Social anxiety disorder (SAD) is a common and debilitating condition marked by intense fear of negative evaluation in social situations. It often co-occurs with other psychiatric disorders, and in particular Autism Spectrum Disorder (ASD). The exact cause of SAD is unclear, though biological, environmental, and genetic factors are believed to contribute. Recent research highlights the involvement of neuropeptides, neurohormones, and immune system components in SAD development, suggesting complex interactions between psychological and biological factors, with a growing focus on inflammation’s role. This study aimed to investigate potential biochemical correlates of SAD in individuals with ASD, their first-degree relatives (BAP group), and healthy controls (HCs), focusing on inflammatory markers, neuropeptides, and growth factors.

Twenty-four adults with ASD, their relatives, and HCs, for a total of 72 participants, were assessed. Biochemical parameters were analyzed using enzyme-linked immunosorbent assays (ELISA), and social anxiety symptoms were evaluated via the Social Phobia Spectrum—Self Report (SHY-SR) questionnaire.

Individuals with ASD exhibited significantly higher SHY-SR scores compared to the BAP and HCs. Subjects in the ASD group tended to make greater use of anxiolytics in order to improve their social interaction skills. Additionally, a specific pattern of correlation and association was found between biochemical variables and specific SAD symptoms, suggesting a potential role of inflammatory pathways in SAD pathophysiology.

Our results confirm the presence of greater social phobic symptoms in subjects with ASD, and support the hypothesis of a role of the inflammatory cascade in the maintenance of the disorder.

Social anxiety disorder (SAD) is one of the most common anxiety disorders and is associated with significant impairment and societal costs. The association between SAD and mortality remains poorly understood, partly because in epidemiological research it is rarely studied independently from other anxiety disorders. In this population-based matched cohort and sibling control study, we estimated the risk of all-cause and cause-specific mortality in individuals with SAD.

From a population of individuals born from 1932 and living in Sweden between 1997 and 2020, we identified all cases of SAD (Swedish ICD-10 code F40.1) in the National Patient Register. Each of these individuals was matched on sex, birth year and county of residence with 10 individuals who had never received a diagnosis. Mortality data were extracted from the Cause of Death Register. Risks were estimated using Cox proportional hazards regression models. Models adjusted for sociodemographic covariates and other lifetime psychiatric disorders. We also identified all clusters of full siblings and conducted within-sibling comparisons to account for unmeasured familial confounding.

The matched cohort included 57,360 individuals with SAD and 573,600 unexposed individuals. During the follow-up, 2355 deaths were registered within the exposed cohort vs. 7800 deaths in the matched cohort (crude mortality rates, 5.25 and 1.73 per 1000 person-years, respectively). The full cohort was followed up for a mean of 7.87 years (standard deviation 5.23). In models adjusting for sociodemographic variables, individuals with SAD had a 2.24-fold increased hazard of all-cause mortality (95% confidence interval [CI], 2.13–2.35). The increased risk was observed for both natural (adjusted hazard ratio [HR], 1.62; 95% CI 1.52–1.72) and unnatural causes of death (HR, 4.18; 95% CI 3.82–4.58). The results were robust to additional adjustment for psychiatric comorbidities, but the magnitude of the associations was attenuated, particularly when adjusting for substance use disorders. In the sibling cohort, 39,993 individuals with SAD were compared with their 64,640 unaffected siblings. While the estimates were also attenuated, they remained statistically significant (HR for all-cause mortality, 1.40; 95% CI 1.36–1.45).

Individuals with SAD face an increased risk of mortality, attributable primarily to unnatural causes of death, such as suicide, but also to natural causes, even after adjusting for socioeconomic variables. Psychiatric comorbidities, particularly substance use disorders, and shared familial factors may also contribute to this excess death. Further study of underlying mechanisms may inform prevention and early intervention strategies to reduce mortality in this vulnerable population.

The Kahramanmaras Earthquakes (2023) are the largest and most devastating earthquakes in the history of the Republic. The effects of these earthquakes are particularly deeply felt among younger generations and trigger various psychological factors. Therefore, the aim of this study is to measure the levels of post-traumatic stress disorder (PTSD), social phobia (SP), generalized anxiety disorder (GAD), and depression on separation anxiety disorder (SAD) among adolescent earthquake survivors affected by the Kahramanmaras Earthquakes (2023).

In the study, the data were obtained using a survey method. A total of 605 adolescent earthquake survivors exposed to the Kahramanmaras earthquakes were reached. The research was analyzed using structural equation modeling (SEM).

Surprisingly, according to the research findings, there was no significant and positive relationship between SP (β = −0.006, P > 0.05) and Depression (β = −0.117, P > 0.05) on SAD.

Consequently, while PTSD and GAD had significant and positive effects on SAD in those adolescent earthquake survivors affected by the Kahramanmaras Earthquakes (2023), SP and Depression did not have significant and positive effects on SAD. Therefore, it is recommended that future studies examine the effects of SP and Depression on SAD more comprehensively and in detail through qualitative research.

