Research suggests social anxiety disorder (SAD) results from a combination of factors – including both nature and nurture. From a scientific perspective, this means considering biological dispositions such as our genetics alongside environmental components. It is unattainable to single out one factor that causes SAD, and it is more likely to be a combination of factors, which can vary for different people. Any of these factors may trigger the disorder in a specific individual at a particular point in time – anyone can develop SAD.
SAD can affect both adults and children, with symptoms typically beginning in adolescence. The average age of onset is early to mid-teens with most people having developed symptoms of the condition before they reach their twenties – 90% of cases of SAD occur by age 23. There is a small percentage of people who develop the condition in later life.
Different people and researchers find different explanations to what causes SAD more helpful than others. We have summarised some of these theories below:
1. Genetic factors: Through research using twins, studies have shown that genetics play a significant role in the development of SAD. Genetic factors are estimated to contribute to around 30-40% of the risk for developing SAD (Stein et al., 1998). This suggests there is a genetic predisposition.
2. Brain structure and function: Differences in brain structure and function have been observed in individuals with SAD. The amygdala, which is involved in processing emotions (particularly anxiety and fear) is often hyperactive in people with SAD. The prefrontal cortex, which regulates emotional responses, may not function properly in those with the disorder.
3. Environmental factors: Some people can identify when their social anxiety began and may associate it with a particularly difficult or embarrassing time in their life. Traumatic or embarrassing experiences during childhood or adolescence, such as bullying, rejection, or abuse, can contribute to the development of SAD. These experiences may lead to the development of negative beliefs about oneself and others, as well as a heightened fear of social situations.
4. Learned behaviour: Observing or experiencing social rejection or criticism can reinforce social anxiety. This can be from anyone, including parents, family, teachers, or friends. If a person grows up in an environment where social interactions are viewed as scary, dangerous, or to be avoided, then they may develop SAD as a learned response. Other people may describe themselves as always having been shy, however their behaviours and avoidance have progressed to become more and more limiting – this behaviour can maintain symptoms of SAD. Furthermore, some studies suggest a quarter of first-degree relatives of people diagnosed with SAD also met the criteria compared to a comparison group, although this may also support the argument of genetic predisposition. (Stein et al. 1998)
5. Biological factors: Neurotransmitters allow neurons to communicate with each other throughout the body and enable the brain to provide a variety of functions. Neurotransmitters such as dopamine and serotonin are involved in regulating mood and anxiety, therefore neurotransmitter dysfunction may contribute to the development or exacerbation of SAD. Research is still evolving to fully understand the exact mechanisms and imbalances of neurotransmitters in SAD.
It is important to note that while these factors may contribute to the development of SAD, each individual’s experience is unique, and not everyone with these contributing factors will develop the disorder. It is not something you necessarily have or have not, it can be seen like a spectrum with different people experiencing different types and severity of symptoms. Sometimes it can be context specific and for some may only occur in specific types of social situations. You can see our pages on treatment at What is CBT?.
References
Heimberg, R. G., Stein, M. B., Hiripi, E., & Kessler, R. C. (2000). Trends in the prevalence of social phobia in the United States: a synthetic cohort analysis of changes over four decades. European Psychiatry: The Journal of the Association of European Psychiatrists, 15(1), 29–37. https://doi.org/10.1016/s0924-9338(00)00213-3
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the national comorbidity survey replication. Archives of General Psychiatry, 62(6), 593–602. https://doi.org/10.1001/archpsyc.62.6.593
Lederbogen, F., Kirsch, P., Haddad, L., Streit, F., Tost, H., Schuch, P., Wüst, S., Pruessner, J. C., Rietschel, M., Deuschle, M., & Meyer-Lindenberg, A. (2011). City living and urban upbringing affect neural social stress processing in humans. Nature, 474(7352), 498–501. https://doi.org/10.1038/nature10190
Liebowitz, M. R., Gorman, J. M., Fyer, A. J., & Klein, D. F. (1985). Social phobia. Review of a neglected anxiety disorder. Archives of general psychiatry, 42(7), 729–736. https://doi.org/10.1001/archpsyc.1985.01790300097013
Schneier, F. R., Fyer, A. J., & Liebowitz, M. R. (2011). The serotonin hypothesis of social phobia. Psychiatry Research, 186(2-3), 243-248.
Stein, M. B., Chartier, M. J., Hazen, A. L., Kozak, M. V., Tancer, M. E., Lander, S., Furer, P., Chubaty, D., & Walker, J. R. (1998). A Direct-Interview Family Study of Generalized Social Phobia. American Journal of Psychiatry, 155(1), 90–97. https://doi.org/10.1176/ajp.155.1.90
Stein, M. B., Goldin, P. R., Sareen, J., Zorrilla, L. T. E., & Brown, G. G. (2002). Increased Amygdala Activation to Angry and Contemptuous Faces in Generalized Social Phobia. Archives of General Psychiatry, 59(11), 1027. https://doi.org/10.1001/archpsyc.59.11.1027
Stein, M. B., & Stein, D. J. (2008). Social anxiety disorder. Lancet (London, England), 371(9618), 1115–1125. https://doi.org/10.1016/S0140-6736(08)60488-2