Etiology Of Social Anxiety Disorder Research Articles

The socially enriched environment test: a new approach to evaluate social behavior in a mouse model of social anxiety disorder.

Social anxiety disorder (SAD) is a common anxiety disorder characterized by a marked fear of social situations. Treatments for SAD, including exposure therapy and medication, are not satisfactory for all patients. This has led to the development of several paradigms to study social fear in rodents. However, there are still some social impairments observed in SAD patients that have never been examined in rodent models. Indeed, social situations avoided by SAD patients include not only social interactions but also public performances and being observed by others. Nevertheless, tests used to assess sociability in rodents evaluate mostly social interaction in pairs. Thus, we developed a new test-a socially enriched environment test-that evaluates sociability within a group of three unfamiliar conspecifics in an enriched environment. In this study, we induced a SAD-like behavior (i.e., social fear) in male mice using social fear conditioning (SFC) and then tested social fear using the socially enriched environment test and the three-chamber test. Finally, we tested the effects of fear extinction and acute diazepam treatment in reversing social fear. Results revealed, in conditioned mice, decreased object exploration in proximity to conspecifics, social interaction, and mouse-like object exploration. Extinction training, but not acute diazepam treatment, reversed SFC-induced behavioral changes. These findings demonstrate that the socially enriched environment test provides an appropriate behavioral approach to better understand the etiology of SAD. This test may also have important implications in the exploration of new treatments.

The Role of Environmental Factors in the Aetiology of Social Anxiety Disorder: A Review of the Theoretical and Empirical Literature

Social anxiety disorder (SAD) is characterised by a marked and persistent fear of social/performance situations, and a number of key environmental factors have been implicated in the aetiology of the disorder. Hence, the current article reviews theoretical and empirical evidence linking the development of SAD with parenting factors, traumatic life events, and aversive social experiences. Specifically, research suggests that the risk of developing SAD is increased by over-controlling, critical and cold parenting, an insecure attachment style, aversive social/peer experiences, emotional maltreatment, and to a lesser extent other forms of childhood maltreatment and adversity. Moreover, these factors may lead to posttraumatic reactions, distorted negative self-imagery, and internalised shame-based schemas that subsequently maintain SAD symptomatology. However, further research is necessary to clarify the nature, interactions, and relative contributions of these factors. It is likely that SAD develops via a complex interplay of biological and environmental factors, and that multiple aetiological pathways underlie the development of the disorder.

Mediation Role of Emotion Regulation Strategies on the Relationship Between Emotional Intensity, Safety and Reward Motivations with Social Anxiety Symptoms, Rumination and Worry: A Structural Equation Modeling

Background: Despite the widespread studies demonstrating the role of emotion regulation in social anxiety and distress symptoms, its mechanism and its relation to more biological basis like motivation is not well known. Objectives: Based on emotion dysregulation model, the present study aimed to assess mediation role of emotion regulation strategies on the relationship between, emotional intensity, safety and reward motivations with social anxiety symptoms, rumination and worry. Methods: Using Quota sampling, 524 participants were recruited from community sample and filled in questionnaires. Data were analyzed using structural equation modeling. Results: The results of SEM supported the mediating role of emotion regulation strategies (attentional control, decentering, awareness, reappraisal, and non-acceptance) in the relationship between motivation (reward and punishment) and emotion dysregulation symptoms (social anxiety symptoms, worry, and rumination). Model examination indicated the good fitness of the proposed theoretical model especially after omitting emotion intensity, as χ2=61.94, df=26, χ2/df=2.38, P < 0.001, CFI=0.97, GFI=0.97, AGFI=0.95, RMSEA= 0.05. Conclusions: These findings emphasize the possible important role of emotion regulation strategies and temperamental traits like motivation in the etiology of social anxiety disorder and their correlate distress symptoms.

Bridging the Gap between Aetiological and Maintaining Factors in Social Anxiety Disorder: The Impact of Socially Traumatic Experiences on Beliefs, Imagery and Symptomatology.