Anxiety disorders are frequent comorbidity in patients with schizophrenia. Their frequency in late-onset psychosis is unknown.

We aimed to study life-time anxiety disorders as well as other psychiatric pathology in patients with late-onset schizophrenia (LoS) and late-onset delusional disorder (LoDD).

42 patients with LoS (age 64,1±9,2, 12% males) and 15 patients with LoDD (n=15; age 69,9±10,9, 14% males ) underwent clinical assessment (PANSS, HDRS-17), cognitive examination (MMSE, MoCA), structured interviewing on life-time pathology. Control group included 24 subjects with no signs of depression or psychosis (age 58,1±10,8, 50% males). Kruscal-Wallis and χ2statistic was used.

Patients with LoS and LoDD had higher frequency of social phobia (50% and 30% compared to 16,7 in control group, χ2 (2)= 6,834, p= 0,033) and more animal phobias (KW χ2 (2)=15,536, p<0,001). The number of habitual anxiety reaction was increased in LoS but not LoDD patients compared to controls (KW χ2 (2)=7,275, p= 0,026) with more severe motor (KW χ2 (2)=8,516, p= 0,014), vegetative (KW χ2 (2)=8,633, p= 0,013 and ideatory symptoms (KW χ2 (2)=6,969, p= 0,031) of anxiety. There was no group difference in life-time frequency of depression. Patients and controls had similar rate of complicated grief, but controls had often no reaction in response to loss and LoS patients responded to loss with manifestation of psychosis (χ2 (6)= 14,473, p= 0,025).

Social phobia and other anxiety disorders are frequent in late-onset psychosis. Symptoms of generalized anxiety are more specific to LoS than to LoDD.

No significant relationships.

Social phobia is frequent comorbidity in schizophrenia. It`s clinical correlates and consequencies for clinical practice in late-onset schizophrenia (LoS) are unclear.

The study aimed to compare clinical correlates and therapeutic options in LoS patient with and without social phobia.

16 LoS patients with social phobia (ICD-11 diagnosis, age 59,6±6,2, 25% males) were compared with 16 LoS patients without social phobia (69,9±10,9, 0% males). Results of clinical assessment (PANSS, HDRS-17), cognitive examination (MMSE, MoCA), CT data were analysed. Type of antipsychotics (conventional\conconventional) was registed, dose of antipsychotics and antidepressants was randed from 1 (low) to 3 (high). Mann-Whitney test and χ2statistic was used.

There was no group differences in age, age manifestation, illness duration, number of psychotic episodes, PANSS and HADRS scores, rates results of cognitive tests, atrophy scores, length of hospital state, types of received antipsychotics. LoS patients with social phobia received more frequently medium and high doses of antipsychotics than LoS patient without social phobia (χ2 (2)=6,432, p=0,040).

Increased doses of antypsychotics in patients with social phobia don`t correlate with severity of psychotic symptoms and nay reflect some treatment resistance as well as misinterpretation of symptoms of social phobia as insufficient retreat of the psychosis. Active detection of social phobia is significant for treatment optimization.

No significant relationships.

Our aim was to develop a brief cognitive behavioural therapy (CBT) protocol to augment treatment for social anxiety disorder (SAD). This protocol focused specifically upon fear of positive evaluation (FPE). To our knowledge, this is the first protocol that has been designed to systematically target FPE.

To test the feasibility of a brief (two-session) CBT protocol for FPE and report proof-of-principle data in the form of effect sizes.

Seven patients with a principal diagnosis of SAD were recruited to participate. Following a pre-treatment assessment, patients were randomized to either (a) an immediate CBT condition (n = 3), or (b) a comparable wait-list (WL) period (2 weeks; n = 4). Two WL patients also completed the CBT protocol following the WL period (delayed CBT condition). Patients completed follow-up assessments 1 week after completing the protocol.

A total of five patients completed the brief, FPE-specific CBT protocol (two of the seven patients were wait-listed only and did not complete delayed CBT). All five patients completed the protocol and provided 1-week follow-up data. CBT patients demonstrated large reductions in FPE-related concerns as well as overall social anxiety symptoms, whereas WL patients demonstrated an increase in FPE-related concerns.

Our brief FPE-specific CBT protocol is feasible to use and was associated with large FPE-specific and social anxiety symptom reductions. To our knowledge, this is the first treatment report that has focused on systematic treatment of FPE in patients with SAD. Our protocol warrants further controlled evaluation.

1. (1) To learn how to deliver all of the core interventions of CT-SAD remotely.

2. (2) To learn novel ways of carrying out behavioural experiments remotely when some in-person social situations might not be possible.

Disease trajectories of patients with anxiety disorders are highly diverse and approximately 60% remain chronically ill. The ability to predict disease course in individual patients would enable personalized management of these patients. This study aimed to predict recovery from anxiety disorders within 2 years applying a machine learning approach.

