Social Stress Reactivity Research Articles

The mediating role of social stress sensitivity on the relationship between hostile attribution bias and paranoia: An experience sampling study

IntroductionHeightened affective responses to daily life stressors, referred to as elevated affective reactivity to stress (or ‘stress sensitivity’), have been proposed as a putative mechanism of schizophrenia. Previous studies on stress sensitivity mainly used a case-control design; given that schizophrenia is heterogeneous its relationship with specific symptoms (e.g. paranoia) is yet to be addressed. In view of the continuum approach of understanding psychotic symptoms, the relationship between stress sensitivity (especially ‘social stress sensitivity’) and paranoia in the general population is important. Supported by emerging evidence of the relationship between hostile attribution bias (i.e. a tendency to interpret others’ actions as hostile and intentional) and paranoia, we hypothesized that social stress sensitivity mediates the relationship between hostile attribution bias and momentary experiences of paranoia.Objectives Using experience sampling method, this study aimed to examine the association between social stress sensitivity, hostile attribution bias and momentary paranoia in non-clinical young adults. We also tested the role of social stress sensitivity as mediator of the relationship between hostile attribution bias and momentary paranoia.MethodsConsented participants free from any past and current psychiatric diagnoses (confirmed with the Structured Clinical Interview for DSM-IV Disorders) completed the measure of hostile attribution bias (i.e. abbreviated Ambiguous Intentions Hostility Questionnaire). Participants then filled in an ESM questionnaire measuring momentary levels of paranoia, social stress (i.e. pleasantness of and preference for being alone or with others) and negative affect on a mobile phone app repeatedly, ten times per day over six days. Social stress reactivity was calculated as the within-moment correlation between social stress and negative affect. The associations between social stress sensitivity, hostile attribution bias and momentary paranoia, and the mediating role of social stress sensitivity, were tested with multilevel modelling.Results The final sample consisted of 131 participants (57.3% female, mean age= 20.36 (SD= 2.93)). The mean compliance rate was 71.9% (SD= 0.16). Social stress sensitivity was positively associated with momentary paranoia (B= 0.03, p= .002). Hostile attribution bias was associated with momentary paranoia (B= 0.41, p< .001), as well as social stress reactivity (B= 0.10, p= .003). The mediating effect from hostile attribution bias to momentary paranoia via social stress sensitivity was significant (ab= 0.05, 95% CI [0.03-0.07]).ConclusionsSocial stress sensitivity was related to momentary paranoia, as well as hostile attribution bias. Our finding suggests social stress reactivity as a potential mechanism underlying the relationship between hostile attribution bias and paranoia.Disclosure of InterestNone Declared

Increased affective reactivity to daily social stressors is associated with more severe psychotic symptoms in youths with 22q11.2 deletion syndrome.

Increased reactivity to minor stressors is considered a risk factor for psychosis, especially in vulnerable individuals. In the present study, we investigated affective and psychotic stress reactivity as well as its link with psychotic symptoms and psychopathology in youths with 22q11.2 deletion syndrome (22q11DS), a neurogenetic condition associated with a high risk for psychosis. A 6-day ecological momentary assessment protocol was used to assess perceived daily-life stress as well as affective and psychotic reactivity to stress in participants with 22q11DS (n = 38, age = 18.4) and healthy controls (HC; n = 53, age = 19.1). Psychotic symptoms, general psychopathology, and coping strategies were also assessed through clinical interviews and questionnaires. Participants with 22q11DS reported higher levels of perceived social stress (b = 0.21, p = 0.036) but lower levels of activity-related stress (b = -0.31, p = 0.003) in their daily lives compared to HC. The groups did not differ in affective or psychotic reactivity to stress, but individuals with 22q11DS who reported increased affective reactivity to social stressors showed more severe positive psychotic symptoms (rs = 0.505, p = 0.008). Finally, avoidance coping strategies moderated the association between stress and negative affects. Our results suggest an increased vulnerability for daily social stress in youths with 22q11DS, and link elevated social stress reactivity to heightened psychotic symptom severity. Given the high risk for psychosis in 22q11DS, interventions should focus on reducing social stress and developing adaptive coping strategies.