A number of key environmental factors during childhood have been implicated in the aetiology of social anxiety disorder (SAD), including aversive social experiences, traumatic life events and parent-child interaction. However, understanding the nature, interactions and relative contributions of these factors remains unclear. Furthermore, the relation of aversive social experiences to the development of key maintaining factors in SAD requires elucidation. The current study aimed to extend previous research regarding the aetiology of SAD by investigating the relationship between key environmental factors in childhood, negative beliefs and self-imagery, and the development of SAD. Social anxiety disorder individuals (n = 40, 87.5% female, Mage = 20.25 years) completed self-report measures of social anxiety symptomatology, traumatic experiences and parenting style. In addition, participants were administered interviews assessing various domains of childhood trauma, as well as negative self-imagery and associated socially traumatic memories. Participants reported a high frequency of early traumatic experiences across all domains (physical, emotional, sexual, social and non-relational), as well as a high degree of parental overcontrol. However, social anxiety symptomatology was most strongly correlated with socially traumatic experiences, and mediation analyses suggest that appraisal of aversive social/peer experiences accounts for the relationship of SAD symptomatology with negative self-beliefs and imagery. These outcomes suggest that social trauma may be a key proximal cause of SAD development, leading to the development of negative beliefs and imagery that subsequently maintain the disorder. These findings have implications for understanding SAD aetiology, and improving treatment outcomes for the disorder. Copyright © 2016 John Wiley & Sons, Ltd. Negative social experiences have been implicated in the development of social anxiety disorder (SAD), but the role of this predisposing factor remains unclear. Compared with other risk factors for SAD, social anxiety symptomatology was most strongly correlated with socially traumatic experiences. Mediation analyses suggested that appraisal of aversive social experiences accounted for the relationship of SAD symptomatology with negative self-beliefs and imagery. These outcomes suggest that SAD individuals would benefit from interventions targeted at processing socially traumatic memories (e.g., imagery rescripting).

Longitudinal associations between social anxiety disorder and avoidant personality disorder: A twin study.

Social anxiety disorder (SAD) and avoidant personality disorder (AvPD) are frequently co-occurring psychiatric disorders with symptomatology related to fear of social situations. It is uncertain to what degree the 2 disorders reflect the same genetic and environmental risk factors. The current study addresses the stability and co-occurrence of SAD and AvPD, the factor structure of the diagnostic criteria, and genetic and environmental factors underlying the disorders at 2 time points. SAD and AvPD were assessed in 1,761 young adult female twins at baseline and 1,471 of these approximately 10 years later. Biometric models were fitted to dimensional representations of SAD and AvPD. SAD and AvPD were moderately and approximately equally stable from young to middle adulthood, with increasing co-occurrence driven by environmental factors. At the first wave, approximately 1 in 3 individuals with AvPD had SAD, increasing to 1 in 2 at follow-up. The diagnostic criteria for SAD and AvPD had a two-factor structure with low cross-loadings. The relationship between SAD and AvPD was best accounted for by a model with separate, although highly correlated (r = .76), and highly heritable (.66 and .71) risk factors for each disorder. Their genetic and environmental components correlated .84 and .59, respectively. The finding of partially distinct risk factors indicates qualitative differences in the etiology of SAD and AvPD. Genetic factors represented the strongest time-invariant influences, whereas environmental factors were most important at the specific points in time.

Intolerance of Uncertainty: A Cognitive Vulnerability Related to the Etiology of Social Anxiety Disorder

Social anxiety disorder (SAD) is characterized by persistent and irrational fears related to the presence of other people and which are accompanied by the persistent belief of being judged or evaluated. The prevalence of SAD in Canada varies somewhat between several sources, but it is known to be a prevalent anxiety disorder. Research has identified significant vulnerabilities implicated in the development of SAD, which include genetic and temperament (i.e., heritable) factors, cognitive processes, dyadic parent–child interactions, personality factors, and adverse environmental experiences. A particular cognitive vulnerability related to SAD and which is garnering more research attention is intolerance to uncertainty (IU). IU is related to insecurities about the unknown and an inability to accept (i.e., tolerate) an unknown and uncontrollable future. IU is responsible for some proportion of the variance in social anxiety symptoms (SAS) that happen before, during, and/or after social encounters. What remains to be determined is how much does IU contribute to the maintenance of SAS and the development of SAD? The author reviews preliminary research suggesting that the cognitive vulnerability of IU plays a role in SAS and in the etiology of SAD. Future research directions are also explored.

