Mentalizing—our ability to make inferences about the mental states of others—is impaired across psychiatric disorders and robustly associated with functional outcomes. Mentalizing deficits have been prominently linked to aberrant activity in cortical regions considered to be part of the “social brain network” (e.g., dorsomedial prefrontal cortex, temporoparietal junction), yet emerging evidence also suggests the importance of cerebellar dysfunction. In the present study—using a transdiagnostic, clinical psychiatric sample spanning the psychosis-autism-social anxiety spectrums—we examined the role of the cerebellum in mentalizing and its unique contributions to broader social functioning.

Sixty-two participants (38 with significant social dysfunction secondary to psychiatric illness and 24 nonclinical controls without social dysfunction) completed a mentalizing task during functional magnetic resonance imaging. General linear model analysis, latent variable modeling, and regression analyses were used to examine the contribution of cerebellum activation to the prediction of group status and social functioning.

Mentalizing activated a broad set of social cognitive brain regions, including cerebral mentalizing network (MN) nodes and posterior cerebellum. Higher posterior cerebellum activation significantly predicted clinical status (i.e., individuals with psychiatric disorders versus nonclinical controls). Finally, cerebellar activation accounted for significant variance in social functioning independent of all other cerebral MN brain regions identified in a whole-brain analysis.

Findings add to an accumulating body of evidence establishing the unique role of the posterior cerebellum in mentalizing deficits and social dysfunction across psychiatric illnesses. Collectively, our results suggest that the posterior cerebellum should be considered – alongside established cerebral regions – as part of the mentalizing network.

To understand caregivers’ perceptions about their children’s mealtime social experiences at school and how they believe these social experiences impact their children’s consumption of meals at school (both meals brought from home and school meals).

Qualitative data were originally collected as part of a larger mixed methods study using an embedded-QUAN dominant research design.

Semi-structured interviews were conducted with United States (U.S.) caregivers over ZoomTM in English and Spanish during the 2021–2022 school year. The interview guide contained 14 questions on caregivers’ perceptions about their children’s experiences with school meals.

Caregivers of students in elementary, middle and high schools in rural, suburban and urban communities in California (n 46) and Maine (n 20) were interviewed. Most (60·6 %) were caregivers of children who were eligible for free or reduced-price meals.

Caregivers reported that an important benefit of eating meals at school is their child’s opportunity to socialise with their peers. Caregivers also stated that their child’s favourite aspect of school lunch is socialising with friends. However, some caregivers reported the cafeteria environment caused their children to feel anxious and not eat. Other caregivers reported that their children sometimes skipped lunch and chose to socialise with friends rather than wait in long lunch lines.

Socialising during school meals is important to both caregivers and students. Policies such as increasing lunch period lengths and holding recess before lunch have been found to promote school meal consumption and could reinforce the positive social aspects of mealtime for students.

Loneliness has become a major public health issue of the recent decades due to its severe impact on health and mortality. Little is known about the relation between loneliness and social anxiety. This study aimed (1) to explore levels of loneliness and social anxiety in the general population, and (2) to assess whether and how loneliness affects symptoms of social anxiety and vice versa over a period of five years.

The study combined data from the baseline assessment and the five-year follow-up of the population-based Gutenberg Health Study. Data of N = 15 010 participants at baseline (Mage = 55.01, s.d.age = 11.10) were analyzed. Multiple regression analyses with loneliness and symptoms of social anxiety at follow-up including sociodemographic, physical illnesses, and mental health indicators at baseline were used to test relevant covariates. Effects of loneliness on symptoms of social anxiety over five years and vice versa were analyzed by autoregressive cross-lagged structural equation models.

At baseline, 1076 participants (7.41%) showed symptoms of social anxiety and 1537 (10.48%) participants reported feelings of loneliness. Controlling for relevant covariates, symptoms of social anxiety had a small significant effect on loneliness five years later (standardized estimate of 0.164, p < 0.001). Vice versa, there was no significant effect of loneliness on symptoms of social anxiety taking relevant covariates into account.

Findings provided evidence that symptoms of social anxiety are predictive for loneliness. Thus, prevention and intervention efforts for loneliness need to address symptoms of social anxiety.

Delineation of changes in neural function associated with novel and established treatments for social anxiety disorder (SAD) can advance treatment development. We examined such changes following selective serotonin reuptake inhibitor (SSRI) and attention bias modification (ABM) variant – gaze-contingent music reward therapy (GC-MRT), a first-line and an emerging treatments for SAD.

Eighty-one patients with SAD were allocated to 12-week treatments of either SSRI or GC-MRT, or waitlist (ns = 22, 29, and 30, respectively). Baseline and post-treatment functional magnetic resonance imaging (fMRI) data were collected during a social-threat processing task, in which attention was directed toward and away from threat/neutral faces.