Oxytocin moderates corticolimbic social stress reactivity in cocaine use disorder and healthy controls

Social stress can contribute to the development of substance use disorders (SUDs) and increase the likelihood of relapse. Oxytocin (OT) is a potential pharmacotherapy that may buffer the effects of social stress on arousal and reward neurocircuitry. However, more research is needed to understand how OT moderates the brain’s response to social stress in SUDs. The present study examined the effect of intransasal OT (24 IU) versus placebo (PBO) on corticolimbic functional connectivity associated with acute social stress in individuals with cocaine use disorder (CUD; n = 67) and healthy controls (HC; n = 52). Psychophysiological interaction modeling used the left and right amygdala as seed regions with the left and right orbitofrontal and anterior cingulate cortex as a priori regions of interest. Moderators of the OT response included childhood trauma history and biological sex, which were examined in independent analyses. The main finding was that OT normalized corticolimbic connectivity (left amygdala-orbitofrontal and left amygdala-anterior cingulate) as a function of childhood trauma such that connectivity was different between trauma-present and trauma-absent groups on PBO, but not between trauma groups on OT. Effects of OT on corticolimbic connectivity were not different as a function of diagnosis (CUD vs HC) or sex. However, OT reduced subjective anxiety during social stress for CUD participants who reported childhood trauma compared to PBO and normalized craving response as a function of sex in CUD. The present findings add to some prior findings of normalizing effects of OT on corticolimbic circuitry in individuals with trauma histories and provide some initial support that OT can normalize subjective anxiety and craving in CUD.

Are shame and self-criticism the path to the pervasive effect of social stress reactivity on social functioning in psychosis?

It is widely known that stress reactivity and social functioning impairment are important difficulties in people with psychosis. However, the specific impact of stress reactivity on social functioning and its underlying mechanisms are still less explored. Social rank variables, such as shame and self-criticism, have been pointed out as relevant in the development, maintenance of several types of psychosocial suffering and, specifically, in psychotic disorders. This study's aim was to explore the associations between external shame, self-criticism, social stress reactivity, and social functioning difficulties and understand the mediator role of shame and self-criticism in the relationship between social stress reactivity and social functioning. Seventy-seven participants with a psychotic disorder filled in self-reported measures of stress reactivity, shame, and self-criticism and were clinically evaluated for social functioning. To study the associations between variables in the study, Spearman correlation coefficients were used. The PROCESS macro was used to test the sequential mediation analyses. All variables under study were associated with each other, and social stress reactivity predicted social functioning difficulties through external shame, whereas self-criticism was not a significant mediator. The present study highlights the role of external shame in the pathway from stress reactivity to social impairment. These results inform recovery-oriented interventions and reinforce the relevance of considering social competitive mentality when working with people with psychosis. Further research is needed to clarify the role of self-to-self relationship in social impairment and to identify other mechanisms aimed at dealing with shame used by people with psychosis.

S45. MENTALIZATION BASED TREATMENT FOR NON-AFFECTIVE PSYCHOTIC DISORDER

BackgroundDeficits in mentalizing – i.e. the ability to understand one’s own and another’s behavior in terms of mental states such as beliefs, feelings and intentions – have been widely observed in patients with non-affective psychotic disorder (NAPD). In turn, robust evidence has shown these impairments to be related to social dysfunction and negative symptoms. However, few treatments have been developed to effectively treat impaired mentalizing, in spite of its increased recognition as an important treatment target. Mentalization based treatment (MBT) is a psychodynamic therapy rooted in attachment theory, originally developed and empirically found to be effective in treating borderline personality disorder. MBT for psychotic disorder aims to improve social functioning in NAPD patients by targeting impaired mentalizing.MethodsThe study is a multicenter, rater-blinded, randomized controlled trial. Ninety patients, who were diagnosed with NAPD by a psychiatrist and whose diagnosis was confirmed by researchers with the CASH, were recruited from community treatment teams in the Netherlands. They were randomly allocated to either treatment as usual plus MBT or to treatment as usual only. MBT consisted of 18 months of group therapy (one hour weekly) and individual therapy (30 minutes per two weeks). Patients had a mean age of 31.48 years (SD = 8.87) and a mean duration since onset of psychosis of 5.53 years (SD = 3.65). The primary outcome variable was social functioning (measured with the Social Functioning Scale). Other outcome variables were positive, negative, depressive, and anxious symptoms, as well as insight (PANSS), quality of life (MANSA), substance abuse, social stress reactivity (Experience Sampling Method), and mentalizing capacity (Social Cognition and Object-Relations System; Hinting Task).ResultsThis will be the first presentation of our trial results.DiscussionThe clinical implications of the results and limitations of the trial will be discussed. Theoretical considerations suggest that mentalization-based treatment could be an effective treatment for social dysfunction and impaired mentalizing in NAPD. If Mentalization-based treatment for psychotic disorders proves to be effective at improving social functioning and mentalizing, it may provide a valuable addition to treatment as usual.

