Objective: Social anxiety disorder (SAD) is a ubiquitous anxiety disorder. Despite being the third most common psychiatric disorder, little is known about the interaction between genetic predisposition and environmental factors in the development of SAD. The available literature on SAD has been compared with data on the genetics and environmental impact on the phenotypic expression of fear and anxiety, and its implicated neurobiology, in order to explore the neurobiology of SAD as understood through the neurochemical dysregulation expressed in fear and anxiety. Method: A systematic review of the literature was employed for the years from 1966 to 2001. Results: SAD does indeed have much overlap with fear and anxiety. This is best demonstrated by the interactions of the noradrenergic and serotonergic systems with each other and the hypothalamic-pituitary-adrenal axis. Conclusion: SAD may well be understood as one potential outcome for predisposed individuals who are exposed to the proverbial 'second hit', or environmental insult, in childhood. Behavioral inhibition may be an early expression of this predisposition, with natural progression to SAD occurring via a disruption of neurochemical homeostasis. Through animal and human data it has become evident that fear and anxiety have shared, as well as distinct, neurochemical and neuroanatomical pathways. These similarities are expressed as symptoms and objective signs that are common to many individuals with social anxiety disorder.
|Original language||English (US)|
|Number of pages||14|
|Journal||Acta Psychiatrica Scandinavica, Supplement|
|State||Published - Oct 1 2003|
- Anxiety disorders
ASJC Scopus subject areas
- Psychiatry and Mental health