Cognitive Constructs and Social Anxiety Disorder: Beyond Fearing Negative Evaluation

Pioneering models of social anxiety disorder (SAD) underscored fear of negative evaluation (FNE) as central in the disorder's development. Additional cognitive predictors have since been identified, including fear of positive evaluation (FPE), anxiety sensitivity, and intolerance of uncertainty (IU), but rarely have these constructs been examined together. The present study concurrently examined the variance accounted for in SAD symptoms by these constructs. Participants meeting criteria for SAD (n = 197; 65% women) completed self-report measures online. FNE, FPE, anxiety sensitivity, and IU all accounted for unique variance in SAD symptoms. FPE accounted for variance comparable to FNE, and the cognitive dimension of anxiety sensitivity and the prospective dimension of IU accounted for comparable variance, though slightly less than that accounted for by FNE and FPE. The results support the theorized roles that these constructs play in the etiology of SAD and highlight both FNE and FPE as central foci in SAD treatment.

High social support buffers the effects of 5-HTTLPR genotypes within social anxiety disorder

An interaction between genetic aspects and environmental stressors has been suggested with regard to the etiology of social anxiety disorder (SAD). However, potential protective interplays which might decrease the risk of SAD have not been considered so far. Thus, we analyzed the interaction between 5-HTTLPR and differing levels of social support regarding SAD. The sample was based on participants of the Study of Health in Pomerania, Germany. We used the triallelic genotype of 5-HTTLPR and longitudinal data of social support. Final analyses were conducted in 79 individuals with SAD and 1,708 without. The diagnosis of SAD was derived from diagnostic interviews in accordance with DSM-IV. Considering the risk of SAD, a general protective effect of high social support was shown independent of variation in 5-HTTLPR genotype. In contrast, the risk of SAD was increased for both genotypes within those individuals with low social support. Additionally, the odds ratio for suffering from SAD was about two times higher for carriers of the l/l genotype compared to those with at least one short allele in those perceiving less-supportive social environments. The findings suggest that SAD is influenced by a protective and a contributing gene×environment interaction. High social support might act in a protective and low social support in an increasing manner on the risk of SAD especially within carriers of the l/l genotype. Therefore, effects of 5-HTTLPR might be buffered by high social support with respect to the risk of SAD.

Testing the diathesis‐stress model: 5‐HTTLPR, childhood emotional maltreatment, and vulnerability to social anxiety disorder

Regarding the development of social anxiety disorder (SAD), a diathesis-stress paradigm including biological vulnerabilities and environmental stressors can be assumed. However, studies dealing with the etiology of SAD did not integrate both aspects so far. We examined a particular diathesis-stress model for SAD in which we included a functional polymorphism of the serotonin transporter (5-HTTLPR) as a genetic vulnerability factor and childhood emotional maltreatment (CEM) as an environmental stressor. Current analyses were based on individuals who participated in the Study of Health in Pomerania. Psychiatric disorders were assessed with diagnostic interviews according to DSM-IV criteria. The triallelic genotype of 5-HTTLPR was determined. Statistical analyses were performed in 78 individuals with SAD and 1,035 without an axis I disorder. Logistic regression analysis revealed that the experience of CEM (odds ratio [OR] 4.56; 95% confidence interval [CI] 2.65-7.84), the l/l genotype of 5-HTTLPR (OR 2.13; 95% CI 1.31-3.48), female gender (OR 3.03; 95% CI 1.80-5.08) and younger age (OR 1.04; 95% CI 1.02-1.06) increased the odds for SAD. The data suggest that CEM, the l/l genotype of 5-HTTLPR, female gender and younger age are risk factors for SAD. This is in favor of the tested diathesis-stress model.