In total, 887 patients with anxiety disorders (panic disorder, generalized anxiety disorder, agoraphobia, or social phobia) were selected from a naturalistic cohort study. A wide array of baseline predictors (N = 569) from five domains (clinical, psychological, sociodemographic, biological, lifestyle) were used to predict recovery from anxiety disorders and recovery from all common mental disorders (CMDs: anxiety disorders, major depressive disorder, dysthymia, or alcohol dependency) at 2-year follow-up using random forest classifiers (RFCs).

At follow-up, 484 patients (54.6%) had recovered from anxiety disorders. RFCs achieved a cross-validated area-under-the-receiving-operator-characteristic-curve (AUC) of 0.67 when using the combination of all predictor domains (sensitivity: 62.0%, specificity 62.8%) for predicting recovery from anxiety disorders. Classification of recovery from CMDs yielded an AUC of 0.70 (sensitivity: 64.6%, specificity: 62.3%) when using all domains. In both cases, the clinical domain alone provided comparable performances. Feature analysis showed that prediction of recovery from anxiety disorders was primarily driven by anxiety features, whereas recovery from CMDs was primarily driven by depression features.

The current study showed moderate performance in predicting recovery from anxiety disorders over a 2-year follow-up for individual patients and indicates that anxiety features are most indicative for anxiety improvement and depression features for improvement in general.

This study aimed to evaluate the discriminative validity of MINI-SPIN (MS) as a screening tool for social anxiety disorder (SAD) in a group of Brazilian university students.

SPIN was collectively applied to 2320 university students. Among them, 656 individuals who fulfilled the criteria for positive MS (N = 473) and negative MS (N = 183) were selected and divided into two groups. The selected subjects were interviewed by telephone using the SAD module of the SCID-IV, used as the gold standard. In order to check interrater reliability, a group of university students (N = 57) was reinterviewed by telephone by a second rater, and another group (N = 100) participated in a face-to-face interview.

The Kappa coefficient among the telephone interviews was 0.80, and a coefficient of 0.84 (P < 0.001) was obtained between the telephone interview and the face-to-face one. For a cut-off score of 6, suggested in the original English version of the instrument, sensitivity was 0.94, specificity 0.46, the positive predictive value (PPV) was 0.58, and the negative predictive value (NPV) was 0.92. For a cut-off score of 7, we observed an increase in the specificity and in the PPV (0.68 and 0.65) while the sensitivity and NPV (0.78 and 0.80) remained high.

MS showed quite satisfactory psychometric qualities. The cut-off score of 6 seemed to be the most suitable to attest the tracking value of the tool. However, the cut-off score of 7 was the most suitable as a minimum parameter for the studied group, with psychometric values more similar to those of the original study.

To perform a psychometric analysis of the Brazilian version of the Brief Social Phobia Scale (BSPS).

Hundred and seventy-eight university students of both genders aged on average 21.2 years and identified as Social Anxiety Disorder (SAD) cases and non-cases was studied, with the structured clinical interview for DSM-IV being used as a parameter. The different instruments were applied in an individual manner in the presence of a rater and of an observer.

The BSPS showed adequate internal consistency (0.48–0.88) and concurrent and divergent validity with the Beck Anxiety Inventory (BAI) (0.21–0.62), Social Phobia Inventory (0.24–0.82) and Self Statements During Public Speaking Scale (SSPS) (0.23–0.31). Discriminative validity revealed a sensitivity of 0.88–0.90 and a specificity of 0.81(0.83 for cut-off notes of 18/19. Factorial analysis demonstrated the presence of six factors that jointly explained 71.79% of data variance. Construct validity indicated some limits of the scale regarding the diagnosis of SAD. Inter-rater reliability was strong (0.86–1.00, p < 0.001).

The BSPS is adequate for use with university students, although further studies in different cultures, samples and contexts are still necessary.

Both psychodynamic group therapy (PGT) and clonazepam are used as treatment strategies in reducing symptoms of generalized social anxiety disorder (GSAD). However, many individuals remain symptomatic after treatment with PGT or clonazepam.

Fifty-eight adult outpatients with a diagnosis of GSAD according to DSM-IV were randomized to 12 weeks PGT plus clonazepam or clonazepam. The Clinical Global Impression-Improvement (CGI-I) Scale was the primary efficacy measure. Secondary efficacy measures included the Liebowitz Social Anxiety Scale (LSAS) total score, the World Health Organization Instrument to Assess Quality of Life—Brief (WHOQOL-Bref) Scale and the Beck Depression Inventory (BDI).

CGI-I data from 57 patients (intent-to-treat population) showed that patients who received PGT plus clonazepam presented significantly greater improvement than those who received clonazepam (P = 0.033). There were no significant differences between the two groups in the secondary efficacy measures.

Our study suggests that the combination of PGT with clonazepam may be a promising strategy for the treatment of GSAD, regarding gains in the global functioning. However the present study failed to detect more specific changes in social anxiety symptomatology between the two groups.