Abstract: Research into autism and mental health has traditionally associated poor mental health and autism as inevitably linked. Other possible explanations for mental health problems among autistic populations have received little attention. As evidenced by the minority disability movement, autism is increasingly being considered part of the identities of autistic people. Autistic individuals thus constitute an identity-based minority and may be exposed to excess social stress as a result of disadvantaged and stigmatized social status. The authors test the utility of the minority stress model as an explanation for the experience of mental health problems within a sample of high-functioning autistic individuals (n = 111). Minority stressors including everyday discrimination, internalized stigma, and concealment significantly predicted poorer mental health, despite controlling for general stress exposure. These results indicate the potential utility of minority stress in explaining increased mental health problems ...

Resilience and the brain: a key role for regulatory circuits linked to social stress and support

Abstract: Given the high prevalence and burden of mental disorders, fostering the understanding of protective factors is an urgent issue for translational medicine in psychiatry. The concept of resilience describes individual and environmental protective factors against the backdrop of established adversities linked to mental illness. There is convergent evidence for a crucial role of direct as well as indirect adversity impacting the developing brain, with persisting effects until adulthood. Direct adversity may include childhood maltreatment and family adversity, while indirect social adversity can include factors such as urban living or ethnic minority status. Recently, research has begun to examine protective factors which may be able to buffer against or even reverse these influences. First evidence indicates that supportive social environments as well as trait-like individual protective characteristics might impact on similar neural substrates, thus strengthening the capacity to actively cope with stress exposure in order to counteract the detrimental effects evoked by social adversity. Here, we provide an overview of the current literature investigating the neural mechanisms of resilience with a putative social background, including studies on individual traits and genetic variation linked to resilience. We argue that the regulatory perigenual anterior cingulate cortex and limbic regions, including the amygdala and the ventral striatum, play a key role as crucial convergence sites of protective factors. Further, we discuss possible prevention and early intervention approaches targeting both the individual and the social environment to reduce the risk of psychiatric disorders and foster resilience.

The role of the microbiome in the neurobiology of social behaviour.

Abstract: Microbes colonise all multicellular life, and the gut microbiome has been shown to influence a range of host physiological and behavioural phenotypes. One of the most intriguing and least understood of these influences lies in the domain of the microbiome's interactions with host social behaviour, with new evidence revealing that the gut microbiome makes important contributions to animal sociality. However, little is known about the biological processes through which the microbiome might influence host social behaviour. Here, we synthesise evidence of the gut microbiome's interactions with various aspects of host sociality, including sociability, social cognition, social stress, and autism. We discuss evidence of microbial associations with the most likely physiological mediators of animal social interaction. These include the structure and function of regions of the 'social' brain (the amygdala, the prefrontal cortex, and the hippocampus) and the regulation of 'social' signalling molecules (glucocorticoids including corticosterone and cortisol, sex hormones including testosterone, oestrogens, and progestogens, neuropeptide hormones such as oxytocin and arginine vasopressin, and monoamine neurotransmitters such as serotonin and dopamine). We also discuss microbiome-associated host genetic and epigenetic processes relevant to social behaviour. We then review research on microbial interactions with olfaction in insects and mammals, which contribute to social signalling and communication. Following these discussions, we examine evidence of microbial associations with emotion and social behaviour in humans, focussing on psychobiotic studies, microbe-depression correlations, early human development, autism, and issues of statistical power, replication, and causality. We analyse how the putative physiological mediators of the microbiome-sociality connection may be investigated, and discuss issues relating to the interpretation of results. We also suggest that other candidate molecules should be studied, insofar as they exert effects on social behaviour and are known to interact with the microbiome. Finally, we consider different models of the sequence of microbial effects on host physiological development, and how these may contribute to host social behaviour.