Patients who received GC-MRT or SSRI showed greater clinical improvement relative to patients in waitlist. Compared to waitlist patients, treated patients showed greater activation increase in the right inferior frontal gyrus and anterior cingulate cortex when instructed to attend toward social threats and away from neutral stimuli. An additional anterior cingulate cortex cluster differentiated between the two active groups. Activation in this region increased in ABM and decreased in SSRI. In the ABM group, symptom change was positively correlated with neural activation change in the dorsolateral prefrontal cortex.

Brain function measures show both shared and treatment-specific changes following ABM and SSRI treatments for SAD, highlighting the multiple pathways through which the two treatments might work. Treatment-specific neural responses suggest that patients with SAD who do not fully benefit from SSRI or ABM may potentially benefit from the alternative treatment, or from a combination of the two.

ClinicalTrials.gov, Identifier: NCT03346239. https://clinicaltrials.gov/ct2/show/NCT03346239

Social anxiety and paranoia are connected by a shared suspicion framework. Based on cognitive-behavioural approaches, there is evidence for treating social anxiety and psychosis. However, mechanisms underlying the relationship between social anxiety and paranoia remain unclear.

To investigate mediators between social anxiety and paranoia in schizophrenia such as negative social appraisals (i.e. stigma or shame; Hypothesis 1), and safety behaviours (i.e. anxious avoidance or in situ safety behaviours; Hypothesis 2).

A cross-sectional study was conducted among Asian out-patients with schizophrenia (January–April 2020). Data on social anxiety, paranoia, depression, shame, stigma, anxious avoidance, and in situ behaviours were collected. Associations between social anxiety and paranoia were investigated using linear regressions. Mediation analysis via 10,000 bias-corrected bootstrap samples with 95% confidence intervals (CI) was used to test the indirect effects (ab) of mediators.

Participants (n=113, 59.3% male) with a mean age of 44.2 years were recruited. A linear relationship between social anxiety and paranoia was found. In multiple mediation analyses (co-varying for depression), stigma and shame (Hypothesis 1) did not show any significant indirect effects with ab=.004 (95%CI=–.013, .031) and –.003 (–.023, .017), respectively, whereas in situ behaviours (Hypothesis 2) showed a significant effect with ab=.110 (.038, .201) through the social anxiety–paranoia relationship.

Social anxiety and paranoia are positively correlated. In situ safety behaviours fully mediated the social anxiety and paranoia relationship. Targeted interventions focusing on safety behaviours could help reduce paranoia in psychosis. Symptom severity should be measured to help characterise the participants’ characteristics.

Cognitive behavioral therapy (CBT) is an effective treatment for patients with social anxiety disorder (SAD) or major depressive disorder (MDD), yet there is variability in clinical improvement. Though prior research suggests pre-treatment engagement of brain regions supporting cognitive reappraisal (e.g. dorsolateral prefrontal cortex [dlPFC]) foretells CBT response in SAD, it remains unknown if this extends to MDD or is specific to CBT. The current study examined associations between pre-treatment neural activity during reappraisal and clinical improvement in patients with SAD or MDD following a trial of CBT or supportive therapy (ST), a common-factors comparator arm.

Participants were 75 treatment-seeking patients with SAD (n = 34) or MDD (n = 41) randomized to CBT (n = 40) or ST (n = 35). Before randomization, patients completed a cognitive reappraisal task during functional magnetic resonance imaging. Additionally, patients completed clinician-administered symptom measures and a self-report cognitive reappraisal measure before treatment and every 2 weeks throughout treatment.

Results indicated that pre-treatment neural activity during reappraisal differentially predicted CBT and ST response. Specifically, greater trajectories of symptom improvement throughout treatment were associated with less ventrolateral prefrontal cortex (vlPFC) activity for CBT patients, but more vlPFC activity for ST patients. Also, less baseline dlPFC activity corresponded with greater trajectories of self-reported reappraisal improvement, regardless of treatment arm.

If replicated, findings suggest individual differences in brain response during reappraisal may be transdiagnostically associated with treatment-dependent improvement in symptom severity, but improvement in subjective reappraisal following psychotherapy, more broadly.

Although the link between alcohol involvement and behavioral phenotypes (e.g. impulsivity, negative affect, executive function [EF]) is well-established, the directionality of these associations, specificity to stages of alcohol involvement, and extent of shared genetic liability remain unclear. We estimate longitudinal associations between transitions among alcohol milestones, behavioral phenotypes, and indices of genetic risk.

Data came from the Collaborative Study on the Genetics of Alcoholism (n = 3681; ages 11–36). Alcohol transitions (first: drink, intoxication, alcohol use disorder [AUD] symptom, AUD diagnosis), internalizing, and externalizing phenotypes came from the Semi-Structured Assessment for the Genetics of Alcoholism. EF was measured with the Tower of London and Visual Span Tasks. Polygenic scores (PGS) were computed for alcohol-related and behavioral phenotypes. Cox models estimated associations among PGS, behavior, and alcohol milestones.