Social Fear Conditioning: A Novel and Specific Animal Model to Study Social Anxiety Disorder

Social anxiety disorder (SAD) is a major health concern with high lifetime prevalence. The current medication is rather unspecific and, despite considerable efforts, its efficacy is still unsatisfactory. However, there are no appropriate and specific animal models available to study the underlying etiology of the disorder. Therefore, we aimed to establish a model of specific social fear in mice and use this social fear conditioning (SFC) model to assess the therapeutic efficacy of the benzodiazepine diazepam and of the antidepressant paroxetine; treatments currently used for SAD patients. We show that by administering electric foot shocks (2-5, 1 s, 0.7 mA) during the investigation of a con-specific, the investigation of unfamiliar con-specifics was reduced for both the short- and long-term, indicating lasting social fear. The induced fear was specific to social stimuli and did not lead to other behavioral alterations, such as fear of novelty, general anxiety, depression, and impaired locomotion. We show that social fear was dose-dependently reversed by acute diazepam, at doses that were not anxiolytic in a non-social context, such as the elevated plus maze. Finally, we show that chronic paroxetine treatment reversed social fear. All in all, we demonstrated robust social fear after exposure to SFC in mice, which was reversed with both acute benzodiazepine and chronic antidepressant treatment. We propose the SFC model as an appropriate animal model to identify the underlying etiology of SAD and possible novel treatment approaches.

Social anxiety modulates amygdala activation during social conditioning

Aversive social learning experiences might play a significant role in the aetiology of social anxiety disorder. Therefore, we investigated emotional learning and unlearning processes in healthy humans using a social conditioning paradigm. Forty-nine healthy subjects participated in a 2-day fMRI differential conditioning protocol. Acquisition and extinction were conducted on Day 1 and extinction recall on Day 2. BOLD responses, ratings and skin conductance responses were collected. Our data indicate successful conditioning and extinction on the neural and subjective level. As a main result, we observed a positive correlation of social anxiety and conditioning responses on the subjective level (valence and fear) as well as on the neural level with significant CS(+)/CS(-) differentiation in the left amygdala and the left hippocampus. Further, significant CS(+)/CS(-) differentiation in the left amygdala was found during extinction and was associated with lower scores in social anxiety. During extinction recall, we found a tendentially negative correlation of social anxiety and CS(+)/CS(-) differentiation in the vmPFC. In sum, we were able to show that social anxiety is related to conditionability with socially threatening stimuli. This could point to an important aspect in the aetiology of social anxiety disorder.

Social anxiety and social norms in individualistic and collectivistic countries

Social anxiety is assumed to be related to cultural norms across countries. Heinrichs et al. [2006: Behav Res Ther 44:1187-1197] compared individualistic and collectivistic countries and found higher social anxiety and more positive attitudes toward socially avoidant behaviors in collectivistic rather than in individualistic countries. However, the authors failed to include Latin American countries in the collectivistic group. To provide support for these earlier results within an extended sample of collectivistic countries, 478 undergraduate students from individualistic countries were compared with 388 undergraduate students from collectivistic countries (including East Asian and Latin American) via self-report of social anxiety and social vignettes assessing social norms. As expected, the results of Heinrichs et al. [2006: Behav Res Ther 44:1187-1197] were replicated for the individualistic and Asian countries, but not for Latin American countries. Latin American countries displayed the lowest social anxiety levels, whereas the collectivistic East Asian group displayed the highest. These findings indicate that while culture-mediated social norms affect social anxiety and might help to shed light on the etiology of social anxiety disorder, the dimension of individualism-collectivism may not fully capture the relevant norms.

Early traumatic life events, parental rearing styles, family history of mental disorders, and birth risk factors in patients with social anxiety disorder

