Objective. To examine the natural course of social anxiety disorder (SAD) in the community and to explore predictors for adverse long-term outcomes. Method. A community sample of N=3,021 subjects aged 14-24 was followed-up over 10 years using the DSM-IV/M-CIDI. Persistence of SAD is based on a composite score reflecting the proportion of years affected since onset. Diagnostic stability is the proportion of SAD subjects still affected at follow-up. Results. SAD reveals considerable persistence with more than half of the years observed since onset spent with symptoms. 56.7% of SAD cases revealed stability with at least symptomatic expressions at follow-up; 15.5% met SAD threshold criteria again. 15.1% were completely remitted (no SAD symptoms and no other mental disorders during follow-up). Several clinical features (early onset, generalized subtype, more anxiety cognitions, severe avoidance and impairment, co-occurring panic) and vulnerability characteristics (parental SAD and depression, behavioural inhibition, harm avoidance) predicted higher SAD persistence and -less impressively- diagnostic stability. Conclusion. A persistent course with a considerable degree of fluctuations in symptom severity is characteristic for SAD. Both, consistently meeting full threshold diagnostic criteria and complete remissions are rare. Vulnerability and clinical severity indicators predict poor prognosis and might be helpful markers for intervention needs.

Background. To examine the role of parental psychopathology and family environment for the risk of social anxiety disorder (SAD) in offspring from childhood to early adulthood, covering an observational period of 10 years. Method. A community sample of 1,395 adolescents (aged 14 to 17 years at baseline) was prospectively followed-up over the core high risk period for SAD onset. DSM-IV offspring and parental psychopathology was assessed using the Munich-Composite International Diagnostic Interview; direct diagnostic interviews in parents were supplemented by family history reports from offspring. Parental rearing was assessed by the Questionnaire of Recalled Rearing Behavior in offspring, family functioning by the McMaster Family Assessment Device in parents. Results. Parental SAD was associated with the offspring’s risk to develop SAD (OR = 3.3, 95%CI: 1.4-8.0). Additionally, other parental anxiety disorders (OR = 2.9, 95%CI: 1.4-6.1), depression (OR = 2.6, 95%CI: 1.2-5.4) and alcohol use disorders (OR = 2.8, 95%CI: 1.3-6.1) were associated with offspring SAD. Offspring’s reports of parental overprotection, rejection and lack of emotional warmth, but not parental reports of family functioning were associated with offspring SAD. Analyses of interaction of parental psychopathology and parental rearing indicated combined effects on the risk for offspring SAD. Conclusions. These findings extend previous results in showing that both parental psychopathology and parental rearing are consistently associated with the risk for offspring SAD. As independent and interactive effects of parental psychopathology and parental rearing may have already manifested in early adolescence, these factors appear crucial and promising for targeted prevention programs.

Parental psychopathology and unfavorable family environment are established risk factors for onset of offspring social phobia (SP), but their associations with the further course, e.g., persistence of the disorder, remain understudied. A community cohort of 1395 adolescents and their parents was followed-up over almost 10 years using the DIA-X/M-CIDI. Parental diagnostic interviews were supplemented by family history data. Parental rearing was retrospectively assessed by the Questionnaire of Recalled Parental Rearing Behavior in offspring, and family functioning by the Family Assessment Device in parents. Persistence measures (proportion of years affected since onset) were derived from diagnostic interviews, using age of onset, age of recency, and course information. Lack of emotional warmth and dysfunctional family functioning characteristics were associated with higher SP persistence, particularly in interaction with parental psychopathology. Predictors for SP persistence differ from those predicting SP onset. Unfavorable family environment alone and in interaction with parental disorders predict higher SP persistence.

Background. To examine the role of parental psychopathology and family environment for the risk of social anxiety disorder (SAD) in offspring from childhood to early adulthood, covering an observational period of 10 years. Method. A community sample of 1,395 adolescents (aged 14 to 17 years at baseline) was prospectively followed-up over the core high risk period for SAD onset. DSM-IV offspring and parental psychopathology was assessed using the Munich-Composite International Diagnostic Interview; direct diagnostic interviews in parents were supplemented by family history reports from offspring. Parental rearing was assessed by the Questionnaire of Recalled Rearing Behavior in offspring, family functioning by the McMaster Family Assessment Device in parents. Results. Parental SAD was associated with the offspring’s risk to develop SAD (OR = 3.3, 95%CI: 1.4-8.0). Additionally, other parental anxiety disorders (OR = 2.9, 95%CI: 1.4-6.1), depression (OR = 2.6, 95%CI: 1.2-5.4) and alcohol use disorders (OR = 2.8, 95%CI: 1.3-6.1) were associated with offspring SAD. Offspring’s reports of parental overprotection, rejection and lack of emotional warmth, but not parental reports of family functioning were associated with offspring SAD. Analyses of interaction of parental psychopathology and parental rearing indicated combined effects on the risk for offspring SAD. Conclusions. These findings extend previous results in showing that both parental psychopathology and parental rearing are consistently associated with the risk for offspring SAD. As independent and interactive effects of parental psychopathology and parental rearing may have already manifested in early adolescence, these factors appear crucial and promising for targeted prevention programs.