Externalizing phenotypes (e.g. conduct disorder symptoms) were associated with future initiation and drinking problems (hazard ratio (HR)⩾1.16). Internalizing (e.g. social anxiety) was associated with hazards for progression from first drink to severe AUD (HR⩾1.55). Initiation and AUD were associated with increased hazards for later depressive symptoms and suicidal ideation (HR⩾1.38), and initiation was associated with increased hazards for future conduct symptoms (HR = 1.60). EF was not associated with alcohol transitions. Drinks per week PGS was linked with increased hazards for alcohol transitions (HR⩾1.06). Problematic alcohol use PGS increased hazards for suicidal ideation (HR = 1.20).

Behavioral markers of addiction vulnerability precede and follow alcohol transitions, highlighting dynamic, bidirectional relationships between behavior and emerging addiction.

Preliminary work suggests anxiety moderates the relationship between irritability and bullying. As anxiety increases, the link between irritability and perpetration decreases. We hypothesize that any moderation effect of anxiety is driven by social anxiety symptoms. We sought to explicate the moderating effect of anxiety, while clarifying relations to other aggressive behaviors.

A sample of adolescents (n = 169, mean = 12.42 years of age) were assessed using clinician rated assessments of anxiety, parent reports of irritability and bullying behaviors (perpetration, generalized aggression, and victimization). Correlations assessed zero-order relations between variables, and regression-based moderation analyses were used to test interactions. Johnson–Neyman methods were used to represent significant interactions.

Irritability was significantly related to bullying (r = .403, p < .001). Social, but not generalized, anxiety symptoms significantly moderated the effect of irritability on bully perpetration (t(160) = −2.94, b = −.01, p = .0038, ΔR2 = .0229, F(1, 160) = 8.635). As social anxiety symptoms increase, the link between irritability and perpetration decreases.

Understanding how psychopathology interacts with social behaviors is of great importance. Higher social anxiety is linked to reduced relations between irritability and bullying; however, the link between irritability and other aggression remains positive. Comprehensively assessing how treatment of psychopathology impacts social behaviors may improve future intervention.

Interpretation bias and safety behaviours (Safe-B) have been proposed as factors perpetuating social anxiety (SA). However, longitudinal research on how they contribute to SA in everyday life is scarce.

The aim was to examine whether interpretation bias predicts daily Safe-B and SA. A mediated moderation was hypothesized, where the relationship between daily social stressors and Safe-B would be moderated by interpretation bias, and Safe-B, in turn, would mediate the association between stressors and SA levels. In addition, it was hypothesized that prior levels of SA would predict higher Safe-B use, especially in co-occurrence with stressors.

An intensive longitudinal design was employed, with 138 vocational training students (51% men, mean age 20.15 years). They completed initial measures of SA and interpretation bias and 7-day diaries with measures of social stressors, Safe-B, and SA. They reported SA levels two months later.

Both stressors and interpretation bias in ambiguous situations predicted Safe-B, which in turn predicted daily SA levels. However, neither interpretation bias nor Safe-B predicted SA levels at the follow-up, and interpretation bias did not moderate the association between stressors and daily SA. In addition, the relationship between stressors and Safe-B was stronger in people with higher initial SA levels.

The results suggest that Safe-B are a mechanism through which earlier SA levels and interpretation bias contribute to higher SA levels in daily life.

Alopecia areata (AA) is an immunological disorder characterised by hair loss. Individuals with AA report high levels of social anxiety. One intervention that holds potential for reducing social anxiety in individuals with AA is mindfulness-based cognitive therapy (MBCT).

Our key aim was to investigate whether MBCT reduces social anxiety in individuals with AA. The study also investigated whether MBCT reduces depression, general anxiety, and increases quality of life and increases trait mindfulness in individuals with AA.

Five participants with AA took part in an 8-session in-person MBCT intervention. A multiple-baseline single-group case series design was adopted. Idiographic measures of social anxiety were measured each day from baseline, through intervention, to follow-up. Standardised questionnaires of trait mindfulness, social anxiety, depression, anxiety, and quality of life were completed at baseline, post-intervention, and at 4-week follow-up.

All participants completed the MBCT course, but one participant was excluded from the idiographic analysis due to a high amount of missing data. The remaining four participants demonstrated reductions in idiographic measures of social anxiety from baseline to follow-up. These effects were larger between baseline and follow-up, than between baseline and post-intervention. Two participants demonstrated significant improvement in standardised measures of wellbeing from baseline to follow-up – they also practised mindfulness most regularly at home between sessions.

MBCT may be effective in reducing social anxiety and improving wellbeing in individuals with AA, although this might be dependent on the extent to which participants regularly practise mindfulness exercises.