The Relationship Between Childhood Traumas with Social Appearance Anxiety and Symptoms of Body Dysmorphic Disorder: The Mediating Role of Sociocultural Attitudes Toward Appearance

Background: Body dysmorphic disorder (BDD) and social anxiety are two concepts related to body dissatisfaction. These concepts have been linked to sociocultural attitudes to appearances and painful experiences in interpersonal relationships. Objectives: The present study examines the relationship between childhood traumas with social appearance anxiety (SAA) and BDD through the mediating role of sociocultural attitudes toward appearance (SATA). Methods: This cross-sectional study was conducted on 415 university students in Tehran, Iran using the convenience sampling method in 2019 - 2020. Data were analyzed using SPSS version 24 and Amos version 21 software. Results: According to our results, while childhood traumas were not directly related to BDD (β = 0.059; SE = 0.31), SAA seemed to play a statistically significant mediating role (β = 0.17; SE = 0.005). Moreover, childhood trauma was related to SAA both directly (β = 0.24; SE = 0.001) and through the mediating role of SATA. In addition, SATA (β = 0.17; SE = 0.005) significantly predicted BDD (β = 0.27, P < 0.001). The assumed model was in good fit with the acquired data (CFI = 0.97, GFI = 0.95, NFI = 0.94, RMSEA = 0.046). Conclusions: Children who have had traumatic experiences may experience anxiety and self-doubt. Thus, childhood traumas are ostensibly related to signs of BDD and SAA through the mediation of sociocultural attitudes. Childhood traumas can also predict susceptibility to rejection in interpersonal relationships. However, no results have been found to mediate rejection sensitivity concerning trauma with BDD and SAA.

Life course traumas, phenotypic aging, and cardiovascular disease: retrospective analysis of 104,939 UKB participants

Background: While childhood and adulthood traumatic experiences have been linked to subsequent cardiovascular disease (CVD), the relationship between life course traumas and CVD and the underpinning pathways are poorly understood. This study aimed to: (1) examine the associations of childhood, adulthood, and lifetime traumas with CVD; (2) examine the associations between diverse life course traumatic profiles and CVD; and (3) examine the extent to which Phenotypic Age (PhenoAge), a well-developed phenotypic aging measure, mediates these associations. Methods: We included 104,939 participants from the UK Biobank who completed the 2016 online mental health questionnaire. CVD outcomes including ischemic heart disease, myocardial infarction, and stroke were ascertained. Childhood, adulthood, and lifetime traumas were categorized into three subgroups (mild, moderate, and severe), respectively. Four life course traumatic profiles were defined as non-severe traumas across life course, non-severe childhood and severe adulthood traumas, severe childhood and non-severe adulthood traumas, and severe traumas across life course based on both childhood and adulthood traumas. PhenoAge was measured using an equation previously developed. Multivariable logistic models and formal mediation analyses were performed. Results: Of 104,939 participants, 7,398 (7.0%) were diagnosed with CVD. Subgroups of childhood, adulthood, and lifetime traumas were associated with CVD, respectively. Furthermore, life course traumatic profiles were significantly associated with CVD. For instance, compared with subgroups experiencing non-severe traumas across life course, those who experienced non-severe childhood and severe adulthood traumas, severe childhood and non-severe adulthood traumas, and severe traumas across life course had higher odd of CVD, with odds ratios of 1.07 (95% confidence interval [CI]: 1.00, 1.15), 1.17 (95% CI: 1.09, 1.25), and 1.33 (95% CI: 1.24, 1.43), respectively. Formal mediation analyses suggested that PhenoAge partially mediated the above associations. For instance, PhenoAge mediated 5.8% of increased CVD events in subgroups who experienced severe childhood traumas, relative to those experiencing mild childhood traumas. Conclusions: Childhood, adulthood, and lifetime traumas, as well as diverse life course traumatic profiles, were associated with CVD. Furthermore, phenotypic aging partially mediated these associations. These findings suggest a potential pathway from life course traumas to CVD through phenotypic aging, and underscore the importance of policy programs targeting traumatic events over the life course in ameliorating inequalities in cardiovascular health.

