Child sexual abuse and social identity loss: A qualitative analysis of survivors' public accounts.

Emerging evidence suggests that social identities are an important determinant of adaptation following traumatic life experiences. In this paper, we analyse accounts of people who experienced child sexual abuse. Using publicly available talk of people who waived their right to anonymity following successful conviction of perpetrators, we conducted a thematic analysis focusing on trauma-related changes in their social identities. Analysis of these accounts highlighted two themes. The first highlights the acquisition in these accounts of unwanted and damaging identity labels. The second presents child sexual abuse as a key destructive force in terms of important identity work during childhood. Discussion of this analysis centres on the pathological consequences of social identity change. Both the loss of valued identities and the acquisition of aberrant and isolating identities are experienced and constructed as devastating by those affected by child sexual abuse. This has important implications, not only for those impacted by child sexual abuse but for how abuse is discussed in society, and how it is approached by policy makers, educators and individuals working with survivors and their families.

PROTOCOL: Group-based interventions for posttraumatic stress disorder: A systematic review and meta-analysis of the role of trauma type.

This is the protocol for a Campbell systematic review. The primary objective is to assess the effects of group-based treatments on posttraumatic stress disorder (PTSD) symptomology in people diagnosed with PTSD (by a clinician or screening instrument) or referred to a PTSD treatment group for their symptoms by a medical professional. We will also examine a range of moderators that may affect the efficacy of group-based treatments, including the nature of the trauma (interpersonal, stigmatized) and the group fit (in terms of gender and shared vs. unshared trauma). Further, we will also explore what, if any, group-based and social identity factors are recorded and how they relate to PTSD outcomes.

The effects of secondary stressors, social identity, and social support on perceived stress and resilience: Findings from the COVID-19 pandemic.

Primary stressors are direct outcomes of extreme events (e.g., viruses, floodwater) whereas secondary stressors stem from pre-disaster life circumstances and societal arrangements (e.g., illness, problematic pre-disaster policies) or from inefficient responses to the extreme event. Secondary stressors can cause significant long-term damage to people affected but are also tractable and amenable to change. In this study we explored the association between secondary stressors, social identity processes, social support, and perceived stress and resilience. Pre-registered analyses of data from the COVIDiSTRESS Global Survey Round II (N = 14,600; 43 countries) show that secondary stressors are positively associated with perceived stress and negatively associated with resilience, even when controlling for the effects of primary stressors. Being a woman or having lower socioeconomic status (SES) is associated with higher exposure to secondary stressors, higher perceived stress, and lower resilience. Importantly, social identification is positively associated with expected support and with increased resilience and lower perceived stress. However, neither gender, SES, or social identification moderated the relationship between secondary stressors and perceived stress and resilience. In conclusion, systemic reforms and the availability of social support are paramount to reducing the effects of secondary stressors.

Pandemic threat and group cohesion: national identification in the wake of COVID-19 is associated with authoritarianism.

Authoritarianism emerges in times of societal threat, in part driven by desires for group-based security. As such, we propose that the threat caused by the COVID-19 pandemic was associated with increased authoritarian tendencies and that this can be partially explained by increased national identification. We tested this hypothesis by collecting cross-sectional data from three different countries in April 2020. In Study 1, data from Ireland (N = 1276) showed that pandemic threat predicted increased national identification, which in turn predicted authoritarianism. In Study 2, we replicated this indirect effect in a representative UK sample (N = 506). In Study 3, we used an alternative measure of authoritarianism and conceptually replicated this effect among USA citizens (N = 429). In this US sample, the association between threat and authoritarian tendencies was stronger among progressives compared to conservatives. Findings are discussed and linked to group-based models of authoritarianism.

Social integration: Implications for the association between childhood trauma and stress responsivity.

OBJECTIVE: Childhood trauma is linked to the dysregulation of physiological responses to stress, particularly lower cardiovascular reactivity (CVR) to acute stress. The mechanisms that explain this association, however, are not yet fully understood. METHOD: Using secondary data from the Midlife in the United States (MIDUS) Biomarker Project (N = 1,148; n = 652 females), we examine whether social integration can help explain the association between childhood trauma and lower CVR. Participants completed a standardized laboratory stress paradigm which involved completing executive functioning (Stroop) and mental arithmetic (MATH) tasks. Cardiovascular measurements were continuously assessed using electrocardiogram (ECG) and Finometer equipment. The Social Well-Being Scale (Keyes, 1998) and the Childhood Trauma Questionnaire (CTQ; Bernstein et al., 2003) measured social integration and trauma, respectively. RESULTS: Regression analyses demonstrated that childhood trauma was associated with lower systolic (SBP; ß = -.14, p < .001) and diastolic (DBP; ß = -.11, p < .001) blood pressure reactivity but not heart rate (HR) reactivity. Mediation analyses, using Hayes PROCESS Model 4, showed that higher levels of trauma were associated with less social integration and in turn linked to lower reactivity across all biological indices. Moreover, sensitivity analyses showed that this indirect effect via social integration was evident for emotional and physical abuse, emotional and physical neglect, but not sexual abuse. CONCLUSION: Overall, the results indicated that dysregulated cardiovascular stress responses owing to childhood trauma may be shaped by a lack of social integration. The implications of this, as well as the findings for the individual types of trauma, are discussed. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Moral Identity Predicts Adherence to COVID-19 Mitigation Procedures Depending on Political Ideology: A Comparison Between the USA and New Zealand.