Effects of short-term cannabidiol treatment on response to social stress in subjects at clinical high risk of developing psychosis

Abstract: Stress is a risk factor for psychosis and treatments which mitigate its harmful effects are needed. Cannabidiol (CBD) has antipsychotic and anxiolytic effects. We investigated whether CBD would normalise the neuroendocrine and anxiety responses to stress in clinical high risk for psychosis (CHR) patients. Thirty-two CHR patients and 26 healthy controls (HC) took part in the Trier Social Stress Test (TSST) and their serum cortisol, anxiety and stress associated with public speaking were estimated. Half of the CHR participants were on 600 mg/day of CBD (CHR-CBD) and half were on placebo (CHR-P) for 1 week. One-way analysis of variance (ANOVA) revealed a significant effect of group (HC, CHR-P, CHR-CBD (p = .005) on cortisol reactivity as well as a significant (p = .003) linear decrease. The change in cortisol associated with experimental stress exposure was greatest in HC controls and least in CHR-P patients, with CHR-CBD patients exhibiting an intermediate response. Planned contrasts revealed that the cortisol reactivity was significantly different in HC compared with CHR-P (p = .003), and in HC compared with CHR-CBD (p = .014), but was not different between CHR-P and CHR-CBD (p = .70). Across the participant groups (CHR-P, CHR-CBD and HC), changes in anxiety and experience of public speaking stress (all p’s < .02) were greatest in the CHR-P and least in the HC, with CHR-CBD participants demonstrating an intermediate level of change. Our findings show that it is worthwhile to design further well powered studies which investigate whether CBD may be used to affect cortisol response in clinical high risk for psychosis patients and any effect this may have on symptoms.

Interpersonal life stress, inflammation, and depression in adolescence: Testing Social Signal Transduction Theory of Depression

Abstract: 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.

The role of oxidative stress in cardiovascular disease caused by social isolation and loneliness.

Abstract: Loneliness and social isolation are common sources of chronic stress in modern society. Epidemiological studies have demonstrated that loneliness and social isolation increase mortality risk as much as smoking or alcohol consumption and more than physical inactivity or obesity. Loneliness in human is associated with higher blood pressure whereas enhanced atherosclerosis is observed in animal models of social isolation. Loneliness and social isolation lead to activation of the hypothalamic-pituitary-adrenocortical (HPA) axis, enhanced sympathetic nerve activity, impaired parasympathetic function and a proinflammatory immune response. These mechanisms have been implicated in the development of cardiovascular disease conferred by social isolation although a causal relationship has not been established so far. There is evidence that oxidative stress is likely to be a key molecular mechanism linking chronic psychosocial stress to cardiovascular disease. NADPH oxidase-mediated oxidative stress in the hypothalamus has been shown to be required for social isolation-induced HPA axis activation in socially isolated rats. Oxidative stress in the rostral ventrolateral medulla is also a key regulator of sympathetic nerve activity. In the vasculature, oxidative stress increases vascular tone and promote atherogenesis through multiple mechanisms. Thus, preventing oxidative stress may represent a therapeutic strategy to reduce the detrimental effects of social stress on health.

Depressive Symptoms among Adolescents Exposed to Personal and Vicarious Police Contact

Abstract: Theories of stress and strain, which emphasize the concentration of social stressors among vulnerable groups, suggest that police contact—the most common type of criminal justice contact—can have d...

Migration and schizophrenia: meta-analysis and explanatory framework

Abstract: Systematic reviews and meta-analyses suggest that there are increased rates of schizophrenia and related psychoses in first- and second-generation migrants and refugees. Here, we present a meta-analysis on the incidence of non-affective psychotic disorders among first- and second-generation migrants. We found substantial evidence for an increased relative risk of incidence among first- and second-generation migrants compared to the native population. As heterogeneity of included studies was high, effect estimates should be interpreted with caution and as guiding values rather than exact risk estimates. We interpret our findings in the context of social exclusion and isolation stress, and provide an explanatory framework that links cultural differences in verbal communication and experienced discrimination with the emergence of psychotic experiences and their neurobiological correlates. In this context, we discuss studies observing stress-dependent alterations of dopamine neurotransmission in studies among migrants versus non-migrants as well as in subjects with psychotic disorders. We suggest that social stress effects can impair contextualization of the meaning of verbal messages, which can be accounted for in Bayesian terms by a reduced precision of prior beliefs relative to sensory data, causing increased prediction errors and resulting in a shift towards the literal or “concrete” meaning of words. Compensatory alterations in higher-level beliefs, e.g., in the form of generalized interpretations of ambiguous interactions as hostile behavior, may contribute to psychotic experiences in migrants. We thus suggest that experienced discrimination and social exclusion is at the core of increased rates of psychotic experiences in subjects with a migration background.