Th17/T regulator cell balance and NK cell numbers in relation to psychosis liability and social stress reactivity

BackgroundPsychotic disorders are characterized by a deranged immune system, including altered number and function of Natural Killer (NK) and T cells. Psychotic disorders arise from an interaction between genetic vulnerability and exposure to environmental risk factors. Exposure to social adversity during early life is particularly relevant to psychosis risk and is thought to increase reactivity to subsequent minor daily social stressors. Virtual reality allows controlled experimental exposure to virtual social stressors. AimTo investigate the interplay between social adversity during early life, cell numbers of NK cells and T helper subsets and social stress reactivity in relation to psychosis liability. MethodsCirculating numbers of Th1, Th2, Th17, T regulator and NK cells were determined using flow cytometry in 80 participants with low psychosis liability (46 healthy controls and 34 siblings) and 53 participants with high psychosis liability (14 ultra-high risk (UHR) patients and 39 recent-onset psychosis patients), with and without the experience of childhood trauma. We examined if cell numbers predicted subjective stress when participants were exposed to social stressors (crowdedness, hostility and being part of an ethnic minority) in a virtual reality environment. ResultsThere were no significant group differences in Th1, Th2, Th17, T regulator and NK cell numbers between groups with a high or low liability for psychosis. However, in the high psychosis liability group, childhood trauma was associated with increased Th17 cell numbers (p = 0.028). Moreover, in the high psychosis liability group increased T regulator and decreased NK cell numbers predicted stress experience during exposure to virtual social stressors (p = 0.015 and p = 0.009 for T regulator and NK cells, respectively). ConclusionA deranged Th17/T regulator balance and a reduced NK cell number are associated intermediate biological factors in the relation childhood trauma, psychosis liability and social stress reactivity.

Childhood trauma, psychosis liability and social stress reactivity: a virtual reality study.

Childhood trauma is associated with higher risk for mental disorders, including psychosis. Heightened sensitivity to social stress may be a mechanism. This virtual reality study tested the effect of childhood trauma on level of paranoid ideations and distress in response to social stress, in interaction with psychosis liability and level of social stress exposure. Seventy-five individuals with higher psychosis liability (55 with recent onset psychotic disorder and 20 at ultra-high risk for psychosis) and 95 individuals with lower psychosis liability (42 siblings and 53 controls) were exposed to a virtual café in five experiments with 0-3 social stressors (crowded, other ethnicity and hostility). Paranoid ideation was measured after each experiment. Subjective distress was self-rated before and after experiments. Multilevel random regression analyses were used to test main effects of childhood trauma and interaction effects. Childhood trauma was more prevalent in individuals with higher psychosis liability, and was associated with higher level of (subclinical) psychotic and affective symptoms. Individuals with a history of childhood trauma responded with more subjective distress to virtual social stress exposures. The effects of childhood trauma on paranoia and subjective distress were significantly stronger when the number of virtual environmental stressors increased. Higher psychosis liability increased the effect of childhood trauma on peak subjective distress and stress reactivity during experiments. Childhood trauma is associated with heightened social stress sensitivity and may contribute to psychotic and affective dysregulation later in life, through a sensitized paranoid and stress response to social stressors.

The Interaction between Childhood Bullying and the FKBP5 Gene on Psychotic-Like Experiences and Stress Reactivity in Real Life.