Reducing the spread of infectious viruses (e.g., COVID-19) can depend on societal compliance with effective mitigations. Identifying factors that influence adherence can inform public policy. In many cases, public health messaging has become highly moralized, focusing on the need to act for the greater good. In such contexts, a person's moral identity may influence behavior and serve to increase compliance through different mechanisms: if a person sees compliance as the right thing to do (internalization) and/or if a person perceives compliance as something others will notice as the right thing to do (symbolization). We argue that in societies that are more politically polarized, people's political ideology may interact with their moral identity to predict compliance. We hypothesized that where polarization is high (e.g., USA), moral identity should positively predict compliance for liberals to a greater extent than for conservatives. However, this effect would not occur where polarization is low (e.g., New Zealand). Moral identity, political ideology, and support for three different COVID-19 mitigation measures were assessed in both nations (N = 1,980). Results show that while moral identity can influence compliance, the political context of the nation must also be taken into account.

New group memberships formed after an acquired brain injury and posttraumatic growth: A prospective study.

Predicting positive psychosocial outcomes following an Acquired Brain Injury (ABI) remains a challenge. Considerable research demonstrates that social group memberships can have positive effects on psychological well-being, particularly during life transitions. Social group memberships are argued to help people derive a sense of self. This prospective study examined if social group memberships (number of groups and connectedness with groups) could predict posttraumatic growth (PTG) in those affected by ABI. Thirty-six participants (10 females, Mage = 46.56, SD = 11.46) engaged in community rehabilitation services completed measures at two time-points. Mediation analyses demonstrated that the number of new group memberships (groups formed post-injury) predicted greater PTG at time 2, via stronger connectedness with these new group memberships (controlling for initial PTG). The observed results suggest that a focus on developing and strengthening connections with new group memberships may promote positive adjustment after brain injury.

Individual differences in emotion regulation and cardiovascular responding to stress.

Instructed use of reappraisal to regulate stress in the laboratory is typically associated with a more adaptive cardiovascular response to stress, indexed by either (a) lower cardiovascular reactivity (CVR; e.g., lower blood pressure) or (b) a challenge-oriented response profile (i.e., greater cardiac output paired with lower total peripheral resistance). In contrast, instructed use of suppression is associated with exaggerated CVR (e.g., greater heart rate, blood pressure). Despite this, few studies have examined if the habitual use of these strategies are related to cardiovascular responding during stress. The current study examined the relationship between cardiovascular responses to acute stress and individual differences in emotion regulation style: trait reappraisal, suppression, and emotion regulation difficulties. Forty-eight participants (25 women, 23 men) completed a standardized laboratory stress paradigm incorporating a 20-minute acclimatization period, a 10-minute baseline, and two 5-minute speech tasks separated by a 10-minute intertask rest period. The emotional valence of the speech task was examined as a potential moderating factor; participants spoke about a block of negative-emotion words and a block of neutral-emotion words. Cardiovascular parameters were measured using the Finometer Pro. Greater habitual use of suppression was associated with exaggerated blood pressure responding to both tasks. However, only in response to the negative-emotion task was greater use of reappraisal associated with a challenge-oriented cardiovascular response. The findings suggest that individual differences in emotion regulation translate to differing patterns of CVR to stress, but the emotional valence of the stressor may play a role. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Individual differences in emotion regulation prospectively predict early COVID-19 related acute stress.

Preliminary prospective research suggests emotion dysregulation may confer vulnerability to poor stress responses. The present prospective study extends this research by examining both specific emotion regulation strategies and global emotion regulation difficulties in the context of acute stress following onset of the COVID-19 global pandemic in 119 young adults. As part of a larger study, emotion regulation was assessed prior to pandemic onset (January 2019 - February 2020) using two standard measures (Emotion Regulation Questionnaire, ERQ, Gross & John, 2003; Difficulties in Emotion Regulation Scale, DERS, Gratz & Roemer, 2004). A self-report assessment of acute stress was conducted 2-3½ weeks after the COVID-19 pandemic declaration. Results demonstrated cognitive reappraisal and expressive suppression (i.e., ERQ) were not individually predictive of acute stress; however, there was a significant interaction of suppression by reappraisal. Simple effects indicated suppression was negatively associated with acute stress only when reappraisal levels were high. Greater global emotion regulation difficulties (i.e., DERS), particularly nonacceptance of emotions and limited access to emotion regulation strategies, significantly predicted greater acute stress. These results provide further evidence of the temporal relationship between emotion dysregulation and stress reactions, and also suggest the expected effects of emotion regulation strategies may differ across contexts.