Isolation, social stress, low socioeconomic status and its relationship to immune response in Covid-19 pandemic context

Abstract: The coronavirus disease 2019 (COVID-19) outbreak was first reported December 2019, in Wuhan, China, and has since spread worldwide. Social distancing or isolation measures were taken to mitigate the pandemic. Furthermore, stress and low socioeconomic status in humans confer increased vulnerability to morbidity and mortality, what can be biologically observed. This condition tends to remain during the Covid-19 pandemic. Social disruption stress (SDR) raises important questions regarding the functioning of the immune system, and the release of several stress hormones. A molecular pattern, conserved transcriptional response to adversity (CTRA), is thought to have evolved to defend against physical injury during periods of heightened risk. Chronic CTRA activation could leave an organism vulnerable to viral infections, leading to increased pro-inflammatory gene expression and a suppression of anti-viral gene expression. The activation of such transcriptional status is related to conditions of social stress through either hostile human contact, or increased predatory vulnerability due to separation from the social group and also low socioeconomic status. This review aims to point out questions for government officials, researchers and health professionals to better target their actions during a pandemic and encourage studies for a better understanding of these characteristics.

A discrete serotonergic circuit regulates vulnerability to social stress

Abstract: Exposure to social stress and dysregulated serotonergic neurotransmission have both been implicated in the etiology of psychiatric disorders. However, the serotonergic circuit involved in stress vulnerability is still unknown. Here, we explored whether a serotonergic input from the dorsal raphe (DR) to ventral tegmental area (VTA) influences vulnerability to social stress. We identified a distinct, anatomically and functionally defined serotonergic subpopulation in the DR that projects to the VTA (5-HTDR→VTA neurons). Moreover, we found that susceptibility to social stress decreased the firing activity of 5-HTDR→VTA neurons. Importantly, the bidirectional manipulation of 5-HTDR→VTA neurons could modulate susceptibility to social stress. Our findings reveal that the activity of 5-HTDR→VTA neurons may be an essential factor in determining individual levels of susceptibility to social stress and suggest that targeting specific serotonergic circuits may aid the development of therapies for the treatment of stress-related disorders. Serotonin is important in depression-like behavior. Here the authors show that dorsal raphe neurons that project to the ventral tegmental area are involved in regulating stress responses in mice.

Interactive effects of stress reactivity and rapid eye movement sleep theta activity on emotional memory formation.

Abstract: Sleep and stress independently enhance emotional memory consolidation. In particular, theta oscillations (4-7 Hz) during rapid eye movement (REM) sleep increase coherence in an emotional memory network (i.e., hippocampus, amygdala, and prefrontal cortex) and enhance emotional memory. However, little is known about how stress during learning might interact with subsequent REM theta activity to affect emotional memory. In the current study, we examined whether the relationship between REM theta activity and emotional memory differs as a function of pre-encoding stress exposure and reactivity. Participants underwent a psychosocial stressor (the Trier Social Stress Task; n = 32) or a comparable control task (n = 32) prior to encoding. Task-evoked cortisol reactivity was assessed by salivary cortisol rise from pre- to post-stressor, and participants in the stress condition were additionally categorized as high or low cortisol responders via a median split. During incidental encoding, participants studied 150 line drawings of negative, neutral, and positive images, followed by the complete color photo. All participants then slept overnight in the lab with polysomnographic recording. The next day, they were given a surprise recognition memory task. Results showed that memory was better for emotional relative to neutral information. Critically, these findings were observed only in the stress condition. No emotional memory benefit was observed in the control condition. In stressed participants, REM theta power significantly predicted memory for emotional information, specifically for positive items. This relationship was observed only in high cortisol responders. For low responders and controls, there was no relationship between REM theta and memory of any valence. These findings provide evidence that elevated stress at encoding, and accompanying changes in neuromodulators such as cortisol, may interact with theta activity during REM sleep to promote selective consolidation of emotional information.