AimThe present study employed Experience Sampling Methodology to examine whether the interaction between childhood bullying and FKBP5 variability (i) is associated with the expression of psychotic-like experiences, paranoia, and negative affect, and (ii) moderates psychotic-like, paranoid, and affective reactivity to different forms of momentary stress (situational and social) in daily life.MethodsA total of 206 nonclinical young adults were interviewed for bullying with the Childhood Experience of Care and Abuse and were prompted randomly eight times daily for one week to complete assessments of their current experiences, affect, and stress appraisals. Participants were genotyped for three FKBP5 single nucleotide polymorphisms (SNPs) (rs3800373, rs9296158, and rs1360780) that have been linked to hypothalamus-pituitary-adrenal axis reactivity. Multilevel analyses were conducted to examine the effect of the interaction between childhood bullying and the FKBP5 haplotype derived from these three SNPs.ResultsThe interaction between bullying and the FKBP5 haplotype was associated with positive, but not negative, psychotic-like experiences, paranoia, and negative affect. The bullying x FKBP5 interaction also moderated the association of a social stress appraisal (specifically, being alone because people do not want to be with you) with psychotic-like experiences and negative affect in daily life. Simple slopes analyses indicated that, in all cases, the associations were significantly increased by exposure to bullying in participants with the risk haplotype, but not for those with the non-risk haplotype.DiscussionThe present study provides the first evidence of the interplay between childhood bullying and FKBP5 variability in the real-world expression of psychosis proneness and social stress reactivity. The findings underscore the importance of investigating how gene-environment interactions are involved in mechanistic pathways to the extended psychosis phenotype and lend further support to the increasing relevance given to socially defeating appraisals in the experience of reality distortion.

Mentalization-based treatment for psychotic disorder: protocol of a randomized controlled trial.

BackgroundMany patients with a non-affective psychotic disorder suffer from impairments in social functioning and social cognition. To target these impairments, mentalization-based treatment for psychotic disorder, a psychodynamic treatment rooted in attachment theory, has been developed. It is expected to improve social cognition, and thereby to improve social functioning. The treatment is further expected to increase quality of life and the awareness of having a mental disorder, and to reduce substance abuse, social stress reactivity, positive symptoms, negative, anxious and depressive symptoms.Methods/designThe study is a rater-blinded randomized controlled trial. Patients are offered 18 months of therapy and are randomly allocated to mentalization-based treatment for psychotic disorders or treatment as usual. Patients are recruited from outpatient departments of the Rivierduinen mental health institute, the Netherlands, and are aged 18 to 55 years and have been diagnosed with a non-affective psychotic disorder. Social functioning, the primary outcome variable, is measured with the social functioning scale. The administration of all tests and questionnaires takes approximately 22 hours. Mentalization-based treatment for psychotic disorders adds a total of 60 hours of group therapy and 15 hours of individual therapy to treatment as usual. No known health risks are involved in the study, though it is known that group dynamics can have adverse effects on a psychiatric disorder.DiscussionIf Mentalization-based treatment for psychotic disorders proves to be effective, it could be a useful addition to treatment.Trial registrationDutch Trial Register. NTR4747. Trial registration date 08-19-2014.

Mother–infant dyadic reparation and individual differences in vagal tone affect 4-month-old infants’ social stress regulation

Infants’ social stress regulation (i.e., reactivity and recovery) might be affected by mother–infant dyadic functioning and infants’ vagal tone (i.e., respiratory sinus arrhythmia, RSA). This study investigated the role of a specific dyadic functioning feature (i.e., dyadic reparation) and individual differences in vagal tone regulation (i.e., RSA suppression vs. non-suppression) in relation to social stress regulation in 4-month-old infants. A total of 65 mother–infant dyads participated in the face-to-face still-face paradigm. Social stress reactivity and recovery were measured as negative emotionality during Still-Face and Reunion episodes, respectively. RSA was measured during Play, Still-Face, and Reunion episodes. Suppressors had higher dyadic reparation during Play and higher recovery from social stress compared with non-suppressors. Higher reparation during Play was associated with lower reactivity and higher recovery only for suppressors. Findings suggest a joint role of infants’ RSA individual differences and dyadic reparation in affecting infants’ social stress regulation at 4 months of age.

