Social Anxiety and Its Relationship With the Brain
Social anxiety disorder (SAD) is understood to be a fear of being negatively evaluated in social situations. This disorder can occur at a young age and persist throughout one’s adult life. SAD can be a restricting ailment that causes impairment to an individual’s social and professional functions. Though it affects one’s behaviors and outer actions, there are underlying occurrences within the brain that are responsible for this disorder.
Common adult symptoms of social anxiety are racing heartbeat, dry mouth, shaky voice, blushing, trembling, sweating and nausea, while common child symptoms can be crying or throwing tantrums in public (N.A., 2010). According to Dunlop (2007), social anxiety is prevalent in approximately 13% of the United States population. Most commonly, social anxiety appears between the ages of 10 and 19. While Seedat (2013) states that 80% of those with social anxiety also have a lifetime history of at least one other psychiatric disorder, those typically being panic disorders, generalized anxiety, agoraphobia, and substance use disorders, to name a few. SAD typically consists of a fear of social interactions and performance interactions, such as public speaking or dating (Seedat, 2013). Seedat (2013) continues to explain that even if other disorders are not present, SAD can be associated with significant distress, such as financial problems increased suicidal thoughts, as well as a decrease in school and work performances.
Though SAD affects daily actions and interactions, understanding what is occurring within the human brain can lead to control and social functionality. N.A. (2010) states brain imagining has found that those with social anxiety disorder display greater activity in the amygdala, the area responsible for processing emotions. Advokat (2013) states a neurotransmitter is the connection between two different neurons, the synapse, and the chemical substances through which neurons communicate. Serotonin is a central nervous system neurotransmitter—it is an indoleamine. Advokat (2014) describes indoleamines as a six-carbon ring that fuses to a five-membered ring with four carbons and a nitrogen. It is created in the brain from the amino acid tryptophan; serotonin is a combination of tryptophan hydroxylase and amino acid decarboxylase (Advokat, 2014). Tryptophan is not organically made within our bodies, so we get it from the food we eat, such as poultry, bananas tomatoes, and walnuts.
Serotonin plays an important role in anxiety among other disorders, as well as the regulation of body temperature, sleep, sex, and cardiovascular functions. N.A. (2010) explains that reduced serotonin transmission contributes to anxiety. A receptor is commonly known as the structure within the body that a drug interacts with to produce its effects. There are 14 different postsynaptic serotonin receptors known as 5-HT. Two receptors are found to have structures where serotonin was able to bind to them. According to Hemmings (2016), the serotonin transporter member 4 (SLC6A4) is one of the most widely investigated genes and is believed to be the reason why 5-HT plays the key role in the etiology of psychiatric disorders, namely anxiety and depression. The serotonin transporter (SERT) found on the SLC6A plays a crucial role in the relationship between serotonin and anxiety.
Sakakibara (2013) states there is a short promoter variant in the SERT gene; it is linked to reducing the 5-HT reuptake (absorption by the nerve ending) and is also associated with anxiety-related personality traits. The anatomy of the brain and its neurotransmitters are constantly changing; the brain is constantly remodeling itself to respond to the environment (Advokat, 2014). When anxiety occurs, the amygdala sends out signals that there is danger, and the body must react. The reactions are usually pertaining to the flight or fight response. However, those who have anxiety have such reactions, as racing heart, trembling, crying and so on.
The changes in the amygdala responses typically occur in adolescent years but can become apparent in adulthood. It is believed that as individuals go through change, there are some who experience a reduction in the SERT levels, thus causing anxiety-like behaviors (Sakakibara, 2014); the causes can come from both genetics and the individual’s environment. Dunlop (2007) states selective serotonin reuptake inhibitors (SSRIs) are typically used as first-line pharmacotherapy for SAD; this is associated with response rates with about 50-60% in patients with SAD. The use of SSRIs allows for increased availability of serotonin, therefore, changing the functioning of brain circuits and reduces the symptoms of anxiety (N.A., 2010).
Social anxiety disorder is known as the fear of being negatively evaluated in social settings. SAD can be a restricting ailment that can cause impairment to an individual’s social and professional functions. It is believed that reduced amounts of the neurotransmitter serotonin play a key role in the formation of social anxiety. In order to prevent or aid those with social anxiety, it is not only important we know the symptoms of anxiety, but understand what is physically occurring and changing within the brain.
Advokat, C. D., Comaty, J. E., & Julien, R. M. (2014). Julien's primer of drug action: A comprehensive guide to the actions, uses, and side effects of psychoactive drugs (13th ed.). New York, NY: Worth Publishers
Dunlop, B. (2007). Tiagabine for social anxiety disorder. Human Psychopharmacology. 22: 241-244.
Seedat, S. (2013). Social anxiety disorder (social phobia).19(3): 192-196
Hemmings, S. (2016). Serotonin transporter variants play a role in anxiety sensitivity in South African adolescents. The World Journal of Biological Psychiatry. 17(1): 66-75.
N.A. (2010). Treating social anxiety disorder. Harvard Mental Health Letter. 26(9).
Sakakibara, Y. (2014). Developmental alterations in anxiety and cognitive behavior in serotonin transporter mutant mice. Psychopharmacology. 231. 4119-4133
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