Instructed reappraisal and cardiovascular habituation to recurrent stress.

Instructed reappraisal has previously been associated with a challenge-oriented cardiovascular response profile, indexed by greater cardiac output (CO) and lower total peripheral resistance (TPR), in response to a single stress exposure. The present study builds on this research by employing a stress habituation paradigm where participants completed a speech task twice; in which prior to the second task participants heard reappraisal instructions (i.e., view feelings of stress arousal as something that is beneficial) or control instructions. This paradigm allowed us to (a) test if reappraisal aids cardiovascular habituation to recurrent stress, and (b) examine if reappraisal leads to a within-participant change in CO/TPR responding from an uninstructed task to an instructed reappraisal task. Habitual use of reappraisal was assessed using the Emotion Regulation Questionnaire. The analyses report upon 173 young adults (121 women, 52 men). Cardiovascular parameters were measured continuously using the Finometer Pro. All participants demonstrated similar cardiovascular habituation during the second stress exposure (lower SBP, CO, and HR); suggesting that reappraisal did not aid cardiovascular habituation to recurrent stress. Reappraisal instructions did not lead to a challenge-oriented response compared to both the control group and responses to the uninstructed task. This study is the first to examine the relationship between instructed reappraisal and cardiovascular habituation and identifies that habitual use of reappraisal does not interact with reappraisal instructions to influence cardiovascular responses to stress.

Establishing the validity of a novel passive stress task.

Laboratory tasks used to elicit a cardiovascular stress response in the laboratory can involve either active or passive coping. However, in previous work, passive stress tasks often incorporate a distinct physical stress element, such as the handgrip or cold pressor task, meaning observed changes in cardiovascular parameters may be the result of the physical element of the stressor rather than truly reflecting psychological stress. The present study aimed to establish the validity of a psychological passive stressor; one more analogous to active tasks than those previously employed in laboratory studies. Twenty-six young, healthy adults completed a speech task in the laboratory following a resting baseline period. Twelve months later, they were invited back to the laboratory and watched the video recording of their speech. Analyses confirmed that while both tasks elicited significant SBP and DBP change (all ps < .001), only the active task was associated with HR and CO reactivity (both ps < .001), while only the passive task was associated with TPR reactivity (p = .028). Furthermore, the passive stressor was associated with a mixed hemodynamic profile, whereas the active stressor was associated with a clear myocardial profile. This study confirms that watching a video recording of oneself complete a speech task is associated with a more vascular response profile, a response associated with passive coping contexts.

Effect of pro-inflammatory stimuli on mucin expression and inhibition by secretory leucoprotease inhibitor.

Stimuli-induced expression of certain mucin genes has been demonstrated to occur as a result of ligand-dependent activation of the epidermal growth factor receptor (EGFR). In particular, MUC5AC expression can be induced by cigarette-smoke, neutrophil elastase and lipopolysaccharide (LPS) following activation of tumour necrosis factor alpha-converting enzyme. We now show that a large of number of stimuli relevant to the cystic fibrosis lung - neutrophil elastase, LPS, Pam3Cys-Ser-(Lys)4 Hydrochloride (a lipopeptide analogue), CpG DNA (which mimics bacterial DNA) and cystic fibrosis bronchoalveolar lavage fluid - can activate MUC1 and 2 expression as well as MUC5AC expression in lung epithelial cells via an EGFR-dependent mechanism. In addition, we demonstrate that the immunomodulatory anti-protease, secretory leucoprotease inhibitor, can inhibit stimuli-induced MUC1, 2 and 5AC expression via a mechanism that is primarily dependent on the inhibition of transforming growth factor type alpha release. Therefore, mucin gene expression, induced by cystic fibrosis respiratory stimuli, can be inhibited by secretory leucoprotease inhibitor indicating its potential importance as an anti-mucin agent in cystic fibrosis and other chronic lung diseases characterized by mucus hypersecretion.

TLR-induced inflammation in cystic fibrosis and non-cystic fibrosis airway epithelial cells.

