Aetiology
A combination of biological, familial, experiential, and cultural factors contributes to the risk of developing social anxiety.[14][15] Compared with the general population, first-degree relatives are up to 6 times more likely to develop social anxiety.[16] The concordance rates for monozygotic twins are approximately 24%, and for dizygotic twins they are around 15%.[17] Genome-wide association studies suggest a genetic basis for social anxiety.[18] Temperament factors, such as behavioural inhibition, shyness, introversion, and anxiety sensitivity, have also been implicated as risk factors for social anxiety. Behavioural inhibition in early childhood in particular is strongly associated with later development of social anxiety.[19] Familial factors, such as parental over-control, over-protection, and lack of warmth, may also contribute to insecure attachment styles and social anxiety risk.[14][20]
Adverse life experiences, including transitions, humiliation, losses, and poverty, may also play a role in the development of social anxiety.[14] Conditioning models of anxiety propose that multiple social cues can develop the capacity to elicit anxiety-related symptoms. Learned escape and avoidance behaviours maintain the anxiety, interfere with skill development, and can lead to increasing levels of functional impairment and disability over time. Similarly, safety behaviours, such as only entering into social situations with a trusted companion, averting eye contact, and staying on the periphery of social gatherings, may also maintain anxiety-related impairments.[21][22]
Selective attention to social cues of negative evaluation and internal cues supporting danger perception may develop.[23][24]
Pathophysiology
Social anxiety is characterised by heightened autonomic arousal to social cues and novelty. Threat processing appears to be mediated by the amygdala, with neuroimaging studies showing exaggerated activation in this cortical area upon exposure to novel facial stimuli.[25] Neuroimaging studies have shown reduced activity in the pre-frontal regions of the brain responsible for threat processing, after pharmacotherapy and psychotherapy.[26] Similarly, amygdala activation to novelty has been noted among individuals with a temperamental style of behavioural inhibition.[27]
Other pathophysiological models suggest that exaggerated hypothalamic-pituitary-adrenal axis reactivity to environmental stimuli may be involved in social anxiety disorder.[28][29] Genome studies are emerging, with available research suggesting chromosome 16 as a potential candidate region for social anxiety.[30] Activation in the higher-order visual cortex for selective social stimuli appears to account for significant variance in response to behavioural therapy.[31]
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