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.

To understand the way chemistry influences human communication is important since the reaction to chemosignals has many implications for science and society. For instance, previous research showed a connection between olfaction and affective psychiatric disorders. Olfactory processing may be impaired in subject presenting depression symptoms (DEP). Furthermore, a heightened sensitivity to social odours has been shown in subject with social anxiety symptoms (SAD). This may be due to the partial overlap of brain areas which are involved in olfactory processing and the pathophysiology of these disorders. Yet, more detailed research on the olfactory processing is required.

POTION is an EU funded project within the Horizon2020 initiative that aims to understand the nature of chemosignals in humans and their sphere of influence on social interaction. Within this project, we conducted a preliminary exploratory study examining whether the odours may be utilized to support positive outcomes of psychological therapy. It evaluates the catalyst effect of the odour conditions on the effectiveness of mindfulness meditation for SAD and DEP.

Thirty subjects per patient group (total=60) are randomly allocated to one exposure group (happy or fearful human body odour or clean air) and follow the intervention while being exposed to the odour. Psychological outcome is measured before and after the intervention through the State-Trait Anxiety Inventory and the Profile of Mood State questionnaires. Analysis of variance is performed to assess outcome differences between groups.

Preliminary results on a subsample of 32 patients show a trend of deeper reduction of anxiety symptoms at post-treatment among odour-exposed groups compared to clean air (F(1,17)=11.08, p=0.004).

Final results on the complete sample will be available and presented at the time of the congress.

No significant relationships.

Internet addiction (IA) is a rapidly growing disorder especially among adolescents and young adults. Social anxiety is one of the risk factors for IA. Also, genes involved in dopaminergic and serotoninergic systems are among the candidate genes most frequently associated with IA.

The study aimed to investigate the association between social anxiety level and genetic markers in young adult Internet addicts.

IA group included 44 people (Chen/Chinese Internet Addiction Scale (CIAS) score ≥ 65), 75,0% males), the average age 22,0 [18,0;25,0] y.o. (Md [Q1; Q3]). Healthy control group (CIAS score was less 65) included 120 people, (73,3% males), the average age 23,0 [22,0;24,0] y.o. Psychometric measures: Liebowitz Social Anxiety Scale (LSAS). Genetic markers: rs2072450 in GRIN2A, rs2832407 in GRiK-GluR5, HUMTH01 in TH01(S<9, L>=9 repeats). The impact of genotypes on social anxiety scores was identified using Proportional Odd Logit modeling taking into account group affiliation.

Group of IA reported significantly higher levels in almost all LSAS measures including total score. We found that carriers of the genotypes rs2072450 CC (p=0.004 vs.CA/AA), rs2832407 CC (p=0.023 vs AA), and TH01 SS (p=0.013 vs. LL) scored significantly higher of LSAS total in the IA group. There were no significant differences in the healthy controls group.

The rs2072450(CC) in GRIN2A, rs2832407(CC) in GRiK-GluR5, and HUMTH01 in TH01(SS) genotypes may be possibly associated with higher social anxiety levels in Internet addicts.

The study was supported by the Russian Foundation for Basic Research (RFBR), project #18-29-22079.

Cognitive therapy for social anxiety disorder (CT-SAD) is recommended by NICE (2013) as a first-line intervention. Take up in routine services is limited by the need for up to 14 ninety-min face-to-face sessions, some of which are out of the office. An internet-based version of the treatment (iCT-SAD) with remote therapist support may achieve similar outcomes with less therapist time.

102 patients with social anxiety disorder were randomised to iCT-SAD, CT-SAD, or waitlist (WAIT) control, each for 14 weeks. WAIT patients were randomised to the treatments after wait. Assessments were at pre-treatment/wait, midtreatment/wait, posttreatment/wait, and follow-ups 3 & 12 months after treatment. The pre-registered (ISRCTN 95 458 747) primary outcome was the social anxiety disorder composite, which combines 6 independent assessor and patient self-report scales of social anxiety. Secondary outcomes included disability, general anxiety, depression and a behaviour test.

CT-SAD and iCT-SAD were both superior to WAIT on all measures. iCT-SAD did not differ from CT-SAD on the primary outcome at post-treatment or follow-up. Total therapist time in iCT-SAD was 6.45 h. CT-SAD required 15.8 h for the same reduction in social anxiety. Mediation analysis indicated that change in process variables specified in cognitive models accounted for 60% of the improvements associated with either treatment. Unlike the primary outcome, there was a significant but small difference in favour of CT-SAD on the behaviour test.

When compared to conventional face-to-face therapy, iCT-SAD can more than double the amount of symptom change associated with each therapist hour.