Cystic fibrosis (CF) is a genetic disease characterized by severe neutrophil-dominated airway inflammation. An important cause of inflammation in CF is Pseudomonas aeruginosa infection. We have evaluated the importance of a number of P. aeruginosa components, namely lipopeptides, LPS, and unmethylated CpG DNA, as proinflammatory stimuli in CF by characterizing the expression and functional activity of their cognate receptors, TLR2/6 or TLR2/1, TLR4, and TLR9, respectively, in a human tracheal epithelial line, CFTE29o(-), which is homozygous for the DeltaF508 CF transmembrane conductance regulator mutation. We also characterized TLR expression and function in a non-CF airway epithelial cell line 16HBE14o(-). Using RT-PCR, we demonstrated TLR mRNA expression. TLR cell surface expression was assessed by fluorescence microscopy. Lipopeptides, LPS, and unmethylated CpG DNA induced IL-8 and IL-6 protein production in a time- and dose-dependent manner. The CF and non-CF cell lines were largely similar in their TLR expression and relative TLR responses. ICAM-1 expression was also up-regulated in CFTE29o(-) cells following stimulation with each agonist. CF bronchoalveolar lavage fluid, which contains LPS, bacterial DNA, and neutrophil elastase (a neutrophil-derived protease that can activate TLR4), up-regulated an NF-kappaB-linked reporter gene and increased IL-8 protein production in CFTE29o(-) cells. This effect was abrogated by expression of dominant-negative versions of MyD88 or Mal, key signal transducers for TLRs, thereby implicating them as potential anti-inflammatory agents for CF.

Neutrophil elastase up-regulates human beta-defensin-2 expression in human bronchial epithelial cells.

Human beta-defensin-2 (HBD-2) gene expression is induced by tumour necrosis factor-alpha, interleukin-1beta and lipopolysaccharide. The objective of this study was to investigate the effect of neutrophil elastase (NE), a major pro-inflammatory protease, on HBD-2 expression. HBD-2 gene expression was assessed by reverse transcription polymerase chain reaction in the human bronchial epithelial cell line 16HBE14o- and primary normal human bronchial epithelial (NHBE) cells. Optimal HBD-2 expression was induced with 100 nM NE. Using a HBD-2-luciferase reporter construct, luciferase activity increased significantly in 16HBE14o- cells following incubation with NE. An increase in HBD-2 protein expression was observed in primary NHBE cells after incubation with NE as assessed by laser scanning cytometry. In conclusion, NE up-regulates HBD-2 expression in bronchial epithelial cells.

Increased expression of interleukin-9, interleukin-9 receptor, and the calcium-activated chloride channel hCLCA1 in the upper airways of patients with cystic fibrosis.

OBJECTIVES/HYPOTHESIS: Mucus overproduction is commonly found in airway disease in patients with cystic fibrosis. Interleukin-9 (IL-9) has been shown to mediate airway hyper-responsiveness and mucus overproduction. Recently, the calcium-activated chloride channel hCLCA1 has been described to be upregulated by IL-9 and has been thought to regulate the expression of soluble gel-forming mucins. We sought to examine the expression of IL-9, interleukin-9 receptor (IL-9R), and hCLCA1 in the upper airway of patients with cystic fibrosis in comparison to healthy control subjects and to demonstrate the relationship of IL-9, IL-9R, and hCLCA1 expression with mucus production. STUDY DESIGN: Prospective design. METHODS: Biopsy samples from nasal polyps of four patients with cystic fibrosis, nasal mucosa of six patients with cystic fibrosis, sinus mucosa of eight patients with cystic fibrosis, and nasal mucosa of six healthy control subjects were stained with periodic acid-Schiff (PAS) to identify mucus glycoconjugates. IL-9, IL-9R, and hCLCA1 expression was determined by immunocytochemical study. RESULTS: We demonstrated significant increases in IL-9, IL-9R, and hCLCA1 immunoreactivity in the mucosa of patients with cystic fibrosis compared with that found in control subjects (P <.05). There were no significant differences between the different locations (nasal polyps, nasal mucosa, and sinus mucosa) in the patient group (P >.05). We also observed a significant increase in the number of mucus-producing cells in biopsy specimens from patients with cystic fibrosis in comparison to control subjects. A positive correlation was found between hCLCA1-positive cells and IL-9-positive cells (correlation coefficient [r] = 0.79, P <.05) or IL-9R-positive cells (r = 0.92, P <.05). Moreover, a positive correlation was also present between PAS-positive (mucus-producing) cells and hCLCA1-positive cells (r = 0.64, P <.05) or IL-9R-positive cells (r = 0.64, P <.05). CONCLUSIONS: Increased expression of IL-9 and IL-9R, as well as upregulation of hCLCA1, in mucus-overproducing epithelium of patients with cystic fibrosis supports the hypothesis that IL-9 contributes to mucus overproduction in cystic fibrosis. Expression of hCLCA1 may also be responsible, in part, for the overproduction of mucus. These preliminary findings suggest that hCLCA1 might be an interesting new therapeutic target to control mucus overproduction in airway disease in patients with cystic fibrosis.