Effects of adverse childhood experiences on the association between intranasal oxytocin and social stress reactivity among individuals with cocaine dependence

BackgroundDrug dependence and adverse childhood experiences (ACE) are commonly reflected by dysregulation of the hypothalamic-pituitary-adrenal axis (HPA). Accumulating research indicates that the neuropeptide oxytocin may regulate HPA function, resulting in reductions in neuroendocrine reactivity to social stress among individuals with drug dependence. However, emerging literature suggests that individual differences may differentially impact intranasal oxytocin's effects on human social behaviors. MethodsThis study employed a double-blind, placebo-controlled design to examine the extent to which ACE influenced the effects of intranasal oxytocin (40IU) on neuroendocrine reactivity to a laboratory social stress paradigm in a sample of 31 cocaine-dependent individuals. ResultsACE scores modified the relationship between intranasal oxytocin and cortisol reactivity. While ACE modified the relationship between intranasal oxytocin and DHEA response in a similar direction to what was seen in cortisol, it did not reach statistical significance. ConclusionsFindings are congruent with the emerging hypothesis that intranasal oxytocin may differentially attenuate social stress reactivity among individuals with specific vulnerabilities. Future research examining the nuances of intranasal oxytocin's therapeutic potential is necessary.

Daily life stress reactivity in remitted versus non-remitted depressed individuals

BackgroundLittle is known about how daily life mood reactivity to minor stressors (stress reactivity) might change following major depressive disorder (MDD) treatment. We investigate whether (i) mood states and appraisals of daily stressors change after treatment; (ii) stress reactivity to event, activity, or social stress differs; (iii) stress reactivity depends on severity of residual depressive symptoms; and (iv) stress reactivity in individuals with remitted or non-remitted depression differ from that of never-depressed individuals. MethodsThirty depressed individuals participated in an experience sampling study before and after a treatment period of 18 months; 39 healthy individuals formed a comparison group. Reactivity of positive affect (PA) and negative affect (NA) to daily stressors were measured. ResultsMore residual symptoms were associated with larger NA responses to stress. Compared to healthy controls, participants with non-remitted MDD showed higher NA-reactivity to all stressors. In contrast, stress reactivity to event and activity stressors was normalized in remitted patients. However, they still showed heightened NA-reactivity to social stress. ConclusionsGreater stress reactivity to event and activity stress appears to be state-dependent. The heightened social stress reactivity in remitted patients suggests that sensitivity to social stress may reflect an underlying vulnerability in MDD.

Social stress regulation in 4-month-old infants: Contribution of maternal social engagement and infants' 5-HTTLPR genotype

BackgroundMaternal behavior and infant 5-HTTLPR polymorphism have been linked to infants' social stress reactivity and recovery at different ages. Nonetheless, Gene×Environment (G×E) studies focusing on early infancy are rare and have led to mixed results. AimTo investigate the contribution of maternal social engagement and infants' 5-HTTLPR polymorphism in predicting infants' negative emotionality in response to a social stressor, namely maternal unresponsiveness. Study designCross-sectional, G×E study. Subjects73 4-month-old infants and their mothers took part to the Face-to-Face Still-Face (FFSF) procedure. Outcome measuresA micro-analytical coding of negative emotionality was adopted to measure infants' reactivity to social stress (Still-Face episode) and infants' recovery after social stress (Reunion episode). Maternal contribution was measured as maternal social engagement during the Play episode. Infants were genotyped as S-carriers or L-homozygotes. ResultsThe interplay between maternal social engagement and infants' genotype was found to be predictive of infants' negative emotionality during both Still-Face and Reunion episodes of the FFSF paradigm. The interaction highlighted that maternal social engagement predicted minor negative emotionality during Still-Face and Reunion episodes for S-carrier infants, but not for L-homozygotes. ConclusionsFindings extend previous results on adults and children, highlighting that maternal behavior might be a protective factor for stress reactivity and regulation, especially for S-carrier infants who are at risk for heightened stress susceptibility.

Social stress reactivity alters reward and punishment learning

To examine how stress affects cognitive functioning, individual differences in trait vulnerability (punishment sensitivity) and state reactivity (negative affect) to social evaluative threat were examined during concurrent reinforcement learning. Lower trait-level punishment sensitivity predicted better reward learning and poorer punishment learning; the opposite pattern was found in more punishment sensitive individuals. Increasing state-level negative affect was directly related to punishment learning accuracy in highly punishment sensitive individuals, but these measures were inversely related in less sensitive individuals. Combined electrophysiological measurement, performance accuracy and computational estimations of learning parameters suggest that trait and state vulnerability to stress alter cortico-striatal functioning during reinforcement learning, possibly mediated via medio-frontal cortical systems.