Social Phobias
Aetiology of Social Phobia and Down Syndrome
It is unclear whether there is a continuum between normal and pathological social anxiety or whether they are categorically distinct. A certain degree of social or performance anxiety is ubiquitous and may have some evolutionary adaptive advantage by motivating preparation and rehearsal of important interpersonal events. It is also likely that social anxiety has a role in determining hierarchical ranks in animal groups. In contrast with anxiety in normal subjects, social anxiety does not seem to attenuate during the course of a single social event or performance. Social phobics seem to lack the ability to habituate in social or performance situations. Current theories consider the development of SP to be due to a combination of genetic and environmental factors.
A family study reported significant increased risk for SP in the first-degree relatives of social phobics. In this study, 16% of the relatives of the ‘‘pure’’ social phobics had SP themselves, compared with 5% in the never mentally ill control group. Data from twin studies have identified specific genetic factors and influences as well. Torgersen compared social fears in a small subject sample of monozygotic and dizygotic twin pairs: the MZ twins were significantly more concordant for such social phobic features as discomfort when eating with strangers or when being watched working, writing, or trembling, suggesting a genetic contribution to social anxiety.
In a large study of female twins, Kendler reported significantly higher concordance rates for most phobias in MZ twins when compared with DZ twins. Their conclusion was that there are definite genetics factors in SP, agoraphobia, and animal phobias, but not in situational phobias. A range of early childhood environmental factors may also contribute to the development of the disorder. Social phobics were often noted to report that their parents were more rejecting, overprotective, and lacking in emotional warmth. However, the same parental traits and attitudes have also been identified in a variety of other mental disorders, especially in the overall phobic group.
It is possible that behavioural inhibition in early childhood, defined as having excessive fears of unfamiliar settings, people, and objects, are a general aspecific risk factor for the development of anxiety and phobia. The investigation of SP at the neuro-biological level is still at an early stage. The majority of studies in normal volunteers suggest that -adrenergic blockers are helpful in reducing performance anxiety, which supports the peripheral catecholamine mediation of SP symptoms, and this differently from panic attacks.
Tancer published a placebo-controlled challenge study where probes for the dopaminergic, noradrenergic and serotonergic systems were used: using the cortisol response to fenfluramine as a measure for the serotonergic function, patients with SP showed a significantly greater response compared with controls. These findings could suggest that patients with SP might have a dysregulation in the serotonergic function, namely post-synaptic receptor super sensitivity. In contrast, SP responded to clonidine challenges with blunted growth hormone responses. Significant additional research will be necessary before a clear picture can be constructed of the underlying pathophysiological brain mechanisms of SP.
Finally, Nichols has catalogued a variety of psychological and somatic traits, observed in a SP sample. Examples of these traits are a low self-evaluation, an unrealistic tendency to experience others as critical or disapproving, a negative fantasy-producing anticipatory anxiety, an increased awareness and fear of scrutiny by others, an exaggerated awareness of minimal somatic symptoms of anxiety, and so on. Nevertheless, it is unclear which among these factors are causal, which are consequences of, and which are not even specifically related to SP.