Social Isolation Stress in Adolescence, but not Adulthood, Produces Hypersocial Behavior in Adult Male and Female C57BL/6J Mice.

Abstract: Chronic stress during the developmental period of adolescence increases susceptibility to many neuropsychiatric diseases in adulthood, including anxiety, affective, and alcohol/substance use disorders. Preclinical rodent models of adolescent stress have produced varying results that are species, strain, sex, and laboratory-dependent. However, adolescent social isolation is a potent stressor in humans that has been reliably modeled in male rats, increasing adult anxiety-like and alcohol drinking behaviors, among others. In this study, we examined the generalizability and sex-dependence of this model in C57BL/6J mice, the most commonly used rodent strain in neuroscience research. We also performed a parallel study using social isolation in adulthood to understand the impact of adult social isolation on basal behavioral phenotypes. We found that 6 weeks of social isolation with minimal handling in adolescence through early adulthood [postnatal day (PD) 28-70] produced a hypersocial phenotype in both male and female mice and an anxiolytic phenotype in the elevated plus-maze in female mice. However, it had no effects in other assays for avoidance behavior or on fear conditioning, alcohol drinking, reward or aversion sensitivity, or novel object exploration in either sex. In contrast, 6 weeks of social isolation in adulthood beginning at PD77 produced an anxiogenic phenotype in the light/dark box but had no effects on any other assays. Altogether, our results suggest that: (1) adolescence is a critical period for social stress in C57BL/6J mice, producing aberrant social behavior in a sex-independent manner; and (2) chronic individual housing in adulthood does not alter basal behavioral phenotypes that may confound interpretation of behavior following other laboratory manipulations.

Executive Control, Cytokine Reactivity to Social Stress, and Depressive Symptoms: Testing the Social Signal Transduction Theory of Depression.

Abstract: Social Signal Transduction Theory of Depression hypothesizes that social stress upregulates inflammatory activity, which in turn contributes to depression for some individuals. However, the...

Social history and exposure to pathogen signals modulate social status effects on gene regulation in rhesus macaques.

Abstract: Social experience is an important predictor of disease susceptibility and survival in humans and other social mammals. Chronic social stress is thought to generate a proinflammatory state characterized by elevated antibacterial defenses and reduced investment in antiviral defense. Here we manipulated long-term social status in female rhesus macaques to show that social subordination alters the gene expression response to ex vivo bacterial and viral challenge. As predicted by current models, bacterial lipopolysaccharide polarizes the immune response such that low status corresponds to higher expression of genes in NF-κB-dependent proinflammatory pathways and lower expression of genes involved in the antiviral response and type I IFN signaling. Counter to predictions, however, low status drives more exaggerated expression of both NF-κB- and IFN-associated genes after cells are exposed to the viral mimic Gardiquimod. Status-driven gene expression patterns are linked not only to social status at the time of sampling, but also to social history (i.e., past social status), especially in unstimulated cells. However, for a subset of genes, we observed interaction effects in which females who fell in rank were more strongly affected by current social status than those who climbed the social hierarchy. Taken together, our results indicate that the effects of social status on immune cell gene expression depend on pathogen exposure, pathogen type, and social history-in support of social experience-mediated biological embedding in adulthood, even in the conventionally memory-less innate immune system.

Sleep in the Social World of College Students: Bridging Interpersonal Stress and Fear of Missing Out with Mental Health

Abstract: Introduction: The college years are characterized by psychosocial and biological phenomena that may impact mental health, such as heightened sensitivity to social stressors and compromises in sleep quantity and quality. The current study uses a biopsychosocial approach to examine the associations among interpersonal stress, Fear of Missing Out (FoMO), insomnia, and mental health. Methods: Survey data were collected from 283 undergraduate students (90% female) with a mean age of 21.4 years. A path analysis was utilized to test a mediational model linking interpersonal stress and FoMO with mental health through a mediator of insomnia. We hypothesized that higher levels of interpersonal stress and FoMO would be associated with higher levels of insomnia symptoms, which would in turn be associated with poorer mental health. Results: As predicted, insomnia partially mediated significant associations of interpersonal stress and FoMO with mental health. The association of interpersonal stress with insomnia and mental health was more robust than the association of FoMO with these variables. Conclusions: The pathway from interpersonal stress and/or FoMO, through insomnia, to compromises in mental health may be modifiable through behavioral interventions focusing on coping skills, sleep hygiene, and even technology-related habit changes. Recommendations to help disrupt this pathway, particularly among college students, are discussed.