An Investgation About the Relationship Between Vasopressin and Oxytocin in Persistent Type Functional Neurological Symptom Disorder

Objective Functional neurogical symptom disorder (FNSD) is a somatic symptom disorder with loss of voluntary motor or sensory functions, which cannot be explained by another medical condition. The study aimed to examine the relationship of vasopressin and oxytocin in persistent type FNSD.Methods This study included 27 female patients between the ages of 20–57 who were diagnosed with FNSD according to DSM-5 and 27 healthy controls matched in terms of age and gender. Serum vasopressin and oxytocin levels were measured twice on the same day in fasting blood samples and the results were compared statistically.Results Vasopressin were lower in patients compared to controls while there was no difference between oxytocin levels. Childhood traumas were more common in patient group, and mean oxytocin level was lower in patients who exposed to childhood trauma, compared to controls. No significant difference was found between the groups in terms of vasopressin.Conclusion Changes in vasopressin and oxytocin balance in the pathogenesis of persistant FNSD, may likely to lead to physiological and behavioral consequences. Lower oxytocin levels may also be a marker of exposure to childhood trauma in FNSD. These neuropeptides plays important role in neuroendocrine balance of emotional behavior.

Mediation role of alexithymia, sensory processing sensitivity and emotional-mental processes between childhood trauma and adult psychopathology: a self-report study

Background There is overwhelming evidence for a strong association between childhood trauma and adult psychopathology. This study aimed to investigate the mediation roles of alexithymia, sensory processing sensitivity, and emotional-mental processes in the relationship between childhood traumas and adult psychopathology. Methods The sample consisted of 337 people (78.9% female, 21.1% male) aged between 20 and 64 years. Participants filled the scales online via a Google form. Reading Mind in the Eyes (EYES), Sensory Processing Sensitivity Scale (SPS), Toronto Alexithymia Scale (TAS-26), Childhood Trauma Questionnaire (CTQ), and the Brief Symptom Inventory (BSI) were used. PROCESS (Model 4) macro was used to examine the mediating role of sensory processing sensitivity, alexithymia, and the EYES test results in the relationship between childhood trauma and psychopathology. Results The results of mediation analysis demonstrated that sensory processing sensitivity and alexithymia mediated the relationship between childhood trauma and adult psychopathology. However, the EYES test (mentalization) did not mediate in this relationship. Conclusion This study shows that childhood traumas may relate to more psychological symptoms in individuals with high sensory processing sensitivity and alexithymia. Our study may contribute to the understanding of what may lead to a person’s vulnerability to experiencing psychological symptoms after childhood trauma. It may be crucial that future treatment and intervention programs should include sensory sensitivity and alexithymia. Sensory processing sensitivity and alexithymia can be examined in the treatment of psychological problems of individuals who have experienced childhood trauma.

Psychological predictors of negative treatment outcome with Erenumab in chronic migraine: data from an open label long-term prospective study

Background Monoclonal antibodies (mABs) targeting the calcitonin gene-related peptide (CGRP) pathway represent the first disease-specific preventive migraine therapy. Growing evidence suggests that they are effective in the preventive treatment of difficult-to-treat patients. In this study, we evaluated the psychological predictors of the outcome of treatment with the anti-CGRP monoclonal antibody erenumab in patients with chronic migraine (CM). Methods Seventy-five patients with CM who had already failed at least 3 preventive therapies received erenumab every 28 days for a period of 12 months. Before the first administration, patients received a full psychological evaluation using The Structured Clinical Interview for DSM-5 Clinician Version (SCID-5-CV) to assess personality disturbances (primary outcome), mood and anxiety disorders, and as well specific questionnaires to evaluate alexithymia traits, childhood traumas, and current stressors (secondary outcomes). Results After 12 months of treatment, 53 patients reported a reduction of at least 50% in headache days/per month (Responders), whereas 22 did not (Non Responders). When compared to Responders, Non Responders were characterized by a higher prevalence of personality disorders belonging to Cluster C (avoidant, dependent, and obsessive-compulsive) (77% vs 37%, p = .001). Non Responders were also characterized by a higher prevalence of anxiety disorders (90% vs 60%, p = 0.007), showed more alexithymic traits (51.7 ± 13.7 vs 42.9 ± 14.3, p = 0.017), and reported a higher number of 'at least serious' current stressors (3.2 ± 4.0 vs 0.8 ± 1.4, p < .0001) than Responders. At the multivariate analysis, higher prevalence of Cluster C personality disorders (OR 3.697; p = 0.05) and higher number of ‘at least serious’ life events (OR 1.382; p = 0.017) arose as prognostic factors of erenumab failure. Conclusions Erenumab confirmed its effectiveness in a population of difficult-to-treat migraine. The presence of “anxious-fearful” personality together with current stressors and anxiety represent negative predictors of treatment outcome. Trial registration The study protocol was registered at clinicaltrials.gov (NCT04361721).