Childhood traumatic experiences, rearing styles, familial mental disorders and birth risk factors have been associated with the development of social anxiety disorder. Patients with social anxiety disorder (n=50) and healthy controls (n=120) were investigated using a retrospective interview with 203 questions. The frequency of reports of traumatic childhood experiences was significantly higher in patients than in controls, including separation from parents, parents' marital discord, sexual abuse, familial violence, childhood illness, and other factors. On a 0-10 point 'severe trauma scale' patients had significantly higher mean scores (2.0; SD 1.28) than control subjects (0.82; SD 1.1; p<0.0001). Only 6 (12%) of the social phobic patients, but 63 (52.5%) of the controls did not report any severe traumatic events at all (chi2=24.0; p<0.0001). Compared to controls, patients described their parents' rearing styles as significantly more unfavourable. Patients reported higher rates of psychiatric disorders in their families in general, in particular anxiety disorders, depression, and suicidality. Birth risk factors did not differ between patients and controls. In a logistic regression model, the highest contribution was noted for familial anxiety disorders. Separation from parents also had a significant, but smaller influence. There was only a trend towards a significant contribution of childhood sexual abuse. Violence in the family, parental rearing styles and birth risk factors did not contribute significantly. The present data suggest that the aetiology of social anxiety disorder is multifactorial and that familial mental disorders and separation experiences are the most important contributing factors.

Etiology of Social Anxiety Disorder in Children and Youth

AbstractSocial Anxiety Disorder is a heterogeneous and distressing problem for many children and youth. Unravelling its multiple causes is essential for a full understanding of the condition. This selective review focuses on the etiology and maintenance of SAD, and examines research findings in several key areas of investigation: genetic or hereditary factors (twin and family studies), temperament characteristics (behavioural inhibition), and parent-child interactions (attachment, parenting styles). We conclude that genetic influences, behavioural inhibition and parent-child interactions play significant and interactive roles in the development and maintenance of social anxiety disorder. Other influences are also acknowledged, such as peer relationships, social skills deficits and traumatic experience. Ultimately, an understanding of such pathways should facilitate effective early screening and intervention of children at risk for severe social anxiety.

Family and high-risk studies of social anxiety disorder.

To present data on the role of familial factors in the etiology of social anxiety disorder. Findings presented from a family/high-risk study (the Yale Family Study) and a prospective community study of youth (the Munich Early Developmental Stages of Psychopathology (EDSP) Study). The Yale Family Study demonstrated a substantial degree of familial aggregation of social anxiety disorder and specificity with respect to other anxiety subtypes among adult relatives. The Yale high-risk component and the EDSP Study confirm the association between parental and offspring social anxiety, but did not yield consistent evidence for an association between familial environmental factors and social anxiety. Future studies are needed to examine mechanisms for the specificity of social anxiety disorder aggregation, to identify vulnerability factors for its development and to pinpoint environmental conditions that may enhance or suppress expression of underlying vulnerability.

Social anxiety disorder under scrutiny

Social anxiety disorder (social phobia) is a chronic disabling condition. As with many psychiatric disorders, the condition is likely to have several causes, including genetic and familial factors, early experiences, and cognitive mechanisms. This review will briefly examine the etiology of social anxiety disorder. The approach required during diagnosis of the condition will also be addressed, in particular, the differentiation between social anxiety disorder and other anxiety disorders with similar presentation. The main focus of this article is to review available treatment options for social anxiety disorder, both psychosocial and pharmacotherapeutic. A number of management strategies have shown promise for the treatment of the condition. The International Consensus Group on Depression and Anxiety recently recommended that a selective serotonin reuptake inhibitor (SSRI) should be considered as first-line pharmacotherapy. To date, however, paroxetine is the only SSRI that is licensed for the treatment of social anxiety disorder.

Social anxiety disorder under scrutiny

Social anxiety disorder (social phobia) is a chronic disabling condition. As with many psychiatric disorders, the condition is likely to have several causes, including genetic and familial factors, early experiences, and cognitive mechanisms. This review will briefly examine the etiology of social anxiety disorder. The approach required during diagnosis of the condition will also be addressed, in particular, the differentiation between social anxiety disorder and other anxiety disorders with similar presentation. The main focus of this article is to review available treatment options for social anxiety disorder, both psychosocial and pharmacotherapeutic. A number of management strategies have shown promise for the treatment of the condition. The International Consensus Group on Depression and Anxiety recently recommended that a selective serotonin reuptake inhibitor (SSRI) should be considered as first-line pharmacotherapy. To date, however, paroxetine is the only SSRI that is licensed for the treatment of social anxiety disorder. Depression and Anxiety 11:93–98, 2000. © 2000 Wiley-Liss, Inc.