From stress to depression : development of extracellular matrix-dependent cognitive impairment following social stress

Abstract: Stress can predispose to depressive episodes, yet the molecular mechanisms regulating the transition from the initial stress response to a persistent pathological depressive state remain poorly understood. We profiled the development of an enduring depressive-like state by assessing affective behavior and hippocampal function during the 2 months following social-defeat stress. We measured remodeling of hippocampal extracellular matrix (ECM) during this period, as we recently identified ECM changes to mediate cognitive impairment during the sustained depressive-like state. Affective disturbance and cognitive impairments develop disparately after social stress, with gradual appearance of affective deficits. In contrast, spatial memory was impaired both early after stress and during the late-emerging chronic depressive-like state, while intact in-between. Similarly, we observed a biphasic regulation of the hippocampal ECM coinciding with hippocampus-dependent memory deficits. Together our data (1) reveal a dichotomy between affective and cognitive impairments similar to that observed in patients, (2) indicate different molecular processes taking place during early stress and the chronic depressive-like state, and (3) support a role of the ECM in mediating long-lasting effects on memory. From a translational point of view, it is important to prioritize on temporal phenotypic aspects in animal models to elucidate the underlying mechanisms of depression.

Status Variation in Anticipatory Stressors and Their Associations with Depressive Symptoms.

Abstract: Members of structurally disadvantaged social groups report more frequent exposure to a variety of negative life events and chronic strains, yet little research has examined whether similar patterns exist for anticipatory stressors, or challenging circumstances that loom as potential threats in the future. This study uses data collected as part of a national survey of college seniors (N = 995) to examine how anticipatory stress regarding economic and residential security, exposure to traumatic events, and experiences of discrimination vary by gender identity, race-ethnicity, sexual orientation, and first-generation college student status. Consistent with stress theory, anticipatory stressors are more commonly reported by members of disadvantaged groups. Notably, variation in anticipatory stressors explains a nontrivial proportion of differences in depressive symptoms found across gender identity and sexual orientation categories. Findings signal the necessity of incorporating anticipatory stressors into research in the stress paradigm to further disentangle the contributions of social stressors to health disparities.

Pandemias, COVID-19 y Salud Mental: ¿Qué Sabemos Actualmente?

Abstract: Pandemics are associated with a score of social and medical stressors that create severe disruptions at multiple levels. Pandemics are related to confusion, fears, uncertainty and the probable deaths of friends and loved ones. Also, pandemics are associated with a wide variety of social stressors such as economic and job loss, social isolation, the breakdown of healthcare systems and other pleasant routines. The manifestation of COVID-19 on December 2019 has created innumerable social and personal stressors that incidentally are similar to the pandemic of 1918 that contaminated nearly a third of the world population. In this article, I present recent empirical international studies that have examined the impact of COVID-19 on the mental health of innumerable people’s around the world. The data are consistent: some psychiatric disorders have shown a dramatic increase including anxiety, depression, insomnia and general fearfulness. This finding is generalizable in children, adolescents and adults. Medical professionals that work with COVID-19 patients show a dramatic increase in those psychiatric disorders. On the other hand, the literature has identified some populations at risk of developing a psychiatric disorders, such as previous trait anxiety, being a woman, and having been exposed to a person with COVID-19. I conclude with a conceptual and theoretical approach resuming different multi=level tactics that could minimize the mental health impact of the pandemic.

Stress and Anxiety among Healthcare Workers Associated with COVID-19 Pandemic in Russia.

Abstract: Background Mental health of medical workers treating patients with COVID-19 is an issue of increasing concern worldwide. The available data on stress and anxiety symptoms among healthcare workers during the COVID-19 are relatively limited and have not been evaluated in Russia yet. Subjects and methods The cross-sectional anonymous survey included 1,090 healthcare workers. Stress and anxiety symptoms were assessed using Stress and Anxiety to Viral Epidemics - 9 (SAVE-9) and Generalized Anxiety Disorder - 7 (GAD-7) scales. Logistic regression, Kaiser-Meyer-Olkin two component factor model, Cronbach's alpha and ROC-analysis were performed to determine the influence of different variables, internal structure and consistency, sensitivity and specificity of SAVE-9 compared with GAD-7. Results The median scores on the GAD-7 and SAVE-9 were 5 and 14, respectively. 535 (49.1%) respondents had moderate and 239 (21.9%) had severe anxiety according to SAVE-9. 134 participants (12.3%) had severe anxiety, 144 (13.2%) had moderate according to GAD-7. The component model revealed two-factor structure of SAVE-9: "anxiety and somatic concern" and "social stress". Female gender (OR - 0.98, p=0.04) and younger age (OR - 0.65, p=0.04) were associated with higher level of anxiety according to regression model. The total score of SAVE-9 with a high degree of confidence predicted the GAD-7 value in comparative ROC analysis. Conclusions Healthcare workers in Russia reported high rates of stress and anxiety. The Russian version of the SAVE-9 displayed a good ratio of sensitivity to specificity compared with GAD-7 and can be recommended as a screening instrument for detection of stress and anxiety in healthcare workers.

Chemogenetic activation of an infralimbic cortex to basolateral amygdala projection promotes resistance to acute social defeat stress

Abstract: Tremendous individual differences exist in stress responsivity and social defeat stress is a key approach for identifying cellular mechanisms of stress susceptibility and resilience. Syrian hamsters show reliable territorial aggression, but after social defeat they exhibit a conditioned defeat (CD) response characterized by increased submission and an absence of aggression in future social interactions. Hamsters that achieve social dominance prior to social defeat exhibit greater defeat-induced neural activity in infralimbic (IL) cortex neurons that project to the basolateral amygdala (BLA) and reduced CD response compared to subordinate hamsters. Here, we hypothesize that chemogenetic activation of an IL-to-BLA neural projection during acute social defeat will reduce the CD response in subordinate hamsters and thereby produce dominant-like behavior. We confirmed that clozapine-N-oxide (CNO) itself did not alter the CD response and validated a dual-virus, Cre-dependent, chemogenetic approach by showing that CNO treatment increased c-Fos expression in the IL and decreased it in the BLA. We found that CNO treatment during social defeat reduced the acquisition of CD in subordinate, but not dominant, hamsters. This project extends our understanding of the neural circuits underlying resistance to acute social stress, which is an important step toward delineating circuit-based approaches for the treatment of stress-related psychopathologies.

Risk From Within: Intraminority Gay Community Stress and Sexual Risk-Taking Among Sexual Minority Men

Abstract: Background Sexual minority men remain highly impacted by the human immunodeficiency virus (HIV) with social stress being a clear predictor of their risk for infection. The past several decades of stress research regarding sexual minority men's HIV-risk behaviors has almost exclusively focused on the influence of stress emanating from outside the gay community (e.g., stigma-related stress, or minority stress, such as heterosexist discrimination). However, recent evidence suggests that sexual minority men also face stress from within their own communities. Purpose We sought to examine whether stress from within the gay community, or intraminority gay community stress, might influence sexual minority men's risk behaviors, including HIV-risk behaviors, over-and-above more commonly examined stressors affecting this risk. Methods We tested whether intraminority gay community stress was associated with sexual minority men's HIV-risk behaviors in a large national survey of sexual minority men (Study 1), and experimentally tested intraminority gay community stress's impact on behavioral risk-taking and attitudes toward condom use (Study 2). Results Self-reported exposure to intraminority gay community stress was positively associated with HIV-risk behaviors when accounting for the effects of several commonly examined minority stressors and general life stress (Study 1). Participants who were rejected from an online group of other sexual minority men evidenced greater risk-taking in a subsequent task and reported fewer benefits of condom use than participants who were accepted by the online group, when accounting for state affect (Study 2). Conclusions Sexual minority men's experiences of stress and rejection stemming from their own community may be an important and overlooked predictor of HIV infection and transmission.